Category Archives: Diets - Page 4

What’s New in the New Edition, I: Evolutionary Dieting

Posted by on December 8, 2012 68 comments

UPDATE: The new edition has launched! Books are in stock and shipping. Here is the Amazon page.

Readers of our first edition, like Steven, are naturally wondering what’s new in the Scribner edition.

There’s a lot that’s new. The Scribner edition is 50% longer; almost half of the material is new. Original material is revised and updated.

In a series of posts this week, I’m going to walk through the book and discuss what’s new and original. This post is about Part I, “An Evolutionary Guide to Healthful Eating.” (You can see a Table of Contents for the whole book on our Notes page, or in the Scribd excerpt below.)

Paleolithic Diets: An Evolutionary Story

Loren Cordain uses a striking analogy: he compares the length of the Paleolithic, 2.6 million years, to the length of a football field, 100 yards. By that scale, the Neolithic – the period when grains and farmed foods became a major part of our diet – is about a foot long. The point is that, in evolutionary terms, our relationship with agriculturally mass-produced cereal grains has been relatively short (to say nothing of our relationship with high-fructose corn syrup and soybean oil!). It stands to reason that we’d be adapted to the diet and lifestyle of the Paleolithic, and we agree, for reasons discussed in Chapter 1.

But what was the composition of Paleolithic diets? The Paleolithic was the era of stone tool use, and one of the primary purposes of stone tools was butchering animals, so the Paleolithic roughly corresponds to the period when meat was a significant part of our diet. But plants were also a major part.

The popular Paleo movement presents a fairly consistent view of what a “Paleo diet” is: meat and fish, fruits and vegetables, nuts and seeds. But how close is this “Paleo diet” to actual Paleolithic diets? Did Paleolithic peoples forgo starches? Did they eat almond meal waffles, muffins, and cookies? Looking into the actual Paleolithic diet is the subject of Chapter 2.

Unfortunately, the standard Paleo “evolutionary” argument doesn’t get us very far toward finding the optimal human diet. First, there was no one Paleolithic diet: it varied considerably by time and place. Second, the contention that our hunter-gatherer ancestors “adapted” to the diet they were eating and were optimized for it is open to question. Our biology is not infinitely malleable, capable of adapting to any diet. We could subsist on Twinkies for 2.6 million years, and Twinkies would never become the optimal human diet. How can we know that plants and animal foods gathered and hunted in the Paleolithic were then, or are now, our optimal diet?

Fortunately evolutionary evidence tells us much more about what is healthful for us, and what it tells us is supportive of the Paleolithic diet story.

A Richer Evolutionary Story

Evolution selects every aspect of our biology – how cells work, how organs work, how our brain works.

In the first edition, we gave a few very brief summaries of some alternative evolutionary arguments for the optimal human diet. We found that even very smart readers often misunderstood or didn’t appreciate the strength of these arguments, so we elaborated on them in the new edition.

These arguments are spelled out in Chapters 3-6: The “Cannibal Diet” of Fasting, What Breast Milk Teaches Us About Human Diets, What Mammalian Diets Teach Us About Human Diets, and The “Tastes Great!” Diet.

Why does fasting tell us about the optimal diet? Think about how food is handled. Our food doesn’t go straight from our digestive tract to our mitochondria to be turned immediately into energy. Instead, nutrients from food are incorporated into tissue within a few hours after a meal, and then that tissue is cannibalized to supply energy needs over the following 24 hours.

As a rule, tissues won’t accept just any macronutrients. Cells have a very specific structure, with fatty membranes and protein-rich cytosols; and they have very specific fatty acid profiles in their membranes, and amino acid ratios in their proteins. Cells specifically take up nutrients in the proportions they need, and refuse to incorporate nutrients they don’t need.

So if we evolved to be nourished by self-cannibalization of tissue, then the nutrient composition of our tissues must be close to our optimal diet.

What about breast milk? Most people will agree that this is the optimal food for infants. But many have thought there must be so many differences between infants and adults that breast milk will tell us little about the adult diet.

Not so. We can quantify the differences between infants and adults – they have mainly to do with the large and fast-growing infant brain – and can see which parts of the breast milk are designed to support that brain. We can adjust for those differences, and estimate the optimal adult diet from the composition of breast milk.

What about mammalian diets? I think this is one of the most interesting parts of our book and will be of great interest to pet owners, farmers, veterinarians, zookeepers, and anyone who has to feed animals.

The reality is that evolutionary selection has been operating for far longer than the Paleolithic, and it settled on certain solutions quite early. Multicellular life was common by 500 million years ago, and the basic composition of cells and their extracellular matrix scaffolding hasn’t changed much in that time.

So if our cellular biology hasn’t changed much in 500 million years, then the nutrients needed by cells hasn’t changed much either. That means the optimal diet hasn’t changed much. Yet there is a diversity of animals that occupies every possible ecological niche and type of food. How can a common biology be fed by a diversity of diets? Why are there herbivores, omnivores, and carnivores?

The resolution of this seeming paradox lies in the digestive tract and how it transforms food into nutrients. This allows us to infer from the digestive tract what an animal’s optimal diet is. We can do that for humans, too.

Those three evolutionary arguments were present in capsule form in the first edition, but the next one is entirely new to this edition: a discussion of the food reward system of the brain. Food reward evolved to motivate us to go seek out healthy, nourishing foods. If it evolved in the Paleolithic environment, then it tells us what foods were hard to get in the Paleolithic, but still necessary for health – these were the foods that Paleolithic foragers had to be motivated to work for.

But in our modern world, all foods are easy to obtain; they are on the shelves of supermarkets. So those foods that were hard to get in the Paleolithic are going to be precisely the ones that we overeat today.

The presence of an innate food reward system explains why peoples around the world eat very similar diets – almost always 50% carb, 15% protein, 35% fat, or close to it. If this food reward system evolved for the Paleolithic food environment, which was radically different from the modern agricultural and industrial global food production system, then we can’t trust our unconscious food buying impulses. If we just go to the supermarket and put whatever seems desirable into our cart, we will overeat all the things that our Paleolithic ancestors tended to undereat.

Worse, we will be tempted to eat junk foods designed to appeal to the tastes that signal healthfulness to the food reward system, without supplying the nutrients that actually deliver healthfulness.

On the other hand, this evolutionary argument is encouraging. It tells us that, if we eat Paleolithic foods and if we educate ourselves to select healthy foods in the optimal proportions, then we can be confident that our brains will find our meals to be delicious and satisfying.

A healthy diet is also a delicious and satisfying diet! There is no need to suffer to be healthy. There is no need to suffer to lose weight. If you are suffering on a diet, you are doing something wrong.

Part I ends by circling back to a recurring topic: animal diets. Our pets, zoo animals, and even feral rats living in urban areas and eating our trash are partaking of our ill health. They are becoming obese in parallel with us, and develop cardiovascular disease at similar rates; their wild counterparts do not have these problems. Yet returning zoo animals to their natural diets returns them to good health. Adopting our natural diet works for humans too. Our Perfect Health Diet reader success stories support this claim.

Evolutionary Fine-Turning

The rest of the book also puts some weight on evolutionary arguments. When we look at individual nutrients, we find that the body has evolved mechanisms to bring them close to an optimal level:

  • The body adjusts toward an optimal carb intake. When carb intake is too high, glucose is converted to fat. When carb intake is too low, glucose is manufactured from protein. The Goldilocks level, at which the body neither manufactures nor disposes of glucose, is an indicator of the optimal carb intake.
  • The body adjusts toward optimal fatty acid proportions. In Americans today, omega-6 fats are more than three times more likely to be burned for energy than saturated fats. Yet on omega-6 deficient diets, omega-6 fats are less likely to be burned for energy than saturated fats. This evolved system for regulating the body’s fatty acid composition is clear evidence that Americans eat too many omega-6 fats and too few saturated fats.

Similar arguments from evolutionary biology guide us toward optimal intake of micronutrients, which have degradation or excretion pathways turned on when they are present in excess, and conservation pathways turned on when they are scarce.

Cooperating with Our Bodies to Build Health

The earliest human temptation, if we are to believe the story of the Garden of Eden, was to “be as gods” and define good and evil — healthful and unhealthful — for ourselves. There is an undoubted attraction, we have felt it ourselves, to masterminding our diet and nutrition. We like to think that evolution got it wrong, or optimized for the wrong thing, and that an extreme diet or unnatural intervention can improve our health.

It’s not just extreme dieters who think this way. What is the pharmaceutical model of medicine, but the idea that we can alter the natural functioning of our bodies in ways that will make us healthier?

Sometimes this can work, but usually wisdom and deeper knowledge show us that evolution got it right, that our innate biology works to maintain our health rather than harm it, and that interventions which subvert natural functions tend to do more harm than good.

A more promising approach, we think, is to cooperate with our bodies. This leaves plenty of room for medicine to help – through diagnosis and testing, through antimicrobial treatments, through integrated dietary and lifestyle advice, and through interventions that support natural bodily functions (as, for instance, thyroid hormone replacement in hypothyroidism, or insulin therapy in type 1 diabetes).

It’s this cooperative approach, integrating the best of medicine with the best ancestral health practices, that we think will be most effective at generating good health and long life. We hope our book will illuminate what those “best ancestral health practices” are, and help build a cooperative effort between the natural health movement and the medical community.

Concluding Thoughts & a Book Excerpt

It could be said that our book is an “owner’s manual” for the human body, helping our readers know how to best support their own health by living in accord with our evolved biology.

The great thing is, the way to do this is by eating delicious, satisfying food!

If you’d like to get a feel for the book, check out this excerpt, which Scribner has put on Scribd:
PERFECT HEALTH DIET: How anyone can regain health and lose weight by optimizing nutrition, detoxifying the…

More Evidence for Low-Carb Diets

Posted by on November 30, 2012 49 comments

In our book we point out a number of dietary tactics that appear to substantially decrease risk of cardiovascular disease. They include:

  • Optimizing tissue omega-6 to omega-3 balance by minimizing intake of omega-6 fats and eating an oily marine fish like salmon or sardines once a week.
  • Optimizing various micronutrients including vitamins D and K2, choline, magnesium, iodine, and selenium.
  • Reducing carbohydrate intake to the body’s natural level of glucose utilization, about 30% of total calories.

We cited two main sources for the claim that reducing carbohydrate intake reduces risk of cardiovascular disease:

–          The Nurses Health Study found that risk of coronary heart disease went down steadily as dietary carbohydrates were reduced and replaced by fat. Those eating a 59% carb diet were 42% more likely to have heart attacks than those eating a 37% carb diet. [1]

–          Replacing dietary carbohydrate with saturated or monounsaturated fat raises HDL and lowers triglycerides, changes that are associated with low rates of cardiovascular disease. Blood lipids are optimized when carb intake drops to 30% of energy or less. [2]

I think this is pretty strong evidence. It is not completely bulletproof, because associations don’t prove causation and improving risk factors doesn’t necessarily improve disease risk; but, combined with supportive evidence from cellular biology and clear evidence that evolutionary selection favors a carbohydrate intake around 30%, I consider it convincing.

However, it’s always good to have more evidence; and two new studies provide some. One directly relates utilization of carbohydrates for energy to atherosclerosis, and the other conducted a 12-month clinical trial of a carbohydrate restricted diet.

Carbohydrate Utilization is Associated With Atherosclerosis

Via Stephan Guyenet comes a study that directly links carbohydrate metabolism to atherosclerosis: “Metabolic fuel utilization and subclinical atherosclerosis in overweight/obese subjects.” [3]

The study used intima-media thickness in the carotid artery, which serves the head and neck, as a measure of atherosclerosis. As Wikipedia notes,

Since the 1990s, both small clinical and several larger scale pharmaceutical trials have used carotid artery IMT as a surrogate endpoint for evaluating the regression and/or progression of atherosclerotic cardiovascular disease. Many studies have documented the relation between the carotid IMT and the presence and severity of atherosclerosis.

To assess metabolism it measured the “respiratory quotient” or RQ. RQ is the ratio of carbon dioxide (CO2) generated in the body to oxygen (O2) consumed in the body.

RQ indicates which fuels are being burned for energy in the body. When carbohydrates are burned, the reaction involves carbon exclusively, so for every O2 molecule consumed there is a CO2 molecule created. This makes the RQ 1.0 when carbohydrates are burned.

Fats, however, donate both carbon and hydrogen, and the hydrogens react with oxygen to make water (H2O). So some of the oxygen consumed when fats are burned goes into water, not carbon dioxide, and the RQ when fats are burned is about 0.7. Ketones also have an RQ around 0.7.

Amino acids from protein have variable amounts of hydrogen and carbon, some amino acids are ketogenic and some are glucogenic, and so the RQ of protein depends on its amino acid mix. Typically RQ from different types of food protein is between 0.8 and 0.9.

However, most people eat a fairly consistent amount of protein, around 15% of energy, so the variable that generally determines RQ in practice is the ratio of carbs to fat in the diet. Higher RQ indicates a higher-carb diet.

Another study had previously shown that calorie restriction, which also reduces RQ by replacing dietary carbohydrate with fat released from adipose tissue, reduces the thickness of the carotid intima-media. [4] This study was the first testing whether the RQ-CIMT relationship holds also in subjects not known to be restricting calories.

The study found that indeed it does: the lower RQ, the less atherosclerosis the subjects had. Unfortunately they don’t present data in a visually useful way (a scatter plot of RQ vs CIMT would have been helpful); here is what they do show:

RQ was better than waist circumference or BMI at predicting degree of atherosclerosis. Only age was a stronger predictor of atherosclerosis than RQ.

RQ predicted atherosclerosis equally well in subjects with and without obesity. This tells us two things:

  1. It supports the idea that it was habitual diet rather than recent calorie restriction (which decreases RQ by replacing food-sourced calories with fat from adipose tissue) that generated low RQ and low CIMT.
  2. As the authors say, it indicates “the main role of metabolic factors rather than BMI” in generating atherosclerosis – metabolic factors meaning burning glucose for energy rather than fat.

It is also supporting evidence for one of the more controversial lines of our book, that “mitochondria prefer fat.”

One caution: Most of the subjects in this study were eating diets that were around 50% to 55% carbohydrate, so the study was testing whether it’s better to eat a little above or below this carb intake. It tells us, I think, that a 45% carb diet is healthier than a diet with more than 50% carbs. It doesn’t tell us what carb intake is optimal.

The Clinical Trial

In a trial lasting 12 months, restricting carbohydrates to 600 to 850 calories per day – that is, about the 30% of energy that we recommend – in the context of a slightly hypocaloric diet improved cardiovascular risk factors. [5]

Overweight and obese subjects in the trial lost 2.8 kg (6 pounds) over the year-long trial, so it couldn’t have been severely calorie restricted. Changes in other risk factors:

–          Blood pressure dropped from 121/79 to 112/72;

–          Fasting blood glucose dropped from prediabetic 106 mg/dl to normal 96 mg/dl;

–          Lipids improved, with triglycerides decreasing from 217 to 155 mg/dl and HDL increasing from 39 to 45 mg/dl.

They conclude:

The results of this study indicate that a moderately restricted calorie and carbohydrate diet has a positive effect on body weight loss and improves the elements of metabolic syndrome in patients with overweight or obesity and prediabetes. These results underscore the need to provide dietary recommendations focusing on calorie and carbohydrate restrictions … Our results are in agreement with reports produced by other authors who also assessed a carbohydrate-reduced diet …

Conclusion

A number of simple dietary and nutritional changes appear to reduce the risk of atherosclerosis and cardiovascular disease generally. One of them is reducing carbohydrate intake.

I believe the optimum carbohydrate intake is around 30% of energy. Many studies generate clear evidence of benefits as carbs are brought down into the range of 20% to 30% of energy, especially in metabolic disorders like metabolic syndrome, diabetes, and obesity. It’s good to see that evidence from other diseases, such as CVD, also supports the same carb intake.

Because most people’s diets are flawed in so many different ways, and fixing an individual factor is often associated with a reduction in CVD risk of 40% to 70%, it’s possible that we could reduce CVD risk by 90% or more by implementing all of the dietary optimizations described in our book.

It’s well worth pursuing all these little optimizations!

References

[1] Halton TL et al. Low-carbohydrate-diet score and the risk of coronary heart disease in women.  N Engl J Med. 2006 Nov 9;355(19):1991-2002. http://pmid.us/17093250.

[2] Krauss RM. Atherogenic lipoprotein phenotype and diet-gene interactions. J Nutr. 2001 Feb;131(2):340S-3S. http://pmid.us/11160558.

[3] Montalcini T et al. Metabolic fuel utilization and subclinical atherosclerosis in overweight/obese subjects. Endocrine. 2012 Nov 28. [Epub ahead of print] http://pmid.us/23188694.

[4] Iannuzzi A et al. Comparison of two diets of varying glycemic index on carotid subclinical atherosclerosis in obese children. Heart Vessels. 2009 Nov;24(6):419-24. http://pmid.us/20108073.

[5] Velázquez-López L et al. Low calorie and carbohydrate diet: to improve the cardiovascular risk indicators in overweight or obese adults with prediabetes. Endocrine. 2012 Sep 1. [Epub ahead of print] http://pmid.us/22941424.

Very Low-Carb Dieting: Are the Hormonal Changes Risk-free?

Posted by on October 19, 2012 60 comments

I was in Chicago earlier this week to record a video discussion with Dr Ron Rosedale hosted by Dr Mercola. Ron and I have taken opposite sides in several “safe starch debates” (First installment here; reply to Ron here; Ancestral Health Symposium panel discussed here.) This new discussion was intended to be more cordial and uncover common ground as well as differences.

I was intrigued to see that Ron’s lunch consisted mostly of plant foods which he ate avidly; he said he believes that most people on his diet eat a significant amount of plant foods. I came away with the impression that the Rosedale Diet resembles the ketogenic version of PHD, only with less starch and MCT oil.

One of my objections to Ron’s recommendations has been that very low carb and protein consumption can be stressful to the body. Scarcity of carbs and protein invokes certain starvation-associated pathways – for instance, lower T3 thyroid hormone. We discussed this in “Carbohydrates and the Thyroid,” August 24, 2011.

Ron believes that low T3 on low-carb diets is healthy, and other low-carb advocates, such as Sam Knox, have made similar arguments.

I believe that intermittent fasting, which invokes starvation-associated pathways transiently, is usually health-improving – but that you can overdo it. What happens if you invoke these pathways chronically and continuously?

Prof Dr Andro on the “Athlete Triad”

Some light was shed on this question recently by Adel Moussa, aka Prof Dr Andro, who discussed the “athlete triad” in three posts (Part I, Part II, Part III) at his blog Suppversity.

The athlete triad appears most commonly in athletes who undereat and overtrain. Symptoms include low energy, amenorrhea in women and low testosterone in men, osteoporosis, reduced cognitive ability, and impaired immune function. The syndrome is surprisingly common, especially in female athletes:

Although the exact prevalence of the female athlete triad is unknown, studies have reported disordered eating behavior in 15 to 62 percent of female college athletes. Amenorrhea occurs in 3.4 to 66 percent of female athletes, compared with only 2 to 5 percent of women in the general population. [1]

As Adel discusses in Part II, the athlete triad is characterized by the following hormonal pattern:

  • low estrogen and testosterone levels
  • low T4 and low T3 thyroid hormone levels, often with low TSH and high reverse T3
  • a disturbed circadian cortisol rhythm lacking an appropriate cortisol spike in the morning and a normal decline in cortisol levels in the course of the day
  • low leptin, low insulin, and low IGF-1

Precisely the same hormonal patterns, including lower thyroid hormone levels, higher cortisol, and a suppressed circadian cortisol rhythm, are observed in total fasting and starvation. [2] [3]

These hormonal changes conserve glucose and protein, an appropriate step during starvation. The energy-intensive tasks of immune function and reproduction are temporarily suppressed until energy is more readily available.

Similar patterns of reduced T3 and elevated cortisol excretion were recently seen in a clinical trial of a 10% carb weight maintainance diet. [4] This trial shows that even in the absence of calorie restriction, carb restriction is sufficient to reproduce much of the “athlete triad”/starvation hormonal pattern.

This pattern reaches its most extreme form in anorexia:

[H]ypocaloric diets causes changes in thyroid function that resemble sick euthyroid syndrome. Changes consist of a decrease in total T4 and total and free T3 with a corresponding increase in rT3….

States of chronic starvation such as seen in anorexia nervosa are also associated with changes in thyroid hormone, GH, and cortisol secretion. There is a decrease in total and free T4 and T3, and an increase in rT3 similar to findings in sick euthyroid syndrome…. [T]here is an increase in GH secretion with a decrease in IGF-1 levels…. The changes in cortisol secretion in patients with anorexia nervosa resemble depression. They present with increased urinary free cortisol and serum cortisol levels. [5]

In chronic starvation, hunger is replaced by anxiety and a desire to move. In evolutionary context this urge to be active may have stimulated food-seeking, but in modern life it can exacerbate conditions like the athlete’s triad.

In Part II of his series, Adel made an interesting observation. Chris Kresser often mentions a patient who cured his health problems with pizza and beer. Here’s Chris recounting the story to Kurt Harris:

Chris Kresser: Back around 2000, I was interning for a holistic doctor down in San Diego, and this was before I got into Paleo or anything, and I was, I think, a vegan macrobiotic, for crying out loud, at that point!  So, we had a patient who was just really, really sick, and he was just getting sicker and sicker.  He weighed about 90 pounds.  I think he was about 6 feet tall.  And the doctor had him on a restricted diet, you know, one of those food allergy type of diets where all you’re eating is, like, broccoli, venison, and quinoa.

Kurt Harris:  The Specific Carbohydrate Diet?

Chris Kresser:  No, no, just like a really, you know, they do the IgG food testing, which is kinda bunk anyways.

Kurt Harris:  Yeah, that’s pretty bunk.

Chris Kresser:  And then they find out you can only eat strawberries, broccoli, quinoa, and ostrich!  You know?  And so, he was doing that, and he kept removing foods until he was literally down to, like, broccoli and steamed whitefish or something.  That was all he was eating.  And he just kept getting sicker and sicker.  So, he disappears for about six months, comes back a completely different person.  He’s back up to 160 or 170, which was his normal weight, you know, completely normal complexion.  Literally, we didn’t even recognize him, and the doctor was saying:  What happened?  Was it diet?  And the guy was like:  Yep, it was diet.  And he said:  Was it the candida diet?  Was it the Specific Carbohydrate?  What was it?  And he said:  It was the beer and pizza diet!  [laughter]  And this guy literally, I mean, the guy got to this point where he was like:  OK, if this is my life, I’m fine with just flaring out.  You know, this isn’t worth it.  And if I’m gonna go out, I’m gonna have fun.  And so, he started going out.  You know, he wasn’t ever hanging out with his friends anymore because he was on such a restricted diet, he had no social life, so he just said: Forget it.  I’m gonna drink beer and eat pizza at least three times a week, and then the other times I’m gonna do whatever I want.  And that completely restored his health.

Adel speculates (very plausibly in light of the man’s weight of 90 pounds!) that the patient was suffering from the starvation pattern which is replicated in very low-carb “euthyroid sick syndrome” and the athlete triad. What he needed was more calories, especially carb and protein calories. Pizza and beer are great sources!

Conclusion

It was a pleasure to chat with Ron and Dr Mercola in Chicago. We recorded a four hour discussion, which is going to be edited down to an hour or hour and a half.

We found plenty of common ground. We agreed that there are very real health benefits to low-carbohydrate diets. Low-carb diets are helpful against diabetes and metabolic syndrome, and quickly improve cardiovascular risk markers such as blood pressure, triglycerides, and HDL.

But in biology, good things can always be taken too far. One can restrict carbohydrates (and protein) too much. Extremism in carb restriction may, indeed, be a vice.

References

[1] Hobart J, Smucker D. The female athlete triad. Am Fam Physician. 2000 Jun 1;61(11):3357-64, 3367. http://pmid.us/10865930.

[2] Shimizu H et al. Altered hormonal status in a female deprived of food for 18 days. J Med. 1991;22(3):201-10. http://pmid.us/1770328.

[3] Palmblad J et al. Effects of total energy withdrawal (fasting) on the levels of growth hormone, thyrotropin, cortisol, adrenaline, noradrenaline, T4, T3, and rT3 in healthy males. Acta Med Scand. 1977 Jan;201(1-2):15-22. http://pmid.us/835366.

[4] Ebbeling CB et al. Effects of dietary composition on energy expenditure during weight-loss maintenance. JAMA. 2012 Jun 27;307(24):2627-34. http://pmid.us/22735432.

[5] Douyon L, Schteingart DE. Effect of obesity and starvation on thyroid hormone, growth hormone, and cortisol secretion. Endocrinol Metab Clin North Am. 2002 Mar;31(1):173-89. http://pmid.us/12055988.

AHS 2012: The Safe Starches Panel

Posted by on August 18, 2012 155 comments

Note: The book has come back to me for copy-editing, that’s why blogging is slow.

The “safe starches” panel turned out to be not about starches, but about carbs. Nobody wanted to contest my assertion that some starchy plants are free of toxins after cooking, so the criticism of starchy foods was solely based on perceived risks from their carb content.

The expectation going in was that Drs. Ron Rosedale and Cate Shanahan would be taking anti-starch/anti-carb positions and that Chris Kresser and myself would take pro-starch/pro-carb positions. But as it turned out, we arrayed ourselves on a spectrum. Ron was resolutely anti-carb, repeating his assertion that we’re all diabetics and intolerant of carbs (see Ron’s summary of the panel here); Cate was more moderate. I supported eating ~30% of calories as carbs, with lower-carb ketogenic dieting as a therapy for certain conditions. Chris took the position that there is little evidence favoring any carb intake over another, and that some cultures have been healthy on carb intakes as high as 85% or more. (See Chris’s summary of his remarks.)

A fair part of the discussion was about longevity and aging, and whether carbs contribute to it. This is a topic that has not been explored much in the Paleo blogosphere, and was the most interesting part of the panel for me.

[Photo from Diana Carr on Facebook.]

My Position: About 30% Carbs is Best

I took an evolutionary perspective. Evolution selected for a carb intake around 30% to 35% of calories. At lower carb intakes, protein is converted to glucose by gluconeogenesis; at higher carb intakes, significant amounts of the excess carbohydrate are converted to fat (not in the liver, but in skeletal muscle and adipose tissue; this is why studies examining lipids exported from the liver show minimal glucose to fat conversion).

If it were equally healthy for the body to have some other glucose supply than the one provided by a carb intake of ~30% of calories, then evolution would not have selected for mechanisms to restore this favored glucose supply by gluconeogenesis or lipogenesis. The body would have accommodated other levels of glucose utilization without trying to alter its glucose supply.

Further, we know that when carb intake is below this natural level, gluconeogenesis does not fully make up the glucose deficit; and when carb intake is above this natural level, lipogenesis does not fully eliminate the glucose surplus. As a result:

  • On high-carb diets, cells/tissues utilize more glucose than in the evolutionarily favored state.
  • On low-carb diets, cells/tissues utilize less glucose than in the evolutionarily favored state.

My thesis is that there are undoubtedly negative effects from over- or under-utilization of glucose by tissues; else evolution wouldn’t be trying to mitigate the over- or under-supply by lipogenesis and gluconeogenesis. And we know at the extremes that negative effects do occur:

  • On very high-carb diets, eg macrobiotic diets, lipid deficiencies appear, reflected in reduced serum cholesterol, impaired immunity, and often mood disorders. We’ve blogged about the effects of lipid-deficient diets in infants.
  • On very low-carb diets, we often see deficient production of mucus and tears due to downregulation of mucin production. We’ve blogged about this.

On less extreme divergences of carb intake from the evolutionary norm, there are no obvious acute effects, but the possibility exists of long-term negative effects.

Ron’s Misunderstanding of My View

Ron Rosedale seems to have misunderstood my argument. In his “A Conclusion to the Safe Starch Debate,” Ron asserts that I am concerned only with blood glucose levels. No, not at all: I am concerned specifically NOT with blood glucose levels but with tissue glucose utilization.

Perhaps a metaphor may help. Imagine an oil well facility connected by pipeline to an oil-burning power-plant. Suppose that it is essential to always maintain a certain pressure of oil in the pipeline, or the pipeline will suffer damage. When the oil wells produce more oil – say, because a new well has become a gusher – the power-plant burns more oil in order to maintain the proper pipeline pressure. When the oil wells produce less oil – say, they’re down for maintenance – the power-plant uses less oil. Always the pipeline has the same amount of oil.

Even though the pipeline always has the same amount of oil and the same oil pressure, that doesn’t mean that it doesn’t matter how much oil is entering the pipeline. The whole complex of wells-pipeline-powerplant may work best and be most robust to trouble if a normal amount of oil is being produced at the well end and a normal amount is being consumed at the powerplant end. Extreme levels of oil production may strain the powerplant’s ability to operate – insufficient oil may shut it down, and excess oil may burn it up or strain its facilities.

In the same way, eating too few or too many carbs will not affect the levels of glucose in the blood – these must be maintained above 60 mg/dl if glucose is to enter the brain which is essential for life even under ketosis – but may strain or stress our tissues which must downregulate or upregulate their utilization of glucose to match the flux of carbs into the body.

Cate Shanahan’s Experience

Cate Shanahan mostly discussed her experiences recommending a low-carb diet to her patients. She says that none of her patients have reported glucose deficiency symptoms, such as dry eyes. For me this mystery was cleared up when she said that she recommends her patients get 70 g of carbs daily. I and others have found that 50 g of starch is a sort of magic level that usually eliminates acute symptoms like dry eyes.  So Cate appears to be recommending a level of carb intake that minimizes the risk of acute symptoms.

It wouldn’t surprise me if most of her patients are eating much more than 70 g. We know the food reward system strongly rewards carb consumption, so that nearly every culture on earth eats at least 45% carbs by calories. Quite possibly most of her patients are eating PHD levels, 100 g to 200 g.

Is there a counter-argument to my evolution based view?

To date, I’ve seen two counter-arguments:

(1)   From the low-carb side, chiefly Ron Rosedale: Evolution didn’t optimize for longevity but for fertility, and we want longevity, therefore we should resist adopting the evolutionarily favored diet.

(2)   From the high-carb side, voiced to some degree by Chris Kresser in the panel: Why isn’t a negative effect of high or low carb intakes apparent in epidemiological data? There seem to be healthy long-lived societies with high carb intakes.

These seem to me to be the interesting issues coming out of the safe starch debate. I will only give brief answers here.

Contra Ron: Very low-carb for longevity

I have two replies to Ron’s argument that very low-carb diets will maximize longevity.

First, evolution DID select for human longevity. The maximum human lifespan is double that of chimps and gorillas. Humans have mitochondrial membranes selected for extreme longevity. Both of these points are discussed in our new Scribner edition. This should give us confidence that the 30% carb intake selected for by evolution may well be the carb intake that maximizes longevity. I believe it is.

Second, Ron’s arguments are based on Cynthia Kenyon’s experiments in the nematode worm C elegans, in which she found that mutations to Daf-2, which is an insulin-like receptor in C elegans, extended maximum lifespan. Cynthia Kenyon famously switched to a low-carb diet after these experiments. However:

  • Humans have multiple genes which are analogs to Daf-2, including insulin-like growth factor 1 as well as insulin, and IGF-1 appears to be more strongly related to longevity than insulin in humans. More significantly, insulin actually antagonizes Daf-2 in worms, inhibiting its signaling; calling into question whether Daf-2 biology can tell us anything about the effects of insulin signaling in humans.
  • More importantly, the mutations to Daf-2 extend maximum lifespan in the laboratory, but they shorten expected lifespan under natural environmental conditions. When Daf-2 mutant worms are placed in the soil, they live shorter lives.

I made the second point during the panel. Here is the reference:

C. elegans mutants that live twice as long as wild-type worms in laboratory conditions typically die sooner than wild-type worms in a natural soil. These results indicate that conclusions regarding extended longevity drawn from standard laboratory assays may not extend to animals in their native environment. [1]

Even if Daf-2 mutant worms were an adequate model of human longevity, we would have to confront the issue of the robustness of health and longevity to stressors such as infections.

The death of Roy Walford, calorie restriction practioner and longevity guru, at age 79 from ALS – a disease that is promoted by fasting and calorie restriction – should warn us about the risks of extreme diets. There are pathogens that can exploit every human environment. “Feed a cold, starve a fever”; for different germs you may need different diets.

Evolution selected for a moderate carb intake because it makes us robust against a wide range of threats. Carb restriction, like calorie restriction, might protect us from some threats but expose us to others. In our natural, free-living situation, we’ll come up against every threat sooner or later. Just because an extreme diet may have the potential to extend our lifespan does not mean that it will. It may reduce our expected lifespan by making us vulnerable to new threats. The safest course, I think, is to follow evolution’s guiding hand.

What Does Experience on High-Carb Diets Tell Us?

Chris Kresser cited a number of healthy high-carb cultures, and noted that Okinawans became the world’s longest-lived culture after being forced to an 85% carb diet during World War II and its aftermath. Stephan Guyenet cites this as a telling point of the debate:

One of the most surreal moments happened right after Kresser brought up the Okinawans, the longest-lived culture and one of the healthiest in the world, and cited a paper showing that their traditional diet was ~85 percent carbohydrate, mostly from sweet potatoes.  Shanahan and Rosedale decided, based on thin air, that the Okinawans actually didn’t eat much carbohydrate, and Shanahan even went so far as to say “I don’t believe you”, even though Kresser was staring right at the citation on his laptop!  This is the kind of head-in-the-sand approach to science that we need to move beyond in the ancestral community.

The source for an Okinawan diet of 85% carbs was published in 1949, and the data was gathered during the post-World War II US occupation. This was a time of desperate poverty, and indeed followed years of poverty and famine during the Great Depression and World War II. Let’s not forget that the Chinese civil war was taking place during this period, and the Korean War was about to begin. Shou-Ching’s parents lived through this period, in China and Korea, and it was a time of starvation for them and for many others in east Asia.

All deeply impoverished people around the world eat high-carb diets, because carb-rich plants are the most readily available “fallback foods” in the natural environment and the cheapest calories available on the market. As soon as animal foods become available, cultures around the world migrate to 50% carb diets.

We have testimony from Okinawans who lived at that time telling us how difficult it was to obtain food. Their diet was severely calorie-restricted. I recall one Okinawan centenarian on television stating that they ate many kilograms of vegetables each day, simply because there was nothing else. (It rather resembled the Terry Wahls diet – very micronutrient rich.)

Then, decades later, the Okinawans become noted for their longevity. What produced the longevity – the carbs or the calorie restriction? Most likely the calorie restriction and high levels of nutrition were more important than the carb-to-fat ratio.

Food quality is also a factor. As readers of our book know, we think traditional Pacific islander diets are the healthiest in the world – composed of safe starches, coconut, and fish, very low in sugar and omega-6 fats. Whatever the carb fraction, such diets are healthier than the American diet. If there is a place in the world to survive a starvation diet of foraged and locally grown foods, it is a Pacific island.

My view: It was silly of the anti-carb panelists to refuse to credit the Okinawan data, but it is also misleading to say that the “traditional diet” of Okinawans is 85% carb based on data from a period of starvation and food scarcity.

As I noted in the panel, when people are able to eat as many calories as they wish, carb intake is generally anti-correlated with longevity at a population level: higher carb intake is associated with shorter expected lifespan. This is mainly due to the correlation of higher carb intake with poverty, but it occurs even within smaller samples of countries at similar income levels. For instance, among the European countries, higher carb intake is associated with shorter lifespan.

As I stated in the panel, this is extremely weak evidence for an effect of carbs; there are many confounding factors and population-level data cannot sort these out (the “ecological fallacy”).

Personally, I give more credence to data on centenarian diets. Few supercentenarians eat high-carb diets, so carbs may indeed reduce maximum lifespan, though eating a high-carb diet certainly doesn’t prevent people from becoming centenarians. (Supercentenarians live to 110.)

How carbs affect appetite may be more important than specific biological effects of glucose (or insulin). As the Simpson & Raubenheimer “protein leverage hypothesis” data show, in rodents higher carb diets are associated with higher calorie intake. Perhaps something similar occurs in humans. We know that energy excess and calorie restriction are major factors in longevity.

In short: I personally think that the relationship of carbs to longevity is U-shaped, with longest expected lifespans at a 30% carb intake; and I think available data is consistent with this. But I think the influence of carbs on longevity is small compared to other factors.

Conclusion

I was concerned going in that the panel would merely re-hash old arguments. I think the anti-carb arguments were, for the most part, familiar and weak; but I think the discussion took us to interesting places. I think the issue of the healthfulness of very high-carb diets, and the data from cultures like Okinawans, is a very interesting topic; and I think the issues of aging and longevity are quite interesting. I enjoyed the panel.

There are some health conditions which benefit from low-carb eating. I am grateful to our moderator, Jimmy Moore, for allowing me to enumerate some of the health conditions that have benefited from the ketogenic version of the Perfect Health Diet.

All in all, I think it was a good discussion but if it is to continue either the very low carb advocates will need to come up with better arguments and better evidence, or the topic will have to shift to exploring the merits of high-carb diets – a topic which the ancestral community hasn’t spent much time discussing.

Reference

[1] Van Voorhies WA, Fuchs J, Thomas S. The longevity of Caenorhabditis elegans in soil. Biol Lett. 2005 Jun 22;1(2):247-9. http://pmid.us/17148178.