Thoughts on the Pritikin Diet

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Denise Minger wrote a very thought provoking post on the very low fat Pritikin Diet and how it can help reduce disease including diabetes and cancer. In the first part, I wrote my thoughts on the Kempner Rice diet here. The Pritikin diet is primarily composed of high fibre, high carbohydrate, low-fat, plant based foods. With his close relationship to McGovern, this diet formed the basis of many of the low-fat, carbohydrate based recommendations of the 1977 Dietary Guidelines for Americans.

Over some decades, his colleague RJ Barnard published many studies on this diet and how it could reduce many different diseases – mostly those associated with the metabolic syndrome. For example, this diet could help reduce prostate cancer, reduce insulin and medication usage for type 2 diabetes, reduce LDL oxidation, reduce breast cancer, reduce colon cancer, reduce heart disease, and improve cardiac risk factors.Minger1

Furthermore, there are many traditional societies that ate a similarly ultra low fat, whole, unprocessed vegetable based diet that had low incidence of all these diseases. The Okinawans and the Kitavans come to mind quickly.These are many of the same benefits that low carbohydrate diets also claim. How can very low fat diets have the same benefits as very low carbohydrate diets? Perhaps there are, as Denise suggest, two different kinds of ‘magic’ going on?

The Pritikin results are clearly at odds with the Carbohydrate-Insulin Hypothesis (CIH) which holds that high carbohydrate diets result in high insulin and therefore obesity, T2D, and the rest of the metabolic syndrome. High carbohydrate diets should have the opposite effect as high fat diets.

So, is Denise right? Does the Pritikin diet have some ‘magic’? Here’s a surprise. I almost completely agree with Denise.

The answer is this. Macronutrients, just as with calories is the wrong measure of a diet. This is nutritionism’s greatest blunder. This refers to the fact that trying to reduce the complexity of foods and their effect on humans to some mix of macronutrients (fat, protein and carbs) is completely wrong.

Carb-Insulin-Hypoth

The CIH, depicted above, as it stands is clearly inadequate. There are too many inconsistencies, which I’ve written about in a previous post – unimaginatively titled “The Carbohydrate-Insulin Hypothesis is Wrong“. The Asian diet of the 1990s for example were very high in carbohydrates, but did not lead to obesity. The main problem with the CIH is that it does not take into account the multiple factors that lead to an increased insulin level (you can review my 50ish posts of the Calories/ Hormonal Obesity series for more background).

Increased insulin leads to obesity and the metabolic syndrome. And sure, refined carbs lead to increased insulin, but they are not the only things that do so. This sort of simplistic theory does not account for, among other things, the deadly effect of fructose, the time dependency of insulin resistance, animal protein, fibre, vinegar and fermentation effects, or dietary fat. CIH pretends that the only thing that matters is the amount of carbohydrates. So it’s wrong. But it’s not really incorrect, so much as incomplete. Yes, carbohydrates are a big part of increasing insulin, but they are not the only part.

NewHOT12

A more complete version would look like this – the Hormonal Theory of Obesity. Notice that insulin is still at the core, but there are many inputs and protective factors – only one of which is carbohydrates. There are many things that raise insulin and many things that also lower insulin. The CIH was too simplistic, and therefore, incorrect.GL

In addition, the use of macronutrients instead of foods complicates things significantly. Not all carbohydrates are the same, just as not all fat or proteins are the same. For example, the amylopectin (a type of carbohydrate) produces vastly different effects depending on whether it comes from wheat or from beans.  Amylopectin A is not the same as Amylopectin C. You can see this effect in the Glycemic Index.

Carbohydrates are not all equal. Unprocessed, whole carbohydrates, yes even boiled potatoes have a much, much smaller effect on glycemic load than processed carbs like cornflakes. For carbohydrate foods, there is a close correlation between GL and insulin secretion. So 30 grams of carbohydrates can either be the most healthy looking lunch you’ve ever seen, or 1 hamburger bun. So focusing simply on macronutrients, whether fat, protein, or carbs is simply wrong. We need to talk about foods, not macronutrients.Slide4

So, looking at the more complete Hormonal Obesity Theory (HOT), you can see that insulin is what drives obesity, but carbohydrates are not necessarily what drives insulin. Non-caloric, non carbohydrate factors such as cortisol (stress) can also play a big role in insulin and weight gain.

So the key question with regards to the Pritikin Diet is not how many carbs, or how much fat, or how many calories. The hormone insulin is what drives obesity. Therefore, the key question in this diet, as with all diets is this:

What happens to insulin?

If a high fibre, high unrefined carbohydrate, diet lowers insulin, then we should expect all the benefits of reduced weight and reduction in all of the manifestations of hyperinsulinemia – Type 2 Diabetes, Hypertension, heart disease etc. If a Low Carb High Fat diet also lowers insulin, then we should see all the same results. And guess what? I don’t really care if you eat LCHF or Pritikin – as long as those insulin levels come down, I don’t care. Why? Because you will derive the same health benefits of lowering insulin. This will be highly beneficial in all the diseases of high insulin (metabolic syndrome).barnard_2008_graph

In other words, we need to evolve from a carbohydrate centric view of obesity (CIH) to an insulin-centric view of obesity (HOT).

So let’s look closer at the Pritikin diet, and others based on it, like the Ma-Pi diet. Insulin goes down. A lot. Even though carbohydrate consumption is high.

Why? Well, the Hormonal Obesity Theory explains why. The carbohydrates being eaten are whole unprocessed ones which do not increase insulin as much (low glycemic load). There is little to no fructose. There is lots of fibre (protective). There is less animal protein (insulinogenic).

This is not a high insulin diet! It lowers insulin. Therefore, I would expect that it lowers weight and the rest of the metabolic syndrome as well. And that’s exactly what Pritikin, as well as Neal Barnard and others have shown. Obesity, T2D, and the rest of the metabolic syndrome are simply different manifestations of hyperinsulinemia (too much insulin). Therefore, any diet that lowers insulin will show incredible benefits. This includes the Pritikin Diet as well as the LCHF and Paleo and Atkins diets. Forget about macronutrient composition of diets. I’ve always tried to stress one point – The toxicity lies in the processing, not the macronutrient composition. You could even live in the macronutrient swampland and do well. But you must keep insulin levels low.Kitava-Insulin

So, I do disagree on one semantic point with Denise. I don’t think there are two types of ‘magic’ here. There is only one type of ‘magic’ – lowering insulin results in benefits in a high insulin disease state. But there are two different ways to get there. Both Pritikin and LCHF work fine. Actually – there are multiple ways to get there – Mediterranean, potatoe diet, Zone Diet, Weight Watchers etc.

Can you eat a high carb diet and still have low insulin? Of course. Because carbohydrates are not the only stimulus to insulin. The Kitavans – a traditional Pacific Island society demonstrate this perfectly. Eating a diet that is estimated at 70% carbohydrate – unprocessed, whole foods with almost no sugar, the Kitavans maintained a serum insulin level lower than 90% of a typical Swedish person.

So, you might be wondering, why do I describe my diet as predominantly LCHF with Intermittent Fasting (another great way to lower insulin)? Well, because most people want the Twitter version of my dietary theories, rather than slog their way through 50 or 60 posts (although my upcoming book will make that easier). The closest approximation is LCHF with IF.  It also differentiates it with the failed Low-Fat movement of the last 50 years.

One last point. I absolutely love the fact that Denise entitled her post – A Call for some Evolution of Thought. Because too often we are bogged down in the Low-Fat vs Low-Carb wars. That’s soooo 2007. Or Caloric Reduction as Primary (CRaP). That’s soooo 1982.Or the CIH. That’s soooo 2010. We need to evolve our understanding of what causes obesity. What is the aetiology of obesity? (That was the original title of my book – The Aetiology of Obesity, but the editors hated it. Too nerdy)Imbalance

We need to move forward from the failed ‘Calories causes Obesity’ paradigm. But just as surely, we need to move forward from the failed ‘Carbohydrates causes Obesity’ paradigm. Let’s face the facts head on. We’ve done Atkins. It was not the effortless weight loss promised. The underlying Carbohydrate-Insulin Hypothesis was woefully incomplete. But the Insulin Hypothesis is still intact. Obesity is a hormonal, not a caloric imbalance. But carbohydrates was not the entire story. There is so much more – stress, and sleep, and cortisol, and protein, and fibre, and fat, and fructose, and insulin resistance and vinegar, and fermentation, and the incretin effect.

Forget macronutrient content. It’s not the Fat. It’s not the Carbs. It’s not the Calories. As my friend Amy Berger of TuitNutrition says, It’s the Insulin, stupid!

2017-09-02T11:54:11+00:00 45 Comments

About the Author:

Dr. Fung is a Toronto based kidney specialist, having graduated from the University of Toronto and finishing his medical specialty at the University of California, Los Angeles in 2001. He is the author of the bestsellers ‘The Obesity Code’ and ‘The Complete Guide to Fasting’. He has pioneered the use of therapeutic fasting for weight loss and type 2 diabetes reversal in his IDM clinic.

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bill
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Don’t know where you got your numbers, but
this: http://www.health.harvard.edu/healthy-eating/glycemic_index_and_glycemic_load_for_100_foods
states that glycemic load of white bread is 10 and
GL of grapes is 11.

Glycemic load is too subjective. Who knows
how much a person eats of any food item? The
better gauge of food’s effect is glycemic index.

A much better analysis is Marty Kendall’s site:
https://optimisingnutrition.wordpress.com/2015/10/19/optimal-foods-for-different-goals/

Jane
Guest

Without re-working the math, I would guess that Dr. Fung adjusted the load data according to a constant weight of the items he graphed, instead of the “serving size” as reported on the site at the link you posted. So he may be reporting glycemic load per 100 g.
On the site you link, the serving sizes vary by quite a bit. E.g., the white bread serving size is 30 g, but the grapes serving size is 120 g.

bill
Guest

Jane:

Apparently you have never heard of the “glycemic load.” It is
the “glycemic index” adjusted for the (subjective) typical amount of
any food eaten. Therefore, completely meaningless.

You are back engineering the load to the index.

michael
Guest

So rude, so sure of yourself, and so easily shown to be wrong, all at the same time: https://en.wikipedia.org/wiki/Glycemic_load

bill
Guest
Michael, from your link: “…estimates how much the food will raise a person’s blood glucose level after eating it.” Sounds pretty subjective to me. Again from your link: “Glycemic load estimates the impact…” “…watermelon has a high GI, but a typical serving of watermelon does not contain much carbohydrate, so the glycemic load of eating it is low.” See that? “estimates” and “typical serving.” Pretty subjective, no? And how ’bout this whole paragraph, again, from your link: “For one serving of a food, a GL greater than 20 is considered high, a GL of 11-19 is considered medium, and a… Read more »
Sky King
Guest

Hey, Bill! I think a better guideline than the glycemic index would be the insulin index:

http://www.nutrientdataconf.org/pastconf/ndbc35/4-2_sampson.pdf

bill
Guest

Sky King: Looks great.

Digby
Guest

Thank you for this! I hadn’t seen it before. Very useful.

Jerome Benthamite
Guest
Dr Fung A question: Insulin signals cells to store fat and burn glucose (and other functions). I have been struggling with the question of the function of insulin when on a ketogenic, Atkins type diet, since glucose is already quite low. As you point out in your blog that protein (certain amino acids) stimulates the release of insulin. The insulin index of fish is 59 and meat 51(white bread 100). Since on the ketogenic diet many of these dieters consume more than 100 grams of protein a day, I wonder what’s the function of insulin–lowering glucose would result in hypoglycemia?… Read more »
Amy
Guest

Great question, Jerome. Check out this post for a potential answer. (Not the only one, perhaps, but at least filling in some small piece of the puzzle.) Insulin is anti-lipolytic, anti-catabolic. We do need *some* insulin to counterbalance glucagon, otherwise we’d all completely waste away via unchecked catabolism of both adipose tissue and muscle. This is what happens in type-1 diabetes. http://www.tuitnutrition.com/2015/10/its-the-insulin-3.html

Mark
Guest
It’s my understanding that protein, like carbs, is also turned into glucose when digested, though not as directly and problematically (in general) as carbs are. I suspect that the degree and manner in which protein is converted to glucose is dependent on a lot of factors, just as the insulin response from eating protein is not so well understood (as I think Dr. Fung has mentioned a few times). If this is right (and I’m no expert), then it seems appropriate that the insulin response in a healthy body from eating a specific protein meal would be commensurate with the… Read more »
Jane
Guest

Thank you!!
— for explaining so many metabolic issues with such clarity!
— Elegant & Concise

Jane
Guest

Dr. Fung,

No doubt you have already planned your future posts.

You and Minger both mention the issue of oxidized LDL as related to diet.

I hope that sometime you can address the dietary and metabolic factors that are involved in that oxidation, as well as in raising serum Apo B or LDL particle numbers.

In other words, add to the story about diet patterns and atherosclerosis, body fat, and diabetes.
Perhaps I have missed or forgotten what you have already posted about these issues.

Again, thank you for all your help.

John C
Guest
Thanks for another insightful article. Yet again you have helped me to understand a little more of the overwhelming complexity of nutrition and its effect on health. I’ve been struggling to understand how I did just as well with calorie restriction as with LCHF plus IF. I just found the latter much easier to stick to because it did away with hunger and cravings. I knew that what I was doing worked in practice but I couldn’t find a theory that explained it. LCHF/IF came closest but now CIH is an even better fit. Thanks for putting it into words… Read more »
Tim Heineman
Guest

I find Peter Dobromylskyj’s posts on Denise Minger’s startling findings the most cogent. Try high-fat-nutrition.blogspot.com on October 10th and 14th, 2015.

Adam
Guest

Awesome post and insights, Dr. Fung!

FWIW, I’ve been trying to get people to see the difference between the CIH and lipophilia (the HOT as you call it) for a while. 🙂 Here’s a bit of what I wrote on this subject if you’re interested…

http://www.caloriegate.com/carbs-insulin-hypothesis/how-are-we-ever-going-to-resolve-the-carbs-calories-debate-a-new-perspective

http://www.caloriegate.com/carbs-insulin-hypothesis/carbohydrate-insulin-hypothesiis

erdoke
Guest
Well, your HOT explains how the Pritikin, Ornish, etc. diets work (when they do). However, Denise mentions extreme low fat diets like the one having cooked white rice, sugar and orange juice. The underlying mechanism must be something different for those and Peter over at Hyperlipid might have the right one outlined. Considering all this, adherence and efficiency appears to be a key differentiator for those with serious insulin resistance. I believe more people find LCHF easier to follow and available data also points to higher efficiency, VLC working in ~90 % of people and VLF working in ~60 %.… Read more »
Peter Lawton
Guest

Jason, thanks for your recent calm commentaries on what Denise has invited us to think about, for pointing to what factors are at play. I was happy with the way Denise set about prodding us to think anew, but was quite surprised at the blunt and dismissive rejections put out by some well-known contributors to the “Paleo/ LCHF / Insulin /Real food” conversation. It was scary to see how quickly some apparently thoughtful, progressive people could jump overboard in their haste to write-off an invitation to think.

BobM
Guest
I could see how they could do that. For me, I used to keep my total fat content very low (less than 10% by calories). I basically ate very little meat, no dairy, and only (very) low fat products. It was a freaking horrible thing to do for my body. There may be people who can survive on such a diet, but for me, my blood sugar was out of control (I didn’t know it then, though). I would get angry, depressed, and was constantly hungry. That’s no way to live. It’s also one of the reasons I tried the… Read more »
Wenchypoo
Guest

This explains why the weight I lost at 35 (eating cheaply with whole foods from all over the spectrum) was a whole lot easier to lose than the weight I lost post-menopausal (with LCHF and fasting)–INSULIN! I wasn’t nearly as resistant then as I am now.

Dr. Jason Fung: Absolutely. This is the time-dependence of obesity, which everybody intuitively knows, but is not explained by either the Calorie paradigm or the Carbohydrate paradigm.

John
Guest

How come glycemic load of white bread and whole wheat bread are equal if the added fibers are “protective”?

At least I get a much longer period of satiety by eating whole-grain bread (which I don’t either any more in principle, but…) compared to white bread.

Amy
Guest
Thanks for that shout-out on yet another fantastic post! Couldn’t agree more with what you’ve written here. I’ll be addressing similar issues in the final installment of my insulin series. It’s the *insulin,* but that doesn’t automatically imply it’s the carbs and *only* the carbs. People want black & white answers, but these things are multifactorial. Unfortunately, you can’t do multifactorial in 140-character sound bytes. It requires multiple blog posts and/or entire books, and, sadly, the people most likely to read those are people like yours and my readers, who *already* know how this stuff works and want to learn… Read more »
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Janknitz
Guest
I grew up on Okinawa and I can assure you that Okinawans are omnivores. Their diet is neither “starch based” nor primarily vegetarian–they eat rice, planet of vegetables, meat, fish, and seafood. The primary meat is pork and I can assure you they don’t discard anything–lard is a common cooking fat. Fish and seafood are abundant surrounding this tropical island. For a glimpse of traditional Okinawans foods (setting aside “taco rice” which is an Americanism) check out Anthony Bourdain’s “Parts Unknown” episode that recently aired on Okinawa. There are very poisonous snakes on Okinawa (habu) and Okinawans have even resorted… Read more »
BobM
Guest

Personally, I think stress has an incredible amount to do with it, particularly for heart disease.

Dr. Alister Frayne MD
Guest
Dr. Alister Frayne MD
Hi Jason, Agree totally. For those with the time, Dr. Robert Lustig’s book “Fat Chance” is excellent reading along the same lines (He’s a neuroendocrinologist from UCSF). The role of Ghrelin, Leptin, peptide YY, cortisol remain to be clarified, but can be summed up as “eat real food”. I often measure Insulin levels in my patients, and am constantly surprised by high Insulin levels, in the context of normal or marginally elevated blood sugars – simple dietary advice (steering these folks away from high “Insulinemic Index” foods) is true primary prevention, and they are able to reverse away from beta… Read more »
Bill
Guest
I like your expanded model, but I’m still not sure it can explain all the data. How about the people who eat lots of *refined* carbohydrate and stay very lean. The Kempner Diet may be one example (if your reduced calorie theory of Kempner doesn’t hold up). Another may be Asian diets quite high in refined white rice. I personally know many Asian people who consume impressive quantities of rice three times a day yet remain incredibly lean and seemingly free of metabolic disease over decades. Yes, they do eat some vinegar and veggie fiber, but I doubt that can… Read more »
donny
Guest
“if your reduced calorie theory of Kempner doesn’t hold up.” I’ve looked at a number of sources, and at least for people who needed to lose weight, it does seem to hold up. It wasn’t an eat to appetite approach when weight loss was desired. Sometimes people are described as losing weight spontaneously on the diet–but calories were increased for these people (probably where the sugar comes in, it increases calories, but doesn’t increase the protein load that Kempner was so concerned about). Dr. Don Rosati and his wife Kitti carried the ball for the rice diet after Kempner. Here… Read more »
Amy
Guest

There is probably at least some degree of genetic influence. There are plenty of groups that *don’t* do well on high amounts of refined grains.
http://www.tuitnutrition.com/2015/06/keto-carbs-stop.html

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Maura
Guest
Of note is that Nathan Pritikin committed suicide after developing leukemia and its complications, so yes, he avoided CVD. But how did his diet affect his overal health? Or his mental health? In our n=2 experiment on the Pritikin diet my husband and I had opposite results. He lost 27 lbs on that diet, and I gained a couple. Why such different outcomes? Genetic and our baseline conditions come to mind as possible explanation. He grew up on an American diet, with more sugar and fat and processed foods. He still ate a typical American diet of more processed food,… Read more »
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matt20
Guest

If you look up the foods which have a measured insulin index, your point is well made:

Tortilla, white, corn (San Diego Tortilla Factory, Australia), insulin index 36, carbs 47

Beef steak, grilled (Australia) : insulin index 37, carbs 0

Snickers bar (Masterfoods, USA) : insulin index 37, carbs 29

source: http://ses.library.usyd.edu.au/handle/2123/11945

Morgana
Guest
The problem with using the glycemic index is that we don’t all respond in the same way; blood sugar and insulin response varies from person to person. One person might be able to eat hoards of white rice and have a very small reaction, whereas another person might have a huge insulin response. I do agree that “it’s all about the insulin”, and I also agree that there’s no one right diet for everyone; however, many of us are metabolically damaged, and for us it absolutely IS “about the macronutrients”. This would not apply to people like the Hazda, who… Read more »
NS
Guest

I think it would serve everyone well to go back and reread Protein Power. It has a good discussion of insulin and the effects of carbs, protein, fat, and their various combinations on insulin levels as well as glucagon levels.

Ed
Guest
Surely the most important thing out of all this though is that whilst the Pritikin diet may well work (by reducing insulin) in similar ways to a LCHF diet, in terms of long term adherence a LCHF diet will nearly always win out. Simply because it achieves the insulin lowering effects while at the same time allowing people to eat more calories that satisfy hunger. Pritikin and similar diets the dieter will almost always end up feeling hungry and fall off the wagon in the longer term. LCHF and IF (and a combination thereof) allow one to adhere better because… Read more »
Colin
Guest

Bingo

Martin Willias
Guest

A very recent study underlines Dr Fung’s hypothesis that sugar is much more harmful than other carbohydrates. All markers of metabolic syndrome were reduced in as little as nine days, and insulin by a third. Note that the benefit occurred even though simple sugars were replaced by bread, bagels, etc.!

http://www.telegraph.co.uk/news/health/news/11956249/Cutting-sugar-can-improve-health-in-nine-days.html

Nate
Guest

Thanks for the last two post Dr. Fung. The calories in, calories out theory is like a broken clock. It is right twice a day. The CICO theory is right only when the foods your are currently eating work well with your metabolism at that moment in time. But if your food or metabolism change, then metabolic disease will follow.

However, the hormonal theory is right all of the time and thus encompasses the CICO.

Nate
Guest

BTW, the CIH may be soooo 2010 for Dr. Fung. But for me it is soooo October, 2015.

I would also give a shout out to Dr. Kraft via the excellent The Fat Emperor, http://www.thefatemperor.com

My new campaign slogan is It’s The Insulin, Stupid. Thanks, Amy.

Jeff
Guest
Hi Dr. Fung, I enjoyed this post. I followed an Ornish/Fuhrman style vegetarian diet for many years before switching to LCHF. As someone alluded to earlier, the problem with these diets is you are always very hungry, because you can’t get enough calories from fruits and vegetables. If you want to be a vegetarian and you are afraid of fat you end up eating lots of bread, pasta and other grains to ease the hunger. I did this and peaked with an A1c of 7.4 before cutting back to 25g of carbs a day. The way I interpret glycemic load… Read more »
Thomas Sazani
Guest

As a T2DM, I do better on a LCHF (Atkins-like) diet vs a high fiber, high carb, low fat (Pritikin-like) diet. My LCHF diet still has lots of fiber due to the judicious use of 1/2 cup of beans and an avocado or two per day. In addition, I eat 4 servings of green vegetables per day.

Gary Katch
Guest

http://high-fat-nutrition.blogspot.ca/2015/10/protons-and-ultra-low-fat-once-more.html

The above link is interesting. The writer (you should read *all* his posts!) kicks around some ideas about the metabolic “magic” which may be going on under extreme low-fat. Be aware the first part of the post is very heavy with cellar biology and biochemistry. You can skip that to get to the end conclusions, which I think are a reasonable response to the study that Minger is looking at.

Dr. Samir Anadkat
Guest
Dr Fung I am your fan. And I am deeply greatful for the comprehensive knowledge you have imparted in my understanding of obesity. My question- I routinely do FBG and Fasting Insulin before prescribing dietary therapy for my patients. I also rule out thyroid (by TSH). But there are few patients where IR is quite low, there are no obvious signs of high cortisol and they are still obese. 1. Do you think these kind of patients will benefit more from lower fat in diet vs lower carb? (Here high fiber, low animal protein, use of vinegar and fermented food,… Read more »
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