July 18, 2013


How to make a fat cell less not thin: the lessons of fat flux

Does being in ketosis automatically translate to fat loss?

by Peter Attia

Read Time 16 minutes

One of the questions I most often receive: Does being in ketosis automatically translate to fat loss?

For those too busy to read ahead, let me give you the punch line: No. For those who want to understand why, keep reading (hopefully this is still everyone). This topic is — surprise, surprise — very nuanced, and almost always bastardized when oversimplified, which I’m about to do, though hopefully less than most.  Without oversimplifying, though, this will turn into a textbook of 1,000 pages.

From the ketosis series, or at least the first and second part, along with the video in this previous post, you should have taken away that ketosis is not some ‘magical state of mystery.’  It’s simply a state of physiology where our liver turns fatty acid (both ingested and stored) into ketones.

There seems to be great confusion around ‘nutritional’ ketosis (a term we use to distinguish ‘dietary-induced’ ketosis from the other 2 forms of ketosis: starvation ketosis and ketoacidosis, the latter a serious complication of type I diabetes). But, before I try to dispel any of the confusion, we need to go through a little primer on what I like to call “fat flux.”

One point before diving in, please do not assume because I’m writing this post that I think adiposity (the technical term for relative amount of fat in the body) is the most important thing to worry about.  On the contrary, I think the metabolic state of the cell is far more important. While there is a correlation between high adiposity (excessive fat) and metabolic dysfunction, that correlation is far from perfect, and, as I’ve discussed elsewhere, I think the arrow of causation goes from metabolic dysfunction to adiposity, not the reverse.  But, everyone wants to lose fat, it seems, so let’s at least get the facts straight.

Let’s start with an assertion: Barring the presence of scientific evidence I’m unaware of, and barring surgical intervention (e.g., liposuction), reducing the adiposity of a person is achieved by reducing the adiposity of individual adipose cells, collectively. In other words, the number of adipocytes (fat cells) we have as an adult does not change nearly as much as their size and fat content.  So, for people to reduce their fat mass, their fat cells must collectively lose fat mass. 

Fat flux 101

According to “An Etymological Dictionary of Modern English,” the word flux comes from the Latin word fluxus and fluere, which mean “flow” and “to flow,” respectively. While the term has a clear mathematical meaning in physics, defined by a dot product I promise I won’t speak of, you can think of flux as the net throughput which takes into account positive and negative accumulation.

If we start with a bucket of water and put a hole in the bottom, the result, needless to say, is an efflux of water, or negative water flux.  Conversely, if we start with a bucket – no hole – and we pour water in, that’s an influx of water, or positive water flux.

If that makes sense, then the idea of fat flux is pretty straight forward.  If more fat enters a fat cell (called an adipocyte) than leaves it, the fat cell is experiencing a net influx – i.e., positive fat flux.  And, if more fat leaves a fat cell than enters, the reverse is true: it is experiencing a net efflux, or negative fat flux.

Not surprisingly, a fat cell is more complicated than a bucket.  Basically, though, there are two “inputs” and one “output.” The figure below shows this in some detail. (TAG stands for triacylglycerol, which is another word for triglyceride, which is the storage form of fat.)  The first thing you may appreciate, especially since I’ve highlighted it, is the role insulin plays in regulating the process of fat flux.  Insulin does the following:

  1. Upregulates lipoprotein lipase (LPL), an enzyme that breaks down TAG so they can be transported across cell membranes. Since TAG are too big to bring across cell membranes, they need to be “hydrolyzed” first into free fatty acids, then re-assembled (re-esterified) back into TAG.
  2. Translocates GLUT4 transporters to the plasma membrane from endosomes within the cell.  In other words, insulin moves the GLUT4 transporter to the cell surface to bring glucose into the cell.
  3. Facilitates lipogenesis, that is, facilitates the conversion of glucose into acetyl CoA which gets assembled into fatty acids along with glycerol.
  4. Facilitates esterification, that is, facilitates the process of assembling fatty acids into TAG (3 fatty acids per TAG).
  5. Inhibits hormone-sensitive lipase (HSL) and adipose triglyceride lipase (ATGL), two important enzymes that breaks down TAG into fatty acids and glycerol such that the fatty acids can be released from the fat cell. Once bound to albumin the free fatty acids are free to travel elsewhere in the body for use (e.g., to the liver for conversion to ketones, to the heart muscle or skeletal muscles for conversion to ATP).
  6. Though not shown in this figure, insulin appears to indirectly act on malonyl-CoA, a potent inhibitor of CPT I, one of the most important mitochondrial enzymes that facilitates the oxidation of fatty acids. (CPT I is what enables fatty acids to be shuttled into the mitochondria for oxidation, the process which releases or liberates their energy through electron transport.)

Other hormones and enzymes in the body also play a role.  For example, under a sympathetic response, the so-called “fight or flight” response, adrenaline and noradrenaline (i.e., epinephrine and norepinephrine) activate HSL and ATGL to combat the effect of insulin as an inhibitor of lipolysis, thereby increasing lipolysis, or liberating stored energy from the fat cell.  Glucagon may also play a role in this process, though the exact role is not as well understood, at least not in humans.

So in summary, insulin is indeed the master hormone that regulates the flow of fat (and glucose) into and out of a fat cell.  There are other players in this game, to be sure, but insulin is The General. High levels of insulin promote fat storage and inhibit fat oxidation, and low levels of insulin promote fat mobilization or release along with fat oxidation.

If this sounds crazy – the notion that insulin plays such a crucial role in fat tissue — consider the following two clinical extremes: type 1 diabetes (T1D) and insulinoma. In the former, the immune system destroys beta-cells (the pancreatic cells that make insulin) – this is an extreme case of low insulin.  In the case of the latter, a tumor of the beta-cell leads to hypersecretion of insulin – this is an extreme case of high insulin.  Prior to the discovery of insulin as the only treatment, patients who developed T1D would become emaciated, if the other complications of glycosuria and dehydration didn’t harm them first. They literally lost all fat and muscle.  Conversely, patients with insulinoma often present looking not just obese, but almost disfigured in their adiposity.  Because Johns Hopkins is a high-volume referral center for pancreatic surgery, it was not uncommon to see patients with insulinoma when I was there.  As quickly as we would remove these tumors, the patients would begin to return to their previous state and the adipose tissue would melt away.

For the purpose of our discussion, I’ve simplified the more detailed figure above into this simplified figure, below. I’ve tried to size the arrows accordingly to match their relative contributions of each input and output.

The first figure, below, shows a state of fat balance, or zero net fat flux.

Input #1: De novo lipogenesis, or “DNL” – Until the early 1990’s there was no way to measure this directly, and so no one really had any idea how much this process (i.e., the conversion of glucose to fat) contributed to overall fat balance.  Without going into great technical detail, , arguably one of the world’s foremost authorities on metabolomics and DNL, developed a tracer technique to directly measure this process. If I recall correctly, the original report was in 1991, but this paper is a great summary.  Published in 1995 in the Journal of Clinical Investigationthis paper would go on to become the “citation classic.” This study demonstrated that under eucaloric feeding conditions, with about 50% of energy coming from CHO, DNL did not represent a significant contribution to fat flux. It was about 5%, hence the tiny red arrow under a state of fat balance (i.e., a state where fat entering the fat cell is equal to fat leaving the fat cell). A very important point to be mindful of, however, is this: this represents an average throughout the body and does not differentiate specifically between, say, DNL in the liver and DNL in the periphery (i.e., fat cells). This limitation is not trivial, but rather than focus on the very specific details of this paper, I’d rather use it as a framework for this discussion. (This paper is really interesting, and were it not for the fact that this post is going to be long enough, I would say much more about it.  As such, I will probably do a full post on this paper and related topic in the future. The 1995 paper also examined what happened to DNL during periods of over- and under-feeding CHO and fat.)

Input #2: Re-esterification, or “RE” – In a state of fat balance, RE is largely composed of dietary fat sources that are not immediately used, but rather stored for later use.  (Nuanced point: RE also includes fatty acids that were previously liberated from adipocytes, not oxidized, and are now being recycled back into TAG.  This is a normal consequence of fat liberation.  The fat cell probably ‘deliberately overdoes it’ by liberating more fatty acid from TAG just to be safe; that which is not oxidized is re-esterified.  The exact balance of RE composed from dietary sources versus recycled fatty acids will depend on fat consumption and energy demands of the person. For the purpose of simplicity, this diagram does not show some portion of the L fraction returning to the RE fraction, though this is exactly what is happening in ‘real life.’)

Obviously, though, the relative size of the blue arrow depends on how much fat one is consuming and how many metabolic demands are in place for fatty acids.  The latter is highly determined by dietary composition (see the discussion on RQ, or respiratory quotient, at about minute 31 in this video).

For the real aficionado, there is another wee bit of nuance here. This study, published in 1991 in the Journal of Lipid Research, suggested that the RE process is a bit more complicated than simply re-assembling fatty acids on a glycerol backbone inside an adipocyte.  Based on these experiments, which used a similar* tracer method to the one used by Hellerstein et al. to evaluate DNL, the authors (which included Rudy Leibel, the co-discoverer of leptin) suggested that RE requires an intermediate step outside of the adipocyte in the interstitial and capillary space (figure 8 of the paper demonstrates this very well schematically).

(*) Technically, Hellerstein et al. used a heavy isotope; Leibel et al. used radioactive isotopes.

Output: Lipolysis, or “L” – Finally, in a state of fat balance, lipolysis must be equal to the sum of DNL and RE.  This is true if we are talking about tiny little fat cells or giant ones.  Remember, it’s the balance that matters.

I hope it’s clear from this summary that there are an infinite number of physiologic states that can satisfy the equation of fat balance: DNL + RE = L. For example, someone like me who is in fat balance (i.e., I’m neither gaining nor losing fat mass at this point) on a ketogenic diet with daily fat intake often exceeding 400 grams, has virtually zero DNL, but quite high RE, especially after meals.  Consequently, I have very high L.  If you took a person on a very low-fat diet (e.g., 20% fat, but 65% CHO), they would have modest DNL and low RE, but they would have low L.  We would both be in fat balance, but we satisfy the equation DNL + RE = L by very different means.

OK, so let’s turn our attention to the non-equilibrium states: Net fat influx and net fat efflux.

Fat influx

In a state of net fat influx – accumulation of fat within a fat cell – the following condition must be met (on average): DNL + RE > L.  (I say “on average” because, of course, a fat cell is a dynamic system with constant changes in these parameters.  So, at any moment in time the balance can shift, but over a period of time the equation is correct.)

The next (overly simplistic) figure below gives you a representative state of what fat influx or ‘positive fat flux’ probably looks like.  DNL is higher, but still relatively small, unless overfeeding CHO.  RE is larger than it was in a balanced state, but not necessarily ‘huge.’  Most cases of net fat influx are probably governed by low L.  In other words, fat accumulation is probably more governed by a failure to mobilize (breakdown TG into fatty acids for export and use) TAG than anything else.

Have you ever spoken with someone who is trying desperately to lose weight (fat) who says, “I don’t understand what’s happening…I hardly eat any fat, and yet I can’t lose a pound (of fat)!”  The skinny people in the group scoff, right? Well, not so fast.  It’s quite possible, if the hormones that regulate fat tissue are not working in your favor, to do such a poor job mobilizing fat from fat cells, and oxidizing that fat (see below), that you can be in fat balance, or even fat imbalance with accumulation, despite small DNL and small RE.

If you think about it, lipolysis (L), or liberating fat from a fat cell is a necessary, but not sufficient condition to actually generate the free energy inherent or stored within it.  One more major step is necessary – oxidizing the fatty acid via the process of beta-oxidation. This is where one actually gets the energy (ATP) from fatty acids. The same hormones and enzymes that promote L, directly or indirectly act on other intermediaries that promote oxidation, more or less. The converse is also largely true.

Brief digression: I’m always troubled by folks who have never tried to take care of someone who is struggling to lose weight (fat), and who themselves have never been overweight, but who insist obesity is ‘simply’ an energy balance problem – people eat too many calories.  When eternally lean people preach about the virtues of their ‘obvious’ solutions to obesity – just eat less and exercise more – I’m reminded of a quote (source unknown to me), “He was born on the finish line, so he thinks he won the race.”  You only need to meet one woman with PCOS, or one person with hypothyroidism, or one child with Cushing’s disease to know that adiposity can – and is – largely regulated by hormones.  The fact that such patients need to create a positive energy balance (i.e., eat more calories than they expend) to allow it does not seem to provide a meaningful insight into the mechanism of why.

Fat efflux

In a state of net fat efflux – reduction of fat within a fat cell – the following condition must be met (on average): DNL + RE < L (same caveat as above on the idea of “on average”). Again, looking at the figure, you can see one physiologically common way this occurs, the setting of carbohydrate restriction.  DNL is reduced (probably even to immeasurable levels, depending on the extent of restriction), but RE actually goes up.  The net efflux, however, results from the greater increase in L.

A person in nutritional ketosis, if experiencing fat loss, probably looks like this. (Don’t worry, I have not forgot the opening questions: Does being in nutritional ketosis automatically put you in this state?).  Certainly another state of net fat efflux is starvation.  DNL and RE are both very small, especially DNL, and lipolysis is quite large. This is probably the most rapid state of negative fat flux a human can experience.

So what we do about it?

I do not believe there is only one state, shy of total starvation, which will assuredly put you in state of negative fat flux.  Of course, starvation is not sustainable, and therefore should be taken off the table as a viable long term eating strategy.

What about profound caloric restriction? Yup, this is probably (though not necessarily) going to work, depending on how “profound” is defined.  If defined as a 40% reduction of energy stable intake, it’s probably going to work.  If defined as a 10% reduction, it would be difficult to know without knowing at least two other things:

  1. Baseline level of insulin resistance;
  2. RQ of pre- and post-diet.

What about dramatic alterations in macronutrient composition? This is where the discussion gets really interesting.  Many people, myself included, advocate a diet that overall reduces insulin secretion. The rationale, of course, is provided by the first figure above (from the textbook) and a slew of clinical studies which I will not review here (see Gardner JAMA 2007, Ludwig JAMA 2012, and Shai NEJM 2008 to name a few).

But, the bigger question is why? Why do most (but not all, by the way) people with excess fat to spare who are on well-formulated carbohydrate-reduced diets lose fat? (Notice, I did not say weight, because the initial – and often rapid — weight loss achieved by many is actually water loss.)

Is it because of a physiologic change that leads them to reduce overall intake?

Is it because of a physiologic change that, despite the same intake in overall calories, increases their energy expenditure?

Is it some combination of these?

I wish I knew the answer, but I don’t (universally).  I believe we will know the answer to this question in a few years, but until then, I’m left to offer the best my limited intuition can offer.  In other words, what I suggest below is my best interpretation of the literature, my personal experience that I’ve had with hundreds of other people, and my discussions with some of the most thoughtful scientists in the world on this topic:

Thought #1: I suspect that many people who reduce simple carbohydrates and sugars end up eating fewer calories.  This observation, however, may confound our understanding of why they lose weight.  Do they lose weight because they eat less? Or, do they eat less because they are losing weight? I suspect the later.  In this state, lipolysis — and by extension, given the hormonal milieu, oxidation — are very high, certainly relative to their previous state.  By definition, L > DNL + RE, so there is ample ATP generated by oxidation of the fatty acid.  If you believe (as I do*) that the liver is the master organ of appetite regulation, increases in ‘available energy’ (i.e., ATP) would naturally reduce appetite (though I don’t think we know if ATP per se is the driver of this feedback loop).  But don’t confuse what’s happening. They are not giving up fat from their fat cells because they are eating less.  They are eating less because they are giving up fat from their fat cells.  Big difference.

(*) The especially astute reader will note that this is the first time I have made reference to this point.  I have been heavily influenced recently by the work of Mark Friedman, and a discussion of this point is worth an entire post, which I promise to deliver at some point in the future. If you can’t wait, which I can understand, I highly encourage you to start scouring the literature for Mark’s work.  It’s simply remarkable.

Thought #2: I also suspect that some fraction of people who follow this eating strategy lose fat without any appreciable reduction in their total caloric intake, at least initially. What?, you say, doesn’t this violate the First Law of Thermodynamics? Not at all.  If L > DNL + RE, and the increase in lipolysis (i.e., fatty acid flux out of the fat cell) results in increased oxidation of fatty acids, energy expenditure (EE) would be expected to rise.  A rise in EE, in the face of constant input, is a sign of fat loss. What differentiates those in this camp (I was in this camp) from those above (point #1), is unclear to me.  It may have to do with concomitant exercise.  I have seen unpublished data, which I can’t share, suggesting non-deliberate EE rises more in a low RQ (high fat, low carb) environment when a person is exercising significantly. I’m not stating the obvious – that the deliberate EE is higher – that is clearly true. I’m suggesting resting EE is for some reason more likely to rise in this setting.  Since I’m taking the liberty of hypothesizing, I would guess this effect (if real) is a result of the body trying to keep up with a higher energy demand and making one trade-off (generating more free ATP via more lipolysis) for another (ensuring a constant supply of available energy to meet frequent demands). It is also possible that this increase in free/available energy results in an increase in deliberate EE (i.e., the person who suddenly, in the presence of a cleaned up diet feels the desire to walk up the stairs when they previously took the elevator).  Finally, and perhaps most importantly, whether or not this up-regulation of energy takes place may be dependent on the other hormones in the body that also play a role in fat regulation, including cortisol, testosterone, and estrogen. They could be partly or mostly responsible for this. The literature is quite dilute with respect to this question, but in my experience (feel free to dismiss), it is not uncommon to see a reduction in cortisol and an increase in testosterone (I experienced about 50% in free and total testosterone) with a dietary shift that improves food quality.  The same may be true of estrogen in women, by the way, though I have less clinical experience with estrogen.

Thought #3: As a subset to the point above (point #2), in an ‘extreme’ state of carbohydrate restriction, i.e., — nutritional ketosis — there is an energy cost of making the ketones from fatty acids.  I referred to this as the “Hall Paradox” after Kevin Hall, who first alerted me to this, in this post (near the bottom of the post).  What is not clear (to me, at least) is if this effect is transient and if so, how significant it is.  I recall that during the first three months of my foray into nutritional ketosis, I was eating between 4,000 and 4,500 kcal/day for a 12-week period, yet my weight reduced from 176 lb (about 9.5% bf by DEXA) to 171 lb (about 7.5% bf by DEXA), which means that of the 5 pounds I lost in 12 weeks, 4 were fat tissue. Today, however, I don’t consume this much, closer to 3,800 kcal/day, and one reason may be that two years later my body is more efficient at making ketones and this so-called “metabolic advantage” is no longer present.

(I have always found the term “metabolic advantage” to be misleading, though I’m guilty of using it periodically.  It’s really a metabolic disadvantage if your body requires more energy to do the same work, but nevertheless, people refer to – and argue vehemently about – this phenomenon. The question is not, does it exist?  One look at individual summary data from David Ludwig’s JAMA paper on this topic makes that clear. The questions are, why does it only exist in some people, what relevance does it have to fat loss – is it cause or effect? – and, for how long does it persist?)

Thought #4: For reasons I have yet to fully understand, some people can only lose fat on a diet that restricts fat (and by extension a diet that is still high in carbohydrate, since I’m excluding starvation and profound caloric restriction from this discussion). In my experience (and Gardner’s A TO Z trial seems to validate this, at least in pre-menopausal women), about 20% of people aspiring to reduce adiposity seem to do it better in a higher RQ environment. Using the Ornish diet as the example from this paper, I suspect the reason is multifactorial.  For example, the Ornish diet restricts many things, besides fat. It restricts sugar, flour, and processed carbohydrates.  Much of the carbohydrate in this diet is very low in glycemic index and comes primarily from vegetables. So, I don’t really know how likely it is to lose weight on a eucaloric diet that is 60% CHO and 20% fat, if the quality of the carbohydrates is very poor (e.g., cookies, potato chips).  The big confounder in these observations is that most low-fat diets, though still modestly high in RQ relative to a low-carb diet, reduce greatly the glycemic index and glycemic load, as well as the fructose.

Which brings us to the point…

Does being in nutritional ketosis ensure negative fat flux (i.e., fat loss, or L > DNL + RE)?

Being in ketosis tells us nothing about this equation!  Let me repeat this: It is metaphysically impossible to infer from a measurement of B-OHB in the blood if this equation is being satisfied.  It just tells us that our body is using some fraction of our dietary fat and stored fat (once it undergoes lipolysis) to make ketones, given that glucose intake is very low and protein intake is modest (net effect = minimal insulin secretion).

If you look at the figure below, you see this point (It’s simplified, obviously, and for example, does not show that fat from fat cells can be used directly by skeletal muscles).  Nothing in this figure implies a reduction in the size of the cells at the bottom right of the figure. It’s quite possible, of course, since ketosis results in a large L and implies a very small DNL.  But, if (small) DNL + (very large) RE is greater than (large) L, guess what? Fat flux is net positive.  Fat is gained, not lost. Still in ketosis, by the way (quantified loosely by fasting levels of B-OHB greater than about 0.5 to 1 mM), but not losing fat. (I hope the first attempt at a solution in this setting is obvious by now, notwithstanding the fact that I’ve seen this situation dozens of times with more than one solution, including the ‘obvious’ one — reducing fat intake.)

The other myth worth addressing is that the higher the level of B-OHB, the more “fat burning” that is going on.  This is not necessarily true at all.  As you can tell, I love equations, so consider this one:

B-OHB (measured in blood) = B-OHB produced (from dietary fat) plus B-OHB produced (from lipolysis of TAG) less B-OHB consumed by working muscles, heart, brain.

How does knowing one of these numbers (B-OHB measured in blood) give definitive answers to another (B-OHB produced from lipolysis of TAG)? It can’t. That’s the problem with multivariate algebra (and physiology).

Many people who enter nutritional ketosis do so, I worry, because they believe it “guarantees” fat loss. I hope I have convinced you that this is not true.  Nutritional ketosis is one eating strategy to facilitate negative fat flux, and it works very well if done correctly. It comes with some advantages and some disadvantages, just like other eating strategies.  When I get back to the series on ketosis, I will address these, but for now I felt it was very important to put things in perspective a bit.  Furthermore, I am convinced that it is not the ideal eating strategy for everyone.

Delorean by Marci Maleski is licensed under CC by 2.0

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  • Good article. Quick Q.

    If B-OHB (measured in blood) = B-OHB produced (from dietary fat) plus B-OHB produced (from lipolysis of TAG) less B-OHB consumed by working muscles, heart, brain…

    …then would B-OHB (measured in blood) actually measure low, giving a false negative, in extremely active people with high amount of B-OHB consumed by working muscles, heart, brain?

    • Absolutely, Ben. This is, at least in part, why B-OHB in serum falls precipitously at activity above threshold. Part of the fall is feedback from HGO, but part of it is simply an overuse-relative-to-production issue. You may note in this situation, a paradoxical rise in serum B-OHB post work-out (See my figures of every 2 hours checks in the metabolic chamber and note in particular the levels post both workouts; this was in the video in previous post).

    • Greg Johnson

      Thanks for the wonderful post! Following up on Ben’s question about the B-OHB equation….

      “If B-OHB (measured in blood) = B-OHB produced (from dietary fat) plus B-OHB produced (from lipolysis of TAG) less B-OHB consumed by working muscles, heart, brain…”

      Does this imply that your best chance of correlating a blood measurement of B-OHB to TAG Lipolysis would be in a fasted state in the morning? That is, in an AM fasted state, B-OHB from dietary fat is low (b/c you haven’t consumed any food for ~10hours) and consumption of B-OHB by the muscles is relatively low (b/c you’ve been sleeping). Given that, would the right side of the B-OHB equation above be dominated by B-OHB generated via lipolysis?

      Even if this is the case, I understand having a high L doesn’t allow one to know the net average influx or efflux in the cell.

      Just wondering if I am understanding this correctly. Thanks again!!

      • It might, Greg, but I’m not sure it does so with enough fidelity to warrant “taking to the bank.” I’ve just seen so much variation and so many inter-dependencies, that I can’t really believe any one number is indicative, besides the number that matters — actual mass of fat.

    • PhilT

      I would guess that “efficiency” comes into it somewhere along the line too – a well adapted muscle / brain may get enough ketones into its cells at a lower concentration than a ketone newbie.

  • melancholyaeon

    “It is also possible that this increase in free/available energy results in an increase in deliberate EE .”

    That would be me. I had been on the Atkins diet for about 3 weeks when I passed a noisy gym and saw women lifting weights. I hated gyms, and have my entire life.

    But this day as I walked by, I suddenly thought, “that music’s really good.” And I went in and got a brochure. When I came home with the brochure my husband asked me “Where is my wife & what have you done with her?” I laughed but the next time I went past there, I did go in for the free class because “it just looked like fun!” Then I went back. . .do you know, going to the gym can be really fun?

    • Interesting. I had always been active, so I don’t believe this applied to me, but I’ve heard many suggest what you are suggesting.

    • Dr. Craig

      Peter, any thoughts as to why a keto diet doen’t work for everyone? I think I read elsewhere that it doen’t work for up to 20% of people. Is there any research as to what diet will work for these people, or is there a “second best diet”out there that has the best chance of working for the keto-resistant folks?

  • Vladimir


    I hope you are planning on discussing at some point in the future why some people don’t respond the same
    way when they go on a low carb diet. There are many people like me who have reached a plateau only after
    losing a few pounds. Every time I read about somebody in nutritional ketosis who spontaneously start doing
    intermittent fasting because they are just not hungry, I want to pull my hair out because I’m hungry. 🙁


    • That will imply I’ve figured it out.

    • Helen

      Dr Steven Gundry talks about plateaus in his book “Diet Evolution: Turn off the genes that are killing you” – it’s all part of the normal process.

  • Mark Ard

    Hi Peter,

    First of all, great read. I have some homework after you post new articles. Second, is it possible to really explain #6? The malonyl-CoA inhibition of CPT-1, and to a greater extent that whole pathway, is unbelievably important and deserves its own spotlight. I spent a few hours recently white-boarding it all out because not one of my 4 biochemistry textbooks puts that pathway into context. I had to hodgepodge together the difference between ketoacidosis and ketosis for a group of fellow students who look at the normal pathway and conclude that starvation and/or ketosis is some lesser form of ketocidosis. I’ve sat in rooms with doctors who talk patients out of ketosis because they know the pathophysiology more than the physiology. I’ve even had to suspend my knowledge when it comes to licensing examinations that lump the two together, or consider them gradations of the same disease.

    And a favorite Grey’s Anatomy quote, “Eat when you can, sleep when you can, and don’t mess with the pancreas”

    • First things, first… That quote is actually wrong. It’s the TV version. The real quote, drilled into our heads during internship, was, “Eat when you can, sleep when you can, and never f*** with the pancreas!”
      But, to your question, the 2 best papers I’ve seen on this topic are the following:

      DIABETES, VOL. 51, JANUARY 2002 (Dysregulation of Fatty Acid Metabolism in the Etiology of Type 2 Diabetes)
      Am J Clin Nutr 1998;67(suppl):500S–4S (Glucose–fatty acid interactions in health and disease)

  • Hemming

    Hi Peter,

    Very thoughtful post, I like your style of ‘I’m not claiming I know all the answers, I’m trying to find out and explain what is actually going on’.

    Anecdotally, I’ve been trying to gain weight while being, more or less, in ketosis during the last six months (I don’t measure ketone levels so I can’t say exactly how much of the time I’ve been in ketosis but I’ve been eating a very strict diet) only to realise that I’ve maybe gained 1kg (starting at around 51kg, 177cm). My point is that I’ve been eating around 3000kcal/day for an extended period without gaining weight, alluding to your point that there are so many different factors to factor in (pun intended). I’m not sure this is a positive thing either as I would probably be healthier at a higher weight.

    Moreover, I also experienced how my appetite went away when I first started out dramatically reducing my carb intake. As you also mention, I believe this was due to the mobilisation of the fat I had stored. When I then dropped below 50kg I started feeling like crap and things got really bad. My point about this is that I think it was a combination of calorie restriction (simply eating ‘real food’ alone will work wonders for many in terms of appetite and weight loss, I believe) and a preference for burning fat.

    I just wanted to chime in with some thoughts from the other side of why people usually come here. Keep up the good work Peter!

    Best regards,


    • Thanks, Hemming. In addition the available energy model of appetite regulation, malonyl CoA probably suppresses appetite, too.

  • Ash Simmonds

    So our liver is the Flux Capacitor – but Mr Fusion is what most people think our bodies are – eg picture the scene where Doc Brown is stuffing any old trash into it and says “We need fuel!”.

    That, is calories in/calories out.

    As an aside, Mr Fusion was surmised to run on cold fusion, which your mate Gary Taubes might have some things to say about… 🙂

  • Martin

    Peter, thank you for another great post. Could you clarify your hormonal changes when you adopted your current diet? I thought I had read elsewhere that cortisol rises in a ketogenic diet. As a man I am of course interested in testosterone, so what you said about a 50 % rise sounded interesting. Don’t you think this results from ketosis per se or rather from a high fat / high quality / low carb diet? Much appreciated!

    • Insulin – lower
      Cortisol – lower
      Thyroid – lower
      Testosterone – higher

      These are my results, only, of course.

  • Raph S

    Maintaining adequately ‘low’ insulin levels seems to be 1 of the prerequisites to enter and maintain a state of nutritional ketosis.

    1- Keeping this in mind, how big could someones DNL+RE get in a state of nutritional ketosis (say approximately 1mM) where their adipocytes are in net flax influx?
    2- If this is in fact possible, could you think of a case study or example showing this despite adequately low insulin levels for this ketotic state?

    Or maybe I’m missing something about individual insulin sensitivity…
    Great post Peter!

    • Sorry, Raph, not sure I understand your question.

  • Judy

    Peter, I know you said you don’t know much about how estrogen figures in, but as a middle-aged woman, I have a HUGE interest in it!

    I read somewhere that fat cells either contained estrogen or were somehow linked to estrogen cells so that people with higher body fat had more estrogen. Have you ever heard anything about this and if so, can you point me in the direction of some references?

    • Judy, I’ll get to it in time.

    • Kathy from Maine

      Please, please, please address the issues that menopausal and post-menopausal women face in trying to lose weight when you can. I’m hoping you can offer some advice, because the traditional methods that work for men and work for younger women simply don’t work for us anymore.

      When I hit menopause 8 years ago, I gained almost 50 pounds in 18 months with no changes in eating or activity (I’ve eaten low-carb since the late 1990s). Nothing would take off the pounds. Finally, I was able to take off 35 pounds using homeopathic hcg and kept it off for more than a year. Then, over the past year, I’ve gained back 20 pounds of it. It doesn’t come back gradually, but rather in spurts of about 5 pounds at a time. I’ll stick at one weight for months, and then all of a sudden have a spurt where suddenly I’m 5 pounds heavier, despite the fact that I’m still eating the same menus (typically 30 or fewer grams of carbs per day). I’m not gluten-free yet, but getting there. Also, I do take bio-identical hormones, and my gyno says the levels are good.

      So what does a menopausal woman have to do to lose weight? I’m in “analysis paralysis” at the moment, not sure whether I should go higher in fat, higher in protein, lower in fat, etc. The very-high-fat approach (75-80% fat) doesn’t seem to work for me or for MANY if not most of the women I know in my age group. I know I feel the best when I’m eating around 100 grams of protein a day, but what of the other macros? I’ve tried the low-fat, higher-carb (coming from veggies and a little starch) approach, but I’m so freakin’ hungry all the time I can only do that for a couple days before my body screams out for some good fat.

      Sometimes I feel like I’m not giving my body enough food (I rarely go above 1500 calories, emphasis on fat and protein). There’s argument that if you don’t give your body enough calories/nutrients, you risk starvation mode and your body gets really good at slowing down metabolism, exactly what you DON’T want. It’s hard for me to eat more than that, though. The one thing I love about low-carb eating is that you have a good breakfast, and then you’re not hungry for hours and hours and you don’t even think about food. I hate having to eat every couple of hours.

      OK, I’m rambling now. Suffice it to say, if you could sometime address what women in menopause need to do to lose body fat, you’d make a whole lotta women very happy. Thanks!

    • SusanneL


      Check out my post further down. I’m a premenopausal woman who suddenly started to gain weight when my gynecologist started giving me extra estrogen. While many women suffers from low progesteron, giving estrogen really disturbes the balance of estrogen and progesterone.
      For more information read on the website: mialundin.com

    • PhilT

      http://jcem.endojournals.org/content/89/4/1739.long is about obese post menopausal women.

      “Thus, diet plus exercise training, but not diet alone, is effective in reducing chronic inflammation in obese postmenopausal women. In addition, modification of chronic inflammation is associated with changes in local adipose tissue metabolism in response to diet and exercise.” Includes lipolysis rate measurement.

      Dr M Harvie has done work on intermittent energy / carb restriction in obese female populations of all ages, http://www.ncbi.nlm.nih.gov/pubmed/23591120 is her latest. May be worth a try – 2 consecutive days a week on <1000 calories with restricted carbs.

    • Chris

      Peter, I happened to watch your TED talk and then found your blog from there. I really can’t wait to hear what your research finds on women and how their hormones interact with insulin and such. I never had a “weight problem” until after I delivered my 4th child when I was a few months short of 39 years old. 4 years later, I still have not lost the 40 lbs, I gained in that pregnancy despite being on a 1200 cal “balanced” diet and working out consistently. I did have gestational diabetes with all 4 of my pregnancies, but I also had all 4 of my kids close together starting at 34 and ending before I was 39. I was able to lose the weight between each pregnancy, but that last one did my metabolism in. My OB/GYN just tells me it is hormones and perimenopause. I have changed the foods I eat and am still trying to keep it at 1200 cal and have lost 4 lbs in a week. The fact that I have actually LOST even a pound after that long doing everything “right” is pure bliss! Thank you for your research. Although it often takes me several days to read a blog entry because I’m not a math or science whiz, it has been so worth the effort to understand it.

  • Christina

    I surfed onto your blog “by accident”. I got kicked off the Engine 2 Extra website (fat free vegan eating), because I asked too many questions and have “complex” medical problems. Basically, many of my family members drop dead of MI’s in their early 40’s and 50’s; those who never smoke have bypasses and stents in their early 60’s and 70’s. I also have C282Y homozygous hemochromatosis, which is not a concern. I got my ferritin down from almost 500 to 8 in one year. It’s easy to control. Bloodletting is a miraculous cure. I am 51 and post-menopausal. I exercise regularly – weights 4x/week and cardio 3x/week. My BMI is 25. I gained some weight, especially around my belly, on the fat free vegan diet, but all my lab numbers – fasting glucose, cholesterol, triglycerides, etc. are “great”. Of course they don’t do the “fancy” cholesterol tests in Canada (apo-B, etc.), which I probably need with my family history. I look healthy and young for my age on the outside (as did many of my now deceased family members), but I know that I am a ticking time bomb on the inside. At 50+, my time is running out. Do you think I should try a ketogenic diet? I am willing to experiment on myself. I feel I have nothing to lose.

    • They should do apoB in Canada. You should insist on it. (You can let your doctor know that Allan Sniderman at McGill is basically the guy who figured out what apoB does.) I have no idea if a KD will be best for you, of course.

  • Robbie

    A digression based on my selfish concerns: as a competitive endurance athlete, my aim through trying to reach ketosis has not been fat loss per say (although I have enjoyed this), but the ‘metabolic flexibility’ that you have aimed for. In short, I never want to need another gel shot again. How far can I stray from a strict ketosis-inducing diet before I ‘fall off the wagon’ and lose metabolic flexibility? Or, once I develop greater insulin sensitivity, will my body ‘remember’ this sensitivity once I re-introduce some complex carbs back into my diet?

    • Good question, Rob. I don’t think it’s binary, though (the ketosis part is binary, but I think the metabolic flexibility improves over a range of RQ, IS). At some point — different for everyone, I suspect — you may laps back into glycogen dependence.

  • Jim

    One thing that I dimly recall from my 1970’s medical physiology and biochemistry was the concept of “futile cycles.” These are biochemical cycles that don’t produce anything, net, but do burn energy. It struck me that the lipolysis and re-esterification could be exactly this–if those arrows are both large, isn’t it inevitable that more energy will be burned than if they are both small? Of course I have no idea how large an effect this might be.

    Intuitively I think we all have the idea that our metabolic load is mostly based on activity (obviously wrong but intuitively appealing.) Of my 2200 Kcal/day I’ll bet all but about 400 is “metabolic”: Na-K pumping, circulation, “futile cycles” to maintain body temp, tissue maintenance, digestion, etc. It has always seemed to me that the body could respond to a low calorie diet with minor shifts in temperature generation etc to compensate and that might explain why people can eat less and not lose weight. We are too complex for the calories in calories out model.

    Saw your video on Ted-X. I really appreciate your heart as you recall the patients you saw. In fact I’m seriously considering an article for the Christian medical association called “Judge not” based on what I’m learning here, and what I’ve seen in Mexico where type II diabetes is rampant among the desperately poor. You are doing good work.

    • Jim, I guess it depends on how one defines futile. My free-living EE is about 3,800 kcal/day (by DLW), but my resting (i.e., laying down for 24 hours) EE is about 2,100 kcal/day (in a metabolic chamber). Most of that 2,100 is the energy I require to make ATP to move ions across gradients, contract/relax involuntary muscles, and thermoregulation. But you’re right, most of our energy is not expended during periods of deliberate activity. Thanks for feedback on talk, also.

  • Denise

    Just found your website (thanks to KTAR and a spotlight they did on you). I’m forwarding it to my son (a 2nd year med student), who, like me, believes in science but understands that findings can be misinterpreted and misapplied and may be based on the wrong question.

    Although I have always worried about my weight (although never overweight), I now have found myself in the unenviable position of gaining weight as you did. The first burst happened perimenopausally…understandable but disconcerting. The last burst has happened 5 years later since my synthroid (given prophylactically, not as a result of hypothyroidism) was dramatically reduced when a DEXA scan showed normal bone density to osteoporosis in less than 5 years. Took on a personal trainer (I’ve always been physically active) but continue to grow. The doc said he doesn’t think the change in dosage relates…I’m (of course) insisting that nothing else changed but I did increase exercise on top of my daily 4 mile (in less than one hour) walk, so I’m thinking something metabolically has changed.

    I’m a firm believer in “average” does not mean “individual” and that I will somehow need to find what will work for *me*. No problems with BP, cholesterol, etc., no meds (other than synthroid), no health issues but this has me frustrated. I will take into account your findings and thank you for being willing to think outside the box.

    • You said it spot on, Denise. What works on average or works for me, is not nearly as important as what will work for you. I hope everyone reading this will take a “selfish” view for a moment and realize that the answer to that question is most important. Pending more nuanced research, self-experimentation within the boundaries of scientific evidence is a good place to start.

    • Grace

      Hi Denise

      This website, this woman, is changing lives with science. Check it out. You’ll be amazed by her generosity and incredible discoveries.


    • Bobby

      Interesting read for sure… I am currently doing KD (along with my wife) and honestly, while I do appreciate the lack of lows (and am not a fan of the lack of highs) in terms of energy (I’m more “level’ than the peaks and valleys with my old diet… but I digree. I found that I had the most luck eating “clean” – low fat high protein with plenty of vegetables and low sugar, and just lifting like a madman in the gym. Made it to 183 lbs and while I’m only 192 now (5’10” – really need to get to 170-175)… it just seems like such a long journey.

  • Chris

    In theory 4 you state:

    “In my experience (and Gardner’s A TO Z trial seems to validate this, at least in post-menopausal women), about 20% of people aspiring to reduce adiposity seem to do it better in a higher RQ environment.”

    The title of that A to Z trial is “Comparison of the Atkins, Zone, Ornish, and LEARN Diets for Change in Weight and Related Risk Factors Among Overweight Premenopausal Women”.

    I just wanted clarification on if your theory applies to pre or post-menopausal.

    The reason my interest is piqued in this particular theory has to do with my wife. She has always struggled with her weight and while I’m not privy to the exact diagnoses she’s been given over the years (there were several beginning prior to our marriage…), she does indeed have endometriosis which has required surgery in the past and a cyst has been removed from her ovary so your reference to PCOS caught my attention although I’m not aware of her having that exact diagnosis. Part of her treatment after surgery (15 years ago) was Lupron injections which were described as “chemically induced menopause” by her Dr. at the time. That went on for about a year but she has a needle phobia so it eventually gave way to traditional BC pills that she just takes consistently with maybe 3 breaks a year for a period. Long story short is I suspect her hormones are all out of whack and that’s playing a large role in her weight struggles.

    Personally, I’ve had great success in ketosis. I dropped 30 pounds (170-140) in 3 months. I really didn’t think I had more than 10 lbs. to lose so I was amazed at the results. In particular with how much better I felt. My wife on the other hand didn’t really lose any significant weight over the course of a year, maybe 5 lbs. or so. We eat 80% calories from fat so we’re “all in”. She did experience the other benefits of reduced blood pressure, more energy, etc. so it wasn’t a complete bust but of course, we all would like the added benefit of carrying less fat. I have little doubt that nutritional ketosis is probably the healthiest way to eat but if something like the Ornish diet could work to shed excess fat, I’m sure she’d favor that approach at least in the short term.

    I’ve always thought that her issue was more about the inability to “mobilize” stored fat than it was about being “too efficient” at storing it and this post bolsters that theory. I know I’ve been rambling for a while so I’ll get to a question! She’s only 40 and is still able to have periods but I have a feeling her hormones are more closely aligned with a post-menopausal woman. What hormones do you think play the biggest role in that situation and is there any particular testing we could ask her doctor for? Would it be obvious like testosterone/estrogen or something more obscure?

    This is more of a comment but it would appear that you believe people with a problem on the L side of the equation may fit into a category that does better on the fat restricted (and by extension, higher carb) diets. Did I interpret that correctly? By reducing the RE compared to a low carb, high fat diet, you hopefully don’t introduce more DNL into the equation because L is still the bottleneck.

    It seems like “mobilizing” HSL and ATGL would be key to getting someone with an L problem on the right track. Any thoughts around how to make that happen? Hormones? I’m sure if you knew the definitive answer to that, we wouldn’t be having this discussion!

    • Chris, good catch. The study was in premenopausal women. Typo corrected. I think your suspicion is correct in your wife’s case, though it would hard for me to speculate on exact causes further. Would certainly suggest docs look at full spectrum of IR, all glucocorticoids, plus sex hormones, thyroid completely, including antibodies.

      I don’t think I can say who does better on a low fat vs. a low carb approach, though it does appear that ability to oxidize fat predicts who does better on low carb (high fat). The L side of the equation, I suspect, is where people get into trouble and where the net influx starts.

  • Trisha

    Very interesting post. I need to re-read it to further digest. Reading through the comments I noticed you talk about how a ketogenic diet has impacted your personal thyroid levels. I’m wondering, is there a way to combat lowered thyroid levels while staying on a ketogenic diet.

  • Jane

    Thank you for a very interesting and well written post, Peter. The graphics help to clarify the basic concepts.
    And extra thanks for including the references, both in the post and in your responses to questions and comments.

  • Paul

    Wow – not to trivialize your earlier posts but this is the good stuff as far as I’m concerned. I had already gleaned that a ketogenic diet wasn’t a magic bullet by itself, even though I’ve lost weight (fat) on it. But my post-menopausal wife has not and I’ve plateaued at around 12% bf (according to my bathroom scale). I get really hungry when I’ve tried to fast so either this is my set point or there’s more fine tuning to do. Not that I’m complaining but I haven’t eaten a processed carb or potato in months. What I’m understanding is that it really is (calories in) – (calories out) but the hormones make each of those terms anything but simple.

    Thanks so much for parsing this out for us, I really appreciate the rigor and honesty.

    • Paul, calories in less calories out is always true, it just provides no meaningful insight. Glad this helps.

    • jw

      My apologies if this was covered in another post, but: In your three day stay described in your ihmc video, did all of the measured energies, calories, fluids and solids, inputted and outputted net out with your beginning and ending weight? ( I am assuming that errors were small enough that this could be determined, I have no idea.)

      • On those days I lost about 300 gm of mass, probably fat mass, given my intake and output and nitrogen balance. I did not get into this during the presentation.

  • ER

    Your diagrams and explanations continue to be clear. Thank you for taking the time.

    If someone is in a net fat efflux (and losing weight, whether or not they are in ketosis ), so that free fatty acids are leaving the adipocyte, would you see a significant rise in triglycerides on their lipid profile? Looking at your first diagram, in this situation of efflux, there would be lots of FFAs entering the bloodstream, bound to albumin, would they reform TAGs in the blood (with the need to be carried by a lipoprotein)?

    • Great question. You may see it transiently, but you you may not. The changes in concentration are so timing-dependent, that it probably matters a lot when blood samples are being taken. I do recall one TG level I had during rapid fat loss that was very high, but otherwise I sort of steadily went down from >150 mg/dL to less the 30 mg/dL.

    • Hemming

      When I lost weight my TG also went up just as my albumin is borderline high. My doctor was of the same opinion as you regarding the TG and didn’t comment on the albumin. I’m not sure if it makes medical sense to have a positive correlation between TG and albumin – maybe someone can comment on this.

  • Frank

    Great article Peter!! Really juices me up to go out and learn more!

    I’m 48, male and overweight. I have hypothyroidism and hypogonadism (guess I won the lottery here, but am on medication to correct) and I tried nutritional ketosis for about a month and really did not shed any weight. I was one of those people who believe that just being in ketosis would make me lose weight.

    I would like to confirm my takeaway from this post – I now have to get off my butt and conduct my n=1 experiments to figure out my solution to make L > DNL + RE ! Any suggestion for a place to start?

    Thanks again and keep these great posts coming.

  • Martin

    “They are not giving up fat from their fat cells because they are eating less. They are eating less because they are giving up fat from their fat cells.”

    Looking at things from this perspective feels very refreshing to say the least and it really does explain a lot. When i first came across this idea reading a book on low carb diet by the swedish MD Andreas Eenfeldt it just blew my mind. Thank you Peter for another wonderfully insightful blog post and congratulations on the very touching TED talk you gave earlier. You truly are an inspiration!

    • Thank you, Martin. I hope, of course, you understand that I am not unique in having these ideas. I’m but one of many in a vocal minority.

  • Anne

    Peter thank you for this blog. I found you through your recent Ted talk. I am a 36 yo female c PCOS who has been on Metformin for 16 years. I maintain a BMI between 20-22, I have the easiest time losing or maintaining weight when I do not exercise and stay on a low CHO diet. However, I love to exercise and I find it frustrating that I always gain fat. My question is, do you have an opinion of how the Metformin may be influencing my metabolism when I am exercising (moderate to high intensity for 50 min 4-5x wk)? The Metformin has yielded reductions in my androgen levels, but I am curious now that I have altered my intake of CHO and/or exercise regularly, if the Metformin may be working against me. Thank you for any thoughts you may have.

    • Very interesting, Anne. If the exercise is vigorous, it may be that the inhibition of hepatic glucose output (metformin’s mechanism of action) is interfering with your liver’s ability to detect adequate ATP, which could drive up appetite?

    • Anne

      Note: I neglected to mention that I am not diabetic.

  • Teresa

    Dr. A –

    I recently made a comment to you – (I’m the one who was an altruistic kidney donor) – anyways…I just want you to know that you speak so far over my head and I love it! I really do…it challenges me to think far beyond what I’ve ever been challenged to do.

    Thank you….You are making a huge difference…just by speaking and writing. Thank you! You are bright and I appreciate it.


    • I showed a friend this post a few days ago, before posting it. He said, “Why the hell would you write to so much and in such a technical manner? More people would read your blog if you kept it to 500 words and dumbed it down!”

      To which I responded:
      1. My goal has never been “readership” — I’d rather a few readers who can really diggest than countless who will forget it tomorrow.
      2. The folks who read this blog are self-selecting on intellectual curiosity and passion for this topic
      3. I appreciate your feedback, but I think I’ll keep it as-is.

  • Bhavna Mishra

    Dear Peter
    I have read almost all your posts in the past two weeks after I first heard your Tedtalk. I appreciate the mission of your amazing organisation and obsession with being fitter and removing the food fallacies that plague our generation and beyond. I started my first dietary intervention in Oct 2012 with Dukan- switching to pure lean protein and veggies on alternate days. Having been a vegetarian in first 26 years of my grain laden diet..i found the results pretty encouraging with literally melting away of the body fat, increase in core strength, energy levels, an inherent needl to be physically more active and try out stuff i never wanted to do before. I lost 7 kilos in weight and 3 inches around my waist. My BMI now is 21. After reading your blog I upped the healthy fats and tried ketosis for the last 2 weeks. After an initial further loss in the inches i seemed to backtrack a bit. I was questioning if maybe the fat inflow now was more than the lipolysis and therefore I was probably storing more triglycerides than i was burning while earlier on dukan i was only burning the body fat and so had a net negative on fat equation. That’s when this post came. Does this mean than when attempting to lose body fat via ketosis you need to watch not just relative food percetages but also the total food consumed..sounds like counting calories again. The other bit is in one of your posts where they studied effects of different dietary interventions on a sample of people some people responded better to low GI or even low fat diets. Do you think dukan which is a low GI, low fat diet may work better atleast in some cases to induce nutritional ketosis that has bulk of B-OHB coming from fat deposits rather than dietary fat. Having said this what does intrigue me is the a access to the 100,000 calorie fat reserve in the body that you can possibly unlock on a high fat diet…would this happen even on lean protein low GI diet?
    Thank you

    • It could still happen, as long as insulin levels, on average, are quite low, though probably not quite as effectively (unless the diet was very hypocaloric).

    • Bhavna Mishra

      Dr Attia
      Is it possible to go into nutritional ketosis on a vegetarian diet. What vegetarian supplements would you reccomend in this scenario where you would burn body fat while retaining healthy lean mass?
      Thank you so much for your response and sharing your knowledge.

      • Yes it’s possible, but more work involved, especially for very active people. For sedentary folks consuming relatively little it’s easier.

  • Justine

    Dear Dr. Attia,

    Thank you so much for your blog.

    I read this article by an Australian doctor on obesity this spring: http://www.themonthly.com.au/issue/2013/march/1361848247/karen-hitchcock/fat-city
    and it kind of haunted me. The 700 comments more so.

    The antithesis and antidote was your TED talk.

    In a moment of congruence I was diagnosed as insulin resistant and given a 650 cal ketogenic diet (from the leading obesity doctor in Belgium via a university hospital) and told many things contrary to your site: eat low fat, use fake sweeteners, avoid salt, no nuts. While I’ve lost weight 16lbs/7.2kgs in about a month, I have suffered with zero stamina, probably feeling much like you felt in the beginning of your 12 week experiment. I’ve been adding more bouillon cubes and coconut oil and hopeful for improvements.

    It was info that was somewhat tricky to root around and find on your site, as the navigation/organization is tricky in terms of locating, and sometimes processing (I’m definitely an intellectual but of the liberal arts/social sci variety — in other words no hard or med science background) information, I am still grateful for your labor of love and the fact that you don’t dumb down your writing. And see fit to intersperse your discoveries with potent reminders about humanity, like the story about Woody Sparrow.

    Again, thanks for your blog.

    • Justine, I read this, also, a while back. Needless to say, I think the smugness of this author is deplorable. Think of the quote I referenced in this post, “She was born on the finish line, so she thinks she won the race.” I would be willing to bet she doesn’t take care of too many people suffering from the diseases associated with obesity.

      I have no response to such people and instead I choose to do what I do. Let them do what they do.

      Last comment: is it nearly impossible to undergo a low-salt KD. That would be the first place I would suspect your weakness is coming from. Pick up a copy of Jeff Volek & Steve Phinney’s book “The Art & Science of LC living.” Great “how to” guide on ketosis.

  • Nan

    I can’t claim to understand this article completely, but I gleaned enough to help me see why I don’t seem to get the same results on KD as my spouse, though we are both in our sixties, and reasonably active. I find that I still have cravings, which he says are non-existent for him. I am low normal thyroid which I believe may be a factor.

    • Nan, correction of hypothyroidism can definitely “unleash” your lipolysis potential.

  • JJ

    Great post Peter (enhanced by flux capacitor reference), good balance between giving us enough without losing everyone and also providing enough of the answers without speculating into areas NUSI may look to research.

    I have still to soak it in properly but I wondered if you could please help my simple brain by considering this dumb question. Although a state of Nutritional Ketosis does not guarantee fat loss, all things being equal (calories, daily activity level) is it likely to for most people (on average) lead to more fat loss (or less fat storage) compared to not being in Ketosis?

    Also, I have a kind of OCD for truly understanding things I know I only have a basic understanding of and metabolism has long been an area I am fascinated by (loved biology in school). Are there any 1,000 page text books you could refer me to which would give me a deeper understanding (sadly I am not kidding)?

    • JJ, I think, all things equal that some % of the population when given the choice between a Standard American Diet (SAD) and KD will have less adiposity on a switch. Whether it’s 30% or 70%, I don’t know, but Mark Friedman has suggested that the result of dietary switch from a combo high fat/high CHO (i.e., SAD) diet to something like KD can predicted by pre-existing fat oxidation potential.

  • JJ

    Just noticed Teresa’s post. Please do not ever dumb it down (any more than you really have to) ever! I will have no where else to go for the real story!

    • Tim

      I agree, don’t dumb it down. There are *plenty* of low carb websites that do that.

      I’m a pre-diabetic low carber. Why is it that my body wants to regulate my fasting blood sugar between 100 and 110? Why not lower, like normal people? What can I do to make my body’s *desired* fasting BG lower?

    • James


      Some low-carbers get their fasting BG level higher than normal due to a “physiological insulin resistance”. To get it back to normal, you can do the following:

      Add resistant starch in your diet.

      Resistant starches are not digested in the small intetsine and do not contribute to your BG level at all. They go further down the colon and are fermented by beneficial bacteria. The overall effect of RS on metabolism is quite dramatic: lower fasting BG level, better regulation of BG and insulin spike after a carby meal (so-called “second meal effect”), better sleep, healthy colon (thanks to the short chain fatty acids like butyrate that these bacteria are spitting out).

      You can find RS in something as cheap as raw unmodified potato starch (the fine white powder, Bob’s Red Mill is selling some, it is about 80% RS by weight which you can have as supplement – about 30-40g mixed in water or a smoothie), green bananas and plantains, etc. There’s this guy hosting a blog called freetheanimal.com He described RS and its effects at lengths in some of his articles. It is a fascinating topic and something a lot of type 2 diabetics or pre-diabetics could benefit from.

  • SusanneL

    Thanks for a very (as usual) interesting post.

    Yes the body is for sure complex. I would love, if you by any chance got the time, to dig in the subject of other hormones as well.

    Being a well trained woman of soon 48 years with normal weight (53 kilo, 162 cm tall) i about a year ago started to have those famous “premenopausal issues”; nightsweats and difficulties sleaping. My gynecoligist gave me a description of vaginals containing estrogen. I have never in my life taken som kind of hormones, never been on the birth-controll-pills and other hormones. Suddenly I started gaining som weights, having cravings and felt very weird. Since eating a paleo diet I wasn’t used to have cravings. I thought to myself that I didn’t like how this had turned out so I got out on the internet and started my search. I found out that many women in my age doesn’t have low estrogen but are low on progesterone. Because of that, the body ca’t “use” the estrogen that is in the body. And then given som supplements with extra estrogen makes the body much more hormonally imbalanced.

    I then bought som extra 5-hpt, L-tyrosene and started to use an progesterone cream during my luthealfase (and also quit using the estrogen medication from my gynecologist). Quite soon I feelt extremely well, started to loose those 2 kg I went up, started to taken the orderered estrogen from my gynecologist. I nowadays have no nightsweats what so ever and sleep like a baby

    What I in many words above are trying to say, is that many women may have trouble with overweight because of hormonal inbalance. It may not be all of the solution, but since I experienced this myself (also as welltrained, eating healthy, not smoking and so on…) I think it would be important to hilight this.

    I am also sad that many doctors (sorry Peter!) doesn’t seem to have a clue on this matter, giving many women estrogen and pills against depression, disturbing the bodys natural balance much more. I haven’t come across articles that show any correlation between insuline and hormones such as estrogen, progesteron and testosterone. But I think that they play quite an important roll. Also the hormones of the thyroid glands play such an important roll.

    Love your work
    (and ps. sorry for my poor english since being a sweedish lady 🙂 )

    Susanne L

    • Susanne, I do look forward to addressing these issues down the line.

  • Rosie

    Peter, thank you for all you are doing in seeking real understanding of nutrition and how it affects the human body. One size (diet) so evidently does not fit all! And, has been pretty obvious to so many of us who have been casualties of what up until several weeks ago I would have called a healthy diet – vegetarian and no refined carbs, low fat. But no! For years I have suffered from dramatic energy swings – going from feeling extremely well for 24 hrs and then crashing if I’ve been at all energetic, as I like to be when well (I love to use my body previously being a dancer)and feeling so ill some days that I cannot move physically as I feel as if I have flu/can’t think straight/ low body temp aka Chronic Fatigue type symptoms. This cycle going on and on. A complete nightmare to plan my life and disguise it as it is so boring having to tell people – actually, I’m not functioning today…However, because I have had trauma in my life from a difficult childhood these highs and lows of energy have always been attributed to a mood disorder – from the biochemical positioned psychiatrists I am bi-polar and was recommended to take lithium. I refused. From the psychologists perspective I have Borderline Personality Disorder…Well, maybe both are right…and I very much believe in psycho-dynamic psychotherapy utilising attachment based theory. I have seen this work in my own training as working with abused children; and in my own case with a marvellously empathetic therapist. But it is not enough. There is more to this equation…I have always felt that foods affect me and my mood and sure diet is so much a bigger component, and thanks to the internet and my facility when my brain is functioning to actually think straight, really quite smart and able to grapple with the science when it is presented in a clear and concise way, as you seem to be able to. So, don’t ever dumb down your blog! Other passionate doctors too, are doing the same out there. So wonderful to have you share your knowledge, which is obviously extensive, but also acknowledge that what you know is still not enough; more questions (the right questions) need to be asked and to include everyone in this discussion is so refreshing, and empowering. Hopefully, it will mean people will come to see that their health is so often in their own hands and not to be just some passive bystander in a body that a doctor is meant to prescribe a pill to fix…Sorry, I digress! Anyway, I have been rigourously following a ketogenic diet following Drs Jeff Volek and Stephen Phinney’s advice on Low Carb eating and despite feeling truly awful 48 hrs after starting for about a week and a half, which having read how the body adapts can be expected, to in the third week now and although no real stamina yet, my mind is clear and my mood ‘just right’. No extreme high or low in mood. It is unbelievable to feel ok all day – no dips in energy really. Provided I don’t need to run anywhere. That kind of energy is eluding me right now. But, baby steps, eh? This is obviously too early to see if this can be really helpful long term to managing my moods and energy…but the very sparse amount of literature I am reading is pointing this way. Very few studies have been done with diet and bi-polar disorder and I think time it was really looked at. Keep up the work you are doing Peter. The NuSI seems such an exciting venture. I apologise I wrote so much and ‘off topic’ specific to the post.

    • Thanks for your comments and feedback, Rosie.

  • Jeff Johnson

    Bestest Article Ever

    This is like Christmas in July – you really out-did yourself on this one –

    I always wondered why – exactly – I had to reduce my fat intake to lose weight – even in Ketosis

    • Jeff, so glad this was able to put that in context.

    • Michele

      I’m so glad Jeff asked the question….the same thing was running through my brain.

      Also thanks Peter- it’s finally hit me like a truck that it is not a “bad” thing that I’m not in Ketosis. For awhile, I thought it was the universal answer and to be “good” and losing weight, I had to be in it. Now I know this is not true, although, from the athletic point of view, the idea of metabolic flexibility just sounds so fantastic.

      As for the comment to your friend Peter, Jeff’s question really supports your point #1 and #2. Not only are the posts so mind opening but the comments too!

  • Nathan Young

    Great write up, Peter!

    The whole notion of “energy balance” and our modern obsession with calories can be depressing, so this post is certainly refreshing.

    I look forward to the work you and others are doing which will help us focus on food choices and hormones and the role they play as the primary drivers of our metabolic health.

    • Thank you, Nathan. It will be a long journey, but it takes time to do things well, as I’m sure you (and all readers) can appreciate.

  • L. Amber Wilcox-O’Hearn

    Thank you for the very interesting post!

    I really like the point about the blood levels of B-OHB being unable to tell you definitelively about production or use. I made a similar point about blood sugar measurements being unable to tell you about the rate of GNG (http://www.ketotic.org/2013/01/protein-gluconeogenesis-and-blood-sugar.html), but I never thought about it in this context.

    I’m also intrigued by your enigmatic description of the liver as master appetite regulator. There is a large faction of scientists who think it will turn out to be the brain. It will be exciting to find experiments that help distinguish these hypotheses.

    As always, thank you for being honest about the limits of our knowledge. I have grown weary of people using authority and a good story to overstate their ideas. Even when I think a theory is likely to be correct, it bothers me to see it presented as such prematurely. You are a role model for the responsible scientist.


    • Thanks very much, Amber. I will definitely write about this topic of the role of the liver in appetite control.

  • Max

    Curious as to how fat cells collaborate in terms of which one of them will be releasing fat at any given point, and which once will be storing them if they are not needed in the circulation after an exercise for example. Can fat cells exchange fats between each other or there is some kind of line up or a queue that dictates which cells will be active in storing or releasing a particular lipid molecule. I think when people do crunches they might think that stomach fat is feeding that effort, while in reality it can be the fats in the neck. Just curious about how that decision is made by the body. I presume there is no simple answer.
    Thank You,

    • There is a entire cascade of cytokines that allow cells to communicate with each other but, frankly, much is still unknown.

  • R. E. Hunter

    Thanks for the very educational post, and blog. I have a theory about #2. First some background. After losing 25 lbs on a fairly strict low carb diet (not any particular one), I got careless a couple of times and went overboard on carbs. Each time, my next workout was a disaster. Part way through my normal running distance (3-4 km) I hit a wall – got weak, short of breath, had to quit early and hardly had the energy to do my stretches. That’s when I discovered the term “carb crash”. I believe I went out of ketosis back to purely carb-burning mode. Then, when my blood sugar went too low, I crashed, because I was out of fat-burning mode.

    My theory is that ketosis gives a more consistent energy level throughout the day, at least if there’s a good supply of body fat to burn (which I still have). This keeps the energy level up between meals, resulting in more calories burned through the day. I’ve noticed I don’t hit the late afternoon drowsiness as much as I used to. It also gives me more endurance during exercise, allowing me to burn a lot more calories.

  • Cap’n Jan

    Thanks Peter – you give a lot to us, I hope you know how much it is appreciated.

    I got the reference to ‘flux capacitor’. Dang, I loved that movie! I could never understand the bad reviews, I was hoping for a sequel. Time to watch it again. Oh well.

    Fair Winds,

    Cap’n Jan

    • Cap’n Jan

      Nevermind, of course they did. I just didn’t care for it. ;->

  • np

    Thanks for the article Peter, been following you for over a year now, (you’re still one of the main inspirations for my 18 month old keto diet/lifestyle switch), and I’m still amazed by the quality of your research data. But am I the only one who thinks you have now made the Ketogenic Diet an altogether more complicated affair?

    At the outset we were told, eat less carbs and a min of 60% fat and you’ll lose weight, then we were told…ahh but you can’t over do proteins. And now you’re saying, watch out, but you may have to restrict fats too.

    How are we mere mortals expected to navigate such an increasingly complex set of rules without resorting to hair tearing and much gnashing of teeth?

    • Nigel, one who aspires to enter ketosis does not need to know anything in this post, to be sure. However, if someone is in ketosis, and is not losing fat, this post may offer some helpful insights.

  • Rob W.


    Thanks for another excellent post. Fantastic detail. One question (and I apologize if I missed this in your blog), what organelle is responsible for the conversion of fats to ketones in the liver cells? Lysosomes? Ribosomes? Mitochondria? Thanks in advance.


  • michael

    Hi Dr. A-I was fascinated by your TEDtalk for nutritional interest and for social issues addressed (I’m looking to become a healthcare professional). What are your thoughts on the demonstrated (http://www.ncbi.nlm.nih.gov/pubmed/11167929?dopt=AbstractPlus) decrease of thyroid hormone production / sensitivity as a result of absence of glucose in the diet and blood? I am also curious if you’ve read other concerns (not related to SFA intake / serum cholesterol) about very low carb lifestyle and alternative understandings of weight regulation that center around food-reward and hypothalamic inflammation. I’d also be grateful to hear your thoughts at some point on organ meats, bone broths, and fermented foods.


    • I think it’s another example of how hormones play an integral role in fat balance.

  • Mark

    Hi Peter,

    How is it that foods like dairy, and even protein like whey, which are very insulinogenic don’t seem to promote weight gain in studies, but carbs do? Is it simply a result of overeating the carbs?


  • Craig

    “Do they lose weight because they eat less? Or, do they eat less because they are losing weight?”

    I suppose this is a way to grab people’s attention for a point you are trying to make. But boiling the issue down to this either/or proposition seems simplistic. Why can’t it be both? People overeat and undereat for a variety of reasons; appetite is a powerful driver, but not the only one.

    • The questions is posed directly in response to the observation I referred to. What is their appetite less in this setting? Is it because they are “eating themselves?” I argue, yes.

  • Raph S

    Sorry for the confusion – I was trying to understand if it was indeed possible for someone who is in nutritional ketosis (say approx. 1mM) to also be in a state of net fat influx.

    It seems to me that the insulin levels necessary to maintain this level of nutritional ketosis would be sufficiently low to prohibit net cellular fat influx – is that not the case?


    • Regardless of B-OHB levels, one can still be in positive fat flux.

  • Tiffany

    Thank you, thank you, thank you for taking the time to educate us!!!! I am not a scientist so I have to read and reread your articles, but I learn so much more from your blog than anywhere else on the internet.

    I have been on a very low carb (10-15 carbs/day) and high fat diet for about 18 months. I keep my protein around 60-70g/ day and never more 25-30g/ protein per meal. Almost all my carbs come from the heavy cream in my coffee. I play singles tennis (3 days/week), ride my bike (~30 miles/week) and walk (~25 miles/week). I am 5″ 4″ tall and weigh 128. There is an extra 5-8 pounds on my back, stomach, and upper arms that I would like to lose.

    Am I reading this article correctly? If the only switch I make to my diet is replacing my heavy cream with half and half, could that possibly help me lose those few extra pounds? Would it be worth it to add the extra 2-3 grams of carbs in exchange for the lower the fat content? (1/2 cup of heavy cream has44g/ fat & 3.5g/ carbs. Half/ half has 14g/ fat & 5 carbs)

    I do not want to give up the coffee, and I can’t drink it black. This way of eating has not only helped me lose weight and be able to play sports in the hot, humid southwest FL sun, but the most amazing part has been the freedom I have gained from not obsessing about food all the time. My meals are simple: grill a piece of fish or meat and treat myself with coffee and cream a few times a day. I have tried giving up the coffee and substituting a small side of vegetables at each meal. The side effect is I start thinking about food again. Variety seems to be a downfall for me.

    Any thoughts would be greatly appreciated. And again, thank you so much for giving so much of your time to education.

    • James


      I am not a woman and hormones have a say in these matters. But I was myself in ketosis for a few months and reached homeostasis at a point where I was not too satisfied. What I did (and was not something I planned but was the result of the ketosis) was to skip breakfast and then luncnh entirely. I work out fasted and make sure I get enough “healthy” carbs (à la Primal Blueprint) when I know I will have high intensity workouts. So my fat intake varies wildly from day to day because I no longer track carb or fat limit. What works for me is to work out fasted. I do have coffee in the morning but I like it black. However, heavy cream in it will not screw up the fasted state. But I do not have coffee after early morning because I don’t see the point of kicking the adrenals late in the day … Having reprogrammed my meal timing is the best thing I did after switching to a so-called primal diet (which I follow loosely since I eat chocolate, and a bit of dairy here and there). But reducing the fat and upping the carb has been a good idea as well 🙂 Since I eat in the evening, I have no problem dealing with the carbs and I sleep much better!

  • Paul Arena

    After watching your TED video about a month ago (and then linking to your blog) I literally spent one week straight reading in chronological order your blog posts because everything you say (especially when it comes down to the known biochemistry) is spot on. I love it. DO NOT DUMB IT DOWN. Since then I have been trying to go ketosis keeping carb as low as possible, fat intake high, and about 100 grams of protein. There were a couple of times I got headaches and lightheaded. I was thinking this may not be the diet for me, but then I sucked down a bunch of bouillon and within an hour, boom felt great.

    FYI I am a personal trainer and it is so interesting to ask the clients that are overweight and having trouble losing it what they eat. I tread lightly when trying to convert anybody to this lifestyle because of such fervent pushback from misinformation. I usually refer them to your TED talk then to your blog and then over time educate them on the biochemistry. About half start to “get it” and come around to idea.

    I know somewhere in your blog you mentioned Ketone urine strips. I couldn’t find it. Are they accurate?

    Keep up the great work! You make me want to go to Med school. We need more doctors like you.

    • Paul, the urine strips test Acetoacetate (AcAc), but do so qualitatively. The blood meter tests BHB, and does so quantitatively. I much prefer the latter, but it is more expensive.

  • Kathy

    I have been in ketosis for 3 weeks and have stopped loosing weight. I have therefore been scouring the net for advice as to why this is happening. I just found your site, and am delighted to read all that you have provided.

    I am specifically looking for where you might write about the proper balance between protein, carbs and fats required for ketosis. I understand this may vary person to person, but I don`t know how to calculate a starting fomula. I am a 52 year old female (4 feet 10 inches tall) and 89kg. I found where you suggested 1-1.5 gms of protein per kg of body weight (for me that would be say 100 gms = 400 calories of protein) and less than 50 gms of carbs = say 200 calories of carbs). Would I then assume I should be on a 1200 calorie diet and eat the remaining 600 calories in fat. I have only been eating between 650 and 950 calories because I have not been hungry, but I have read that this will cause my metabolism to slow down……can you please comment on how I determine a starting point, where I make changes if I am not in ketosis (according to a blood monitor), and if eating less than 1200 calories causes a metabolic slowdown.

    Fabulous site and thank you for your time.

    • Perfect timing. Hopefully others can chime in with suggestions.

    • Pam

      Kathy–A good place to begin is with the book “Art and Science of Low Carbohydrate Living” by Phinney and Volek. Another beginning place is http://www.dietdoctor.com/lchf, the website of Dr. Andreas Eenfeldt. That particular page on his site is titled “LCHF for Beginners.”

    • PhilT

      If you aren’t in ketosis then cut the carbs down to 20g and if that isn’t enough drop the protein too. A ratio of fat grams to (protein + carb) grams might be helpful – if it’s too low you won’t be in ketosis. Google Skaldeman or Ketogenic ratio for the maths. Jimmy Moore’s n=1 ketosis experiment had less protein than 1-1.5 grams per kg from memory.

      Most if not all of this “metabolism slowing down” stuff appears to be nonsense prevalent in diet forums and women’s magazines. Find me a clinical trial with 600-800 calorie intake and no weight loss.

    • Kathy

      Thank you to the people who have replied to my question. I imagine us ‘newbies’ keep repeating the same questions! I have been reading copious amounts of information and my ketone monitor arrived last week. I find the protein numbers to be a bit confusing because there is quite a spread, and a variety of numbers quoted. Some will quote total body weight, some lean mass, some height, and then it depends on your activity level. But I will find my ‘sweet spot’ amongst all those numbers.

      Although the urine sticks showed I was in ketosis, my monitor reading was .6. After a 2-3 week stall, my weight had started to move, but I in an effort to get to the 1.5 – 3.0 range I cut back my protein to about 70gms a day, instead of 100. I have also added fat, fat and more fat (somewhat reluctantly) to get me to the 1100 calorie range. For the past 4 days I have been dropping one pound per day and my morning ketones are up from .4 to .9….I shake my head every morning, but am enjoying both the numbers and the challenge of figuring this out.

      Thanks again to those who took the time to comment. Much appreciated.

  • Allen W.

    Dr. Attia,

    Thank you so much for all the great things I have learned from you since I discovered your blog in January. Thanks to you I have eliminated most of the starch from my diet and finally started losing weight. I spend over an hour working out on the elliptical 6 to 7 days per week and was stuck for three months until I cut out the bread, potato’s and most other starches. My wife is type 2 diabetic so when possible I use Glycerol as a sweetener for drinks like home made lemonade so that it will not effect her blood sugar levels if she drinks it.

    How does excess glycerol effect TAG flux? I normally avoid eating anything close to bedtime or from the time I get up until I finish working out so I know my insulin levels are as low as I can get them during my workouts. When I started this routine back in late January it really made a difference and I started dropping pounds every week. I had a bad two month plateau when I achieved an early goal of 24 pounds off and stopped being as careful of how much starch I was eating but I am back on track now. My concern is the RE uses both Glycerol and free Fatty Acids from your blood stream after you work out. Will the glycerol used as a sweetener destroy the balance between the components and keep my efflux of fat from working properly? Does it matter when the glycerol is consumed compared to when I finish my exercise?

    Thank you for all your work, you are an inspiration and a blessing!

    Allen W.

    • Glycerol is brought into the fat cell via the GLUT4 transporter (just as glucose is). More glycerol would promote more synthesis of TG from FFA. So, in short, excess glycerol would promote fat storage (RE), rather than lipolysis (L).

  • Andrew

    Hi Peter,
    I am a long time reader – but a first time poster.
    I have conducted my own n=1 experiment and found something quite interesting. I lost around 10kg on a low carb/high fat/high protein diet over a period of 6 months. Having worked for a pharmaceutical company selling exogenous insulin, the whole aim of my eating regimen was to control by body’s endogenous insulin response to food – and open up the pathways to utilise fat stores.

    Here is the interesting part. After sticking to a low carb diet for 9 months, I regressed back to eating my previously normal high carb diet – and for a number of months did not enter into a state of fat influx. I decided to give my n=1 experiment extra weight by increasing the amount of crap food I put into my system – and still didn’t achieve fat influx for 2-3 months. After this time, fax influx did begin to occur.

    From the results I came to this conclusion. Over the 9 months of eating high fat/high protein, my system made some adaptations to use fat as its primary energy source – which then made it more difficult to enter a state of fat influx for some time after.

    I realise the reasons for this will be due to a complex mix of factors – however I have thought that a possible theory is that it is due to an up-regulation of hormone-sensitive lipase (HSL), adipose triglyceride lipase (ATGL) and CPT-1 that allowed my body to continue to use fat as energy – and therefore not store as much.

    Just thought this may be another component to the Fat Flux Balance!

    Also, thanks for this fantastic resource.

    • Andrew, if I had to guess, I would assume that your 9 months of carb restriction increased your insulin sensitivity (IS). So for the first 2-3 months of your foray into “bad” eating, your cells were still sufficiently IS to partition fuel favorably (i.e., oxidize fat as the highest priority). Eventually, this effect wore off.

  • Tim

    Hi Peter

    Thank you for a very educational post. Could you possibly elaborate on the flux of fat cells themselves? How is the number of fat cells determined in the body? As a person burns fat do actual fat cells eventually get destroyed and reduce in total number or does the fat cell persist and merely shrink in volume?



  • Cooper

    “Do they lose weight because they eat less? Or, do they eat less because they are losing weight?”

    This reminds me of something a heard on “The People’s Pharmacy” [NPR] when they had a guest doctor come on a talk about the different digestion pathways of glucose and fructose. One (glucose) was directly digested in cells, while the other (fructose) was digested by the liver. The pathway through the liver also produced hormones that increased appetite and decreased energy [and causing cirrhosis of the liver].

    So the doctor turned the common phrase “over eating and lack of exercise causes weight gain” on its head to “eating better increases energy levels and suppresses hunger causing weight loss”

    • Yes, I subscribe to that model. As I alluded to in this post, I believe the liver controls appetite, and it does so by sensing changes in energy availability.

  • Caitlin

    Dr. Atta,

    I would request that you also include more posts and research (and, if possible, clinical trials with your NuSI) on the neuroprotective properties of the ketogenic diet. I have come across some scattered evidence that a ketogenic diet has been an effective treatment for brain cancer in conjunction with standard treatments (currently, however, 99% of glioblastoma multiforme patients die within 2 years of diagnosis).

    Here’s an example:

    1.4. Other Clinical Applications of the Ketogenic Diet
    The fact that the KD is considered a proven therapy with relatively few adverse affects and wide clinical experience, particularly in children, led to recent studies investigating new potential uses for other neurological disorders [3]. One of the most intriguing and active fields of research is the effect of a high-fat caloric-restricted diet on the survival of brain tumors cells. Brain cancer cells have restricted metabolic flexibility and are dependent mainly on glucose metabolism. It is hypothesized that mitochondrial abnormalities impair the ability of brain tumors to generate energy from ketone bodies. Unlike normal cells, malignant tumor cells have impaired genetic adaptability due to their genetic abnormalities and, therefore, increased susceptibility to environmental stress, such as fasting or caloric restriction. The same genomic defects that are involved in the creation of brain tumors can be exploited for their destruction [3, 10, 11].
    In 1995, Nebeling et al. [12] reported two young girls with unresectable advanced stage brain tumors who had poor response to radiation and chemotherapy. They were treated with a KD and their response was remarkable, both clinically and according to positron emission tomography follow-up scans. Zuccoli et al. [13] described a patient with glioblastoma multiforme whose tumor, which is very malignant, improved on the KD. Surprisingly, despite the appealing efficacy of this treatment, no further human studies or clinical trials on the KD as a therapy for brain tumors have been conducted. Several laboratory studies in mouse and rat models have recently confirmed that inhibition of brain tumor growth is directly related with reduced levels of glucose and elevated levels of ketone bodies. Moreover, the KD was shown to reduce reactive oxygen species (ROS) in the brain [5]. Cancer cells need high levels of ROS for the induction of angiogenesis and the production of tumor growth factors [11], thus, through this mechanism the KD can be protective.


  • Richard

    Peter –

    You mentioned Ludwig’s JAMA paper. I love that study. However, I think the conclusion misses the most important point – and it’s a point you keep making.

    With the crossover design, each subject tried all three diets. As you noted in another post, most subjects had significantly different results from the different diets. Each diet was the best for some and the worst for others. In some cases the differences were dramatic, and for most subjects the individual differences dwarfed the average differences among the diets.

    Yet that was what the conclusion emphasized – how on average the low-carb diet was slightly better, etc. But who really cares about the average reactions? (Should anyone follow a diet that works better for the majority of other people?)

    The most important finding is that different people can react quite differently to these diets. Therefore, the key conclusion is that each of us should: (1) Experiment and find out which diet is best for us, and (2) follow it!

    (Which is what you keep encouraging us to do.)

    Thanks for that, and for another great post.

  • JJ


    Have just read Mark Friedman’s 1998 paper on fuel partitioning and food intake, I can’t thank you enough for referring me to his work.

    What I am really interested in is the relationship between simple carbohydrate/fat intake (dietary composition) on the body’s ability to metabolize fat efficiently and the change in this relationship over time (including the effect on individual fat and glucose fuel pathways). This could hopefully provide some insight into which type of diet different individuals are more likely to be suited to and how this could change over time.

    Is this a research area NuSI is likely to consider? Also if there are any of Mark’s papers in particular that you like, I would be eternally grateful if you could point me in the right direction. Otherwise, I will tried to read as many as I can find!

    • A recent chapter her wrote in 2008 titled “Food intake: control, regulation, and the illusion of dysregulation” is exceptional. I think the text is Appetite and Food Behavior. Go back to about 1976 for some of the real gems.

  • JJ

    Much appreciated!

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  • Hi Peter,

    Thanks for the great post. Just a few questions about ketosis, macronutrients and hormones as I’m thinking…

    1. You mentioned that being ketosis doesn’t guarantee weight/fat loss, my thought is ketosis means our body could be more efficient with lipolysis but if our pancreas/ liver is not yet fully adapted to digesting high amount of fat, the excess fat would still be stored as fat? Or is there a fixed amount of fat that a liver can handle at one time??

    2. Re your mention about ketosis and hormones, I am quite interested in the fact that your cortisol level has decreased and would love to hear your thought on low carb, leptin and cortisol.

    Reason is I have gone very low carb (unintentionally, <30g including alcohol consumption) since April, I lost about 4kg in 3 months and decreased 5k running time with increased energy until 3 weeks ago, I hit the wall and my period has been 2 weeks late (sorry for TMI) plus 2kg weight gain in 2 week! Could it be just the low-carb/alcohol combination that has overworked the liver or do you think women general need more carb than men in terms of fat loss, normal menstruation and better athletic performance?

    3. Weight loss – it baffles me as I no longer know how much a person should consume regarding to the macronutrients. Is it just about hunger and activities control and therefore we lose fat from consuming less calories? Just imagine not every Olympic swimmer can handle Michael Phelps' diet….

    Also, there are days I experience constant hunger albeit a 2500+kcal fat/ protein based diet and I'm a 5'6/59.5kg female but sometimes hunger stops at the moment I ingest some carbs. Do you think it's leptin and other hormones regulation that plays a more important role in weight/ fat management?

    It would be fantastic if you can write a post to discuss hormones/ hypothyroidism/ adrenal fatigue in the near future!


  • I love love love this post. Before you posted this I had to figure this out on my own. I have helped many people in my community lose weight with ketosis but have had trouble with post-menopause women. It will definitely be interesting to find out more about this. I’m also curious about your theory on the liver regulating appetite. I know there are quite a few bodybuilders now that use keto-diet to cut to 5% body fat. I personally get to about 10% and once I drop below that start feeling miserable. I’m also interested in why that is (shouldn’t I still be feeling alright since I have access to my fat stores?) Oh Peter, if you could only make updates like this everyday! You have no idea how much my curiosity tortures me! Thanks for the post. Look forward to the next.

  • Isaac

    Thanks for another great post, I was greatly looking forward to this post on the topic for a while. Would you consider making another diagram with the adipocyte and the arrows that includes small sub-captions for each arrow that correspond to it’s effect on that particular arrow? Does that make sense? Sorry if it sounds confusing, I’m just trying to figure out the best way to word it. Basically, have little sub-points that denote how an item increases/decreases that arrow. The list doesn’t have to be all inclusive/exhaustive but serve as a basic reference as each person tries to figure out what needs to be (or can be) tweaked to get a desired outcome. Obviously, I think one can figure this out from reading all the quality text you have throughout the blog but I always found it handy in biochem/physiology courses to be able to reference a figure (diagram) that can go along with all the text. Thanks again Peter, I always get excited when my e-mail prompts me about a new post!

    • Isaac, have it. Feel free to download a copy of the diagram and made the additions. I’m sure others would like it.

  • Joseph

    I tried to post this on your heart disease risk related article, but comments are disabled, so I hope you don’t mind.

    I appreciate that you can’t give out medical advice on specific cases, but I’m looking for a more general view. What is your take on low sodium diets for those diagnosed with congestive heart failure? If you’ve already written about this, I’d appreciate direction to it. I understand that NK means higher sodium requirements so I was just wondering your take. Thanks Peter

    • I think the best evidence today (which is modest at best) is consistent with this view — i.e., those with CHF are best avoiding sodium and reducing plasma volume.

  • Richard S.


    I agree that you shouldn’t “dumb down” these posts. Many of us love the detail, and we like knowing there’s good science in your work, even if we don’t always understand it.

    Still, having said that, I think we need to simplify the key message. There can be great value a simple truth, or a memorable sound bite.

    I was talking to some folks about my no-carb diet at a party last weekend. I could see their eyes glaze over as I went on about insulin resistance, etc. Finally, at one point I called the growing epidemic “carbohydrate poisoning.” The glaze vanished and the conversation perked up. They were all curious and wanted to know what I meant. I explained that over time, many people have a severe reaction to eating too many carbs for too long. For millions, the result is insidious weight gain and a host of medical problems including metabolic syndrome, T2 diabetes, etc.

    Then I asserted (I believe correctly) that the single most effective cure for carbohydrate poisoning and all those related ailments was to drastically cut carbs. To that they all nodded — not a word of disagreement. (If you are being poisoned, then of course the first thing you should do is stop taking the poison.)

    I know, you’re a doctor and a scientist. There may be reasons why “carbohydrate poisoning” is not be the best term. But to gain popular appeal and help millions of people get it quickly, we need simple terms and concepts like that one.

    What do you think?

    • I agree, but when I’m having the same conversation with people I refer to it as a “carbohydrate intolerance” — we all have different levels of this. Some (e.g., my wife) appear to have none. Others (e.g., me) appear to have a great deal.

    • Richard S.

      Well, you are the doctor. Plus this is the blog that changed my life when I found it last September. I’ve become a disciple of this movement and I have referred friends and family to your work. I wish I could do more, especially as I look around as see this growing epidemic.

      My background is in marketing, so perhaps that’s how I can help. It’s not polite to argue with someone on their blog, and “carbohydrate intolerance” might be more accurate from a medical perspective. But from a communication perspective, the word “intolerance” is nowhere near as powerful “poison.” (It will remind people of things like lactose intolerance — unpleasant for those of us who have it, but not a serious medical issue. It won’t kill me.)

      In short, when it comes to powerful messages and marketing punch, “carb intolerance” might get a 4 out of 10. Calling this an epidemic of prolonged “carbohydrate poisoning” is probably a 10.

      (Just want to help. I know you’ll do what you think is right.)

      • Richard, no need to change your views based on my mine. There is no “right” answer here. I don’t disagree with your point about the punch it packs.

  • Marrena

    I think you aren’t getting the full picture. I think that obesity, outside of a controlled laboratory setting, is mainly caused by nutritional deficiency. I am quite obese, and just recently found that my copper level was low. It didn’t show up as dangerously low on the blood test, just borderline low. I started supplementing with extra copper and was surprised to notice that my appetite has dropped dramatically. Before, I could have eaten plates of food without getting full. It was like the nutritional deficiency shut off the “full” feeling in my brain, I assume until I had eaten enough food so that the trace amounts of copper in the food were sufficient to keep me from dangerously low copper levels. In that sense, being fat kept me healthy. Now my appetite matches that of a normal person, and I feel overfull after a large meal.

    In other words, I think many of us have the obesity equivalent of scurvy. Even though we eat food, maybe even healthy, organic food, because our soil is so depleted (and the feed we feed our livestock is similarly depleted), most of us are living in a state of chronic mineral deficiency. The studies of healthy, thin cultures are of cultures that engage in small-scale farming with soil preservation, often up in the mountains where mineral levels are higher in the soil. I’m not sure if for everyone it is copper deficiency causing obesity, but I think it is something that should be researched.

    • Chris Adams

      this sounds like paul jaminet’s thesis…

  • Teresa

    Dear Dr Attaia,

    Like many others I ‘found’ you after your TED talk. At last, someone who makes sense – even if I don’t understand half of what you say on first reading (sometimes second & third readings also!). But please, please, don’t ‘dumb down.

    A quick question. Can you suggest a basic ‘palette’ of tests that you feel are useful/essential to have? You often mention a variety of blood, etc, tests in your blogs. Here in England my NHS doctor would keel over if I went and asked for them all! Obviously you, as a doctor, don’t have the same considerations to be made.

    If it makes a difference to your answer I’m 50, went through the menopause at 32 (no diagnosis made), and doubled my weight in the next two years (thyroid’s fine). I have kept a food diary for five years and average 1400 calories a day, but my weight remained constant within about 3lbs either side of 15 stone. I was fed up with being told to eat less and exercise more as I KNEW that wasn’t working and that something else was wrong. Your TED talk made perfect sense, so I gave up sugar. Result is that in three weeks I have lost 9.5lbs without feeling hungry.

    I hope you can give an answer to this question. Thank you so much for what you’re doing, we all appreciate it.

    • Teresa, I would suggest basic chemistry, but also include fasting insulin, TG, cortisol, CRP, LDL-C, HDL-C. If they can, I would also strongly lobby for apoB and ACTH. This assumes, of course, your doctor is comfortable interpreting the results for you.

  • Iris

    Hi! Thank you so much for all the information on this blog! I’m a newcomer here, and am delighted with all the learning I can do here!

    I’m pretty sure this is not the best place to ask this question, but I wasn’t sure where I should post new questions. I am really hoping you might write an article on fiber. I noticed that you are planning to write an article on “How can carbohydrate restriction be healthy if it means eating less fiber?”, but would you consider writing an article on whether fiber is at all necessary? I’ve always been told that fiber is an absolute must for regularity… but I would like to hear if you have anything to say about this assumption.

    Thank you, again, for such an illuminating blog!

    • I’ve addressed this in a few comments, but basically the “case for fiber” is pretty weak in cancer reduction and heart disease. There is a case to be made, however, for bowel comfort, though dietary fat, salt, hydration, and other factors play at least as great a role.

  • Lindsey


    From your site and the phenomenal Phinney and Volek books I read that the ideal range for blood ketones is 1.5-3 mmol/L. In one of their books, it shows a ketone level chart that shows a curve where levels over 3 mmol/L approach starvation ketosis and then at much higher levels, keto acidosis. Is there any literature that you’re aware of that looks at the effects of ketone levels above 3, but lower than the amount present during keto acidosis?

    I ask because after reading their books, I began a reduced carbohydrate diet this week and I’m only 4 days in. Being a geek, I bought the Precision Xtra and the (expensive) ketone strips to measure ketone levels and I’ve received readings of 5.4, 6.7, and 5.7 mmol/L. Is there any literature that suggest these readings should be harmless? Or is there incentive to add carbohydrates to achieve levels between 1.5-3? It’s referenced at the ideal range, so is there some knowledge that something negative happens above 3 mmol/L? Also is there any indication of what might amuse those heavy levels in such a short time period? I read that keto adaption takes a few weeks, and that it takes a while for blood ketone levels to rise above .5 mmol/L. I’m a 29 year old woman, 5 weeks post partum and breastfeeding. My carb intake hasn’t been super restrictive either as there isn’t much in the way of literature on ketosis and lactation. I’ve been eating dark chocolate, berries, fresh cherries daily. My ketone readings are a mystery to me!

    • DKA does not typically occur until BHB levels reach north of 15 mM. More importantly, they are virtually impossible to consider in the face of a working pancreas. Does seem odd, though. Perhaps your meter is not calibrated correctly?

    • PhilT

      You can get test solutions for the Precision Xtra to check it on both glucose and ketones.

      I think keto acidosis also requires high blood glucose, hence the meter flagging a high glucose for you to test for ketones. http://endoemergencies.org/sample-chapter.html

      http://www.anaesthesiamcq.com/AcidBaseBook/ab8_2.php says of starvation ketosis “The acidosis even with quite prolonged fasting is only ever of mild to moderate severity with ketoanion levels up to a maximum of 3 to 5 mmol/l and plasma pH down to 7.3”

    • Kathy

      Just a note that the expensive ketone strips are available through universal drugstore for $2 a piece. They come from Canada, so may be a longer delivery time. Am I allowed to say that on this site??

  • Dan Hackam

    Peter, I find I readily lose weight when I cut calories from my diet. I’ve done that in a few different ways – skipping whole meals, removing food items from meals, etc. I know you say it’s not about the calories but rather the amount of non-complex carbs that are in the diet, but it seems to me that consumption of very calorie-dense low carb foodstuffs could contribute to obesity. What is your opinion on that?

    (I can lose as much as 5-6 lbs in less than a week by doing this. I weigh myself reliably in a fasting state each morning after voiding. The weight is a key indicator for me to go hard on diet or ease up a little. Physical activity leading to expenditure of calories could be a factor here but I think much less so.)

    I respect and value your input.


    • Dan, it would be hard to imagine a scenario, outside of near or total starvation, where ones fat mass could change by 5 to 6 pounds in a week. My weight, too, fluctuates by this much at times, but it’s clearly movements in water (e.g., more or less retention due to inflammation resulting from over- or under-training, illness, travel, supplementation). An actual fat deficit of 2 pounds in one week is VERY significant.

  • George @ the High Fat Hep C Diet

    Some good writing here and a very useful discusion.
    Just a little addition to the hepatic DNL discussion; this is around 5% normally, but if the liver is diseased can increase to 25%. A lot of the glucose in such a scenario is not used to synthesise palmitate, but to convert palmitate to oleate; the supply of oleate means that palmitate is more likely to be converted to TGs, less likely to be oxidised. (palmitate alone cannot be made into TGs, is instead a PPAR-alpha ligand)
    Now, we have diets that produce NAFLD quite consistently these days; fructose plus enough linoleate to drown out the fat-burning signalling from DHA. So the rate of hepatic DNL is sneaking up.
    Info derived from this book: http://books.google.co.nz/books?id=T_Jwh1OmYV8C&printsec=frontcover#v=onepage&q&f=false

  • Gandalf

    Hi Dr. Attia!

    ‘ When I get back to the series on ketosis, I will address these, but for now I felt it was very important to put things in perspective a bit. Furthermore, I am convinced that it is not the ideal eating strategy for everyone.’

    Did you mean it’s not ideal for people/athletes doing higher intensity workouts? I noticed on my N=1 performance drop in NK. I can up fat as much as I want but running or biking over 80% max HR and longer lifting workouts suffer. I can’t get max performance like eith carbs and can easily overeat fats, hopping I’ll perform better my next workout. But it doesn’t happen.

    • No, I meant what I said. If I meant it’s not for athletes, I promise I would have said so. I understand what you’re describing, and experienced it for about 18 months. However, the effect is gone and I appear to have no difficult reaching anaerobic peaks I did 2 or 3 years ago. Adaptation seemed to take me a while.

  • Amy B.


    Thanks for yet another incredible post. I think I speak for all your readers when I say how much we appreciate the amount of time and dedication that clearly goes into the research behind your posts. If it’s a choice between more frequent but less in-depth forays versus posts that are fewer and farther between but so meticulously researched and detailed, I’ll opt for the latter every time.

    I’m fascinated (and simultaneously annoyed, discouraged, and inspired,) by the ever-changing theories and explanations behind obesity as science digs deeper. And even more so, as interested parties (yourself near the top of this list) continue to dissect the information. Thank goodness for curious minds that are *not* satisfied by simple and straightforward — but often INCORRECT — answers. I shudder to think where metabolic research as a whole would be today if no one had ever spoken up and said, “Hey, wait a minute…I *am* eating less and moving more. Why aren’t I losing weight?!” Or, “Hey, doc, weren’t my cardiovascular markers supposed to *improve* on this low-fat, high-grain diet you put me on? How come they’re getting worse?”

    One more point before I get out of your hair…
    I find it ironic that even among the people who visit your blog–and are presumably aware of just how unbelievably complex metabolism is–there are those who ask how many calories they should be eating, or how many carbs, fat grams, etc. If only it were that simple, folks. (No one ever seems to ask how much sleep they should get, or how much they need to calm down behind the wheel in traffic. Or how a day off, lounging in a park with a hammock and a good book could lower their cortisol levels. I *wish* it were only a matter of what we do or do not cram down our pieholes.)

    • Amy, thanks so much for sharing these insights. I’ve never intended this blog to be for the casual reader, and I do think it attracts the absolute smartest and most curious readers out there. From what I’ve noticed, those looking for bumper stickers don’t still around long. I mean, who in their right mind would read this 4,000 word post on fat flux if they thought they only needed to know how many calories to eat!

  • Kathy

    Peter, July 27th you commented to Dan that

    ‘it would be hard to imagine a scenario, outside of near or total starvation, where ones fat mass could change by 5 to 6 pounds in a week’.

    Jimmy Moore (livin the vida low carb) writes that he lost 100 pounds in the first 100 days of following the Atkins diet. At 2 lbs. of fat per week he would have lost 28.56 lbs. of fat. If you subtract a generous 15 pounds for water fluctuations (he was quite heavy at the start), you are still at 56.44 of unexplained loss. Are you saying that this weight would most likely have been loss of lean mass?

    I am new to the process and one of my fears is that I preserve lean muscle mass. I have been on less than 20 carbs for about 6 weeks now. Keeping my carbs consistant, I have just reduced my protein to move my blood ketones from .6 to .9 (so far) in an attempt to get into optimal ketosis of 1.5 – 3.0. I have lost almost 8 lbs. in the past 12 days while drinking the same amount of water (but I understand my body may handle the water differently).

    QUESTION: At what point should I start to be concerned that the loss is lean muscle mass? Also, this might be a silly question, but is protein the only variable in maintaining lean mass, or does the number of calories/fat come into play.

    As usual thanks,


    • I guess anything is possible, and I’m not sure what Jimmy started at, but it’s far outside of the norm.

  • Joe

    Hi Peter,

    Thank you for taking the time to share all of your knowledge. You’ve provided a great service for all of us searching for unbiased accurate information.

    I would like your take on someone adopting nutritional ketosis that is also dealing with a-fib. There seems to be conflicting information as to NK being harmful, causing more problems.

    • NK could make a-fib if electrolytes are not managed carefully, especially potassium and magnesium. I have not seen research around this, though, just a few clinical observations.

    • Debbie

      I have a friend who is a lone A-fibber. He controlled his A-fib with large – on the order of several grams of Mg, K and Na. He has also been NK for 4 years. The electrolytes are a major answer for him – when the electrolyte levels are low he goes into A-fib, high he does not. The NK does not seem to be part of the answer for him but he does not get altitude sickness and has more fun exercising when he is NK. He does not need as much water skiing above 11,000 feet and he only eats morning and night. He prefers the NK state. He has type 2 diabetes and Alzheimer’s in his family so he figures that besides the better performance at recreational sports, he may be slowing down the progression toward these conditions.

  • JJ


    I assume there are likely to be a number of factors which will determine how well an individual is suited to a ketogenic diet. I do not wish to get hung-up on a tenth-order term but there is one factor I would like to like to propose.

    I understand there are a number of studies which have shown individuals who sleep longer and/or who have better quality sleep tend to eat and weigh less (I have seen it postulated this has to do with leptin and ghrelin regulation). Before I completely changed my own diet I had significant problems with sleep and no matter how much (normally cereal) I ate often late at night, I always seemed to wake up in the middle of the night starving and felt completely exhausted the following day. This in turn could theoretically have resulted in me eating more and gaining more weight than if I had enjoyed better quality sleep.

    Do you think this is a factor worth considering i.e. how well an individual sleeps or if they have any difficulties with sleep (obviously there are a number of other lifestyle factors which influence quality of sleep itself)?

    As I noted above, I do not wish to overemphasise this effect particularly if it is a side-effect of some other much more important factor.

    • One should be a bit wary of these data. They are very associative and contain zero causal information. I can think of a dozen reason why those who sleep more, and sleep with better quality, have less adiposity, including but not limited to the ones you mention. That said, if you’re not sleeping well, absolutely resolve that issue! Hint: Vit D deficiency needs to be corrected.

  • JJ

    Apologies for not explaining, sleep quality has been much better adopting low carb diet.

    It’s amazing you mentioned Vitamin D as I recently had this tested due to my skin type, environment and occupation (often work in office basement) and I was found to be deficient.

    Points taken, just wanted to throw one in the mix for your view.

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  • Gabriel G

    Hi Peter,

    I have a question about keto adaptation. In one of your videos you mention that it takes about two weeks to reach a keto adaptive state. After you are keto adapted, if you fall out of ketosis because you ate too many carbohydrates on a given day, does it take another two weeks to return to keto adaptation?

    Also–I might be confused on this point–is there a difference between keto adaptation and being in ketosis? If there is, is there a reason to prefer being keto adapted?

    Thanks! Love your blog!

    • No, usually quicker. Adaptation probably takes longer than 2 weeks, also. The more I study this, the longer it appears to take for full functional adaptation. 2 weeks is generally good for day-to-day stuff, but not necessary high-end performance.

  • Amanda

    Hi Peter,

    This probably belongs in one of your posts focussing on sugar, but I thought you might find it interesting. It is Australian, out of the University of Adelaide and on Australian public television last night. The site below has the video segment (also downloadable) and the transcript:


    • Yes, quite interesting, isn’t it. Hard to believe this stuff is good for us.

  • Shankar

    Hi Peter, I greatly respect how you are educating all of us fatsos to lose weight. I have been on keto for around 2 weeks now and already lost close to 15 lbs. My main issue is this, I travel maybe once or twice a month for work. Can you kindly write an article on what you eat when you travel. It will be so very kind of you.

  • carolyn

    Present for you on your journey of self healing and discovery have you found Ray Peat yet? he’s the man for the man with an open mind – dr of physiology and what he knows about the cell is amazing! http://raypeat.com/articles/articles/sugar-issues.shtml ( been there done that and wish i’d found him sooner ) it is easier to listen to him if you google up some of the interviews he has done around the place. Goodluck with your studies.

  • JC Santos

    Thanks Peter, useful as always.

    I know you have this on your “coming soon” session, but I’ve been struggling to find the scientific basis behind it. Why protein overconsumption jeopardizes ketosis maintenance?

    Thousands of LCHF dieters make this “common” mistake (protein overconsumption) especially when starting the diet, given the common sense against fat consumption (seems you’ve incurred in that same mistake yourself) and results show that shifting a fraction of your caloric intake from proteins to fat (keeping protein intake around 1-1.5g/kg) enhances ketosis and weight loss.

    However, as per my understanding (please correct me if I’m wrong) aminoacids can only be processed into glucose in the liver via gluconeogenesis (GNG), and it seems that there are no indications that GNG is a supply-driven process (higher availability of protein, higher level of GNG).

    So what am I missing here? How do we get to the common “25-40% of our protein intake is processed as carbs” affirmation?

    Thanks so much in advance!
    p.s. sorry for jumping into something already listed in the “coming soon” section, but a single line (let’s call it a teaser) would be quite helpful…

    • It is GNG, and probably insulin, too. Protein also stimulates insulin release and insulin inhibits conversion of FFA to BHB.

  • Carol

    I have been reading HFLC diet information extensively for weeks; numerous different sites including many of your blogs, writings and responses to many posts your site. I also have read Gary Taubes 2 books (‘Why we Get Fat/ Good Calories/ Bad Calories).

    I saw something you wrote in one response (i.e.- “I had a coronary CT in 2009 which prompted this intervention.”), that has intrigued me to comment in hopes you will have some opinion on the best diet for me.

    I have a strong family history of CAD (father- MI @40, mother- hyperlipidemia/ MI/CABG early 70’s, brother- CABG early 40’s). Since my twenties, I have always trended with high total chol, LDL but High HDL that I thought I was controlling fairly well with healthy diet ( 🙁 ) of complex carbs/LF/ minimal processed foods) and exercise. I have always been active, thin ( BMI < 22 my whole life). This year, I've had advanced lipid testing twice since Jan. (2nd time after starting Niaspan after 1st test). Now, I am at a loss as to how to eat??? I have discordant results, Apo- B is better but still high, LDL-P normal. Unfortunately, I have Apo E 3/4.

    So, would you recommend the HFLC diet and see what my lipid response is to that? Or go to LCLF??

    Thanks for any input. Keep up the great work; my husband is on board with your diet (he's metabolic syndrome, which I'm sure will change with diet).

    • Carol, in all but the most obscure cases, LDL-P drives risk, rather than apoB, so if LDL-P (by NMR) is at goal based on your history, your doctor should be pleased. “At goal” will need to be defined by your doctor. For some people, that may be as low as <800 nmol/L, while for others it may be <1,200 nmol/L.

  • Carol

    I also meant to say I had a CAC with a 369 score!! (Which is why I was prompted to write you because of your post about your scan).

    Thanks Peter; you are doing great work.

  • Verna

    Hi Peter,
    I am on a diet which begins with 3 weeks of almost no carbs (less than 3g) and gradually adds back 10g per week to determine the optimal level for weight loss. The first week I lost 4kg (which I assume is water) and have since been standing still. I have tested my urine with ketostix, which also shows no ketosis. (in week 2 it turn slightly pink, but week three nothing). I have been sticking to this so strictly and am quite dissapointed that it isnt working. I also havent had any of the symptoms of ketosis. What could be the cause for not reaching ketosis? Should I start reintroducing carbs (10g) before I have actually reached ketosis?

    • I assume you mean 10 gm per day, not per week, right? My best guess is that you’re consuming too much protein. Very hard to be in NK with more than about 120 gm of protein in your diet.

  • Janaki

    Dr. Attia – Thanks for the blog, the right amount of information for people like me who are not doctors but crave the detail! I am a nursing mom, have 3 kids, and work as a management consultant. Needless to say, the first thing that goes out the window is my workout, against my instincts! My problem is, I am “pre-diabetic” with a history of diatebetes in my family. Over the last 5 years, I have tried every workout possible, every diet possible, but I lost a few pounds initially and stall. Being a vegetarian makes it harder too. Anyway, long story short, I need to fix my “pre-diabetic” state and have enough energy for my kids. I tried the higher fat, low carb levels, gained much from the increased energy levels, but lost 0 lbs. Also, I worry (not to my real question), if it is ok for my baby to be drinking breast milk while I am in ketosis. (The cave women did this right? They only ate meat !) So it should be ok for my baby? Please point me to something on this, or formulate your own hypothesis, I will take anything.

    • Janaki, the main goal should be to fix your IR first, and worry about what the scale says second. There are enough hormonal changes in your body right now, that weight loss may be tough.

    • Janaki

      What about breastfeeding while in ketosis? Do you think that ketones can get into breastmilk?

      • When I don’t answer a question, it’s usually for one of two reason: I’m not qualified to answer; the question is a request for medical advice, which I am legally not permitted to provided.

  • Wayne

    How do you fell about the association of Omega-3 Fatty Acids being linked to increase risk in Prostate Cancer?

    • I read the study a few weeks ago, and did not find it at all compelling. Read the commentary of Bill Harris on Lecturepad.org for a great review.

  • Sean

    Hi Peter,

    After losing about 80 lbs on Atkins in 2002, I am now trying NK again to lose weight. I abandoned it in 2003 for two reasons. 1) I started feeling really awful during workouts 2) It was freaking my wife out because she thinks that low-carb is really unhealthy. Over the past decade I gained all that weight back in spite of running three times a week, etc. etc. The high carb=high insulin response makes a good deal of sense.

    So I am back in NK again. It feels great! I took the “new” advice of supplementing my sodium and I have had little trouble with my workouts. However, my wife is still freaked out. I have addressed some of her fears, but she has two questions that I have not been able to answer:

    1) What of the loss of antioxidant benefits from a diet high in greenery? Is that just propaganda?

    2) What of the proportionally higher consumption of nitrates? I have found that many convenient low carb meats are filled with nitrates, and we are both worried about higher cancer risk. I know that it is possible to avoid nitrates while doing low carb, but it takes alot more work.

    Thanks, Peter. I appreciate the work you do, including your N=1 human Guinea pig experiments. It is truly meaningful.

    • Sean, not sure you need to abandon greenery. I’m pretty sure I eat more salad than 99% of Americans, though I’m in ketosis. That said, I don’t find the evidence compelling that dietary antioxidants do anything (vs. the effect being the removal of things that do harm).
      Ditto on the nitrates. That is, no need to consume them in any great quantities, but no compelling science they are as bad the propaganda would have us believe.

    • Sean

      Thanks, Peter. I suppose it is just a matter of challenging firmly entrenched beliefs through honest scientific inquiry.

    • Amy B.

      Hi Sean,

      Don’t forget that cholesterol is an antioxidant!
      Also: glutathione, the body’s “master antioxidant” is actually a peptide (made from amino acids) and you get more amino acids from protein foods than from, say, lettuce & spinach. 😉

      Colored fruits & veg aren’t the only ways to get antioxidants. I’m not saying whether someone would be better off including them or not; just pointing out that they’re not the only game in town.

  • Norm

    Hi Peter,

    First of all many congratulations and thanks for all your contribution to make people’s life.

    Before posting my questions I would like to briefly explain the context please. I’m 6ft, 32 years old male. The lightest ive been was 95KG that was 10 years ago. The average ive been is around. 110 KG. The heaviest ive been is 119KG that was a year ago when I started to count and restrict my calories to 1600 a day to lose weight. I did not restrict carbs or sugar (i had a sweet tooth). With this I managed to lose about 14KG during 5 months wit moderate exercise 3/4 times a week but during this I had been constatntly fighting with craving and hunger. I stalled at 105KG and started to gain weight upto 111KG. So I lost hope with calorie deficit approach. Four months ago I discovered low carb which lead me to read up on it including ofcourse Gary Taubes. Having been on low carb since then about 70gm per day I weigh 98 KG. A few weeks ago I dropped carbs to under 50gm per day. My calorie intake on low carb has been around 1800 a day that is without restricting them, ive to force myself to go over 2000 a day. Before starting low carb my TGHDL ratio was under one and my fasting blood glucose was 4.2 which makes me think probably im not insulin resistant.

    My Questions:

    1.Could it be that the weigh Ive lost on low carb is in fact due to eating less calories?

    2. If Im not insulin rgsistant, why have I been gaining weight?

    3. On low carb is it ok to have around 1800 calories a day that is without consciously restricting cals?

    4. My hunger has really gone down? Is it because of being in ketosis?


    • Thank you, Norm, for your kind words. I’ll try to address.
      1. Certainly. Caloric restriction often results in shift of dietary nutrients (and often reductions in all F/C/P), so could be multiple things explaining effect.
      2. Hard to answer without knowing more, but certainly as many as 30% of those overweight are NOT insulin resistant.
      3. Not sure I understand question. The calories are what they are.
      4. Possibly, or possibly because your liver is sensing no need to eat as much if you’re mobilizing so many internal stores of fat.

  • Alex

    Hi, great article, really helped me understand the fat flux biochemical fundamentals better.

    Sorry if this question is off-topic and a bit obvious but how does a high fat diet facilitate fat loss? i.e. why doesn’t the body use dietary fat preferentially over activating lipolysis? In other words, why would lipolysis be activated at all if dietary fat is ample. Sorry if this question is amateur hour but it’s been bugging me a while as something that sounds so simple but I can’t seem to find an answer to.


    • It probably does during a fed state, but a LCHF diet will still promote lipolysis outside of a fed state due to hormonal changes.

  • Dave

    Hi Peter,
    I was wondering a couple things. Have you tested testosterone levels pre and post ketosis and have you noticed any increase or decrease in sex drive pre and post ketosis?
    Thanks for your time,

    • Yes, my testosterone rose quite a bit (about 250 to 450), BUT there is a huge confoudner, so I have no idea if it was ketosis per se, or the the reduction in my training volume. I’ve been very low my whole adult life, and looking back assume it was due to a combination of excessive exercise and poor diet.

  • Norm

    Thanks Peter for a prompt response to my previous post. If you could kindly shed some light on the following please :

    If Insulin is the FAT regulator, why some overweight people are NOT insulin resistant?

    On low carb, am I under eating by taking around 1800 calories per day as Ive to force myself to go over it? ( im 6ft tall, male, 32 years and trying to lose weight).

    Many thanks

    • Any number of factors, including genetic of course, that prevent negative fat flux. Other hormones are often part of the problem, such as androgens, glucocorticoids, and thyroid. Basically, if the HPA axis is off, fat accumulation can and often occurs.

  • Jeff

    With a few weeks between major cycling events I decided to experiment with going from low carb (approx 100g/day) to VLC <20g/day also keeping an eye on protein 100g day.

    After 12 days I've noticed a drop in peak power.

    After the first few days intervals 2×20@80-85% FTP (275 watts) felt normal, the second day of intervals 2×20 same watts felt difficult but I suffered through, the third day of intervals (day 9 VLC) I was unable to complete the interval session. Endurance power was unchanged at 200-230 watts for 2 to 3 hours.

    Yesterday after a recovery day I had a lot of difficulty with a harder session 5min@285watts/30sec VO2Max/5min@285watts two sets, the first set was hard between sets I drank approx 8oz UCan 15min between sets. The second set I was unable to finish the second 5min.

    Do you have any insight into performance at the beginning of keto phase and performance, I'd like to gain the metabolic flexibility you describe. Can I supplement with more carbs on days with difficult workouts or races and still reach ketosis or do I need a sustained 2 to 4 weeks VLC. Will the peak power come back once I reach full ketosis.

    As a track racer and TT/Individual Pursuit specialist I will need that peak power as well as being able to stay at FTP for up to an hour at a time.

    Should the Ucan supply me with enough glucose to complete difficult workouts like I described? or will I need more carbs than UCan alone can supply.

    What would be a strategy for "carbing up" prior to a diffiult training or race day if that is even possible and still reach ketosis

    FYI on the test strips I still only show trace amounts of ketones, after approx 12 days I've noticed no change in weight or %BF always between 155-160 lbs, 5ft 9in.


    • Jeff, I experienced this exactly. Similar numbers, too. In 12 weeks I can fully adapted aerobically (and actually made huge gains), but — and I hope you’re sitting down — it took me probably 18 months to exceed the anaerobic performance I had prior to ketosis. UCAN will definitely help, but I still think the cells need to re-learn how to access which fuels, and when to do it. Of course, my experience says nothing of what yours might look like. You may adapt quicker.
      BTW – based on your last comment you may have a different issue. That is, you may not be in ketosis at all. You may be in “no man’s land” — too little glucose and too little BHB. First step is counting your protein intake. That’s usually the issue.

  • Joan

    I’ve had my brain in your blog for 3 days now. We threw away 3 lbs of sweets from our cupboards this evening. We – my husband and I. The last 7 months, I have done nothing else but try to find out why I am broken. Because I’m ill. I have always been ill.

    I’m fat (obviously). My mum is fat, my grandmother was fat, my brother is fat. They are not American and neither did any of us grow up with processed food, fizzy drinks or any of the “sins” that should’ve caused our bodily mishaps. Faremers, hardworking, traditional, poor. ALl that jazz. Brother, mother, maternal grandmother all have Type 2 diabetes. I don’t. Not yet. But I have been a zealot with my diet since January 2009. I lost over 50 kilo (How much exactly, I don’t know, ‘cos my scales couldn’t weigh me to begin with) and landed on 64 kilo. Haven’t been 64 kilo since I was in 3rd grade! Anyway, I say “landed” because no matter what I did – HA! – yes, I know now I that I didn’t do the right thing – but I did as I had been told would solve ALL my problems in life – and suddenly, the weight would not budge. Not a gram. I ate and eat 1200-1400 calories a day and was as active as I could be with my fibromyalgia, PMDD, and the masses of other pathetic health issues I was SURE would go once the fat had gone. Needless to say, they did not. In fact and to my surprise, it got worse. I got worse! Then I fell pg. And BAM! Still on a 1200-1400 calories diet, I gained 40 kilo! That’s not possible. It’s impossible. That’s NOT how the body work. Calories in, calories out. You must be lying. You are eating on the sly. You’re not “doing it right.”

    During my other two pregnancies and on an unrestricted diet (whilst morbidly obese) I gained about 7 kilo. That’s not even the weight of the pregnancy itself! So WTF? (Pardon my language).

    My math had broken! My math IS broken!. Since giving birth and still, I remain stuck at 86 kilo. And not just that – I am now so ill I can barely lift my baby to change him.

    My NHS doctor… well, he suggested a thyroid problem. Tested my THS and as that came back normal, sent me away with a prescription for morphine and antidepressants. I declined. I paid for private doctor. He also tested my thyroid and found my T3/reverse T3 shockingly low. But he didn’t know what to do with this information – was scared of the Standard Practise, which looks at THS, T4 and T3 only and suggested I diet and exercise to get better. He actually said that as a doctor, his must important mantra was “do no harm”. So, I guess, in my case, it prevented him from doing good. I’m still looking for a doctor. Maybe. Or maybe I can go it alone like I did with my first (but flawed) weight loss.

    But it’s my hormones. And I fear I’m born with a vulnerability. And that environmental factors and “good” but oh so wrong diet have exacerbated my situation. And I feel like I’m staring into the abyss. It feels insurmountable. For several reasons, but mainly because I have never – and I mean never – had support from any health care professionals I have been in contact with. If you’re fat, you’re fair game. Dysmenorrhea and menorrhagia? It’s ‘cos you’re fat. Feeling blue? It’s ‘cos you’re fat. Aches and pains? It’s ‘cos you’re fat. Lose weight, and you’ll see – all will be good. Never even once did anyone suggest that the reasons I’m fat might be the same reason as is causing the other problems. I didn’t even realise fat could be a symptom. I believed it was My Fault. And I have spent the 33 years Hating Myself. What a waste! What a sad, sad waste.

    And now that I know better, I feel more alone than ever, because I realise that now, the support from the medical professionals is further away than it ever was. Now, I’m one of the Crazy People, who believe in Crazy Theories that go against Recognised Science. I’m on my own. Well, I’m not. I have you and the other crazy people on the internet to back me up. And of course my never faltering and lean and eats what he likes husband, who supports me so much.

    He’s a good man. He was always confused by my size. “But you hardly eat anything.” he’d say even when we first met. “You can’t be big because of your diet. There must be something else going on.” He likened it to dark matter. Scientist knew it was there long before they could prove it because of the way other elements of the universe were acting. Dark matter had to exist. And I guess all these years, we’ve been looking for My Dark Matter. The thing that was “breaking my body-math”.

    Being fat sucks. Not because of the health implications. Nope. It’s because of the social implications. I can’t eat an ice cream in public or I will get comments and *tut-tut*. I can’t go shopping without ppl peering at my shopping choices. What they’re trying to glean from them, I’m not sure. They’ll see nothing but organic-fairtrade-food pyramid-compliance. In fact, bar a few years of student life, they would have never seen anything but organic-fairtrade-food-pyramid-compliance.

    I feel a little betrayed. Lied to. But my eyes are being opened. It hurts a little, all this light suddenly coming in. It’s pretty hardcore stuff. I’m struggling to compute it all. I’m sure I’ll be struggling even more to implement it. But I’m pretty fierce and I’m also immensely angry, and there’s nothing quite like anger that can make people do what they didn’t think they could!

    But actually, what I came here to say was thank you. You are saving lives of that I am certain. I’m hoping mine will be next.

    • George

      That sounds terrible, I hope you make some progress soon. Have you seen http://www.perfecthealthdiet.com? Maybe you should start with his advice – be well nourished. Make sure you’re getting all the right nutrients in appropriate quantities.

  • Joan

    Sorry for all the spelling mistakes. My brain, being part of my body – just doesn’t work very well any more. I used to be an accomplished academic. Now I can barely manage a comment on a brilliant blog. My apologies. Hope it doesn’t detract from the dishevelled ramblings too much. I started my period today. Does that count? You know what they’re like, those hormonal women! 😉

  • Jeff

    Thanks for the respomse, i have tried to keep protein under 100g, i did read both Phinney/volek books, trying to get my fat from butter, cream, avacados, olive oil. I haven’t been eating excessive amounts of meat usually one serving per meal, 2 or 3 eggs for breakfast, yogurt once a day.

    I seemd to have most of the other classic symptoms of ketosis, lots of trips to the bathroom,appetite supression. I also have some muscle ache that i dont attribute to my current training load.

    My experiment my have to wait for the winter off season but even that is very short for me usually only 4 weeks between cyclocross nationals and beginning training again.

    In your opinion can an athlete better utilize fat as a fuel source without reaching ketosis?

    Also you said over a year ago if you were training for the TDF this wouldn’t be your nutritional plan, would you change your mind about that now? Do you think something like that could be done? Bicycle racing is such a different animal than triathlon or ultra endurance running.

    • In the end, unless plasma levels of BHB are elevated (0.5 mM is the bar minimum, but the real benefits don’t really kick in, especially for exercise until you’re in the 1 to 3 mM range), nothing else matters. As far as TDF, complicated question I can’t address at this time.

    • Jeff

      Peter, sorry for the stupid question, how are you measureing BHB, with a blood glucose meter? Any recommendations for what kind you like?

      • Precision Xtra measures both glucose and BHB (different strips, of course).

  • Norm

    Hi Peter,

    Would a LCHF diet reduce insulin sensitivity ?


  • EdR


    I saw your you-tube “Peter Attia: What if we’re wrong about diabetes?” I have T2D and am holding my blood sugar in check with diet and exercise (no drugs). If there is any way I can help in your efforts, please let me know.


    • Thank you so much. Please visit NuSI’s site (nusi.org) for information about what we do.

  • Damon Amato

    I’ve seen you mention that too much protein can prevent you to be in ketosis. I weigh 210lb and have been at ~60-80g protein/day and <30g carbs and 140-170g fat for two weeks and am in no mans land. Blood ketones were .2mmol/L post prandial today. Is that really still too much protein? It's spread over 2-3 meals during the day.

    • No it should not be. Typically up to 120 gm or so is fine for males. Strange.

    • Sean

      Carbs can be hidden in many, many places. They often are not on labels. Some spice mixes are really high in carbs. Even sweetener packets have about a gram of carbohydrate each in them.

  • Damon Amato

    I’m not sure if that makes me feel better or worse. I can’t really find much research as to why that would happen. Are you able to consult hypothetically? No meds or conditions. I can’t think of a single reason why I’m such an outlier.

    • I hear you. Without doing a detailed assessment of everything you’re eating, including a measured assessment of what you’re eating and what kind of activity you’re undertaking, I can’t really speculate.

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  • Todd Williams

    Love this site and the work you do. I’m very excited to see what you (and Taubes) come up with in the next few years. My question is about insulin resistance: It seems to me that being resistant to insulin is a good thing–your body is less willing to respond to the signals from insulin to store fat. Am I just interpreting this wrong?

    • Initially the body may “think” this, but ultimately, this mechanism is more problematic.

    • Richard S.


      Here’s what I know (or think I know) on this topic:

      In this video, Dr. Tara Dall explains the problem of being insulin resistant: http://www.youtube.com/watch?v=qL6aXRwuMgg .

      In other words, after eating carbs your body HAS to bring your blood sugar down (or you’re in deep trouble). So your body will keep producing insulin until your blood sugar drops (that is, unless one is diabetic and cannot produce enough insulin anymore, in which case one needs to get it externally). In the insulin-resistant person, their blood sugar often drops too far and the body’s self-defense mechanism kicks-in to bring blood sugar back up to normal. It does that by making us hungry — especially for carbs.

      (In my case, most days I could go until supper without being hungry and without eating. But after supper I would have all the symptoms Dr. Tall talks about — I’d feel tired, light-headed, and have cravings, especially for carbs. That would start just an hour or so after eating. Why? My body was producing too much insulin after the meal and dropping my blood sugar too low.)

      How did some of us get this way? Most people think genetics has a lot to do with it. Many of us also think a lifetime of over-exposure to carbs is a primary cause of insulin resistance. (Our bodies are trying to defend themselves again, in this case from all the carbs.) I’ve started to call it “carbohydrate poisoning,” though a better term might be acquired carbohydrate intolerance.

      How do you cure it? Cut out the carbs as much as you can. (Dietary fat alone creates no insulin response, and protein creates a little, though it is different for other reasons.) Without the carbs, one can finally get off the insulin rollercoaster. And over time, it seems that some of us can recover and be less insulin resistant.

      At least, that’s what I understand now. I hope that helps!

  • Colin Chambers (CellYourSole)

    Fascinating article Peter. Thanks for the in depth explanation.

    I’m particularly interested in exercise and it’s effect in regulating insulin. Particularly it’s role in making cells more responsive to insulin reducing the amount of insulin required to trigger the required responses of sugar transport. In turn this requires a smaller insulin response by the body to achieve the same result. I explain it more at http://cellyoursole.blogspot.co.uk/2013/05/heart-disease-and-diabetes-move-out-of.html. That’s my understanding so far. I was focusing on regulation of sugar. Not fat. I had forgotten this role.

    Promoting activity is important to me because the food and activity situation has been turned on its head in the last century. Activity used to be normal and food used to be scarce. Now it’s food that’s everywhere and activity is scarce. The effect is more complicated than is generally realised. Obviously more calories being consumed than burnt is a result but it also seems to me that we’re less able to recover from the challenges of the day. Activity forces our body to maintain itself and thus recover properly each day. Hence activity forces cells to listen to insulin by creating a need to regulate energy properly.

    That’s a quick overview of where my research is leading me. I’m wondering if you know much about exercise and insulin and it’s wider role in fat regulation. It’s mainly viewed simply as a process to burn calories. I feel that’s simplistic. Few seem aware that it can directly affect a cells ability to respond to insulin when present. There are many other effects but that seems most relevant to this post.

    I like your style and thoroughness. Activity doesn’t seem to get due attention in medical circles, nutrition seems to take priority. So I’m interested to hear your views. Am I misinterpreting the evidence? Maybe you’ve got a good understanding on exercise and it’s effects. Maybe I’ve added another angle you can look at. Particularly something people can do for themselves without popping pills.


    • Exercise, certainly if strenuous, blunts the insulin response somewhat, but the real drawback of hyperinsulinemia during exercise is the inhibition of lipolysis.

  • Mathieu Gagné

    Nice article as usual!

    I was reading about the resveratrol researches in past years after watching a David Sinclair talk this week. He was explaining how resveratrol mimics caloric restriction impact on longevity by activating the sirtuin gene and I wondered if this was recurrent with Ketosis? It seems they are developping analog drugs that would be more powerful than revesratrol and it seems a big deal. From what I understand, this gene is implicated in the signal to produce ketone? I’ve found those 3 papers explaining it a bit, but I thought you might have an interesting opinion on that subject:

    “Sirtuins: a conserved key unlocking AceCS activity”
    “SIRT3 deacetylates mitochondrial 3-hydroxy-3-methylglutaryl CoA synthase 2 and regulates ketone body production.”
    “Effect of Dietary Macronutrient Composition on AMPK and SIRT1 Expression and Activity in Human Skeletal Muscle”

    In the last paper, they conclude in the abstract: “Our data indicate that a relative deficiency in carbohydrate intake or, albeit less likely, a relative excess of fat intake even in the absence of caloric deprivation is sufficient to activate the AMPK-SIRT 1-PGC1? energy-sensing cellular network in human skeletal muscle.”

    Do you know if there was any animal longevity experiments on ketogenic diet similar to those who study caloric restriction?

    • Caloric restriction is tricky, but by definition it restricts more than just calories. It reduced absolute levels of all macronutrients.

  • Sabine

    Not losing weight on a strict ketogenic diet?

    Could the actual problem be a lack of patience?
    My own weight loss was not without many plateaus, and some necessary adjustments (hidden carbs and sugars, longer breaks over night, etc.). Sometimes nothing happened for months, no weight loss at all, and I thought I had reached my set-point. But, as I felt so much better overall, i continued eating ketogenic. Suddenly, I would enter another brief weight loss phase, and so on, until I stayed around 120 lbs for the last couple of years, less than I weighed as a teen.
    ( I am also watching my omega 6 intake, as this seems to have some effect on my well-being.)

    Could it be, that the body, at least the bodies of some people need more time to regenerate and adjust? Are the studies too short? Do people give up prematurely, and do we come to the wrong conclusions because of this?

    The situation reminds me of a paper by Chris Masterjohn, where he discussed the effects of omega six laden vegetable oils, and that they increase the incidence of cancer. This fact was missed, because the effect starts to show up after about 7 years, and even the long-term studies only went for about 5 years.

    Would the effectiveness of a ketogenic diet (without cheating or inadvertent mistakes) be universal for humans, IF they would stick with it long enough?

    • Dan

      Sabine, I thoroughly agree with you. Patience and persistence are the appropriate response. It may take over a year to thoroughly normalize bodily homeostasis after beginning a ketogenic diet. It certainly took that long for me. And there are clear oscillations – both up and down – in weight that tend to come and go for weeks at a time. People do not become obese overnight and it is a little hard to expect they will become lean within the same timespan. Most overweight/obesity is a gradual process spanning years.

  • Anthony V

    Such a great read and very easy to understand thank you. I just have one question that may or may not be able to be answered in a simple response. I have recently been consuming less than 30g carbs, about 1.5g/kg of protein, and 75% of total calories from fat a day. I am much leaner for sure. I understand that by lowering my carbs I am lowering my DNL, although I am still a little confused as to how consuming a high % of calories from fat (about 250-300gm/fat/day) is “helping” (if at all) with my fat efflux? (sorry if you already answered this in a previous post or in this post)

    • If you kept protein and carb constant, and lowered fat intake, you would likely get leaner. The question is, could you do that without increasing your appetite significantly?

  • Norm

    Hi Peter,

    I would really like to know your take on gynechomastia? Is going under the knife only option? Would appreciate your guidance in this regard.


    • Not until you have your estradiol checked! You have this because you’re shunting too much testosterone into estrogen. Surgery is not the treatment for that.

  • Norm

    Ok, thanks. What do I exactly ask my GP to do then please? Would really appreciate your guide on going about fixing it please.

    Many thanks

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  • Tom Michels

    Is there some reason the blog post is blank other than the comments and discussion?

  • Gabriele

    Dear Peter,

    I’ve been in ketosis for almost an year now and have been experiencing hypothyroidism and high cholesterol (only TC is “relatively” high at 313 while TG=50 and HDL=87). I started with a paleo low-carb diet and then shifted to a very low carb diet (the only carb I ate for 7 months was half of an avocado a day which is actually a fat more than a carb). This helped me a lot to fight my SIBO but at the same time my thyroid levels dropped. My problem was with the conversion from T4 to T3 (and tired adrenal glands). So I first supplemented with T3 only to balance rT3 and FT3 and then (after 3 months) I used desiccated thyroid. During the first 3 months I added back into my diet some carbs (sweet potatoes). It was a “trauma” for me. I’m thin (whatever I eat), but the sensation of being in ketosis (which you described perfectly in a talk I found on YT) is addictive.

    I see that several low-carbers find their FT3 to lower without any hypothyroid symptoms. It seems to be a good sign, meaning your engine needs less fuel to burn. But in my case, FT3 wasn’t the only marker to be out of track plus fatigue, dry skin, digestive problems, insomnia and so on.

    Now, that my thyroid is OK, I’m back into ketosis. I would like to know what are your thoughts about this. I mean, do you think what happened to me will happen again if staying in ketosis due to some “genetic” reasons or is there any way to prevent hypothyroidism while staying in ketosis?

    Thanks a lot,
    Gabriele from Italy

    • It’s a good question. There is no doubt that TSH, T3, and T4 can and often do change with dietary change. Most of the time these changes in numbers are not accompanied by clinical symptoms (the only ones worth treating). In your case, clearly the symptoms needed treatment. I don’t know the answer to your question, though.

  • Norm

    Hit Peter,

    I read somewhere that being on low carb diet does not give proper fasting blood glucose levels, to get actual fasting blood glucose level one should be consuming at least 150 grams of carbs for 3 days at least? My fasting glucose levels were 93 mgdl today (ive been on low carb around 50 grams per day since April). After 2 hours of my break fast of 3 eggs omelette cooked in butter, whole roasted chicken leg, 15 grams of roasted salted peanuts and 8 grams carbs worth of dark chocolate my blood glucose level was 106 mg/dl.


    • Certainly correct as far as OGTT, and maybe true as far as fasting glucose (i.e., it may be artificially elevated). Peter D (Hyperlipid) wrote a nice piece on this phenomenon, which I linked to in another comment asking about this point.

  • Jim Layton

    Great information on your blog–but what about cheating with the sugar alcohol bars touted by Atkins. Will they influence any of the hormonal pathways that will ruin an otherwise strictly compliant diet. They taste too good to be helpful!

    • Different for everyone. I don’t like those bars personally, though I do (especially on long bike rides) really enjoy Quest bars, which contain small amounts of alcohol sugars. I seem to tolerate these very well, as do others.

  • Timothy

    Great article! So does this circumstance actually kill off fat cells or just reduce their mass? Like do they experience apoptosis?

  • spar

    Peter, would you suggest to supplement with selenium, iodine and maybe liver on Keto?

    • Salt seems sufficient for most, plus or minus magnesium.

  • Jack

    Hi Peter,

    I recall reading from Dr. Atkins’ book that ketones that are not utilized gets flushed out through the kidneys and ends up in urine. Maybe this is the reason people lose weight while on ketosis. Would this mean that ketone bodies don’t undergo RE?

    Great blog!

    • I’ve measured this, as have several others. The amount is trivial. In 24 hours of collected urine, I excreted less than 1 gm of AcAc (about 3 kcal worth).

  • TFrey

    I recently started an adult epileptic on a ketogenic diet. She has been intolerant of multiple meds secondary to side effects and, as a consequence, has had refractory, catamenial epilepsy. She is a urology nurse and has ready access to urine test strips. She has been following her urine ketones which I understand to be a less desirable method. Since it is available to her, I think we are going to judge things by this and her clinical response. My question has to do with her spilling bilirubin (“moderate”) into her urine. I haven’t been able to find information on this. Is this to be expected? She is largely vegetarian if that matters (it is a taste preference so she hasn’t had a problem adding some animal products to her diet). I appreciate any light you can shed on this. Thanks in advance.

    • Not sure, but certainly would look at serum bili. Possible Gilbert’s if mildly elevated with no obstructive etiology.

  • Norm

    Hi Peter,
    After being on low carb for 4 months, I checked my BOHB for the first time today. After waking up 0.4 mmol (technically out of kerosis as it is below 0.5mmol ? ). Before dinner im at 2.1 mmol. I can clearly tell from my brain energy when in ketosis which I experience from mid morning till mid night.

    Could I be in and out of ketosis so quickly?

    Am I doing any harm to my brain when not in ketosis but on still under 50/60 grams of carbs?


    • Harm might be too strong a word, but many people (though not all) report feeling tired or sluggish in this setting. I was/am definitely one of these folks, which is why I termed it “no man’s land,” if one is in this state for days on end. Being here for hours (which most people are from time to time) is usually unnoticeable.

    • Hemming


      Do you mean that you don’t have ‘enough’ ketones in your body to fuel exercise and/or mental activity but at the same you don’t have ‘enough’ glucose to fuel it either? Should you eat more fat to get more energy in this situation?

      • If transient, not an issue. If ongoing for days, best to get in to NK or start eating more CHO.

    • Hemming

      Peter, thank you for the reply. As a follow up to that. Is it possible for a lean person (some % body fat threshold for simplicity) to not produce enough ketones even though they eat limited carbs and protein but not enough fat either(the relative amount of fat might be high but the absolute is not)? So that there is neither an endogenous or exogenous source of fat and this would prevent them from producing enough ketones to not end in “no-man’s-land”

      • Possible, but I have not seen this studied. The issue certainly would not be a lack of fat — even someone with 5% body fat has plenty — it would be more about homeostatis. Starving (lean) people still produce ketones of 7 mM.

  • spar

    Peter, What do you think about inefficiency at recycling vitamin C from its oxidized form, dehydroascorbic acid or DHAA – leading to Kidney stones?
    Would you advise against Vitamin C supplementation on Keto?

    • I’ve never seen evidence for the benefit of supplementing vit C, E, or A in any state except extremes.

  • Meirav Heim

    Thanks for this post. As with most of your longer and more complicated posts, I’ve read it three times already, each time getting more comfortable with the terms and procedures. It makes a lot of sense.
    I’d like to ask you to write about fiber and complex carbs, as I’m not sure what to make of those. I’ve used the searched and looked at the upcoming topics list, and couldn’t find it. If you have a good reference to information on the subject in the meanwhile, I would be grateful.
    Thank you and all the best!

    • DO


      Colpo has written an interesting piece about fibers (actually whole grains but fiber is part of the topic) at 180 degree health:


      In any case, my n=1 is this: I don’t care much about fibers, but I do eat foods with resistant starch, which is well known for its health benefits.

      • AC does a great job on this one, hitting most of the high points.

  • Norm

    Thanks Peter.
    How many grams of carbs would a brain need (in addition to the glycogen produced by the liver) per day if not using ketones?
    If you wanted to increase carbs intake which ones would you go for?

  • Jennifer

    Hello Dr. Attia:
    I am very interested in your ideas and quite impressed with your ability to elegantly deliver complex information in a way that is readily comprehensible. I do have a couple of questions, however, and did attempt to search for them before I asked. I will apologize now if the subject has been addressed and I was unable to locate it. What is you view on trans fats? Do you think that the process of hydrogenation alters the way the body processes this fat?
    Thank you

    • Trans fats occur in nature, of course, but in relatively small amounts. I think the question you’re asking is, “What about large amounts of trans fats?” Well, the only way to get large amounts of trans fats is when they are added to highly processed junk food. So in reality, if one is avoid garbage food, one will not be confronted with much trans fats. The data implicating trans fats are largely cohort / observational, so I have no idea if they are harmful on their own when consumed in large amounts. The good news is we don’t actually have to for any reason.

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  • spar

    Hi Peter,

    How long after a meal do you test for Ketones? or is it best to just test it in the morning once a day? When you do get into no man’s land as you call it, would MCT oil or Leucine bring you back to Ketosis faster?

    • Completely dependent on what I’m looking for. Best “baseline” is AM fasting, but sometimes, if I’m trying to investigate something, I might check several times per day. To your last question, MCT, or better yet >98% pure caprylic acid can help.

  • Norm

    Hi Peter,
    1. Just to follow up gynachomastia issue, from my blood results I got these levels:

    THS 1.2 mU/L
    Oestradiol 111 pmol/L
    Prolactin 214 mU/L
    Testosterone 19.7 nmol/L
    Cortisol 247 nmol/L.

    2. Being on HFLC diet for just over 4 months my LDL-C has increased from 3.93mmol/L to 5.59mmol/L, HDL-C has increased from 0.97mmol/L to 1.04mmol /L and my triglycerides have decreased from 0.9mmol/L to 0.8mmol/L. Increase in LDL was expected but i’m wondering if improvement in HDL and Trigs is good enough in 4 months time? My CRP has increased from 2mg/L to 3mg/L and my ESR is 19mm/h, isn’t HFLC diet meant to decrease inflammation?


  • BobM

    About three months ago I switched from a low-carb diet to a keto genic one. It was a time of beacon, butter and barbecue and the weight came off quickly. I lost 28 pounds in 10 weeks. At that point, I had a blood test. When the results came back, I saw a slight improvement in the Trigs and HDL. But my LDL more that doubled to 162.

    This got me thinking and wondering. You mention in this post that fat cells contain triglycerides. Does it also contain cholesterol? By burning all that fat in a relatively short period of time, am I releasing additional cholesterol into my blood stream that will have to be cleared?

    Thank you in advance.


    • Short answer is “not really,” at least not in the way that I think you’re asking. (Technically, all cells contain cholesterol, but this is a different story.) But it is often reported in weight loss that LDL-C (and maybe even LDL-P) rise, though unclear for how long.

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  • Anna

    If ketosis increases testosterone, could that explain my increase in acne since being on a ketogenic diet?

    • I have no idea, but I would not consider that hypothesis #1.

  • Gary

    Hey Pete,

    I know this is an old topic here, but I thought this question relevant and I’m sure others would be curious as to your response. I saw a discussion on a low-carb facebook page where someone argued that fat can’t make you fat because it doesn’t evoke an insulin response. The person was lambasted for saying that, and a lot of CICO/Loe Fat folks said she was wrong because of a compound called acylation stimulating protein (ASP) which stores dietary fat in the fat cell with ZERO rise in insulin levels. In other words, fat can be stored without insulin. I’ve yet to hear you talk about that. They were saying that it proves that the reason low-carb diets work is because of the lowered caloric intake and had nothing to do with insulin itself. This post here (http://www.bodyrecomposition.com/fat-loss/how-we-get-fat.html) was also used to make the argument. Here is an excerpt of the article, which basically makes his argument for him.

    1.) Carbs are rarely converted to fat and stored as such
    2.) When you eat more carbs you burn more carbs and less fat; eat less carbs and you burn less carbs and more fat
    3.) Protein is basically never going to be converted to fat and stored as such
    4.) When you eat more protein, you burn more protein (and by extension, less carbs and less fat); eat less protein and you burn less protein (and by extension, more carbs and more fat)
    5.) Ingested dietary fat is primarily stored, eating more of it doesn’t impact on fat oxidation to a significant degree

    Could you comment on:

    1.) ASP and the claims that reducing insulin doesn’t lead to fat loss because ASP can, and does do teh same thing.
    2.) The link above from bodyrecomposition.com where the author links studies that supposedly, “prove” that low carb only works because of caloric reduction.

    I know you are busy, but I think these are important questions, the first one especially.

    • Gary, the folks on both side of this are a little bit right and a little bit wrong. This is why I wrote this post (i.e., to avoid long debates on this commonly misunderstood topic). Most of these points (except the ASP one, which even the experts in that field can’t make sense of) are addressed in this post, but it will require a few reads.

    • Yossi Mandel

      For anyone else interested in reading the specifics of the confusion of ASP that Dr. Attia mentions, the most recent review is here: http://pharmrev.aspetjournals.org/content/65/1/500.full.pdf on page 528-532.

  • Norm

    Even if we assume it is the calorie deficit ONLY that causes weight loss, still in my experience one is worse off with higher carbs in the diet as compared to the higher fat. 100 calories of fat will satisfy me a lot more than 100 calories of carbs. Fat wins when it comes to satiety and we know how important satiety is in terms of food consumption. What about spikes in blood glucose and insulin due to carbs? What about interplay of insulin and leptin? Carbs and sugar probably are the main culprit when it comes to brain’s approach to food and overeating.

  • Rebecca

    In response to thought #4- could it be possible that these people would thrive on a high fat diet if they had adequate bile production? Possibly these people have the most sluggish livers of all of us & therefore do not produce enough bile for fat emulsification. Maybe that’s an obvious thought. Thanks for the work you are doing. I am learning a lot from your blog.

  • Curzon Dax

    I suspect the optimal way is Low Insulin/High Leptin. While low insulin opens the doors to higher fat loss and lower fat accumulation, leptin accelerates the process.

    It also explains why satiety matters.

    • See previous comment. Only in leptin deficient individuals (who are dramatically obese) does a high level of (exogneous) leptin work to raise EE and suppress appetite.

  • Curzon Dax

    “Certainly another state of net fat efflux is starvation. DNL and RE are both very small, especially DNL, and lipolysis is quite large. This is probably the most rapid state of negative fat flux a human can experience.”

    I suspect that’s where leptin research may help. With high leptin (and satiety) lipolysis should be accelerated, hence “marginal satiety” with a combination of low carbs(low insulin) might be the optimal solution.

    • Leptin does not appear to do much when it is high, only the reverse. In other words, low leptin is a signal to eat, but high leptin is not a signal to stop/not eat.

  • Curzon Dax

    Apologies for having a third post. Let me offer my hobbyist research notes on it, in case it offers more. Further apologies if it offers nothing more.

    “On Leptin and why Satiety matters:

    Leptin itself is directly proportional to the amount of white fat and to a much lesser extend other parts of the body (brown adipose tissue, placenta (syncytiotrophoblasts), ovaries, skeletal muscle, stomach (the lower part of the fundic glands), mammary epithelial cells, bone marrow, pituitary, liver, gastric chief cells and P/D1 cells in the stomach).

    Hence its base amount is mainly regulated by the amount of body fat, it won’t alter easily without conscious effort or other external means.

    However, it will reduce in amount when in starvation/very-low-calorie diets [2 studies found supporting it following leptin’s wikipedia article].

    Leptin is detected by a part of the brain (Hypothalamus) and – directly – does the following things:

    a) In the Hypothalamus, it decreases the activity of neuropeptide Y neurons, that when active promote fat storage and hunger.

    b) It decreases the activity of Agouti-related peptide that promotes hunger and reduces energy expenditure.

    c) In promotes the release of ?-Melanocyte-stimulating hormone (?-MSH) which promotes Melanogenesis which among other things decreases appetite.[source for it found on wikipedia].

    Hence being on very low calorie (not carb or high fat) diets can bring a decrease in leptin which in turn does bad things, conversely, satiety will keep leptin at higher levels, promoting easier fat loss and a healthier life.”

    It’s mainly from following sources and links from the wikipedia article for leptin.

  • Olga

    All I want to say is that I LOVE YOU! Keep up the good fight. We all deserve better doctors. Thank you for what you are doing.

  • 1.21 GIGAWATTS!!!

    That is all.

  • Razwell

    Hi Dr. Attia,

    Excellent article. The overly simplistic caloric hypothesis of obesity is indeed dead. It is only promoted by the deeply ignorant who need to see their world in simple black and white, instead of shades of grey. It is only promoted by snake oil salesmen who are unaware of contemporary obesity science and the hellish complexity of human physiology. Real scientists acknowledge uncertainty and unknowns.

    There is much the caloric hypothesis cannot explain:

    * For example , even successful gastric bypass patients still have a very substantial amount of body fat. Sure they are smaller in size ( which varies among individual to individual) but still obese- only less. Their body fat percentage would be surprisingly high, despite a reduced *overall mass*- mass being the key word here rather than fat tissue per se. They probably lost a lot of muscle too. To add insult to injury, this poor result is their “reward” for only eating 800 to 1,000 calories! How unfair is that? These patients are eating ONLY 1/3 of what normal to thin people eat- regular non-obese among the population. I have played basketball against “successful” patients ( some close friends, other strangers ) and their backs literally feel as soft as a pillow as they back me into the basket ( I hand check with my forearm) . This is indicative of high body fat. Basically many or most of them are left with a smaller version of their previous self, but still considerably fat. I have seen many patients first hand over the years. Their bodies are loaded with fat in every nook and cranny. Their body composition is nowhere near a person who was never obese- just regular- let alone a truly lean individual such as , say, Allen Iverson or Evander Holyfield etc.

    This is not to criticize these patients at all. I applaud their efforts and sympathize with them. Rather, it is an indictment of the dogma of modern medicine. These patients are victims of the poor treatment options. That said, currently it sppears to be the best we have. But it does not work anywhere near as well as advertised as Dr. Jeffrey Friedman has noted many times publicly during his lectures.

    *Another example is world class Olympic endurance athletes and swimmers ( often female) getting liposuction for stubborn body fat that is completely resistant to diet and their immense exercise regimes. Their are YouTube videos of procedures to prove this really happens. Fat does act like a tumour it seems.

    Science is moving toward the regulation/dysregulation of fat cells, as well as the chemical behavior of fat cells’ receptors. This is a hypothesis “with legs.” The first law of thermodynamics is being completely abused and misused by numerous well known Blog authors who attack Gary Taubes ( and myself). I have personally confirmed this with some of the best physicists in the world. They all agree with Gary’s thermodynamics explanation to a tee . even if it is indirectly. Dr. Christopher Jarzynsky ( world renowned pioneering non- equilibrium thermodynamics scientist) personally told me by e-mail that ” the loss and gain of fat/muscle are extremely complex biochemical processes best understood within the framework of physiology. It’s NOT a matter of basic thermodynamics.” Many M.I.T. professors recommended Dr. Jarzynski to me.

    I think both Gary Taubes and yourself do an excellent job of ” reasoning from evidence ” – which is what we do in science. The both of you step outside of the box and try your best to get to the bottom of it . I think you guys are doing what Richard Feynman suggested when dealing with a complicated problem- “think like a Martian.” Looking at the problem completely anew as if you never saw it before. 🙂

    I wish NuSi much success. Don’t worry about the Internet “gurus” who attack Gary’s work. Just ignore them. They are all charlatans. My buddy, Urgelt of Youtube, is highly scientifically literate and intelligent. He identified numerous Bloggers as hucksters immediately. In fact, the well known and infamous Bloggers who constantly critcize Gary are almost comical in their lack of understanding of science. Having learned from Urgelt, I see this more clearly than ever. Urgelt respects Gary’s science journalism work a lot and recognizes him as a person who understands science well.

    Best wishes,


    • Thanks for the perspective, Raz.

    • Tom

      Interestingly, the calories hypothesis might be coming back from well, a bit unexpected direction, cf. e.g.two quotes from a short article from a well known site:


      “the presence of excessive nutrient intake and subsequent systemic metabolic dysfunction is not controversial”

      “Evidence for the metabolic effects of immunity on the loss of tolerance suggest that over-nutrition may be a crucial component of this process, and could effect the mucosal barrier, as evidenced by the presence of dysbiosis and intestinal permeability in obese patients.”

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  • Edward

    Hi Peter,

    The quote, “He was born on the finish line, so he thinks he won the race,” sounds suspiciously like something Yogi Berra would say.

    Where would one find >98% caprylic acid in a consumable form? Most of it is 66% max in softgel form.

    MPBio has it here: http://www.mpbio.com/product.php?pid=02100391, 99.5%, but they treat it like you would have to be insane to put it in your mouth, seeming to consider it to be a hazardous material, and want nearly $40 for 25 ml. How much would you consume and how frequently?



    • Purest form of caprylic acid is from a chemical company, such as Sigma chemicals. They sell 99%, but it’s quite costly. Not sure I see a need for this.

  • Edward

    I was asking due to your September 1 response to spar: “To your last question, MCT, or better yet >98% pure caprylic acid can help.” As a solution to getting back into ketosis, after being in “no man’s land.” Thanks.

  • Norm

    How can one get rid of gynachomastia when hormones which usually cause it come out as normal and weight loss does not make much of a difference? Any info/links would be appreciated. Thanks

  • Norm

    Peter, it came as 111pmol/L (40-162), which is apparently normal so are testosterone and prolactin.

    • That’s about 30 pg/mL, so, yes, pretty normal. Maybe look at E1 and E3, though unlikely.

  • Norm

    Will do peter, many thanks

  • Maryann

    Merry Christmas Peter! God bless you and your family!

    Thank you so much for all of your super-human efforts on our behalf…I know the blog is the last on your list; but, somehow you manage your monthly post. Even if in the future you just did a post without the comments, I would be so grateful. I know you can’t do this forever.

    Thank you for all you teach us!


    • Thanks so much for understanding, Maryann. I’m happy to keep up what I can.

  • Robert


    I really enjoyed your TED talk and love reading all the detail on your blog. I have been on a ketogenic diet for the past month and it seems to be working. Prior to my diet, my blood metrics revealed slightly high uric acid levels. What kind of risk (if any) is there by consuming more fat? I am hoping that this diet will actually reduce the uric acid levels. Also, I have OSA (obstructive sleep apnea) and am using a BiPAP machine at night. Will CPAP/BiPAP have any negative affect on weight/fat loss?


  • Christine

    In my experience, there are several flaws in the low-fat processed diet that many of us have accepted.
    I have discovered from my own experience and from helping clients, that people lose weight not by restricting fat as much as eating healthy fats such as nuts, oils, avocados, and wild-caught salmon, and reducing/eliminating refined starchy carbs, which the body processes as glucose. For most people, the sugar control diet helps them lose weight and establish healthy eating habits for life.

  • newbie

    Every time I reread a slew of your posts, I glean new insights – I cannot thank you enough.

    Looking at your equation……..B-OHB (measured in blood) = B-OHB produced (from dietary fat) plus B-OHB produced (from lipolysis of TAG) less B-OHB consumed by working muscles, heart, brain.

    I read this post (again) on the heels of Ketosis I and II, , as well as IFIK. Can you envision a scenario where someone is in nutritional ketosis, is in hour 15 of Martin Berkhan style(leangains) 16 hour fast, about to start the 8 hour eating window, and you check their insulin/bs/ketones – where BS would be relatively high for this fasted state (say 5.5), insulin is incredibly low (fat floodgates are wide open), and ketones are only 0.2 – in other words, fat efflux is occurring, the glycerol backbone is being used to make glucose and most of the available ketones are fueling basic cellular metabolism so the ketone level is low? Does this make metabolic sense?

    • It’s possible, especially if metabolic demand during the fasted period is very low, and as a result the liver is making very little BHB.

  • newbie

    RE – IFIK – If you don’t mind my asking, did you check your B-OHB when you were feeling hungry on fast days, pre-exercise? If you have that result, would it be fair to say you would have been doing sedentary computer type activity?

  • mark

    This may not be the right place to ask, but I haven’t found any info on what might be a maximum dosage of coconut oil / MCTs. Can you tell me or point me in the direction to look for the info? What are the dangers of exceeding 6 tablespoons of coconut oil per day? I usually use ~4 tablespoons in my morning coffee and maybe 2 more in a cup of hot tea later in the day. I’m 58 YO T2 eating a ketogenic diet for nearly 2 years and use coconut oil to help meet my fat needs. I put in a little over 3000 miles on bicycle last year, was pretty sedentary before that. Am looking toward maybe doubling that this year and was wondering about increasing coconut oil a little. Is there any benefit of the timing of coconut oil intake?

  • Jeff Johnson

    Insulin – Ketosis – Weight Gain

    Insulin will be produced by the body regardless of any and all diets – you can’t stop this – even in Ketosis – some people will gain weight according to their calorie load

    For Such People the only anwser is to Control Hunger and there-by reduce Calorie Load

    Controling Hunger is best and is probally the only way accomplished – by reducing Fat Intake

    Overly Obese Women and many men pay should pay attention to the above sentence – most women have an RMR(resting metabolic rate) around 1500 calories – many of these women eat that much and more and wonder why there not losing weight – even in or around Ketocic levels – and Insulin production is probably the reason

    Protein should be used to control hunger whether the amount results in Ketosis or not – ( – 80 to 200 grams) – animal fats should be reduced to something like 1/2 pat butter – 1/4 slice cream cheese – 2

    tablespoons sour cream – 2 tablespoons raw milk and some low carb yogurt (4 carbs per serving – Kroger Brand) and eating raw nuts(almonds-peanuts -sunflower seeds – many of the calories in the raw nuts will not be absorbed becuase the body can’t break them down – but all the dairy fat and meat fat calories will be absorbed

    The main reason for reducing fat is to control hunger and secondly to reduce the chances of the body storing this fat

    Ketosis or Low Carb by it-self simply will not work for many people – they will store ingested fat even in these conditions – Protein to satiety – low carbs – and lowered fat intake – and reduced calories below RMR is a reasonable solution

    Salt intake

    Even at levels just above Ketocic may require more salt – 4 or 5 teaspoons sea salt in an empty green olive bottle with mostly water but some vinegar and black pepper added is one way of getting it

    I personaly have to add 2 to 5 teaspoons sea salt daily to my diet ot eliminate cramping and I’m just above being in Ketosis generally

    Not a well written comment – (mine – this) – but I have other things to do besides think up literary gems

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  • Chris

    Hi Peter, thanks for your detailed explanations. Here’s a related question. I’ve been a heavy carb user for a long time and have some symptoms of metabolic syndrome. I’ve changed to a low carb diet and 3 weeks in feel cleaner, smoother energy, more alert and am losing weight and waist inches. So far so great.

    I do long distance walking, typically 30+ mile routes. I would say this is mostly aerobic with some more anaerobic parts in places (steep climbs in mud, for example). So I need to train my body to start burning fat as much as possible for this activity. But after years of abuse it’s primed to burn glycogen as soon as the going gets even slightly tough.

    So how do I teach it as efficiently/quickly as possible to get better and better at upregulating fax oxidation? What can I do to really help drive that process now that I’m in a low carb low insulin state? And do I need to keep doing it or will staying low carb ensure it stays learned?

    Thanks again

    • It takes time, but RQ will migrate to match FQ, and that’s the biggest step. Sounds like you’re on the right course.

    • Chris

      Thanks Peter, sorry but I cannot find what FQ means on your blog. The only reference to it is here. Do these stand for Respitory Quotient (fat vs glycogen use) and Fat Quotient (ie simply how much fat vs how much carb in your diet?

      If so you are saying that eating more fat, not necessarily doing more aerobic exercise, is what upregulates fat oxidation pathways more than anything? This seems counterintuitive to me. Sorry if I’ve misunderstood you.

      • It’s the “RQ” of your diet if you burned the food. The more fat in the diet, the closer to 0.7, the more CHO, the closer to 1.0

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  • John

    Hi Peter,

    I half-accidently stumbled upon your blog, and your analytic approach has given me the long awaited inspiration to try low carb diet for losing weight. Thanks for that!

    May I ask if you have personal experience or know of reliable reseaech of any side effects of low carb diet (not a diabetic, not doing extreme intensity sports) E.g. how would you comment this http://news.bbc.co.uk/2/hi/health/4435046.stm Would you agree they have a relevant point to consider?

    Thanks in advance!

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  • Kevin

    Great article by the way! It’s nice to see someone “show their work” instead of just make statements. 🙂

    What I take away from this is (but maybe I am misinterpreting)…

    1. Fat really is the bad guy (fat makes you fat) IF it is in the presence of insulin since DLN is always relatively much lower than RE.
    2. Fat is the good guy if not in the presence of CHO/insulin.
    3. Hormone level differences among people have a big effect on what diet someone should follow.

  • Norm

    Hi Peter,

    1. In a low carb / ketogenic setting if one is attempting to lose weight and does not feel hungry do they need to be concerned about caloric restriction and consequent hpothyroid/down regulation of metabolism? Do they use hunger as a guide or kind of force themselves to eat enough calories?

    2. Apart from reducing fat intake and addressing hormonal issues is there anything else one can try to accelerate fat oxidation? For example low intensity exercise or intermittent fasting?

    3. The fat to be reduced: is it specific as SAFs or MUFAs?


    • 1. Hunger is probably the best guide
      2. Hormones rule
      3. Depends on dietary intake, but ideally, it’s the storage form of triglyceride

    • Yossi Mandel

      Do you have any recommendations for where we can read up on #3 – what you mean by storage form of TAG and how dietary intake will affect that, beyond the standard divisions of SFA, MUFA and PUFA? Or what terms to search for to find it?

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  • James

    Hi Peter

    Please could you elaborate on why so many people have such positive results in reducing body fat while under a ketogenic diet?

    Reading your previous articles they sounded like they were in favor of ketosis (atkins diet etc) yet when I read this article it seems against it?

    Surely on a low carb, high fat diet once the body utilizes fats as its primary source of energy your fat stores begin to deplite? If this is not due to a ketogenic diet how else can this be achieved when under ‘normal’ diet with carbs being primary source they (glycogen)are utilized first and then once they are depleted your body uses a mixture of muscle mass and fat which is far from ideal?

    • Not sure why you’re interpreting this article that way. This post is simply a statement of facts. No judgement or emotion intended.

  • Mike Roberts

    >They are not giving up fat from their fat cells because they are eating less. They are eating less because they are giving up fat from their fat cells. Big difference.

    This leaves me confused as the two activities are very different. You can chose to eat less, but you cannot simply choose to give up fat from your fat cells (note: if you can, I’m impressed). The way these sentences are written imply that the only way anyone will be able to eat less is if they are already giving up fat from their fat cells. Clearly, I’m missing something.

    • Your understanding is likely correct over the long run. If a fat cell is “hanging on” to fat, as far as the body (esp. the liver) “knows” you are starving, and appetite goes up. One can only fight this for so long.

  • Sumit Bhatnagar

    Hi Peter,

    I really like your blog and I was hoping you could please tell me something about this ketosis mystery. My question may sound silly to you since I am not from medical background but I am really interested to know this and no one on Internet seems to have an answer for this..

    My question is –

    When you are in Ketosis, i understand that it is the process of your liver turning fat into ketone bodies. I fail to understand one key point is that these ketones are made up of my own body fat or the high amount of fat i am eating while on low card diet. If ketones are made up of my own body fat, why do i need to consume so high amount of fat in the first place? What happends to dietry Fat then? Is eating high amount of fat really neccesary to induce ketosis?

    • Made from both, but to answer your question, if you stop eating, just from your body — this is called starvation ketosis.

    • Hemming

      At some point you’ll have used so much body fat that you need to eat some fat. Having been very underweight I can assure that you can’t live on your stored body fat when you’re that low in body fat percentage despite people claiming that I’m still carrying 30,000-40,000 calories of fat.

  • Nan

    For those interested, here is the obit for Dr. Coleman, co-discoverer of the genetic leptin role in weight:


  • Norm

    Hi Peter,

    1. If the brain needs 120-150 grams of carbs how can it run optimally out of ketosis at a lower number of carbs?
    2. For how long generally does the insulin stay raised after eating carbs?
    3. Is it better to restrict carbs to one meal or spread them over 3 meals in terms of their effect on insulin?


    • 1. Ketones offset this need. That’s the point.
      2. Depends on the person and the carb source
      3. “better?”

    • Vicente

      Hi Norm,
      I am far from being a MD, but from what I have read:
      1) Your brain does NOT need 120-150g of carbs. It needs a few grams but it can also use ketones.
      Even if our brain couldn’t use ketones our liver can create glucose from fats: in other words you don’t need 150g of dietary carbs even if your brain where unable of using ketones.

      Question 3) is insteresting. Is the peak value of glucose/insulin what causes the damage or is it the AUC the important factor and several meals can cause the same effect? Is there a glucose/insulin threshold it is better not to reach or does their effect follow a smooth curve? Intuitively spreading carbs in several meals should be better or at least equal than eating all of them in one meal: the more stable your blood glucose, the better.

  • Norm

    Sorry Peter, I was menat to ask if restricting carbs to one meal was better than spreading them over 3 meals in terms of insulin secretion. Thanks

  • Norm

    Hi Peter,

    What do you think about ASP (Acylation Stimulating Protein) which apparently stores fat without raised insulin? Could this explain weight gain/stall on a LCHF diet for some people?


  • Norm

    Sorted. Gary kindly pointed me to the email exchange between Keith Frayn and Fred Hahn over ASP.

  • Marco

    Hi! My name is Marco and i am an student 22 years of age, living in Sweden. I was wondering on your take on Bioenergetics and their take on HFLC. They smash the idea of HFLC here ->

    Do you think it is pseudoscience when it comes to biological matter where endokrinology explains things better? I am freaked out of the debate since i wanted to pursue biochemistry for their authenticity to explaining everything on a micro scale, all the way from the cell. I thought that was were the explanations could be found for solving huge problems in the world. Do you recommend studying something else or are their take on HFLC somewhat valid?

    “Eating a high-fat low-carb diet (HFLC) tends to increase levels of free fatty acids (or non-esterified fatty acids, NEFA) in the blood. While this is usually the goal of any HFLC diet, it mimics the “stress”metabolism seen in those with diabetes, obesity and old age (Frayn K, et al. 1996). However, insulin resistance isn’t necessarily induced on a hypocaloric HFLC diet because fatty acid oxidation “keeps up” with fatty acid mobilization.Free fatty acids suppress mitochondrial respiration (Kamikawa and Yamakazi, 1981), leading to increased glycolysis (and the production of lactic acid) to maintain cellular energy.

    Lactic acid along with the longer chain fatty acids inhibit the regulatory enzyme pyruvate dehydrogenase (Bradley N, et al. 2008), which is activated by insulin and links the metabolism of glucose via glycolysis with the Krebs cycle in the mitochondria. The inactivation of pyruvate dehydrogenase (PDH) reduces the production of carbon dioxide (increasing lactic acid through lactate dehydrogenase) whereas carbohydrates have the opposite effect.

    • Vicente

      Marco, are you sure that the words in the link you posted are not placed at random?

      Nevertheles, let’s assume they are not and let’s talk about science:

      1) Make a guess: “HFLC diets support mitochondrial dysfunction”
      2) Make a prediction (?)
      3) Design an experiment to test your prediction (?)
      4) Analyze the results (?)

  • Marco

    Or it seems endokrinology as of Ray Peat among others also support glukose as healthy and the PUFA’s more dangerous in the equation.
    “If Dr. Budd’s thinking (and results) had been more widely accepted when his publications appeared, thinking about “diabetes” might have led to earlier investigation of the syndromes of stress and tissue wasting, with insulin being identified as just one of many regulatory substances, and a large amount of useless and harmful activity treating hyperglycemia as the enemy, rather than part of an adaptive reaction, might have been avoided.”


  • Marco

    Here comes the last quote – sorry spamming Peter but i am intrigued to see if you done simplicity to early and reductionism to a hard complex biological matter question.

    Carbs are needed to activate inactived T4 thyroid gland and much much more. Excessive Triglycerides from eating bad fats that have been oxidised which many overdo on HFLC or to much SFA and MCT contribute to over inflammation in the body. When you then enter ketosis, you enter a slower metabolism as fat burns slower than glycogen. Say goodbye to performing HIIT, Crossfit, Soccer and many more activities that actually build type IIb fiber muscles that keep you from storing fat, while builds muscle when you have glycogen levels intact and fueled.

    I love intermittent fasting with fats such as coconut and macademia nuts but to much fat in the body can mimic the exposure under training with triglycerides, the same oxidative way like A.G:E products?

    If you do intermittent fasting with cooked greens in blender with fats and berries (they say not to mix fats with sugar but you can ferment the berries with salt and lemon to reduce sugars) is prone to be beneficial to balance thyroids and limit methionine and triglycerides oxidative processes i think, cause you only refeed fats on fasting days. Carbs and protein on training days, fats on IF days. What do you think about that?

    • PhilT

      Low carb / ketogenic eaters have a normal blood sugar, so your hypothesis needs to explain why things like thyroid function depend on ingested carbohydrate as opposed to the endogenous glucose available in nutritional ketosis.

  • Marco

    Vincente, i am not qualified to engage in a personal experiment cause i can’t on a cellular level, test for true causality. These experts which studies i linked at no random place, was given reference to my concern with LCHF, as i adressed to peter and everybody on the blog. My take is ” moderate carbs, moderate fats on fasting days with 2 meals to not overeat and indulge in stimulating the sensitive actions of insulin” and everyother training day to have “moderate protein, moderate carbs with very little fat”. A refeed strategy for energy needs but overall health by balance conflicting theories of food intake. Moderation as Peter, Ray Peat or any other expert out there, can make statements now that will be devestating when new science paradigm enters later on. I think the paradigm will come when one is an expert of general science in every field – if one has the abillity to study biochemistry, endokrinology, neuro etc. etc. etc. Every studyfield shows different results by huge standards.

    • Vicente

      The authors of the article are “experts”? I don’t believe that. Their reasoning is so poor…

      Just a couple of examples: they talk about miochondrial energy efficiency and you can’t find the word “ketone” in their speculations.

      Another one, they say that “consuming a HFLC diet mimics a diabetic’s metabolism” so as long as “an increase in lactic acid is a common feature of diabetes”, HFLC diets are energetically inefficient and “when energy production becomes “inefficient” reactive oxygen species (ROS) are produced in large amounts”. Even if that speculation were true, the reasoning seems BS to me.

      IMHO, a piece of garbage.

  • Marco

    Thanks for your comment Vincent. You seem to reason well and question things well. They are acclaimed experts, at least in the public eye but i may need more scientific approach to myself question these claims. As of now, i don’t so thanks for contributing Vincente! 🙂

  • Marco

    As a thank you gift, i would like to share this medicinal context for how to lower risks with LCHF with spices for (in case Attia and researchers in the same field have gotten LCHF wrong). This study is done on overweight but otherwise “healthy” people so may not be the best chosen group as they are likely to already have high drawing abbillities for triglycerides i suppose. But anyhow:

    “According to Penn State researchers, eating a diet rich in spices, like turmeric and cinnamon, reduces the body’s negative responses to eating high-fat meals. Sheila West, associate professor of biobehavioral health, Penn State, who led the study said that people eating a high-fat meal end up with high levels of triglycerides (a type of fat) in their blood.We found that adding spices to a high-fat meal reduced triglyceride response by about 30 percent, compared to a similar meal with no spices added.”

    I should add that bioperine from black pepper, oils and cooking activates a far more bioavailable tumeric.
    Cinnamon i prefer to add to raw hot chocolate with goat milk (just slow-boil the milk seperate). Have a great day!

    • Vicente

      “Sheila West, associate professor of biobehavioral health, Penn State, who led the study said that people eating a high-fat meal end up with high levels of triglycerides (a type of fat) in their blood”.

      Low-carb high-fat diets do NOT raise triglycerides. Read “Systematic review and meta-analysis of clinical trials of the effects of low carbohydrate diets on cardiovascular risk factors”. Obes Rev. 2012 Nov;13(11):1048-66. Epub 2012 Aug 21″.

      She is probably not wired to think scientifically.

  • Marco

    Wow, thanks for the reference. I guess we really need Peter and you Vincente and that mindset to set an end to flaw-based statements. You all really motivates me to study really hard now and ask the right kind of questions in research later in life, by involing more data before statements are made in my limited field of research…

    Have a great day!

    • Vicente

      Hi Marco,
      Peter is a MD and a nutrition expert. I am neither of the two.

      You don’t need me, specially since my personal experience (LCHF diet has made wonders in my quality of life) makes me a clearly biased source. Read the scientific articles that report clinical trials and intervention studies in humans (I would ignore other kinds of scientific articles) and choose what you think is best for you.

      Have a nice day

  • Marco

    http://www.abioenergeticview.com/2-3 I debunk this if nutritonal ketoss is done right but i do have a question about the gains of nutritonal ketosis in testo production…

    I get this in my mailbox (a series of bioenergetic views on LCHF). Peter take the BIG picture in the whole of his nutritonal ketosis which i don’t see them doing above. Peters diet is healthy as it includes low methionine content indirectly by a low protein diet (excessive methionine increase R.O.S and the “fight or fly” exhaustive stress gene. But from a nutritional standpoint in regards to testo production, the IGF-1 are clearly raised by fatty acid consumption as free testosteron is excreded right?
    That is good for balancing Intermittent fasting that induces IGF-1 and autoghapy which then rejuvenates old damaged neuron cells, and cells in the mitocondria. But does eating much fat – Nutritonal ketogenic fasting – increase autoghapy for the worse and inhibit the induced IGF-1 by increasing free testo?

    I ask cause i want to limit testo as much as possible and gain complex of female attributes regarding muscle. They have thinner, longer and a more elegant storage of the muscles – they dont gain as much volume. I have trained for fast muscle fibers and heavy weight training with 55kilo weighted Dips, 150 kilo squat before i accumulated damage and injured my leg from bad standpoint both execution wize and inflammatory rich diet. I now have lost that huge volume of my body but my arms are still big enough compared to girls. I weight like 68 kilo and am 1.80 cm. I think i have the wrong muscle fibers that do benefit skeletal but not my identity esthetically. For my goal of being more thin in muscle volume with a balance of 1 day HIIT, 1 day really high reps strenght training with low weights, and one day to to calisthetics for 20 minutes, and approach lower testo by:

    Lose IGF-1 one day with fasting and lower fats and benefit autoghapy for HEALTH and Longevity
    Increase IGF-1 the other day by GOAT colostrum powder?

  • Marco


    The article discusses IGF-1 as a marker increased only by short high intensity training. And i know Peter performs at this levels sometimes besides longer marathon training. But isn’t a shorter lifespan with much higher life quality prefered over induced IGF-1 longevity by diet, excercise and from the AGE DHEA & TESTO DECLINED after 25 with skeletal loss after age 30? And if the answer is yes for you, then is LCHF really the ideal for HIIT and heavy weight training? I know that if you wait for insulin responses with the postworkout meal, excluding carbs, the skeletal and hypertrofy can benefit even more according to some research, including Mercolas. But for the thyroid gland and recovery overall, is not overall some carbs from blueberries, sea buckthorn berries with omega 7 and lastly, goat milk or sheep milk with folate and b12 and taurine rich, prefered benefits to neurological health and thyroid health, over LCHF all the time? Can’t one switch to heavy training with Soccer HIITS and carb rebounds 80g 3hours after, and 40g at night to stabilise blood sugar, and the next day, get into intermittent fasting with coconut milk and organic cooked + juiced greens along that?

    Can’t one alternate or does this induce getting into NK several days?

    The growth factor IGF-1 and the anabolic hormones growth hormone and testosterone stimulates
    protein synthesis and tissue regeneration. IGF-1 can be decreased by mild aerobic exercise at the la
    threshold which is approximately 50% VO2 max. This would be beneficial in cases where the patient has
    increased risk of cancer. Exercising at levels higher than 60% VO 2 max will increase IGF-1 and high resistance exercise will also increase IGF-1. Growth hormones are stimulated by high intensity exercise both short sprint exercise and resistance exercise if it provides high tissue stress.
    Resistance exercises with high workloads are the most effective way to stimulate the release of test
    osterone. Clinically it may look like IGF-1, growth hormones and testosterone can only be stimulated later in
    the treatment program when the patient has progressed into higher resistance exercise protocols”.

  • Marco

    You know what – let me simplify: I wanted to raise IGF-1 without testosterone in order to gain a more female skinny complex. This cannot apparently be done but i can offset chronically high testo production and balance my lifestyle so i have a higher chance. I think IGF-1 is needed to be raised in order to achieve that fat loss, but reduced type II fast and heavy weight training, is i think, required for not bulking up volume when having raised IGF-1. IGF-1 is still highly benefical for my goal as it helps collagen, firmness, greater fat loss, etc. etc.

    I wanted to eat carbs 3hours after training and late at night – this spikes the insuline somewhat and apparently, the IGF-1 is at the highest the first 1-2 hours during sleep. So i thought i could stabilise my blood sugar by eating carbs late at night and yes, this does that but also induces IGF-1. I thought the body handled fat very poorly at night but now i see in context of IGF-1 and satiety for better sleep, why Peter and many is recommending fat at night (disclaimer for peter: i don’t know for sure his recommendations but i THINK it was similar to what i wrote above).

    So a traing with 50% vo2 max which induces IGF-1, and decreased dietary fat & protein which induce IGF-1 and testo, with some days of explosive soccer HIIT to increase IGF-1, with dietary Goat colostrum powder, more protein and dietary fats to increase IGF-1. I think it is the best way to get lean in a “skinnier” way as a guy. A chronically high testo and muscle volume is what i am seeking to exclude. I wrote this in case anyone can benefit from my reasoning. Sorry if being somewhat Off Topic!

  • Marco

    Another post but i am so motivated so hope this come across. Peter Attia, have you considered the negative side effects of overconsuming SCA and MCT fats in your NK diet because they lead to 30% higher needs of Choline, than a dietary moderate PUFA-diet? There are over 69 found Phosphoslipids in Krill Oil but still you supplement Carlsons liquid fish oil as you stated in an interview, overloading triglyceride converting-work in the liver?
    I recommend that you investigate in Choline further for pregnancies if you can because your credentials and position at the moment in the public eye, can really draw much needed attention to global problems of ADD, ADHD, poor study results, lower focus abbillities, depression, suicides etc. – all derived from Choline deficiency and probably overeating MCT’s by thus increasing the needs of Choline. Apparently, the need of 550mg daily as a male, is just a guess and hypothesised of being to small so this is already an issue with vegans and non-egg or liver eaters.

    Choline is what really keep cortisol markers away well as depression and anxiety. It also regulates the metabolism and hinders acumulating a fatty-liver profoundly according to many resource studies found by googling. The daily Lipid Blog is one of them. Mercola states that “Prior research has concluded that choline intake during pregnancy “super-charged” the brain activity of animals in utero, indicating that it may boost cognitive function, improve learning and memory, and even diminish age-related memory decline and the brain’s vulnerability to toxins during childhood, as well as conferring protection later in life1.

    Interestingly, the higher choline intake led to changes in epigenetic markers in the fetus. Specifically, it affected markers that regulate the hypothalamic-pituitary-adrenal (HPA) axis, which controls hormone production and activity. The higher intake of choline contributed to a more stable HPA axis, which in turn meant lower cortisol levels in the fetus. The changes in fetal genetic expression will likely continue into adulthood, where they play a role in disease prevention”.

    Epigenetic Changes May Last for Generations / http://articles.mercola.com/sites/articles/archive/2012/10/08/choline-consumption-during-pregnancy.aspx

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  • Pål Jåbekk

    Thank you so much for another fine post on a fine blog. So glad to see Friedmans work being mentioned. His work was an eyeopener for me during my studies. Discussions pertaining to hunger and satiety often focus too much on the signals (leptin, ghrelin, PYY etc.) and too little on the source of the signal which seem to be highly related to ATP production. Anyway, keep up the good work!

  • Yossi Mandel

    I just realized an exception to this:

    “How does knowing one of these numbers (B-OHB measured in blood) give definitive answers to another (B-OHB produced from lipolysis of TAG)? It can’t.”

    When water fasting (supplemented, of course) the BHB in the blood is only the result of fat burning, as no fat is being consumed. Let’s say it’s after 3 days of water fasting, if it truly takes 3 days for food to clear the body as noted in allergen testing.

    • True, but not the case I was referring to. I’m addressing nutritional ketosis, not starvation ketosis.

    • Yossi Mandel

      To go even further in limiting this, it’s only when the bhb level is 2-3, somewhere between 5 and 10 days of fasting, that it is a useful measurement of how much is being burned. Above that, the bhb level may rise to 6 and above, but that only reflects lipolysis and how many ketones are available for the body to use and not actual use. Only those original 2-3 mmol of ketones are being used, the rest is present just in case and is not excreted or taken up by the brain, muscles etc. And then insulin kicks in again to limit ketone production to something below 10, so lipolysis decreases. Presumably once glucose or protein intake starts again, those last 4+ mmol of ketones in the bloodstream are stored again. So the real benefit of water fasting would be from when bhb levels hits 2 until it exceeds 3 as after that metabolism drops in response. After that nutritional ketosis is called for to keep metabolic rate up. (If I made a mistake somewhere there, please point it out as it would be very useful.)

      Would make a neat esoteric article explaining: Why is nutritional ketosis superior to starvation ketosis for weight loss?

  • Chris

    Great photo! That’s that flux capacitor from Back To the Future! 😀 did you like that movie doc? it’s my favorite

  • Norm

    Hi Peter,
    In a low carb/keto diet setting, cutting dietary fat sounds counter intuitive if one is following their hunger because if their bodies are releasing fatty acids accordingly, dietary fat would be adjusted via hunger signals unless they are force feeding themselves which makes me think that it could be something other than insulin that is inhibiting release of body fat for oxidation? So cutting fat might lead to hunger or short term weight loss at the cost of lower energy expenditure?

    For those who have stalled, could it be that their energy expenditure has decreased (due to weight loss or maybe thyroid) and now their bodies are not tapping into their stored fat as before? Can eating even more help in this scenario by increasing energy expenditure? Or may be adding more carbs if they directly affect thyroid?

    • Hard to say because there are many mechanisms at play. T4 conversion to rT3 may be partly responsible in weight-reduced folks.

  • Mike Nunan

    Dear Peter,

    First of all, thank you for the amazing resource you have created here, which I have been digging into for the past couple of months with great enthusiasm. While the books of Phinney and Volek gave me a good start into the practicalities of NK, the Q&A material on your site has filled in a multitude of details. To find such a wealth of high quality information is wonderful enough, but coming as it does from someone whose priorities are to do with using good science to help further the wellbeing of others – that’s something very special indeed. All power to you and Gary Taubes for what you are setting out to do with NuSI especially.

    I do have a couple of questions relating to your discussion above with Hemming, about the need for dietary fat to support ketosis. I have been taking regular blood BHB readings and that has been helping me get a feel for how different eating and training habits impact my level of ketosis. I’m surprised to see that (so far) nothing raises BHB levels more than total fasting. Going without food throughout a highly active rest day recently, I hit a morning BHB level of 5.7mM the following morning (at which point I hadn’t eaten for 32 hours). A couple of hours after that I ate what I thought was a highly ketogenic breakfast of 110g raspberries 100g heavy and clotted cream plus a couple of fish oil capsules. Two-and-a-half hours later, my BHB level had dropped to 3.8mM. Ok, there were 7-8g of CHO in the raspberries, but I still expected my BHB levels to stay up around where they were first thing. On a more normal day I might see a waking BHB level of around 1.2-1.6mM, do a fastest Crossfit session then eat lunch, after which my afternoon readings will often drop below 1.0mM for a considerable period. I’ve been careful over protein intake but the combined effect of a high-intensity workout and eating anything at all seem to combine to knock me out of NK on almost a daily basis. Plus, if my BHB (and presumably also therefore FFA mobilisation) levels are highest when fasting, and I wish to be leaner (currently around 13% BF, aiming for 8-10%), then it seems counterproductive to consume much dietary fat, as per Hemming’s comments above. I’m not talking about running some huge energy deficit that might slow metabolism, but the notion of consuming 2000kcal/day in fat when there are plenty of stores available and being mobilised seems illogical. Any thoughts or suggestions?

    My second question leads on from the first, but is actually more fundamental, and while I feel slightly silly asking it, I looked long and hard for an answer here and via every other research medium I could muster, but still have come up blank. My question is, what is the underlying purpose of being in nutritional ketosis? Is ketosis just a proxy for low insulin level? Or, do you believe that by maintaining high serum BHB levels (particularly during training efforts of a high enough intensity that they would mostly rely on glycogen) we can encourage adaptations away from CHO metabolism towards use of a combination of ketones and FFA? Or, is there yet another aspect to the reasoning that I’ve missed? My observation from the meter is that really high-intensity workouts (particularly those involving sprint/interval structures with rest periods between) result in a massive blood glucose rises – from 4.9 to 11.8mM (i.e., 86 to a whopping 212mg/dl) on one occasion a couple of weeks ago – and this when fasted. Clearly as much as I would like to be spending the whole week in NK, my liver has other ideas when I am triggering major catecholamine releases with heavy Crossfit sessions. Research has confirmed that the BG rise is mostly from glycogenolysis rather than GNG (which makes sense, as GNG is a relatively slow process) but nothing in the literature that I’ve found has mentioned what happens to insulin levels in this scenario. It would be seem a safe guess that they’re also elevated, and that this causes a great deal of the circulating glucose to be converted back to muscle glycogen. This is a very anti-ketogenic environment and I find myself wondering whether I shouldn’t just “go with the flow” and introduce some dietary CHO and additional protein around workouts, given that I’m very likely being pushed out of NK anyway.

    (Sorry, this post has turned out much longer than I intended. That’s the trouble with complex and nuanced subjects I guess!)

    Warm regards,

    Mike (London, UK)

    • peter

      Two really superb questions Mike,
      I look forwards to Peter’ answers. it is interesting to note that the more that one goes down this road, the more one has such questions.

  • Rod Clifton

    Excellent article.

    I’m still trying to fully decipher it, I must admit.

    I’ve personally lost 47 pounds, about 20% of my overall weight, and I’ve done it over the past year without changing any of the food I eat. Instead, I restricted how much I ate in the form of cutting out one meal, all snacks, and any drink with sweetener or sugar in it. (I don’t eat breakfast, but I have two meals between 1-8pm)

    In addition, I exercise 3-4 times a week.

    For me, the answer has always been, burn more calories than you’re taking in. Maybe that sounds too simplified, but I’ve lived it for over a year.

    This diet isn’t as restrictive as it sounds. In addition, I eat anything in sight every other Friday from the moment I wake up until I go to sleep (if I want to…I don’t always want to).

    I have about another 7 pounds to lose, and I think I’m going to have to finally cut carbs down.

  • Michael

    Hi – I’ve been on a LCD for about 2 months and have lost about 6lbs. My problem is that my body fat scale (WithThings) doesnt actually reflect a drop in body fat. I know these scales use water to help measure body fat against adipose tissue in the body. Does being in a Ketogenic State (Diet), throw off the calculation? My jeans fit better so I know my body composition is changing. I suppose that’s the best test for results.

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  • Seth

    Peter, so if fatty acids enter the fat tissue via RE and DNL where they are assembled into TAG and then broken down into fatty acids and released back into the blood stream via lipolysis to be either oxidized or recycled via RE, what might cause a person not to be able to oxidize fat assuming they restrict carbs and/or are ketotic? How is beta oxidation inhibited or encouraged?

    As a follow-up, since ketones are a by-product of fat oxidization, is it possible to be ketotic if your fat is not oxidizing and is simply being recycled.

    Thanks, Seth

  • thompsonpat

    On the question of sensitive populations… I’m of Amerindian descent and my husband is European. we seem to thrive on very different diets – though his love of carbs does impact his dental health. I’m wondering if being Indian –only a few generations out from traditional diet –and close to menopause is a kind of double whammy w typ American Diet. I’ve always framed my craving for fat as “bar food” – but in truth I’m a scratch cooker – if I make leg of lamb the bones are broken and used for stock. this article http://www.westonaprice.org/health-topics/guts-and-grease-the-diet-of-native-americans/ helped me in reframing “fat” (not in your detailed scientific way) but as full use of the animal mentality. I also got advice from a Chinese medicine practicioner that bone broth would ease the transition to menopause. And (n=1 & possible placebo effects) drinking bone broth seems to have really helped reduce hot flashes. so far my personal experience and your writings seem more or less in synch.

    the point of confusion for me is that the Chinese medicine practicioner argued that some carbs are good for menopause transition. I wonder why that might be?

  • Paul Arena

    Is it possible to accumulate fat without insulin (e.g. type 1 diabetes)?

    • Without ANY insulin, probably not, or at least not much, but late stage T1D is extreme. Before the discovery of insulin such patients died completely emaciated–no fat and no muscle.

  • Anna

    Dr. Attia,

    I have been doing the ketogenic diet for about 2 months now, after finding your videos on YouTube. I feel great, have more energy, fewer cravings, and have lost weight. The first month I lost 14 lbs. The next month, 6 lbs. Now I am stalled at about 1 lb a week. I work out 4 days a week doing resistance, total body workouts with bursts of cardio. I am 5’8″ and 40 lbs. from healthy weight range. I use ketostix and keto calculator to ensure I am in ketosis, and am almost always in the mauve=eggplant color range. I am very careful with the macros (<30 net carbs, 90-100 protein, and the rest natural fats for 70-80%. Calories about 1300-1700 on workout days. I do daily IF as well, with a 6-8 hour feeding window. I am wondering what you do with your clients when their weight loss slows on Ketogenic diet, and how long before you consider them in a "plateau" that could indicate the need for changes. I am happy to do more IFIK if it will help, or to reduce or add calories. I just do not want to assume that the constant nutritional ketosis state is no longer working for me. I know I am very insulin resistant and gain weight with the slightest reintroduction of carbs in the diet. Can you speak to when to make changes, such as a fat fast, twice a week intermittent fasting, or trying something other than Ketosis with the assumption that it may be an indication that there is no longer appropriate fat flux?

    • Anna

      I meant to say that I am only losing about 1/2 a lb. a week the last couple of weeks, not 1 lb.

    • Anna, 1 pound of fat loss per week is excellent progress. According to the work of Kevin Hall, it can take 3 years to reach steady-state reduced weight (though most of the weight loss occurs in the first year). Keep up the good work.

  • Mark Crawford

    Peter, I’m 59, 160 lbs, Late Onset Type 1.5 diabetic and very active. My A1c was getting worse, up to 7.5+, so 8 weeks ago I took the Keto plunge. My blood glucose numbers were great for the first 3 weeks but then insulin resistance skyrocketed in the last 2-3 weeks. I’m waking up with 200+ blood sugar and taking more insulin now than before I was eating 70% fats. So I don’t know what to do, really. I was reading about “free fatty acid overload’ that can be a insulin blocker and using Niacin with some fruits and vegtables- by Ricky Everett. Do you know anything about that? Also, if you any lo carb doc close to Middle Tennessee, I’ll go in a minute. Even travelling now would be OK. Thanks, Mark

    • Takes me weeks to sort this out with my patients, but “typical” pattern of success involves metformin, CHO restriction (but not necessarily KD), and maybe GLP-1 agonists. But this is where you need a great doc. Sorry I don’t know any out there.

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  • Aviv

    Hi Peter,
    Been a long time my friend.
    I know I asked you this before, and you approved it, but just wanted to confirm it one more time – I want to translate most of this post into Hebrew, and post it on my blog, with full credit to you and a link to your website of course.


    BTW, you have a pretty big fan base in our ketogenic community in Israel 🙂

  • Ray

    Hi Peter,
    as always yet another highly informative article. Thank you for your dedication.
    But it confused me. I’ve recently (2 months ago) embrace ketogenic lifestyle and lost 6 kg excluding the 2,5 kg water weight. During that time I didn’t exercise except archery session for 4 hours once a week.
    The evidence of fat loss is obvious. I’ve gone from belt hole number 2 to number 5 which is 8 cm loss in waist measurement.
    Yet the body fat percentage measured by Omron Body Fat Monitor shows no change at 22%. I was sure it’s not muscle wasting because I don’t feel weaker or sluggish. Do you have any suggestion what constitute my weight lost?

    • Not sure how accurate that device is for measuring body fat.

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  • Tysen

    Dr. Attia,

    I’ve read several of your posts so I didn’t really know which one to post my question, but decided on this one.

    I’m still a little confused with conservation of energy and the ketogenic diet. I understand that carbohydrate restriction will cause a decrease in the insulin secretion. Since insulin increases fatty acid synthesis in the liver and a decrease in TAG breakdown, less circulating insulin would be beneficial that along with less glucose will shift the body’s energy source to fat. But at the end of the day I’m still failing to see the difference in net energy to a high carb diet with that has the same caloric level. (i.e. If one requires 2500 calories and consumes 2400 calories there will be an energy debt that will be taken from fat/muscle/glycogen stores. Those 2400 calories can be any combination of macronutrients)

    The only thing that I can think of is would the body excrete non-metabolized nutrients during a ketogenic diet which would lead to the energy equation needing to include “energy excreted” to the equation like the following: Energy consumed – Energy burned – Energy excreted= net Energy consumption. I guess that the fact that you can detect ketones in the urine and acetone on the breath would be evidence that some energy is being wasted via excretion but is that the only thing responsible for the advantageous fat loss ketogenic diets have over standard low-fat diets?


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  • Jerry Bruton

    Dr. Attia,
    My question is in regards to fat oxidation measured by grams per minute verses exercise intensity (%V02 max).
    If you have such a measurement, what has been your experience? I think .60 grams per minute is the maximum for a person on a non-ketogenic diet.

  • Jacob

    What turns a carb from A cellular to B? Why is whole wheat bread or blended fruit considered A cellular even if your also eating the fiber?

  • Michael Cornman

    Hi Peter,

    I have a question that is slightly off topic for this blog post, but still relevant to fat efflux. If someone experiences chronic insulin spikes that hinder their ability to breakdown stored fat for energy, does that make them more likely to suffer from deficiencies in fat soluble vitamins?

    I understand that vitamins D, E, K, and A are all stored in the liver and in adipose tissue. To access the stored fat-soluble vitamins, does the body have to release stored fat or can it access it through other means?

    Funny story about how this question actually came about. This morning I was sitting in the sun writing my med school personal statement. The major topic of the essay is about my experience as a personal trainer using a ketogenic diet to help clients lose weight and alleviate themselves of chronic disease. I actually used a quote from one of your blog posts in the essay…thanks for that! But anyway, I realized that I was getting a little too much sun and thought about vitamin D production and storage…at the same time that I was writing about weight loss/fat efflux. Thought you’d enjoy the mental loop.

    I also wanted to thank you for all of your hard work on this blog and work in nutrition field in general. This blog changed my perspective on health, nutrition, scientific methodology, and medicine. It also pointed me in the right direction to find research from great scientists, like Phinney and Volek. Finding your blog was definitely one of the initiating factors that lead to my decision to pursue a career in medicine.

    Thanks Peter!

  • Ryan

    Dr. Attia,

    Thank you for taking the time to put this information and your experiences online, it is extremely helpful to beginners like me. I do find myself confused by the “information blender” between high carb and low carb diets. There is a video on the high carb/no meat protein website that outlines how high fat diets increase insulin resistance by blocking the signaling pathway between insulin receptors and glucose transport vesicles in individual cells. Obviously, I’m trying to lower my triglycerides so this came across as a shock when doing research on a high fat diet. Keep up the good work you do!

    P.S. – Here is the video, http://www.forksoverknives.com/fat-insulin-resistance-blood-sugar/


    • A high fat diet probably does increase IR in the presence of (relatively) high carbohydrate. High insulin + high fat is a bad combo (it’s called, the “standard American diet,” of course).

    • Norm

      Hi Ryan,

      The video did not mention what would happen to glucose uptake and insulin when muscles are filled with glycogen and can’t take any more glucose. Also, glucose tolerence gives very little information without measuring insulin levels. Insulin resistance is very complex issue; it is both desirable and harmful depending on the context. With regards to fat in the blood, you will find this study ineteresting:


    • Tyler

      On the subject of the standard American diet, I wonder what exactly is a high fat, high carbohydrate diet?

      It could be interpreted to mean a low protein diet. But Americans are near the top when it comes to per capita meat consumption – and also have a high consumption of cheese and other milk products – so I don’t think there’s a lack of protein, in the country, per se.

      Certainly a lot of the packaged foods people eat throughout the day fit the bill for high fat, high carbohydrate. (Same thing goes for desserts.) Yet, interspersed throughout those junk-food excursions appear to be meals that make up for the protein scarcity of cookies, cake, and chips.

      It’s a weird dietary pattern.

  • Alyspaleo

    Hey Peter,

    Maybe you can help me with my extreme difficulties losing weight on a ketosis /paleo /any diet really, and continued weight gain on very low calorie diets (800-1200-1400-1500-1600)

    You mentioned you have seen the extreme problem if insulinomas. I don’t think I have one, as my hypoglycemia has been on going for as long as I can remember. Including hating fruit and sweets as a child. And a family history of hypoglycemia with no one ever developing diabetes. (excluding one who had a pancrectomy).

    My fasting blood sugar is 55-75
    My triglycerides are 34
    My Albumin is 3.3
    With high fasting insulin, excellent cholesterol and very low testosterone for a woman.

    I maintained a bmi of 27 since I was 15 always on a diet. But recently ballooned to obesity in a very short time on propranolol, likely due to its clear contraindication to never be given to those with asthma or hypoglycemia. (prophylaxis tx for chronic migraines). After a year, I haven’t been able to lose any of this excessive gain.

    My postprandial hypoglycemia typically occurs within 45 minutes of eating, this includes all levels of carbs 0-75g. I do feel more neuroglycopenic hypoglycemia when there are more then 20g carbs in anything consumed. Remarkably, my postprandial blood sugar rarely exceeds ~100 when check very frequently.

    I have been actively asking doctors and Endocrinologists for help for the past 15 years and they will not treat my hypoglycemia problems, trouble losing weight or hyperinsulinemia. (and all of the dieticians they have sent me to have no idea how to manage my hypoglycemia, and none of their suggestions help me lose weight)

    1) How can I lower my insulin levels that don’t seem to have any correlation to dietary intake?

    2) Knowing insulin inhibits lipolysis. And certain hormones (growth hormone, catecholamines, glucagon, ACTH, corticosteroids, T3) aid in the stimulation of HSL with in adipose tissue…. Is there any hope in trying to increase HSL stimulation to overcome hyperinsulinemia? Or is it simply better (healthier) to reduce insulin?

    3) Since I can’t explain it to my doctors, but is it odd, or is there a physiological reason I’m almost never hungry? Is there some reason for abnormal ghrelin/ leptin in my hyperinsulinemia hypoglycemia? Even in hypoglycemia, I only remedy it with food consciously because I have neuroglycopenic symptoms. Typically food makes me feel worse, so I am prone to avoid.

    Thank you for any wisdom you can give on this atypical situation!

  • Barb

    I read your article a couple times on how to create fat efflux but I’m missing something. I see that we can lower DNL by eliminating carbs, and we can increase our RE by eating more fat but I can’t figure out from what you wrote what we can do to directly control the rate of our lipolysis. It seems like you are saying we need to start by cutting the carbs and increasing our fat and see what happens over time. Its the results (losing fat, gaining fat or staying the same) that tells us we have the right combination of behaviors to cause the sum of these two things to be less than our lipolysis and we adjust them until we get it right – or rather in most cases we adjust the fat intake until we get it right. Is that correct?

    I would really like to do something that works directly on my rate of lipolysis and it sounds like exercise may have bee the trick for you – right? I also read elsewhere that taking Ursolic acid would help speed up lipolysis directly. Can you comment on that?

    Thanks for you help.

  • Debra

    I have been following a keto diet with reduced calories with regular and I have not lost weight. I thought this was imposible and that I was “screwing up” somewhere. But your article seems to explain how (although I got a little lost) You talk about less faty fat cells. Perhaps I missed this point, can you actually “get rid of” a fat cell? And if not, once a fat cell as been “plump” does it have some kind of “memory” wherein it will tend to fatten up faster once carbs and suger are reintroduced. I am worried because although I can keep up this diet for months eventually I will want to eat pasta and bread and bananas – even if its a little – I miss these things terribly.

  • Alaa

    Hi Peter,
    I read most of the articles here, I would love to meet you in person one day as you inspire me !
    I have done a slow carb diet where I consumed a lot of meat and eggs with red beans and lentils, I lost around 12 kg but my visceral fat is still there, so now I want to try nutritional ketosis as I am convinced it is the way to go for me, I fit 4 of the 5 indicators you prescribed for metabolic disorder.
    problem is for me right now : I did not find a step by step plan on your site to do this, I get that everybody is different but is there a book or a plan you recommend that can help me do this in organised way ?

    thank you so much for enlightening the general public about health tips, if it were not for you, such information would be available only to the rich.

  • Laura

    Thyroid, hypothyroidism post as related to KD, pretty please with sugar on top?

  • Vanessa

    Hi Dr.
    I wrote a big question and comment and I don’t know why isn’t here. Did u get it?it was concerning about my eating disorders problems and my case of gaining lost without a reason

  • Chris

    Thanks Dr. Attia:

    Thank you for your article, I have not thought about insulin and ketosis for a while and it lead me to think about your patients that are having trouble entering into ketosis and staying there. I would suppose that one possible reason would be increased insulin resistance. There are several possible solutions for lowering insulin resistance but what comes to mind is Pterostilbene upregulating GLUT4, http://www.ncbi.nlm.nih.gov/pubmed/25998070.

    N=3 Experiments confirm increased insulin sensitivity

    As a relatively cheap GRAS substance this seems like it might be worth a try I think for some people.

    And as an added bonus!

    Pterostilbene also has a number of anti-inflammatory effects, http://www.ncbi.nlm.nih.gov/pubmed/?term=Pterostilbene+asthma . My obesity was exacerbating my allergic asthma making exercise more difficult. An added bonus to Pterostilbene was that it seemed to shut down my asthma. (Ketosis may also be playing a part but I am seeing a time/dosage relationship.)


    Thanks for your website I have enjoyed your articles.


  • Maryann

    Hi Peter,

    Is a 14 -15 hour IF enough to lose weight or does it need to be 16-8? Would some almond milk in coffee ruin the fast (I read that less than 50 calories is ok). Is coconut oil in coffee ok ? I know the calories are way over 50 but I thought maybe it is metabolized differently and would be ok. Thank you if you have the time to answer and thank you for all you do.

  • Dougie

    Hey Peter,

    I’ve just come up with an awesome analogy that I think summarises this. Forgive me if I sound condescending by saying you’re welcome to use it (trust me, I am so far below you), but I think it sounds cool.
    To all the mechanics out there (many of my family included) and car enthusiasts, I apologise if it’s oversimplified.
    If there’s any holes in it, or if it outright makes no sense (like why I wasnt born 30 yrs ago……..mullets and AC/DC suit me!!!), please let me know.

    “So fat accumulation (ie, obesity) is more than just a calorie imbalance, it’s a hormonal imbalance.
    To lose fat (to use technical terms, induce a fat efflux), the release of fat from our fat cells must be greater than the uptake of fat into our fat cells.
    To get technical again, lipolysis must be > de novo lipogensis (conversion of glucose to fat) and re-esterifcation (storage of dietary fat and fat already circulating in the blood).
    Eating less calories than we burn doesn’t necessarily increase lipolysis/fat release (and thus, beta oxidation, fat burning). But certain hormones do regulate our fat accumulation. Insulin is probably the most important hormone in that it promotes carbohydrate oxidation, DNL (a little) & RE (a lot), and inhibits lipolysis.
    Bottom line – hormones are chemical messengers, very similar to neurotransmitters, which instruct our body what to do with our fat stores. To loose fat, we must release more of it from our fat cells than we are taking in. Without being able to release it and transport it to the mitochondria, we can’t burn it for energy

    And here comes the analogy:
    Cars are similar to the human body in that they have a fuel tank (adipose tissue), an engine (mitochondria) and a means of transporting the fuel to the engine (lipolysis and the blood). The car is instructed by the driver (the hormone, or set of hormones) to take in fuel, as the driver inserts the head of the bowser into the fuel cap.
    Car takes up fuel, just like when we eat our bacon, eggs and snags.
    When either the fuel cannot get to the engine (lipolysis is inhibited), or the engine cannot function properly to burn the fuel (beta-oxidation is inhibited/impaired), then the car will not be able to lose weight or function very well.
    Hypothetically, if a car’s fuel tank could expand just like our adipocytes, I’m sure it would in this situation”


    And thanks for another great in-depth post!

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  • Ali

    As a 200lb severely insulin resistant Diabetic, I have discovered that (short of water-fasting) the ONLY way I can lose weight is to radically reduce both carbohydrates AND fats.

    Having faithfully followed LCHF for 8 years – and not only GAINING well over 30lbs but also plagued with worsening IR to the point that even injected insulin hardly worked, I was at my wits end. The LC mantra seems to be ‘eat high fat, and if that doesn’t work, eat MORE fat…..!

    But for some people, that is tantamount to adding fuel to the fire.

    Yes, carbohydrate eaten in excess is a problem, but why make obese people who already have a ton of fatty acids floating round their bloodstream, add to the burden…? Some obese or overweight people may have IR mild enough that dumping the carbs – and so reducing the extra glucolipolysis from excess carb consumption – is enough to enable them to lose weight regardless of how much fat they ingest.

    But others, especially the severely IR, whose bodies are almost certainly clogged to the brim with toxic fat already, may well need to follow some kind of PSMF for some time to clear everything out and enable the body to reset itself hormonally. The obese do not need to ingest lots of fat – they are lugging ample stores around with them continuously…..

  • osama

    thank you so much for enlightening the general public about health .

    iam type 2 diabitic and in ketosis since one year ,

    haw long can i stay in ketosis ?

  • Steve Martin

    Hi Dr Attia,

    You mentioned some data you can’t share that suggests that “non-deliberate EE rises more in a low RQ (high fat, low carb) environment when a person is exercising significantly”

    Are you in a position to share more about this? It seems to match my personal experience of an LCHF diet coupled with regular high intensity exercise. The combination of the two seemed to significantly accelerate loss of body fat. My ketones got as high as 5.8 mil/L and my blood sugar as low as 1.8. With zero discomfort or ill effects as far as I can tell.

    I would really love to read any studies in this area.

    Many thanks for your wonderful work!

    • Actually, I’m not sure if those data are yet published. Will need to check.

  • Jenna

    This was a great post! Very interesting. I’m wondering, would your advice to someone who has been in nutritional ketosis for about half a year, who has lost 30 Lb, has about 50 Lb more to lose, and who has been on a plateau for about 3 months, be to restrict calories on top off being in ketosis?


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  • Margarita

    I am really glad I have found your blog! I am 33 and alllwayd have been running. But lately (after a second child) I am struggling with some weight (based on my stomach), hypothyroidism, high sugar and high cholesterol and rheumatoid arthritis. I knew I had to change diet! And I became vegan 80-10-10 , from one side I felt much better with my arthritis and overall, but my weight were just going higher. Now I have found your page and started ketogenic diet; my weight is going down, but I feel bad, I can’t run (just don’t have strength), I feel just a stout in my stomach, like a hole, where nothing is satisfying…I am a bit lost of what should I do? I really need an advise..I am completely lost!
    Best regards, Margarita

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  • Federer Fanatic

    Please discuss the mathematical modeling of these topics? Perhaps, as part of subseries on your site for nonmathphobics :-)?

  • MaRy VP

    Thank you Peter!!! This is the answer I was looking for since I started Keto diet 5 years ago. I was doing everything right, a lot of strength training and still, fat didn’t go away until I started IF.

    I am a big fan of your work, thank you again for sharing this with us.


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