Category Archives: Disease - Page 6

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.

Chocolate: What is the Optimal Dose?

Posted by on November 3, 2012 146 comments

Bret asked us how much chocolate is needed for good health:

I have a question about having dark chocolate daily. Does it need to be every day or what is the mininum grams per day. I have been having around 35g a day of 70% but I wondered if less would be ok or not having it at all.

This is a great time for this question, since Halloween candy will be running out soon, and those on tight budgets may be tempted to skimp on their chocolate. Should they?

Chocolate Is Not Considered Essential … Yet

Chocolate has not yet been recognized by the Food and Nutrition Board of the National Academies as an essential nutrient. We haven’t either: Our food plate lists it among “pleasure foods,” which are healthful but optional.

However, we are becoming ever-more chocolate friendly. In the new edition of our book, we list chocolate among our “supplemental foods” which we recommend consuming regularly. But our suggested dose is “as desired.” Perhaps we should narrow that down a little.

Chocolate Against Cardiovascular Disease

We’ve previously warned of the danger of chocolate deficiency, based on a systematic review that found: “The highest levels of chocolate consumption were associated with a 37% reduction in cardiovascular disease and a 29% reduction in stroke.” [1]

Here’s a visual summary of their findings:

The review authors report that every study accounted for chocolate intake in a different way, so they could only compare the groups with highest and lowest chocolate consumption in each study, not specific doses of chocolate.

Chocolate Against Diabetes

Bret was concerned about the sugar in chocolate, but if this is a problem, it’s outweighed by the benefits of chocolate. A Japanese study found that the rate of diabetes was reduced by 30% in those who consume the most chocolate. [2]

Chocolate Against Dementia and In Support of Cognitive Function

Several studies [3, 4] have found that chocolate consumption reduces risk of dementia and enhances performance on tests of cognitive function.

One of them found that cognitive function was optimized with a relatively low dose of chocolate – ten grams per day:

The associations between intake of these foodstuffs and cognition were dose dependent, with maximum effect at intakes of approximately 10 g/d for chocolate and approximately 75-100 mL/d for wine, but approximately linear for tea. [3]

The other found that cognition improved with intake of cocoa flavanols up to quite high doses – elderly given 1 g/day cocoa flavanols performed significantly better on cognitive tests than those given lower doses. [4]

Unfortunately I don’t know what fraction of chocolate is made of flavanols. I’m guessing it’s not more than a few percent, in which case this research suggests the optimal dose of chocolate may be 50 g/day or more.

Chocolate in Support of Circadian Rhythms

Most authors attribute the benefits of chocolate to their flavanols, which are thought to improve endothelial function and increase blood flow to the brain, among other effects.

However, there are other active compounds in chocolate, include peptides that interact with the opioid receptor. The opioid receptor has a role in circadian rhythms, which is one reason low-dose naltrexone (which blocks opioid function at night) works. It’s possible that eating chocolate during the day may support circadian rhythms via opioid receptor stimulation, especially if the peptides can reach the systemic circulation.

Indirect evidence that this may be beneficial comes from a Russian study in which exorphins (opioid receptor ligands) were injected into rats:

The chronic intraperitoneal administration of the peptide at the same dose of 5 mg/kg significantly increased exploratory activity, decreased anxiety, and improved learning. [5]

I don’t know how much chocolate would have to be eaten to achieve a similar exorphin dose in humans, but I imagine it’s large.

Chocolate in Support of Nobel Prizes

So how shall we resolve the issue of optimal chocolate dose? For me, the decisive evidence comes from a recent study by Franz Messerli published in the New England Journal of Medicine.

Based on chocolate’s support for cognitive function, he decided to see if chocolate consumption was related to another measure of cognition – Nobel Prize awards per capita. He counted Nobel Prizes and compared them to the recipient’s country’s chocolate consumption. These were his findings [6]:

There is clearly a strong correlation. The correlation coefficient is .79; p < 0.0001.

The correlation coefficient if Sweden is removed increases to .86 – which is suspicious:

Given its per capita chocolate consumption of 6.4 kg per year, we would predict that Sweden should have produced a total of about 14 Nobel laureates, yet we observe 32. Considering that in this instance the observed number exceeds the expected number by a factor of more than 2, one cannot quite escape the notion that either the Nobel Committee in Stockholm has some inherent patriotic bias when assessing the candidates for these awards or, perhaps, that the Swedes are particularly sensitive to chocolate, and even minuscule amounts greatly enhance their cognition. [6]

Those dastardly Swedes! Giving themselves more Nobel Prizes than their chocolate consumption warrants!

But I apologize, I’ve been diverted. The key point is, is there an optimum chocolate consumption?

the dose–response curve reveals no apparent ceiling on the number of Nobel laureates at the highest chocolate-dose level of 11 kg per year. [6]

11 kg/yr is an average of 30 g/day. So benefits are still increasing at that dose.

Of course, this was only a population level study. We still need to measure the doses in individual laureates to gain confidence. But anecdotally, there appears to be a correlation:

“I attribute essentially all my success to the very large amount of chocolate that I consume,” said Eric Cornell, an American physicist who received the Nobel Prize in 2001. “Personally I feel that milk chocolate makes you stupid. Now dark chocolate is the way to go. It’s one thing if you want like a medicine or chemistry Nobel Prize…but if you want a physics Nobel Prize it pretty much has got to be dark chocolate.”

Dark chocolate is, indeed, the PHD-approved form of this highly beneficial food.

Conclusion

This dose-response data might not be strong enough to define an RDA, but I’m going to take a stand: Bret’s intake of 35 g/day is healthy. Indeed, it’s right in line with the Nobel Prize-maximizing chocolate intake of the Swiss.

In regard to your last question, Bret – can you eat less chocolate, or none at all – the answer is clear. Yes, you can. But you must accept the consequences. You probably won’t be winning the next Nobel Prize for Physics.

References

[1] Buitrago-Lopez A et al. Chocolate consumption and cardiometabolic disorders: systematic review and meta-analysis. BMJ. 2011 Aug 26;343:d4488. doi: 10.1136/bmj.d4488. http://pmid.us/21875885.

[2] Oba S et al. Consumption of coffee, green tea, oolong tea, black tea, chocolate snacks and the caffeine content in relation to risk of diabetes in Japanese men and women. Br J Nutr. 2010 Feb;103(3):453-9. http://pmid.us/19818197.

[3] Nurk E et al. Intake of flavonoid-rich wine, tea, and chocolate by elderly men and women is associated with better cognitive test performance. J Nutr. 2009 Jan;139(1):120-7. http://pmid.us/19056649.

[4] Desideri G et al. Benefits in cognitive function, blood pressure, and insulin resistance through cocoa flavanol consumption in elderly subjects with mild cognitive impairment: the Cocoa, Cognition, and Aging (CoCoA) study. Hypertension. 2012 Sep;60(3):794-801. http://pmid.us/22892813.

[5] Belyaeva YA et al. Effects of acute and chronic administration of exorphin C on behavior and learning in white rat pups. Moscow University Biological Sciences Bulletin Volume 64, Number 2 (2009), 66-70, DOI: 10.3103/S0096392509020035. http://www.springerlink.com/content/qt537481061656gt/?MUD=MP.

[6] Messerli FH. Chocolate consumption, cognitive function, and Nobel laureates. N Engl J Med. 2012 Oct 18;367(16):1562-4. doi: 10.1056/NEJMon1211064. Epub 2012 Oct 10. http://pmid.us/23050509.

Look AHEAD Scientists: Trying to Move the Deer Crossing

Posted by on October 22, 2012 78 comments

The Look AHEAD: Action for Health in Diabetes trial has been halted two years early. Here’s Gina Kolata in The New York Times:

The study randomly assigned 5,145 overweight or obese people with Type 2 diabetes to either a rigorous diet and exercise regimen or to sessions in which they got general health information. The diet involved 1,200 to 1,500 calories a day for those weighing less than 250 pounds and 1,500 to 1,800 calories a day for those weighing more. The exercise program was at least 175 minutes a week of moderate exercise.

But 11 years after the study began, researchers concluded it was futile to continue — the two groups had nearly identical rates of heart attacks, strokes and cardiovascular deaths.

It’s clearly a negative result for “eat less, move more” as a health strategy for obese diabetics.

Was “Eat Less Move More” Harmful?

A few Paleo bloggers are not surprised; indeed, Peter Dobromylskyj speculates that all-cause mortality – which Ms. Kolata and the NIH press release do not report – may have been higher in the “eat less, move more” intervention group:

It seems very likely to me that more people died in the intervention group than in the usual care group, but p was > 0.05.

Call me a cynic, but I think they stopped the trial because they could see where that p number was heading.

Peter may be a cynic but cynics are sometimes right, and I will bet that he’s right about this. In general, calorie restriction and exercise are better attested against cardiovascular disease than against other health conditions, so if death rates from CVD were identical in the two arms after 11 years, it’s quite likely death rates from other causes were higher in the intervention arm.

Our Theory

We discuss in our new Scribner edition two reasons why “eat less, move more” can backfire:

  • On a malnourishing diet, “eat less” means even greater malnourishment. Less of a bad diet is a worse diet.
  • Excessive exercise may over-stress the body and harm health. In diseased people, the volume at which exercise becomes excessive may not be that high.

On the other hand, ultimately some form of “eat less, move more” is needed if optimal health is to be attained:

  • An energy deficit – eating less than the body expends – is necessary to lose fat mass, and obesity is probably incompatible with optimal health.
  • About 20 to 30 minutes of exercise per day at the intensity of running or jogging is needed for optimal health, probably due to the role of daytime activity in entraining circadian rhythms (see “Physical Activity: Whence Its Healthfulness?”, October 11, 2012). Most people would need to “move more” to achieve this.

So the challenge in weight loss is two-fold: It’s necessary to adopt a healthy diet in which malnourishment doesn’t occur despite calorie restriction, and to find a healthy level of exercise that improves health without overstressing the body.

Look AHEAD: Bad Dietary Advice

The Look AHEAD Study Protocol tells us what the intervention group was told to do.

From page 29, here is the diet advice:

The recommended diet is based on guidelines of the ADA and National Cholesterol Education program [96,97] and includes a maximum of 30% of total calories from total fat, a maximum of 10% of total calories from saturated fat, and a minimum of 15% of total calories from protein.

This gives 55% carbs and probably 10% omega-6 fat. The omega-6 intake is far too high – for weight loss and good health, omega-6 intake should be less than 4% – and so is the carb intake – for diabetics, reducing carbs to 30% or less is highly desirable.

From page 30, here is the exercise advice:

The physical activity program of Look AHEAD relies heavily on unsupervised exercise, with gradual progression toward a goal of 175 minutes of moderate intensity physical activity per week by the end of the first six months. Exercise bouts of ten minutes and longer are counted toward this goal. Exercise is recommended to occur five days per week.

Moderate-intensity walking is encouraged as the primary type of physical activity.

I think this is reasonable advice. It translates to 35 minutes per day for 5 days. The intensity is quite low. This level of exercise is hardly likely to be excessive; indeed, it’s probably grossly insufficient for optimal health. It represents about a mile and a half of walking per day, five days per week. This may have been a homeopathic level of activity.

There is another reason the exercise may have produced no observable benefit. Since I believe the health benefits of exercise occur primarily through circadian rhythm entrainment, it’s likely that daytime exercise is much more beneficial than night-time exercise. Night-time exercise might be ineffective or even harmful to health if it disrupts circadian rhythms.

Unfortunately many people find it difficult to find time during the day for exercise. If the walking was performed at night, even the modest benefits of the activity may have been lost.

Weight and Health: What’s the Direction of Causation?

The one “success” of Look AHEAD was that it brought about some weight loss: the intervention group lost 5% of their original weight.

We know that obesity is associated with poor health. Since causation implies correlation, the existence of this correlation suggests that either (1) obesity causes poor health, (2) poor health causes obesity, or (3) some third factors cause both obesity and poor health.

The Look AHEAD study presumed (1) – that obesity causes poor health. The “eat less, move more” intervention was wholly directed at weight loss. If obesity is the cause of poor health, Look AHEAD should have improved health. It didn’t. This tells us that the direction of causality is either (2) or (3). Obesity doesn’t impair health; other factors that impair health cause obesity.

It’s easy to make faulty inferences about the direction of causation. The Look AHEAD scientists made the same mistake this woman did:

Conclusion

The basic flaw in the Look AHEAD study was that it was designed to bring about weight loss, and hoped that weight loss would improve health.

A better intervention would seek to improve health through a more PHD-like diet and through circadian rhythm therapies. Successful health improvement would, more than likely, lead to weight loss.

For the overweight and for diabetics, the focus should not be on weight, but on health. Improve health, and weight loss will follow. Focus on weight with a simple-minded “eat less, move more” intervention without tending to the quality of your diet and lifestyle, and you might be doing yourself more harm than good.

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.