July 3, 2012

Understanding science

Good science, bad interpretation

Read Time 9 minutes

In 2012, the Journal of the American Medical Association (JAMA) published a study entitled Effects of Dietary Composition on Energy Expenditure During Weight-Loss Maintenance. While I’m guessing most readers have not read this study, I’m pretty sure most of you have heard about the results as it was all over the news this week.

I was fortunate enough to read an embargoed copy two weeks prior to publication with the caveat that I could not speak about it until it was released publicly. Furthermore, I’m friends with one of the reviewers who told me months prior that “a very interesting paper was going to hit a highimpact factor journal very soon.”  Completing my disclosure, I had become acquainted with the senior investigator on this study, Dr. David Ludwig at Harvard.

This study sought to test an important question:

When an overweight or obese person loses weight, how does their choice of macronutrients impact their tendency to regain lost weight?

This is important, of course, because as most of us know that while losing weight is difficult, keeping it off is even more difficult.  In fact, as the authors point out, only about 15% of people who lose 10% of their bodyweight can maintain the weight loss for up to one year.  The obvious question is why?

You’ll recall from this post, that we must always obey the First Law of Thermodynamics.  In other words, we accumulate stored energy (e.g., fat mass) when we are in a positive energy balance and we lose stored energy when we are in a negative energy balance.

Energy balance is a function of two variables:

  1. Energy input – what we eat
  2. Energy output – what we expend

Furthermore, energy output can be broken down into four sub-components:

  1. Resting energy expenditure (REE) – the amount of energy expended to stay alive at rest (e.g., energy required for basic cellular function like ion transport and respiration)
  2. Thermic effect of food (TEF) – the amount of energy required to process and digest food (I also include in this category the amount of energy lost as undigested material in stool)
  3. Activity energy expenditure (AEE) – the amount of energy expended by exercise and non-exercise movement (I consider these as two forms of expenditure)

The sum of REE, TEF, and AEE is called, appropriately, total energy expenditure (TEE).

Of these, REE is the dominant “sink” of energy output in most people, and it is generally proportional to bodyweight.  I’ll cover the importance of this momentarily.

The traditional model of obesity, the so called “calories-in-calories-out” model, says that obesity is caused by the energy input terms exceeding the energy output terms.  In the words of one prominent obesity researcher, “While it is mathematically true that someone who has gained weight has consumed more energy than they have expended, using the First Law to explain why someone gains weight is of little help.  The First Law is descriptive but not explanative.”

I couldn’t have said that better myself.  The mistake most folks make when using the First Law to explain weight gain (versus using the First Law to describe weight gain) is that they lose sight of the fact that these variables – input, REE, TEF, AEE – are linked.  They are dependent on each other.  They don’t exist in isolation.

Proponents of the Alternative Hypothesis argue that intake (i.e., food) plays a role on hormones and enzymes in the body that have a resulting impact on energy output, and even subsequent input.  For example, eating one food over another can increase or decrease appetite, increase or decrease REE, increase or decrease AEE, and even impact TEF.  While the effect on each of these may be modest in isolation, even small changes over the course of days can result in significant changes over months or years.

What does all of this have to do with this study?

The figure below shows how the study was conducted.  This was a prospective design 3-way crossover study of 21 overweight or obese subjects with an average BMI of 34.4.  Each subject underwent a 20-week run-in phase, which is very common in weight-reduced studies.  During the run-in phase all baseline measurements are collected, including body composition by DEXA, TEE by doubly-labeled water, substrate utilization by respiratory quotient, and plasma levels of various blood markers (e.g., lipids, blood chemistry, hormone levels).  No, unfortunately, lipoprotein particles were not counted.

During the 12 week weight loss phase caloric intake was reduced until each subject lost 12.5% of their starting (stable) weight.  For the final 4 weeks of the run-in phase energy intake was again calibrated to hold their now-reduced-weight stable.

 

The figure below summarizes the data from Table 1 of the paper, showing the breakdown of macronutrients during the run-in phase and the subsequent 3 dietary interventions, each lasting 4 weeks.  Again, each subject did each diet for 4 weeks due to the 3-way cross-over design.  In other words, each subject spent a total of 32 weeks in the study (20 weeks of run-in and 3 x 4 weeks of each intervention diet).

 

How did the diets impact energy expenditure?

The figure below shows the change in REE and TEE measured for all groups.  There was no difference in total physical activity or exercise, so presumably there was no appreciable change in AEE.  I could not find a mention of TEF, suggesting it was not measured.   These figures are a bit ugly, but they convey helpful information.  Each dot represents an individual subject and the lines joining each dot allow you to see the change for each subject across the 3 diets.  The blue box shows the mean change (middle of the box) with the 95% confidence interval above and below.  The height of the box is therefore two standard deviations.

 

 

A few things stand out from these results:

  1. The group consuming a very low carbohydrate diet had a higher REE and TEE than the low GI group, which had a higher REE and TEE than the low fat group. In other words, the fewer carbohydrates in the diet, the higher the resting and overall expenditure.  This is actually the sine qua non of the alternative hypothesis: something beyond the actual number of calories is playing a role in how the body expends energy.
  2. As expected, given that each subject was starting from a weight-reduced state, the REE was lower for each group, relative to their baseline.  REE is highly (though clearly not entirely) dependent on body mass.
  3. There is enormous variation between subjects by diet type.  For example, at least one subject saw a dramatic increase in TEE on the low GI diet versus the other two, while another saw the greatest TEE on the low fat diet.  This speaks to a theme I iterate on this blog: be willing to self-experiment until you find what works for you. 

How did the diets impact metabolic parameters?

The table below shows the changes in hormone levels and metabolic syndrome biomarkers.

One thing that really jumped out at me was that it is quite likely that not one of the subjects in the study met the formal criteria for metabolic syndrome.  MS requires at least 3 of the 5 parameters (blood pressure, waist girth, fasting glucose, HDL-C, and TG) exceed threshold.  The thresholds are as follows:

  1. BP > 140/90 [No subject met this at baseline]
  2. Waist girth > 40 inches (men), >35 inches [Not reported, but let’s assume at least some subjects met this]
  3. Fasting glucose > 100 mg/dL [Not reported, but let’s assume at least some subjects met this]
  4. Fasting TG > 150 mg/dL [No subject met this at baseline]
  5. HDL-C < 40 mg/dL (men), < 50 mg/dL [No male subject met this, but it’s possible some female subjects did]

This may speak to the age of the subjects, which averaged 30.3 years, but I would have expected a worse set of baseline metabolic parameters. It also speaks to the point that just because someone is obese doesn’t mean they have metabolic syndrome and vice versa.

 

Tables are a bit cumbersome, so I took the liberty of graphing some of these results, mostly because I just can’t resist playing with think-cell (PowerPoint without think-cell is simply a tool for torturing people.)

I’ve explained p-values before, but let me explain the two types of p-values reported above and below.

P_overall is the p-value testing the hypothesis that the mean outcome of the three diets was equal.  The smaller this value, the more likely the differences were not due to chance.  As a general rule, if the p-value is greater than 0.05 we say the difference is “not significant.”  Most use a more stringent requirement of 0.01 to hit the mark of statistical significance.

P_trend is the p-value testing the hypothesis that the mean outcome of the three diets showed a trend from low fat to low GI to low carbohydrate.

 

Not surprisingly, the low fat group experienced a significant reduction in HDL-C.  It’s been documented many times that dietary fat raises HDL-C and dietary carbohydrates reduce HDL-C.

Each group also experienced a reduction in triglyceride (TG) level.  Since we know carbohydrates, not fat, raise TG, you may wonder why this was even the case in the low fat group, which actually increased carbohydrate intake.  I suspect it was a carbohydrate “quality” issue.  I’m guessing the baseline levels reflect more sugar consumption than the low fat phase.  Nevertheless, and again not surprisingly, the high fat-low carbohydrate group experienced the greatest improvement in plasma TG levels.

 

 

Insulin sensitivity was measured according to a protocol in this paper.  The protocol uses time blood draws after an oral glucose challenge.  The higher the index, the greater is the insulin sensitivity.  Each diet improved both hepatic and peripheral insulin sensitivity and both the overall differences and the trends were significant.

If insulin is the most important hormone regulating fat metabolism and accumulation, leptin is certainly a close cousin.  Leptin is a hormone secreted by fat cells that plays an important role in regulating appetite and some metabolic functions.  High levels of circulating leptin can be suggestive of leptin resistance which, like insulin resistance, tends to be a marker for metabolic derangement.  I’ll write a lot about leptin in subsequent posts.   While leptin sensitivity was not directly measured as insulin sensitivity was, the significant reduction in circulating leptin levels suggested it was also improved in all groups, though greatest in the low carbohydrate group.

How did the diets impact inflammation?

Two markers for inflammation were evaluated in this study, C-reactive protein (CRP) and plasminogen activator inhibitor-1 (PAI-1).  Neither is particularly sensitive in the way, say, Lp-PLA2 is (this was discussed in the cholesterol series). Nevertheless, they give us some indication of how much overall inflammation exists in the body.

 

Each group experienced a significant decline in both PAI-1 and CRP, and there was no significant difference between the groups for either marker.  However, the trend was (barely) significant favoring the low carbohydrate group for PAI-1 and favoring the low GI group for CRP.  Sorry low fat, you didn’t win either.

I know what you’re thinking because it was the first thought that ran through my mind when I saw this table:  What?  Is this meaningful or is it an example of statistical chicanery?  I’ll let you decide, but I’m pretty sure I know the answer.

Because I know some of you will ask, I will comment in a subsequent post on the changes seen in TSH, T3, and cortisol.  These topics deserve a post of their own.

What should have been taken away from this study?

This study reproduced a number of results which have been noted for decades:

  1. Low carbohydrate, high fat diets reduce TG and raise HDL-C more than other diets.
  2. Low carbohydrate, high fat diets improve insulin sensitivity more than other diets.

It never hurts to hammer those findings home again, but the really dramatic finding of the study was the impact of macronutrient balance on REE and TEE.   At previous count (circa 2011), 81 studies over the past 80 years involving 4,094 subjects for more than 1.2 million subject-days have attempted to ask this question – many of them attempting to “prove” that all calories are created equally.  While none (i.e., not one) have refuted the alternative hypothesis, most of them had enough methodologic limitations that it was difficult to know for certain if the type of food – rather than the number of calories – was playing an important role.

This study, while still limited (e.g., short duration, small sample size), makes one of the more compelling cases that all calories are not created equally.

What was taken away from this study?

The embargo on this paper was lifted at 4:00 pm EDT on Tuesday, June 26, 2012.  Within about 30 minutes I was being bombarded with news stories that, if you hadn’t read the study, as virtually no one actually does, would suggest that the low carbohydrate diet was the “worst” of the three diets tested.  This was not universally true, in fairness to the media, but there was no shortage of this sort of commentary:

USA Today

…the authors note a downside to the low-carb diet: it appears to raise some risk factors for heart disease.

Marion Nestle, a nutrition professor at New York University, says longer studies conducted among people in their own environments, not with such controlled meals, have shown “little difference in weight loss and maintenance between one kind of diet and another.”

George Bray, an obesity researcher at Pennington Biomedical Research Center in Baton Rouge who has also studied this topic and who wrote the accompanying editorial in JAMA, says that other studies “show that you can do well on any diet as long as you stick to it. Adherence is the major key for weight loss and maintenance. There is no magic in any diet.”

The New York Times

…the low-carb diet “also had marked problems. It raised levels of CRP (c-reactive protein), which is a measure of chronic inflammation, and cortisol, a hormone that mediates stress.”

The Wall Street Journal

…the low-carb diet had the biggest boost in total energy expenditure, burning about 300 calories more per day than those on the low-fat diet — about the same as an hour of moderate exercise. But that bump came at a cost: increases in cortisol, a stress hormone, and a measure of inflammation called CRP, which can raise the risk of developing heart disease and diabetes.

Some of these comments were patently false (e.g., “the low carbohydrate diet raised levels of CRP” according to the New York Times), reflecting utter incompetence, but most of them commit a different journalistic sin: They miss the forest while machinating on one leaf.

Tragically, most people (unfortunately this includes physicians, dietitians, and politicians) have neither the time nor scientific discipline to wade through these studies and understand their implications.  Instead, they rely on “reputable” journalists to translate for them.

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281 Comments

  1. Hopefully, it is not against protocol here to note that Gary Taubes is featured on this week’s EconTalk podcast:

    http://www.econtalk.org/archives/2012/07/taubes_on_why_w.html

    (I am sure it is great, but I won’t have a chance to listen to it for a few days…)

    I figure that this only fair as it was Gary’s original interview on EconTalk back in November:

    http://www.econtalk.org/archives/2011/11/taubes_on_fat_s.html

    That was the AHA! moment for me and led me to read his books and eventually discover Peter’s site.

  2. Peter,

    I have been reading a lot of research articles about the effects of hormones on the body at the cellular level (as well as Good Calories, Bad Calories) and their effects on lipoprotein lipase in storing fat in adipose tissue. Research by a woman named Greenwood talks about how when progestin is added to Zucker rats the LPL activity on the fat cells increases. Does this mean that women who are on birth control that contains progestin (or progesterone) will likely have difficulty losing weight even if on a low-carb diet? Insulin would no longer be present to shuttle the glucose/fat/protein to the fat cells, but progesterone’s affect on LPL (the gate keeper to the cells) might combat the gains that could be made on a low carb diet. I ask because I have been doing the low carb diet for 5 months now, 20-25g of carbs daily with an increase in fat in the recent months (cream cheese, coconut oil, etc). Granted I am 5’11 and weigh 150lbs (where I should be for my BMI), but I would like to tone up and lose the excess fat. However, my weight has not budged and I was curious to know if it had to do with the progesterone in my birth control? Do you know much about other hormones’ affects on fat metabolism?

    • Corrie, the effect of hormones on LPL is significant as you note. The effect of E and P on LPL (in addition to insulin’s dramatic effects) may partially explain fat differences in men and women, and pre- and post-menopausal women. However, there could be many reasons to explain the lack of weight loss. Figuring it out would require a lot more detective work.

    • I read through your personal testimony and read about your results. Did you notice once you began a more drastic Carb restriction that it was difficult to slim down in your abdominal area, or that it took longer? Since you mentioned that’s where your body chose to store fat. How long did it take to get to the waist size you are now? Do you think there is a set point for everyone as far as weight goes? Maybe there’s a certain weight that your body likes and doesn’t want to lose anymore fat? Or is there always room for improvement on a high fat low Carb lifestyle, it just requires a more strict restriction of carbs, or possibly resistance or weight exercises added with it?

      • I think there certainly are set points. It’s taken 3 years to take 5 inches off my waist in a manner I deem “sustainable” for me, and it has not been a monotone decrease, either. There are many plateaus, of course, so you’ve got think LONG term…as in a lifetime of change and tweaking.

    • Thanks very much for this, Andrew. Kind of amazing that NYT would run a LOOOONG piece on this featuring someone who hadn’t read the paper *without* contacting the author of the study…then only give him 150 words to respond. Better than nothing, I guess.

  3. Has anyone considered the worlwide impact of these diets on the Earth? Can we support this for everyone or are we just talking about an elite class that can personally afford these menus along with our big screen TV’s and iPhones? Are there other healthy options?

    • Lots of folk have, but largely with incomplete and inconsistent science. I think this is an important question, but it is a distant second place to the first-order question: what should we be eating to be healthy. If we don’t know the answer to that, what difference is sustainability? These issues get confused too often.

    • Yeah, that’s a fair question, Keith, and it’s one I seem to hear a lot from family and friends. Like “well, there’s not enough land on earth or air in the sky for all the animals we’d need and methane they’d fart out if everyone ate as much meat as you, John” Sustainable choices are things I want to consider as I continually tweak my diet, but on the other hand, I also don’t want to be that guy who says “Yeah, sure, LCHF with lots of animal proteins/fats is better for you, but it’s not sustainable…so let’s keep eating stuff that makes us obese, gives us heart disease, diabetes, cancer and kills us prematurely. After all, that’s more sustainable. You see my struggle?

  4. great articles. just also read the cholesterol blog. just got home today with my new heart stent due to a clogged artery (plaque). Now , how do I now continue to convince myself, my doctors and family, that despite needing this stent , which really came at a shock to me. discovered the blockage when i increased my exercise regime. I am s. fla and am not feeling like I will get any help maintaining a low-carb, high protein regimen . how do I get my doctor on board with me ? immediately the statins are out and have been read the riot act !

  5. I am encouraged by seeing medical people like yourself actively involved . maybe when it goes more mainstream, it would benefit all of us, you have the advantage of access to the proper tests of true measure of health, not some cookie cutter formula and knee jerk “standard ‘ test’s we all get shuffled into.
    my breakfast in the heart wing this morning was scrambled egg with a piece of pound cake?? oatmeal?? lunch was something breaded , white rice, margarine? how are we to get /stay healthy when this is their idea of “good eats” for me? it is maddening ! hope to get some support, feel like , now my life REALLY depends on it!

  6. I found this statement confusing: “Not surprisingly, the low fat group experienced a significant reduction in HDL-C. It’s been documented many times that dietary fat raises HDL-C and dietary carbohydrates reduce HDL-C.”

    If dietary carbs reduces HDL-C, why is it “not surprising” that low fat reduces “HDL-C.” Sorry for the confusion.

  7. Just a minor statistical quibble: when you say “The blue box shows the mean change (middle of the box) with the 95% confidence interval above and below. The height of the box is therefore two standard deviations.” shouldn’t the last part be “two standard errors” (i.e., SD / sqrt(N))?

  8. The 1000 dollar question should maybe be: “WHY do people (researchers, the media) often try to angle their conclusions towards the angle “Low Carb Is Dangerous” even though the data says something else?” Is it (putting on my tin foil hat) the Sugar Lobby? Or is it just the old Fear of Fat that lingers on? This is something I haven’t seen anybody discuss.

  9. I am very interested in your futher comments on TSH, T3, and Cortisol. I am almost 4 months into a Ketogenic Diet – initially started to support my husband who has Type I Diabetes and is having great success with his BG readings. I have Hashimoto’s Thyroiditis and while my lipid profile (done two months into diet) was excellent by all standards…my TSH was low (and went lower still); my T3 was low; and my 24 hour urine Cortisol was high. I am seeing my endocrinologist next week and coincidentally came across this post. Would love some info in hand when I see her.

    Your quote from above article:
    “Because I know some of you will ask, I will comment in a subsequent post on the changes seen in TSH, T3, and cortisol. These topics deserve a post of their own.”

  10. Just a notion about a experiment.

    One of the things I’d love to see highlighted in an expertimental design is a stunningly important distinction between low carb weight loss diets and effectively everything else…which is that everything else is calorie or portion limited and low carb is classically ad libitum within accepted foods. The importance of this is glossed over in designs that compare the results of weight loss diet regimens. Since these designs take each regimen at face value the critical fact that one group is forced to eat less than it chooses and the other is not is rendered unimportant.

    The two buffets experiment:

    One nice resort or cruise ship…6 weeks, two different kinds of buffets 3 weeks each.

    Participants get a free long resort vacation with all food free in exchange for agreeing to a lot of testing and monitoring (which is designed to be as unobtrusive as possible.)

    Participants aren’t allowed to bring in any food. All food is provided at the resort’s buffet which is open much of the day. Participants are not made aware of the purpose of the study. Various resort activities are also provided and activity is monitored.

    One buffet is designed by Dr.Attia, one by a well known representative of the mainstream…say Dr.Ornish. Each side has control of the menu and presentation…but of course no control of what or how much any participant eats. Participants are not in any way told to restrict their eating…other than the control inherent in the fact that the only food is at the buffet…eating is completely ad libitum. Both Attia and Ornish menus strive for food variety, quality and presentation over the entire study that meets appropriately high resort standards.

    One of the things measured is what everybody eats and how much. I picture a scale with a camera that takes a second to register who, what and how much.

    Participants activity levels are measured and everybody gets several full physicals with bloodwork…etc. hey it’s the price of a long free resort vacation.

    The study is interested in the the effect of diet composition in an unconstrained completely ad libitum setting on physiology. There is absolutely no effort to seek weight loss or any other outcome…the only variable is the buffet.

    Half the period is Attia buffet, Half is Ornish buffet. Three weeks each. Everything remotely reasonable about the participants is monitored.

    If the Alternative hypothesis is correct, the nature of the choices in the Attia buffet will have a significantly different impact on the participants than the choices in the Ornish buffet. Since the partipants are not “dieting”, not seeking to lose weight and in fact are unaware of what’s being studied…no distortion is introduced by one experimental group being restricted while the other is not. The same participants are exposed to both buffets for an extended period allowing within subjects tests.

    If the Attia buffet has lobster tails in butter, flilet mignon, asparagus and hollandaise ….and the participants entirely at liberty choose to eat less of it…would the lipid hypothesis – calories are calories – folk say it was because it was was so boring and unappetising?

    • Mark, that’s a very elegant idea. If the low carb cruise had better results (just focus on weight loss), there would be at least 3 NOT mutually exclusive explanations:
      1. They consumed few calories (perhaps because they were less hungry; for others, perhaps “bored”)
      2. They were more active, either deliberately or spontaneously
      3. In a lower insulin environment, they increased lipolysis relative to re-esterification and this was manifested by an increase in REE (a la David Ludwig’s JAMA paper).
      Of course, any combination of the his would work, too.

  11. I think it could provide pretty solid data about 1 and 2.
    People in AI resorts typically wear little ID bracelets anyway. In this case they are bit bigger and have a QR code on top and a little pedometer/pulse reader on wifi. There are workers standing there to help in the buffet anyway…they monitor and assist with the simple protocol which is every time they get a new plate of food they put it on a convenient scan station. The station weighs it subtracting the weight of the plate, scans their bracelet and takes a photo of the plate. Later people follow a protocol to enter data about foods and portion weights…and the menu data has exact nutritional numbers for each dish. When they are finished the plate is run through again to subtract the uneaten portion. It’s not accurate to the microgram but it’s a pretty fair aproximation of what every participant is eating which is a whole lot better than many designs.

    The pedometer/pulse reader provides constant data and of course it’s used with a lot of detailed data about each particpant…height, weight, age, etc. That would provide a pretty decent metric for activity level…not calorie by calorie but decent.

    As towhat they were thinking…for a lot of reasons it would be good to have an experimental psychologist in on the design. A worker with a ipad taking daily surveys…if well designed could go a long way to answering that. They would just seem like obsessive consumer satisfaction surveys. Less hungry or bored ought to show up pretty clearly in a good design. It’s not that subtle a psychological question in this context.

    Neither of these data streams are very intrusive. Most casual observers would barely notice them. The devices and coding are pretty basic stuff cobbled together out of common cheap digital devices.

    One potential confound is if particpants have some idea what’s actually being studied…and if they have some existing opinion or bias about the outcome. This is another reason for experimental psychologists. This can be detected and dealt with.

    One odd possibility is that the study could make some extra money to help reduce expenses …and help provide a layer of misdirection at the same time. This kind of captive audience is used by both companies selling stuff and market reasearchers. You could sell an hour or so a day of your captive audiences time to outsiders. This would provide a very plausible cover story misdirecting attention away from possible confounds if participants have an idea what’s really being studied. A hour a day of focus group or timeshare condo sales and nobody would be looking for further explanations of what’s really going on.

  12. Pardon if my comment makes no sense, great article btw… I’ve posted about this study and a rather smart guy mentioned how he didn’t like the study. For one stated that the DEXA results “went missing” or something like that. Do you have any updated thoughts on this study?

    thanks

    • They only did baseline DEXA. No subject had follow up DEXA due to the short duration of the study. Nothing went missing. It was never intended. The follow up version of this study, which will be much longer, will include this and more.

  13. I have recently started on a ketogenic diet after seeing one of your youtube interviews. The area of concern I have is with flow mediated dilation (FMD) studies conducted with various fats. How does that square with CVD risk?

    Mike

  14. The testing Vogel has done using FMD seems to indicate that a high influx of fat causes inflammation in the blood vessels…at least temporarily. Apparently it takes several hours for the vessels to return to their normal cross sectional area. If one is regularly consuming saturated fats (as I am now) do I need to worry about chronic inflammation at each meal?

    • You’re going to have to send me the exact paper Mike. I get about a hundred “what do you think of this” emails a day. Hope you can appreciate writing this blog is the lowest priority of my life (family > NuSI > training > …. > blog). If I’m going to spend a minute answering a question, don’t make me chew up the minute looking for the paper.

    • I don’t get this journal without paying, so can only read abstract. Not able to comment without really understanding this methodology. I’ve never found studies like this to be especially helpful, unless they can be translated to meaningful outputs.

  15. This study seems to portion the blame of this observation on high levels of serum triglycerides which overall as I have observed personally and from what other people and studies have demonstrated seems to dramatically decrease on a High Fat low Carbohydrate diet.

    • That’s certainly a problem with it, since there is no debate in the literature (or all practical experience) that isocaloric replacement of carb with fat decreases TG and raises HDL-C. There may be a 1-5% exception to this rule based on apoC-III deficiency. So out of the gate this seems odd. Perhaps there was something else in the meal? Perhaps the technique is measuring an artifact? Perhaps this effect is so transient as to not be clinically meaningful? Or maybe it’s all true. Who knows.

  16. It seems they introduce carbohydrates into the testing that I have seen i.e., bread with olive oil. In any case, I intend to proceed experimenting with LCHF (into my 2nd week). I will test my ketones with a meter and also get my blood tested for the parameters that have been discussed. My previous HDL level was 34 (TCL = 140) based on a mostly plant based diet. I expect an improvement there. Thank you for such an informative site!

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