Thoughts on the Pritikin Diet

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.

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.

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.

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.

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.

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).

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.

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)

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!

2017-10-27T20:10:41-04:0046 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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