If I held a crystal ball 10 years ago, I’m not sure I would’ve believed it if it showed me the increased interest in the ketogenic diet would look like the figure below. That’s 2 logs, folks.
Admittedly, I started my journey on this path in 2009, with a deep dive into ketosis in the Spring of 2011, but it seemed so obscure! (For a timeline of what I did, I think I covered it somewhere in this talk…yes I’m too lazy to actually confirm this by skimming through it.) All told I spent approximately 3 years in the strictest state of nutritional ketosis (NK) with one very memorable deviation when I had 6 or 7 full-sized and upsettingly decadent desserts circa September 2013. I believe the diet helped me transition from metabolic syndrome to metabolic health and I certainly thought it could benefit other people. This nutritional state could gain some steam, I thought.
I was well aware of the dearth of mainstream knowledge of NK, and particularly the conflation of NK with diabetic ketoacidosis (DKA), a pathologic state that results from the complete or near absence of insulin, which is what prompted my writing and desire to share my journey. And I was once in the wanker category of folks who spoke with “authority” about ketosis, despite knowing somewhere between zero and nothing on the topic. I remember exactly where I was sitting in a clinic at Johns Hopkins in 2002 during my residency explaining to (admonishing, really) a patient who was on the Atkins diet how harmful it was because of DKA. Not only that, the ketogenic diet could be seen as the antithesis of a “healthy” diet by conventional standards. I could see how this was a difficult proposition for many to acknowledge.
The beautiful part of good science is its self-correcting nature. The ugly part is this self-correcting nature often moves at a glacial pace—and it’s not linear. We often view history century-by-century and see what amounts to continual progress in medicine. But we live our lives—and consume information—day-by-day, exposed to the peaks and valleys of medical wisdom.
Looking back on my earlier posts on ketosis—and explaining what I eat, for example—makes me both chuckle and cringe. I remember how bizarre the diet seemed to many readers and the general public at the time. I also remember digging into the literature and learning, for example, that my alma mater, Johns Hopkins had been using the ketogenic diet to treat pediatric epilepsy for almost a century…and being so embarrassed about admonishing that patient I saw in my residency.
Since then, it’s safe to say I dove down the rabbit hole. The more I learned, the more I grew tired of reading so much misinformation on the topic. While there are more thoughtful people and articles on the subject of ketosis these days (e.g., here’s a thoughtful video on ketosis and ketogenic diets from one of my most important ketosis mentors, Steve Phinney, a co-founder of Virta Health1Disclosure: I’m an investor in, and advisor to, Virta Health.), there are still pieces like the one Vox published this month, that doesn’t exactly do the topic justice.
Like many variables in diet, health, and disease, it behooves us to look beyond the bumper sticker explanation. I want to highlight a couple of posts I wrote, to attempt to provide a little more nuance and understanding to the subject: “Ketosis — advantaged or misunderstood state?” Parts I and II. Part I follows below. I’m hoping to write more on the topic in the not-too-distant future since there’s been a number of intriguing papers published recently (certainly since 2012). But I also wanted to bring these back into focus in light of the information I’m seeing more of on the interwebz. (You can also visit the Ketosis section of the site to view more articles on the subject.)
Because I know people will ask, I have not been on a ketogenic diet “regularly” since about mid- to late-2014. The reasons are too nuanced to describe here, but my deviation is not because I lost confidence in its efficacy. With nearly a decade of clinical experience, I can safely say I was an outlier (in the best sense) with respect to my physiology and response. I was leaner, and more mentally and physically fit during this three year period than during any other period of time as an adult, and my biomarkers were as good as they had ever been. I’ve also seen the benefit of ketogenic diets first-hand on my patients and my own sister, a remarkable story I hope to share one day. But I’ve also been humbled by my inability to explain why some people have suboptimal or even negative responses to NK. I would say, all things considered, my knowledge of ketosis is greater today than when I was writing about it voraciously, but my confidence in my understanding of it, might actually be lower. As the saying goes, the further one goes from shore, the deeper the water gets.
—P.A., April 2018
(Part I: originally posted November 26, 2012)
In part I of this post I will see to it (assuming you read it) that you’ll know more about ketosis than just about anyone, including your doctor or the majority of “experts” out there writing about this topic.
Before we begin, a disclaimer in order: If you want to actually understand this topic, you must invest the time and mental energy to do so. You really have to get into the details. Obviously, I love the details and probably read 5 or 6 scientific papers every week on this topic (and others). I don’t expect the casual reader to want to do this, and I view it as my role to synthesize this information and present it to you. But this is not a bumper-sticker issue. I know it’s trendy to make blanket statements – ketosis is “unnatural,” for example, or ketosis is “superior” – but such statements mean nothing if you don’t understand the biochemistry and evolution of our species. So, let’s agree to let the unsubstantiated statements and bumper stickers reside in the world of political debates and opinion-based discussions. For this reason, I’ve deliberately broken this post down and only included this content (i.e., background) for Part I.
What is ketosis?
Ketosis is a metabolic state in which the liver produces small organic molecules called ketone bodies at “sufficient” levels, which I’ll expand upon later. First, let’s get the semantics correct. The first confusing thing about ketosis is that ketone bodies are not all – technically — ketones, whose structure is shown below. Technically, the term ketone denotes an organic molecule where a carbon atom, sandwiched between 2 other carbon atoms (denoted by R and R’), is double-bonded to an oxygen atom.
Conversely, the term “ketone bodies” refers to 3 very specific molecules: acetone, acetoacetone (or acetoacetic acid), and beta-hydroxybutyrate (or beta-hydroxybutyric acid), shown below, of which only 2 are technically ketones. (The reason beta-hydroxybutyrate, or B-OHB, is not technically a ketone is that the carbon double-bonded to the oxygen is bonded to an –OH group on one side, technically making B-OHB a carboxylic acid for anyone keeping score.)
Now, back to the real question at hand. Why would our body make these substances? To understand why or when the body would do this requires some understanding of how the body converts stored energy (the food we eat or the energy we store in our body, i.e., fat or glycogen) into phosphate donors. For a refresher on this process, please refer to the video in this post, specifically the section from 2:15 to 13:30.
The ATP issue
As you may recall, about 60% of the energy we expend, say 1,800 kcal/day for someone consuming 3,000 kcal/day in weight balance, is purely devoted to keeping us alive by generating enough ATP (“energy currency”) to do 2 things: allow ion gradients to function and allow muscular relaxation. So, obviously, we can’t tolerate – literally even for one minute – insufficient ATP production. In fact, one of the most potent toxins known to man (cyanide) exerts its effect on this process by inhibiting the electron transport chain which generates the bulk of the ATP our body produces. Even the most transient interruption of this process is fatal.
Take home message #1: No ATP, even for 1 minute, equals no life.
The brain issue
The brain is a particularly greedy organ when it comes to energy requirement. To put this comment in perspective consider the following: though our brain represents only about 2% of our body mass, it accounts for about 20% of our energy expenditure. (In children, by the way, this may be closer to 40-50% of basal metabolic demand.) So, beyond the ATP issue, above, there is a substrate issue with the brain as neurons derive most of their energy from glucose. While there is emerging evidence that neurons can also oxidize fatty acids directly in small amounts and may even prefer lactate (over glucose), these two substrates do not approach the levels of consumption by neurons that glucose does. So, for the purpose of this discussion, let’s just focus on the need of the body to provide glucose to the brain.
You’ll recall, from the point I made above, that my brain requires about 400 to 500 kcal of glucose per day (100 to 120 gm). You’ll also recall (from the video, above) that I can store about 100 to 120 gm of glucose in my liver. While I can store much more in my muscles, (on the order of about 300 to 350 gm), because muscles lack the enzyme glucose-6-phosphatase, glucose stored in muscle as glycogen is unable to re-enter the bloodstream and is meant for the muscle and the muscle alone to use. In other words, muscle glycogen is a stranded asset of glucose in the body to be used only by the muscle.
So, if I’m deprived of a dietary source of glucose, I depend solely on my liver to release glycogen (a process known as hepatic glucose output, or HGO). How long can HGO supply my brain with sufficient glucose? It depends on a few things that impact both the “source” and the “sink” of glucose. Other competing sinks for glucose (e.g., activity level, thermogenic needs) and sources (e.g., glycerol and gluconeogenic amino acid availability) can make a difference for a while. But, in a state of starvation we’ve only got about one to three days before we’re in trouble. If our brain doesn’t get a hold of something else, besides glucose, we will die quite unceremoniously.
Take home message #2: No glucose for 24-72 hours equals the need for something else the brain can use instead (that is not fat or protein, since neurons can’t oxidize fat and the last thing we want to do is start muscle wasting at a geometric rate).
The Krebs Cycle
This poses a real evolutionary dilemma. We need an enormous amount of energy just to not die, but the single most important organ in our body (also quite energy hungry in its own right) can’t access the most abundant source of energy in our body (i.e., fat) and is, instead, almost solely dependent on the one macronutrient we can’t store beyond a trivial amount (i.e., glucose). Obviously our species wouldn’t be here today if this were the end of the story. But, to understand how we survived requires one more trip down biochemistry memory lane. In the figure below (also included and described in the video) I gloss over a pretty important detail.
How, exactly, does our body take pyruvate (from glucose) or acetyl CoA (from fat) and generate so much ATP? The answer lies in the beauty of the Krebs Cycle, which feeds into a process called the electron transport chain (or ETC), I alluded to above. Since the adage ‘you can’t get something for nothing’ is as true in biochemistry as it appears to be in life, to get all that ATP (i.e., stored energy in the form of the phosphate bond), we need to give up something. What the ETC does give up, as its name suggests, is electrons. Through a series of redox reactions the ETC trades the stored energy held by electrons going from higher to lower energy states in exchange for the chemical energy stored in the bonds of the third phosphate group on an ATP molecule.
To think of it another way, if you start with stored energy – glucose or fat, for example, which if burned in calorimeter will give off varying amounts of heat – and you’re willing to convert their carbon, hydrogen, and oxygen molecules into another form with less energy – water and carbon dioxide which, if burned, produce very little heat – it’s a fair trade! The ETC is simply the vehicle that allows our body to make the switch.
In a car, by contrast, it’s much simpler. The engine combusts the hydrocarbon (e.g., gasoline) directly and in one flash liberates the heat contained within the hydrogen-carbon and carbon-carbon bonds in exchange for carbon dioxide, water vapor, and a few other things.
If you take a look at the figure, below, you’ll get a sense of the moving pieces involved in this cyclic transfer process. Molecules shuffle back and forth, around the cycle, and kick off spent carbon (carbon dioxide, termed “waste”) and reducing agents (e.g., conversion from NAD+ to NADH) for the ETC.
Under conditions of abundant glucose (and sufficient insulin sensitivity) the brain is primarily converting glucose to pyruvate (left side of figure). Pyruvate is then shuttled into the mitochondria and converted into acetyl CoA with the help of a very important enzyme called pyruvate dehydrogenase (PDH). I’m going to come back to this enzyme, in part II of this series, because this is where the story gets very interesting. Acetyl CoA (which is also a direct byproduct of fatty acid breakdown) is then combined with oxaloacetate and so begins the Krebs Cycle, which generates all the reducing agents to feed the ETC and generate massive amounts of ATP.
Where do the ketones come in?
In the absence of acetyl CoA (several ways this can happen, including substrate shortage, as I’m describing here) we evolved a cool trick. Our liver can make – out of fat or protein, though we much prefer to use fat so we can spare our protein and prevent severe muscle wasting – something called beta-hydroxybutyrate, one of the 3 ketone bodies I described above.
B-OHB and acetoacetate (see figure below from this paper by Cahill and Veech, 2003) are produced by the liver from long and medium chain fatty acids and released into the bloodstream.
Acetoacetic acid and B-OHB live in reversible equilibrium (on the left), but once acetoacetate is converted to acetone (on the right) there’s no going back.
Now take a look at the figure below, from this 2001 paper. This is another rendition of the figure above showing the Krebs Cycle, but here you can see where B-OHB and acetoacetate enter the picture.
The reason a starving person can live for 40-60 days is precisely because we can turn fat into ketones and convert ketones into substrate for the Krebs Cycle in the mitochondria of our neurons. In fact, the more fat you have on your body, the longer you can survive. As an example of this, you may want to read this remarkable case report of a 382 day medically supervised fast (with only water and electrolytes)! If we had to rely on glucose, we’d die in a few days. If we could only rely on protein, we’d live a few more days but become completely debilitated with muscle wasting.
The graph below, also from the Cahill and Veech paper, shows the blood chemistry of a person starving for 40 days. Within about 3 days, a starving person’s level of glucose stops falling. Within about 10 days they reach a steady-state equilibrium with B-OHB levels exceeding glucose levels and offsetting most of the brain’s need for glucose. In fact, the late George Cahill did an experiment many years ago (probably would never get IRB approval to do such an experiment today) to demonstrate how ketones can offset glucose in the brain. Subjects with very high levels of B-OHB (about 5-7 mM) were injected with insulin until glucose levels reached 1 mM (about 19 mg/dL)! A normal person would fall into a coma at glucose levels below about 40 mg/dL and die by the time blood glucose reached 1 mM. These subjects were completely asymptomatic and 100% neurologically functional.
The last point I’ll make on the starving patient is that, as you can see in the figure below, the glucose level normalizes at about 65-70 mg/dL (about 3.7 mM) within days of fasting, despite no sources of exogenous glucose. Why? Because with so much fat being converted into B-OHB and acetoacetic acid by the liver, a significant amount of glycerol (the 3-carbon backbone of triglycerides) is liberated and converted by the liver into glycogen. As an aside, this is why someone in nutritional ketosis – even if eating zero carbohydrates – still has about 50-70% of a normal glycogen level, as demonstrated by muscle biopsies in such subjects.
Take home message #3: We evolved to produce ketone bodies so we could not only tolerate but also thrive in the absence of glucose for prolonged periods of time. No ability to produce ketone bodies = no human species.
Last point of background: Everything I’ve just presented is based on data from starving subjects. If one restricts carbohydrate intake, typically to less than about 20-50 gm/day (dependent on timing and carbohydrate composition), and maintains modest but not high protein intake (because protein is gluconeogenic – i.e., protein in excess will be converted to glycogen by the liver), one can induce a state referred to as “nutritional ketosis” with similar physiology to what I’ve just presented without resorting to starvation. Why you’d do this is something I will discuss later.
One other housekeeping issue: Ketosis versus DKA?
In a separate post, I explained the difference between nutritional ketosis (NK) and diabetic ketoacidosis (DKA). If this distinction is not clear, I’d suggest giving this separate post a quick skim for a refresher. DKA is a pathologic (i.e., harmful) state that results from the complete or near absence of insulin. This occurs in the setting of type 1 diabetes or very end-stage type 2 diabetes, and often as the result of a physiologic insult (e.g., an infection) where the patient is not receiving sufficient insulin to bring glucose into his cells. A person with a normal pancreas, regardless of how long he fasts (including the fellow I reference above who fasted for 382 days!) or how much he restricts carbohydrates, can not enter DKA because even a trace amount of insulin will keep B-OHB levels below about 7 or 8 mM, well below the threshold to develop the pathologic acid-base abnormalities associated with DKA. Let me reiterate, it is physiologically impossible to induce DKA in anyone that does not have T1D or very, very, very late-stage T2D with pancreatic “burnout.”
Embarrassing admission: I remember exactly where I was sitting in a clinic at Johns Hopkins in 2002 explaining to (admonishing, really) a patient who was on the Atkins diet how harmful it was because of DKA. I am so embarrassed by my complete stupidity and utter failure to pick up a single scientific article to fact check this dogma I was spewing to this poor patient. If you’re reading this, sir, please forgive me. You deserved a smarter doctor.
In Part II of this post I’ll tackle the questions I know folks still have on their mind (below). Until then, re-read this post to make sure you really understand this physiology. You’re already 10 steps ahead of the next person.
- Is there a “metabolic advantage” to being in ketosis?
- Are there dangers of being in ketosis?
- What are the most important things you need to know about getting into (or staying in) ketosis?
Hi Peter, I found a study linking ketogenic diets to arterial stiffness: http://www.seizure-journal.com/article/S1059-1311(13)00339-7/fulltext#sec0010
What do you think about that? Is it something to worry about.
It’s an interesting study. I was surprised to see TG so much higher on the KD group. Where there is some variability in LDL (or LDL-P, apoB) in response to KD, there is almost uniform reduction in TG. In this cohort TG was more than 2x the control! So something was going on here and I suspect it may be the formulation of the KD, which they don’t specify.
This study has also a very funny conclusion: “This supports that arterial stiffness is an early marker of vascular damage.”.
How does showing that patients, that are on a ketogenic diet, have increased arterial stiffness parameters demonstrate that arterial stiffness is an early marker of vascular damage? The only way to demonstrate that conclusion would be to follow up a group with increased arterial stiffness in comparison to a control group and to show that the first group has higher rates of in Stroke, MI or other-CV-events.
Yes, another good point. I’d go a step further to day that I am not aware of a causal relationship between “stiffness” and vulnerable plaque–which is the issue of concern.
I have a question – my husband and I have been on the ketogenic diet for two weeks with no weight loss. We have been eating mostly protein and fat – steak cooked in butter, italian sausage (no sugar/carbs), etc. Our carb intake is most days less than 15g and we drink plenty of water, moderate exercise. What are we doing wrong?
I use free online carbohydrate measurements of daily carb intake, You may find that something you are eating has more carbs than expected. I only say this because you say there is two people in this, the best food measuring software that I have found is online ‘Fitday’. In any case I would bring up my fats higher than you have, I am lazy and have epilepsy and it has worked out fine. My suggestion is to measure your intake correctly, because before this I was in the same boat <50 carbs is enough.
I made your mistake before I developed a reaction to butter. When you intake butter you intake fat, but you also intake lots of carbohydrate and tyrosine, the tissue-creation protein. “Clarify” your butter into ghee, and use the ghee to fry your meat. Also, you can just eat the chilled ghee straight, because you need to increase your fat intake.
How to clarify butter…….
I’d say you’r eating too much protein.
Because the MCTs in coconut oil get shipped to the liver and turned into ketone bodies, they are often used in epileptic patients to induce ketosis while allowing for a bit more carbs in the diet.
“Take home message #3: We evolved to produce ketone bodies so we could not only tolerate but also thrive in the absence of glucose for prolonged periods of time. No ability to produce ketone bodies = no human species.”
It always sounds like glucose is the primary fuel and ketones are secondary. It appears to me that ketones were meant to be the primary fuel and glucose only generated internally in small amounts. Grain crops were probably the prime reason for the flip-flop.
After all my reading it would seem that higher levels of glucose in the blood is somewhat damaging hence the reason for insulin-stimulated glucose uptake. This would appear to be a defense mechanism against too much glucose. yes/no?
Ketones probably become primarily beyond a week of starvation, at least as suggested by Cahill’s starvation data.
In addition to blood glucose remaining stable while in nutritional ketosis, is it also common not to experience spikes in postprandial glucose levels due to lack of carbs (e.g. BG consistently in the 80s 1, 2, and 3 hours after eating)? I’ve been experiencing this, and am very interested to find an explanation.
1 month ago I started phase 1 of a low-card diet. During this time I drank no alcohol. I’m just a social drinker, I had 5 beers over 6 hours. This usually doesn’t have any effects on me. Does my alcohol tolerance drop, and if so are there any medical studies on this because I have been unable to find any.
Brian, most people report this, but I’m sure exactly why (admittedly I haven’t spent much time looking).
I have a question that I’ve been searching for an answer for to no avail.
Does each meal have to be in certain percentages, let’s say 70% fat, 25% protein, 5% carbs, or does the entire daily intake have to be the 70/25/5?
A typical breakfast is one egg, one ounce of cheese, one ounce of nuts. For ease of explanation, let’s just say all three meals are that. So would each meal have to be exactly this, or could I eat three eggs for breakfast, three ounces of cheese for lunch, and three ounces of nuts for dinner? I don’t know what the, I guess, metabolic rate is for the breakdown of food, so I don’t know if it wouldn’t matter if I just ate the entire percentage within a certain feeding period, say 12 hours, or if it’s a constant, short-term breakdown and, therefore, all percentages have to be maintained constantly for constant breakdown.
Help me, Obi-Wan Ketobi, you’re my only hope.
Hopefully this is the right place to ask this question. Ive been doing the 5:2 diet made popular by Michael Mosley for about 3 months now. I fast for two consecutive days and its essentially less than 100 kcal. I will have about 2 cups of coffee with skim milk (no sugar). Im pretty sure I go into ketosis by the second day. Ive noticed that if I touch my stomach (actually any part of my body really) with my hand that it feels hotter than it would normally. Ive not measured this in any formal way but Im pretty sure its not my imagination. Is this a known phenomenon? Do you run “hot” during ketosis?
Some have reported what is known as thermogensis from ketosis. Possibly regulated by FGF21.
Hi Peter I heard you on Tim Ferriss podcast and I am now experimenting with the ketogenic diet (KD) because both my parents have diabetes.
Can going on KD help with mental health issues? Considering telling some friends who suffer from bipolar to try this diet if it can help them.
I’ve heard several anecdotal reports of this, but I have not seen any clinical trial data.
Hello Peter and thanks for sharing all this wealthy and healthy information. My question is regarding Kambucha and Ketogenic diet. I brew homemade Kambucha and there is a substantial amount of sugar used in the process. My brews run a little sweeter than normal and I’m assuming I shouldn’t be drinking it while on the diet? Kimchi also has a substantial amount of carbs. I like the benefits that both these items have on my gut flora. What is your opinion on this topic and is there any other substitutes either than taking oral supplements?
Thank you, Peter, for the very informative information you’ve given on your site. I hope you can give me some insight on the question I have.
I need to know if it’s okay for people with Type 2 diabetes to use ketosis as a means of losing weight? I am on Metformin, 2000 mg a day and have not had any problems so far. I just worried now if it’s too good to be true that I feel this good and losing weight and yet damaging my body without knowing it???
KD is a very effective tool for people with T2D.
I love the mental benefits and fat loss while I am in nutritional ketosis. I tend to keep my blood ketone levels between 1.5-3 mm. I have one problem, however. I compete in Crossfit, and I find it extremely difficult to train at a high intensity while in ketosis. I almost feel as if I could pass out any second. I have been trying different things for about a year now and I can’t seem to figure it out. Any Advice?
I’m wildly carbohydrate intolerant and am a pre-diabetic even though I exercise a lot and have body fat around 13%. I’ve put myself on a very low carbohydrate diet (only from vegetables). My morning blood glucose has gone from an average around 115 to low 90s, high 80s after two weeks on the diet. I bought some keytone test strips but so far haven’t seen a positive result. I’m curious how long does it typically take or does that vary wildly person to person and is there generally a morning glucose level where one would start to think they are in ketosis?
Test strips, the blood test strips? Try modifying the amount of protein you eat the night before. See if reducing it a bit helps.
This might help https://www.marksdailyapple.com/why-am-i-getting-low-ketone-readings-on-a-ketogenic-diet/
I’m currently in year12 and am doing the elective The Biochemistry of Movement in Chemistry, and am completing an assessment on low-carbohydrate diets and exercise, and was wondering if you could provide any tips or advice? I understand if you’re too busy though. Thanks
Jeff Volek has written quite a bit about this topic.
hello peter ,thank you for info,please guide me what are those ideal blood glucose level numbers in ketosis and how to find out we are in ketosis.thank you
Hey Dr. Attia.
First off, thanks for all your research over the years. It’s eye opening to say the least.
I’ve a question if you’ve time to answer it.
Have you ever heard of The Carb Nite Solution?
Another doctor (Dr. John Kiefer) claims that the best way to lose weight is a combination of ketosis and carb loading. Basically after the introduction phase of ketosis (11 days), for a 6 hour window you eat what you want. Then you revert to keto again for 6.5 days, and the last halfday you carb load again. And on it goes.
According to Dr. Kiefer, your metabolism slows down the longer you’re in ketosis, and this carb loading spikes your metabolism to reignite optimum fat burning.
Conversely, you showed a slide in your presentation(s) where it displayed a huge jump in your metabolism when you were in long term ketosis with no carb loading in the interim.
I’m currently 14 days into ketosis, and my sweet tooth is kicking in! The thought of a carb nite is very appealing, but if it’s going to knock me out of ketosis for a couple of days for no boost in fat loss, I’d be disgusted with myself.
Have you any thoughts on the matter?
Thanks in advance.
I loved your article on ketogenic diet. My daughter is on it for epilepsy. (She’s 21). I got to thinking about the ketogenic diet and insulin, etc. When my daughter had her first seizure at age 9, it was mid morning and she had eaten a late breakfast. I wondered that day if it was because she had low blood sugar. We have always eaten healthfully…whole foods, low sugar, and are also vegetarian. Anyway, I always keep my mind open to a cure for seizures…and was thinking about all of this. The ketogenic diet (ratio of 2:1) has worked beautifully a Nd we are so grateful. Thanks for the research you are doing.
A close friend of mine was diagnosed in June with a brain tumor on her speech center. It’s since been successfully removed – the surgeon was quite proud that he was able to “get it all”. Great! It was determined that the tumor was secondary and from a melonoma, possibly from a large birthmark on her forehead that was removed not long after her birth. A subsequent PET scan and full-body exam found no evidence of cancer. Because of the near-miss with the tumor and the fact that while growing up in Australia she acquired more than her fair share of skin damage, I’ve recommended she adapt some form of ketogenic diet to “starve” whatever cancer cells might be lurking, in addition to it’s other health benefits. From what I’ve learned from various sources – including Dom D’agostina, cancer cells need glucose and/or glutamine, without this fuel they can not live or proliferate – do I have this correct? OK, now my question: If I’m not consuming carbs and am producing ketones, why can’t my pre-cancer or actual cancer cells simply feed on the glucose that I seem to have ever-present in my blood – during disciplined periods of good ketone-friendly eating my fasting blood sugar is around 80 mg/dL. I’ve recommended the diet to her, but am hoping she doesn’t ask me this question. What am I missing?
Hi Dr. Attia,
I am 54 and my husband and I started at a Longevity clinic about a year ago. At that time my IGF1 level was 68 where their ‘ideal’ range is 159-195. I was placed on a triple amino supplement combo to take 3 at nite before bed on an empty stomach (l-arginine, l-lysine and l-orthine). No matter – my labs yesterday said my IGF1 level was 56.3… it has continued to drop throughout the year. I did start ketogenic eating in combination with intermittent fasting 6 months ago and lost 10 lbs… I feel great! But the #’s seem discouraging. My provider has offered the growth hormone stimulator semorelin that I have researched. Any thoughts about taking this ? and is 56.3 way to low for someone my age? (I get the longevity thing, but I also want to be healthy 🙂 Thank you!
I just discovered this blog. I came here through a google search on your name after watching your moving TED talk about judgment over obesity and diabetes. My father is a Type 1 diabetic (probably a MODY, since it runs in the family). I am concerned for his health because of his diet. He has developed a pattern of eating as many carbs as he wants (fruits, rice, rotis lots of milk products) and then adjusting his insulin dose to sorta nullify the effect of his eating. I am from India and I don’t know about other countries but physicians spend very little time delving into the nutrition of their patients. So my father does not get a proper scrutiny at the doctors office. Now I have 2 questions from reading your post:
1. How does the biochemistry of glucose synthesis work in the absence of insulin? I mean with a fixed dose of external insulin, can a diabetic person reduce his carb intake significantly? And here, I am not even talking about hardcore keto people such as all of you. I am just wondering what happens if a person with type 1 reduce carbs under a monitored dose of insulin?
2. The current practice which my father has developed (of using insulin to reduce his blood sugar synthetically) seems wrong to me. I think between the time he checks his glucose his vital organs receive blood with an consistently elevated glucose. So even if it is 3-4 hours a day, is it enough to cause serious damage?