Category Archives: Perfect Health Diet - Page 3

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.

Higher Carb Dieting: Pros and Cons

Posted by on February 2, 2012 160 comments

Last week’s post (Is It Good to Eat Sugar?, Jan 25, 2012) addressed what I see as the most problematic part of the thought of the health writer Ray Peat – his support for sugar consumption.

Apart from this difference, “an extreme amount of overlap is evident,” Danny Roddy notes, in our views and Peat’s. Both perspectives oppose omega-6 fats, support saturated fats, favor eating sufficient carbs to normalize metabolism, support eating nourishing foods like bone broth, and oppose eating toxic foods like wheat.

If there is another difference between our ideas and Peat’s, it’s that “Peat-atarians” often eat more carbs. Danny puts it:

Paul and Peat have similar recommendations for carbohydrate consumption. Paul’s recommendations hover around 150 grams while Peat usually recommends 180-250 grams, but he himself eats closer to ~400 grams.

So I thought it might be worth looking at the issue of overall carb consumption.

Carbs for Hypothyroidism

In Is There a Perfect Human Diet? (Jan 18, 2012) we noted that diseases can change the optimal diet. In some diseases it’s better to lower carb consumption, but in others it’s better to increase carb consumption. The example we gave is hepatitis; hepatitis B and C viruses can exploit the process of gluconeogenesis to promote their own replication, so high-carb diets which avoid gluconeogenesis tend to slow down disease progression.

Another disorder that might benefit from more carb consumption is hypothyroidism. A number of people with hypothyroidism have benefited from Peat-style carb consumption. Here is ET commenting on last week’s post:

As someone following the PHD with a good dash of Peat, I really enjoy this post and the comments. Thank you Paul….

Paul says that “I’m not persuaded that it’s a desirable thing to keep liver glycogen filled at all times, but for some health conditions it may be good to tend that way, like hypothyroidism.” Well, according to Chris Kresser, 13 of the top 50 selling US drugs are either directly or indirectly related to hypothyroidism. If going by either the low body temperature/low pulse diagnostic, and/or some kind of pattern on the serum tests (Anti-TG, TPO, TSH, free T-3, free T4, total T3, total T4), we are talking a significant proportion of the population, especially women, being hypothyroid in some form….

Many with low T3 have a conversion problem from T4 in the liver (80% of T3 is converted from T4 in the liver and kidneys – only a small portion is coming from the thyroid gland).

Is it a good idea to NOT try to fill the liver glycogen in such a pattern? For those who have lived with the consequences of low T3 (adrenaline rush, waking up in the middle of the night, fatigue, tendency to orange-yellowish color i the face etc.), and had improvements on a more Peat like diet, I do not think so.

The way to fill liver glycogen, of course, is by eating more carbs.

I’ve previously noted that increased carb consumption upregulates the levels of T3 thyroid hormone (Carbohydrates and the Thyroid, Aug 24, 2011):

T3, the most active thyroid hormone, has a strong effect on glucose utilization. T3 stimulates glucose transport into cells, and transport is the limiting factor in glucose utilization in many cell types. In hyperthyroidism, a condition of too much T3, there are very high levels of glucose utilization. Administration of T3 causes elevated rates of glycolysis regardless of insulin levels.

The body can reduce T3 levels by converting T4 into an inactive form called reverse T3 (rT3) rather than active T3. High rT3 levels with low T3 levels lead to reduced glucose transport into cells and reduced glucose utilization throughout the body.

This means that eating more carbs raises T3 levels, and eating fewer carbs lowers T3 levels.

For a hypothyroid person, then, eating more carbs is an alternative tactic for increasing thyroid hormone activity. It may provide symptomatic relief similar to that achieved by supplementing thyroid hormone directly.

Perhaps the two are complementary tactics that should be done together. Taking thyroid hormone pills will increase glucose utilization, creating a need to eat more carbs. A mix of the two tactics may be optimal.

UPDATE: Mario points out that most cases of hypothyroidism in advanced countries are due to Hashimoto’s, an autoimmune disease probably triggered by infections or gut dysbiosis, and eating more carbs will tend to flare any gut dysbiosis and thus aggravate the thyroiditis. Meanwhile, supplemental thyroid hormone tends to reduce antibody activity.

Carbs for Mood

Another interesting comment came from Jim Jozwiak:

Paul, this discussion gets to the crux of what I do not understand about the Perfect Health Diet. You are speaking as if refilling liver glycogen is a good thing, and it undoubtedly is, because mood is so much better when there is sufficient liver glycogen because then the brain is confident of its power supply. Also, you acknowledge that safe starch would eventually replenish liver glycogen after muscle glycogen is topped off. So why not eat enough starch to replenish liver glycogen? It is not so difficult to figure out how much that would be. Have some sugar, feel what replenished liver glycogen is like, then titrate safe starch gradually meal-by-meal to get the same effect. When I do it, and I am not an athlete, I get 260 grams of non-fiber carb per day, which is considerably more than you usually recommend. Have you tried this experiment and found the result unsatisfactory in some way?

Jim has experimented to find the amount of carbs that optimize his mood, and found it to be 260 g (1040 calories). On a 2400 calorie diet, typical for men, this would be 43% carbs.

If Peat typically recommends 180 to 250 g carbs, as Danny says, then on a 2000 calorie reference diet that would be 36% to 50% carbs.

Those numbers are strikingly similar to another statistic: The amount of carbs people actually eat in every country of the world.

Here is a scatter plot of carb consumption vs per capita income by country. Dietary data comes from the FAO, income is represented by GDP per capita from the IMF:

At low incomes people eat mainly carbs, because the agricultural staples like wheat, rice, corn, and sorghum provide the cheapest calories.

As incomes rise, carb consumption falls, but it seems to approach an asymptote slightly below 50% carbs. The lowest carb consumption was France at 45%, followed by Spain, Australia, Samoa, Switzerland, Iceland, Italy, Austria, Belgium, and Netherlands.

We can guess that if money were no object, and people could eat whatever they liked, most people would select a carb intake between 40% and 50%.

This is precisely the range which Jim found optimized his mood.

The Longevity vs Fertility and Athleticism Trade-off

I won’t enumerate studies here, but animal studies indicate that higher carb and protein intakes promote fertility and athleticism, while restriction of carbohydrate and protein promotes longevity.

In our book, we calculate the daily glucose requirements of the human body at around 600 to 800 calories, or 30% to 40% of energy on a 2000-calorie diet.

So a 30-40% carb diet is a neutral diet, which probably places minimal stress on the body.

A 40-50% diet is a carb-overfed diet, which probably promotes fertility and athleticism.

A 20-30% diet is a mildly carb-restricted diet, which probably promotes longevity.

Do we see diminished longevity with higher carb consumption in human epidemiological data? I think so.

It’s useful to compare European countries, since they are genetically and culturally similar. There is a correlation between carbohydrate intake and longevity. Here is a list of life expectancy among 46 European countries. Neglecting little countries like Monaco, San Marino, and Andorra, that are not in my carb database, the countries with the longest life expectancy are also the ones with the lowest carb consumption: Italy first, France second, Spain third, Switzerland fourth, and Iceland sixth are all countries with carb intake below 50%. Sweden, at 50.8% carbs, placed fifth in longevity.

Did Evolution Hardwire a Preference for Carbs?

We know that the brain has an innate food reward system which tries to get people to eat a certain diet. What carbohydrate intake is it likely to select for?

Experiments on the food preferences of insects and rodents give us clues. The paper “Macronutrient balance and lifespan,” by Simpson and Raubenheimer, cited some time ago by Dennis Mangan, summarizes evidence from animals for the influence of macronutrients on lifespan. A good example is the fruit fly; protein has the dominant effect on lifespan, with low protein favoring longevity and high protein favoring fertility. The flies eat so as to maximize fertility:

The response surface for lifetime egg production peaked at a higher protein content than supported maximal lifespan (1:4 P:C, Figure 1A). This demonstrates that the flies could not maximize both lifespan and egg production rate on a single diet, and raises the interesting question of what the flies themselves prioritized – extending lifespan or maximizing lifetime egg production. Lee et al. [3] answered this by offering one of 9 complementary food choices in the form of separate yeast and sugar solutions differing in concentration. The flies mixed a diet such that they converged upon a nutrient intake trajectory of 1:4 P:C, thereby maximizing lifetime egg production and paying the price of a diminished lifespan.

This seems to be the evolutionary preference in mammals as well as flies. When unlimited food is available, animals tend to overfeed slightly on carb and protein, sacrificing lifespan for increased fertility and athleticism.

Jim reported improved mood on a 43% carb diet. Is it due to the filling of liver glycogen raising metabolism? Due to a sensation of enhanced fertility, libido, and athleticism? Or simply due to greater satisfaction of the brain’s reward system?

Yet another factor may also be involved.

Might Stress Be Mistaken for Enhanced Energy?

Peat favors sucrose as a carb source, which is why Danny Roddy recommended orange juice and Travis Culp soda. I argued in last week’s post that it would be better to eat a starchier diet so that the carb breakdown would be at least 70% glucose, less than 30% fructose and galactose.

Eating a higher-carb diet fills up liver glycogen, removing the most rapid fructose disposal pathway. This makes a high-carb sucrose-based diet rather stressful for the body; it has to dispose of fructose rapidly to avoid toxicity, but has limited ability to do so.

We can see the stressfulness of sucrose by its effects on the “fight-or-flight” stress hormones adrenaline (epinephrine) and noradrenaline (norepinephrine). Here is a study that fed high-fat, high-starch, and high-sucrose diets for 14 days to healthy non-obese subjects, and measured the hormonal response [1; full text]. This paper was discussed by the blog Proline (hat tip: Vladimir Heiskanen). The results:


On high-fat and high-starch diets, adrenaline and noradrenaline levels are low; they are consistently elevated — almost doubled — on the high-sucrose diet.

This makes sense; as Wikipedia notes,

epinephrine and norepinephrine are stress hormones that underly the fight-or-flight response; they increase heart rate, trigger the release of glucose from energy stores, and increase blood flow to skeletal muscle.

These hormones trigger the release of glucose from liver glycogen, thus freeing up room for fructose disposal.

Note that this result contradicts an assertion by Danny Roddy:

I consider the ability to refill glycogen (minimizing adrenaline & cortisol release) to be an important factor in health.

Refilling glycogen is not the same thing as minimizing adrenaline release. The requirement to dispose of fructose may trigger adrenaline release.

The reason I bring this up is not to renew the starch vs sugar discussion; but rather to ask if this “fight-or-flight” response to sugar consumption may not be partially responsible for the perceived mood and energy improvements on a Peat-style diet.

Indeed, one of the peculiar aspects of Ray Peat’s health advice is his recommendation to increase pulse rates well above normal levels. In his article on hypothyroidism, Peat states:

Healthy and intelligent groups of people have been found to have an average resting pulse rate of 85/minute, while less healthy groups average close to 70/minute.

I would have thought 60 beats per minute was normal, and when I was more athletic my pulse was typically 48 beats per minute.

One of the effects of adrenaline and noradrenaline is to speed up the pulse rate. If Peat really does eat 400 g of carbs per day, predominantly from sucrose, then he may be achieving his high pulse rate from an “adrenaline rush” that helps dispose of an excess of fructose.

If, indeed, this is a source of improved sense of well-being on Peat-style diets, it may be a double-edged sword. Chronic stimulation of the “fight-or-flight” hormones to aid in fructose disposal may have long-run negative consequences.

UPDATE: I’m reminded of this video, showing the adrenaline-promoting effects of sucrose consumption:


Starch would not have had the same effect, and would surely be healthier in the long run.

Summary

It is possible that higher carb intake may increase thyroid hormone levels, fertility, and athleticism, and enhance mood in some people. These gains do not come without cost. Notably, they probably involve a sacrifice of longevity.

If the benefits of higher carb intake are sought, it is best to achieve them by eating starches primarily, not sugar.

Conclusion

In our book, we recommend a slightly low-carb diet of 20-30% of calories. If we were re-writing the book now, we would probably be a bit less specific about what carb intake is best. Rather, we would say that a carb intake around 30-40% is neutral and fully meets the body’s actual glucose needs; and discuss the pros and cons of deviating from this neutral carb intake in either direction.

For most people, I believe a slightly carb-restricted intake of 20-30% of calories is optimal. Most people are not currently seeking to have children or engaging in athletic competition. There is good reason to believe that mild carb restriction maximizes lifespan, and most people desire long life. As we’ve noted, supercentenarians generally eat low-carb, high-fat diets.

But the spirit of our book is to educate, and let everyone design the diet that is best for them. And there is room for difference of opinion about the optimal carb intake.

References

[1] Raben A et al. Replacement of dietary fat by sucrose or starch: effects on 14 d ad libitum energy intake, energy expenditure and body weight in formerly obese and never-obese subjects. Int J Obes Relat Metab Disord. 1997 Oct;21(10):846-59. http://pmid.us/9347402. Full text: http://www.nature.com/ijo/journal/v21/n10/pdf/0800494a.pdf.

Is It Good to Eat Sugar?

Posted by on January 25, 2012 188 comments

A few “Peat-atarians” – followers of the iconoclastic health writer Ray Peat – have accused us of being too skeptical of fructose. They think we should promote sugar consumption.

Here’s Travis Culp:

I think fructose is only conditionally problematic and that the consumption of it alongside glucose at a time of low liver glycogen is highly advantageous. In fact, I would go so far as to say that (somewhat slowly) drinking a can of soda upon waking (as disgusting as that is) would not result in any real glycation, insulin resistance, elevated TGs etc…. I think it’s beneficial to eat something really sugary upon waking …

Here’s Danny Roddy:

Peat has stated that … fructose … “powerfully” refills glycogen …

I would consider the ability to refill glycogen (minimizing adrenaline & cortisol release) to be an important factor in health …

It’s true that the ability to refill glycogen is essential for health; some genetic glycogen storage disorders are fatal in early childhood. But everyone who lacks a glycogen storage disorder has the ability to refill glycogen from multiple sources. In addition to fructose, glucose sugars and starches refill glycogen, as does milk sugar (a compound of glucose and galactose).

So the question is which combination of dietary sugars (a) is best at refilling glycogen and (b) makes the healthiest diet, all things considered?

Sugar Composition of the Diets

Both Danny and Travis framed their arguments as criticisms of our diet. They are really arguing that a Peat-style sugary diet is healthier than a PHD-style moderate-starch diet.

So before going further, let’s look at the sugar content of the diets we’re comparing.

First, note that PHD is not a zero-fructose diet. As an examination of the PHD Food Plate shows, PHD includes many fructose-containing plant foods – fruits, berries, and vegetables such as beets, onions, carrots, and squashes – plus “pleasure foods” like chocolate.

Also, PHD is not a zero-dairy diet, so for many practitioners it will include some milk sugars which are half galactose and half glucose.

In my diet personally, probably about 55% of carb calories come from starches, 30% from fruits, berries, and sugary vegetables, and 15% from dairy products such as yogurt. In terms of simple sugars, this translates to about 77% glucose, 15% fructose, and 8% galactose.

Not every Perfect Health Dieter will have the same sugar proportions; there is no obligation to consume dairy, and the relative proportions of starchy and sugary plants will vary according to taste. But let’s take mine as characteristic PHD proportions.

In a Peat-style diet, in contrast, the breakdown of sugars is near 50% glucose and 50% fructose.

So we aren’t comparing fructose against glucose, but a 77% glucose 15% fructose diet against a 50% glucose 50% fructose diet.

Why the Focus on Refilling Glycogen?

Why do the defenders of sugar focus on its ability to refill glycogen?

The reason is that fructose is treated by the body as a poison. Dietary fructose is shunted to the liver for disposal by conversion to glycogen, fat, lactate, or pyruvate.

Fructose is treated like a poison because it is dangerous. High doses of fructose have observable harmful effects even in short-term studies. Fructose does no good to the liver while it’s there, in fact fructose combined with polyunsaturated fats very effectively creates liver disease. Fructose in any other organ does harm; for instance, fructose promotes cancer growth.

Given fructose’s rapid disposal, any benefits from fructose have to be attributable to the glycogen or other products it is turned into. If fat, lactate, or pyruvate (a glucose product) provided benefits, dietary fats or starches would do the same, without the risk of fructose toxicity or fats getting stuck in the liver due to choline and methionine deficiency. So if fructose is to have benefits, it has to be via glycogen.

Here, then, is the challenge Peat-atarians face. Fructose has many proven harms. It has only one possible benefit: its ability to help re-fill liver glycogen. Peat-atarians have to show two things:

  1. That a diet with Peat-like sugar proportions – roughly 50% fructose, 50% glucose –is better than a diet with PHD-like sugar proportions – 15% fructose, 8% galactose, 77% glucose – at refilling liver glycogen.
  2. That better re-filling of liver glycogen improves the healthfulness of the diet.

How Do Sugars Perform at Refilling Glycogen?

Danny provides no citations for his claim that fructose “powerfully” refills glycogen. But Danny’s commenters help him out.

Daz, drawing upon a New York Times report, offers two studies [1] [2]. Cliff offers several more [3] [4]. Let’s see what these tell us.

The first study, “Fructose and galactose enhance postexercise human liver glycogen synthesis” [1], looks at athletes depleted of liver glycogen by intense cycling, and assessed the effectiveness of three sugar drinks at replenishing liver glycogen. The three drinks were:

  • 2/3 maltodextrin, 1/3 fructose;
  • 2/3 maltodextrin, 1/3 glucose;
  • 2/3 maltodextrin, 1/3 galactose.

Maltodextrin digests to glucose, so all three drinks are majority glucose. The athletes drink 275 calories of these drinks per hour for 6.5 hours after exercise. Galactose is non-toxic, but like fructose tends to be taken up by the liver.

Liver glycogen was measured every two hours with carbon-13 magnetic resonance imaging. Here were the results:

So 67% glucose / 33% galactose did the best, 67% glucose 33% fructose was close behind, and 100% glucose lagged.

Why does the 100% glucose drink underperform? One reason is that fructose and galactose, but not glucose, are preferentially targeted to the liver:

A factor of potentially larger magnitude in enhancing liver glycogen synthesis is the differential postabsorptive fates of fructose and glucose. Glucose is a relatively poor direct substrate for liver glycogen synthesis (24,27). Much of it is released from the liver into the systemic circulation to be stored as muscle glycogen (3,7). In contrast, fructose is primarily taken up by the liver … [1]

The second paper, “Superior endurance performance with ingestion of multiple transportable carbohydrates” [2], did not measure liver glycogen replenishment; instead, it gave its cyclists sugary drinks every 15 minutes throughout an intense 2-hr cycling test, and compared performance. Three different drinks were used: a 67% glucose 33% fructose drink, a 100% glucose drink, and a water-only control group. Performance was best with the 67% glucose 33% fructose drink, intermediate with the glucose drink, and worst with the water drink. The results suggest that the 67% glucose 33% fructose drink was better for liver glycogen replenishment, and that liver glycogen replenishment aided the cyclists’ performance.

The third paper, “Effect of different post-exercise sugar diets on the rate of muscle glycogen synthesis” [3], isn’t available to me electronically, so we’ll have to work from the abstract. It looked at muscle glycogen, measured using biopsies (ouch!), rather than liver glycogen.

It first assessed the effect of different amounts of glucose. It found that 0.7 g/kg body weight of glucose given every 2 hours would maximize the rate of muscle glycogen synthesis. For an 80 kg man, that works out to 56 g or 224 calories of glucose per two-hour period, or 112 calories per hour. Above this amount, the rate of muscle glycogen synthesis is unchanged.

It then compared three formulations at this same 0.7 g/kg body weight dose: 100% glucose, 100% sucrose (50% glucose, 50% fructose), and 100% fructose. Muscle glycogen synthesis rates were:

  • 5.8 mmol/kg/hr with 100% glucose
  • 6.2 mmol/kg/hr with 50% glucose, 50% fructose
  • 3.2 mmol/kg/hr with 100% fructose

If we fit a quadratic curve to these points, it predicts a peak rate of glycogen synthesis with 70% glucose, 30% fructose:

Athletes Agree: More Glucose Than Fructose

Of course, endurance athletes know that it’s beneficial to replenish glycogen during endurance events like marathons and triathlons.

Some authorities, including Tim Noakes, an exercise physiologist who has run over 70 marathons, believe that liver glycogen rather than muscle glycogen is the gating factor in marathon performance. From “The Science of Carbohydrate Loading” by David Peterson:

Remember also that muscle glycogen is committed to be used by muscle and cannot assist in maintaining blood sugar levels. Therefore should no additional carbohydrate be ingested during prolonged exercise, the task of maintaining blood glucose levels rests firmly on the liver’s glycogen stores and gluconeogenesis (the manufacturing of glucose from plasma amino acids). Oxidation of blood glucose at 70-80% VO2 max is about 1.0 g/min or about 60 g/hour. Therefore it can be predicted that even with full glycogen stores, a less conditioned athlete’s liver will be depleted of its carbohydrate within an hour and three quarters of continuous moderate intensity exercise. (Interestingly, the daily carbohydrate requirements of the brain and nervous system alone are enough to deplete the liver glycogen stores within 24 hours.) Once liver glycogen levels begin to drop and exercise continues the body becomes increasingly hypoglycemic (low blood sugar) mainly because blood glucose is depleted faster than it is replaced by gluconeogenesis. Professor Tim Noakes considers liver glycogen depletion and subsequent hypoglycemia to be the primary factors affecting fatigue and performance during extended duration races and especially in instances where muscle glycogen levels are low as well.

So marathoners and other endurance athletes will want to replenish liver glycogen as rapidly as possible during a race. What mix of sugars do they use?

The popular product is carbohydrate gels that can be swallowed at the same time water is taken. Here are the top carbohydrate gels sold on Amazon:

So the sugar mix ranges from 67% glucose to 100% glucose. No product uses 50% fructose.

Presumably, athletes have done a great deal of personal experimentation and know that these ratios do, indeed, optimize the speed of glycogen replenishment.

When athletes have no need for speed, as when they are carb loading before a marathon, then they eat starches like pasta and bread, not sugar. So to maximize total glycogen status, regardless of speed of filling, a carb mix close to 100% glucose works just fine.

Glycemic Control

The fourth paper, “Acute fructose administration decreases the glycemic response to an oral glucose tolerance test in normal adults” [4], is about how a bit of fructose affects the glycemic response to an oral glucose tolerance test.

It showed that a 9% fructose 91% glucose test (7.5 g fructose, 75 g glucose) produced a lower glucose area under the curve and higher insulin response than a 100% glucose test. Here’s the glucose response:

In general higher insulin and lower glucose is healthier than the reverse, so this is considered an improvement.

Summary of the Data

What these papers show is:

  • Glycogen replenishment proceeds the fastest with a mix of sugars consisting of about 70% glucose and 30% fructose or galactose.
  • Although this wasn’t tested, we can guess that a mix of fructose and galactose would be more effective than fructose alone, since it seems that utilizing multiple carbohydrate pathways is what drives the speedier glycogen replenishment. So the fastest glycogen replenishment might occur with something like 70% glucose 15% fructose 15% galactose.
  • Muscle glycogen replenishment is maximized with a carbohydrate intake of 100 calories per hour.
  • Athletes agree with the research, using carb gel packs that contain typically 30-40 g carbs with a composition of 67% to 100% glucose, 0% to 33% fructose.
  • Glycemic response to a large dose of carbohydrate may be improved by eating a 9% fructose 91% glucose mix.

From these data, I infer that for glycogen replenishment in liver or muscle, a PHD-style carb mix of 77% glucose, 15% fructose, 8% galactose is probably equal or superior to a Peat-style carb mix of 50% glucose, 50% fructose.

Conclusion

For athletes in the midst of a race, or in need of rapid recovery for a second race on the same day, speedy glycogen replenishment may be the endpoint to optimize. If so, they should eat a sugar drink composed of roughly 70% glucose and 30% fructose and galactose.

This is closer to PHD diet ratios than to Danny Roddy’s recommendation of orange juice or Travis Culp’s recommendation of soda!

But for others, speed of glycogen replenishment is hardly likely to be the parameter to optimize. There are unlikely to be significant benefits for non-athletes from replenishing glycogen 6.5% faster, as was found in the muscle glycogen study [3].

Speedier glycogen replenishment is almost the only known benefit to fructose consumption. It’s possible that low fructose doses, about 9% of carb calories (perhaps 2-3% of total calories), may improve glycemic control. This is a lower fructose fraction than is found in PHD, and far below the fructose fraction recommended by Danny and Travis.

Given the known risks of fructose consumption, especially with chronic intake at high doses or in conjunction with polyunsaturated fats, it seems prudent to err on the low side. It seems to me that the Peat-atarians have failed to provide any evidence at all in favor of a higher fructose intake than is provided by the fruits, berries, and sugary vegetables recommended by the Perfect Health Diet, save for athletes in the midst of a race or post-race recovery.

References

[1] Décombaz J et al. Fructose and galactose enhance postexercise human liver glycogen synthesis. Med Sci Sports Exerc. 2011 Oct;43(10):1964-71. http://pmid.us/21407126.

[2] Currell K, Jeukendrup AE. Superior endurance performance with ingestion of multiple transportable carbohydrates. Med Sci Sports Exerc. 2008 Feb;40(2):275-81. http://pmid.us/18202575.

[3] Blom PC et al. Effect of different post-exercise sugar diets on the rate of muscle glycogen synthesis. Med Sci Sports Exerc. 1987 Oct;19(5):491-6. http://pmid.us/3316904.

[4] Moore MC et al. Acute fructose administration decreases the glycemic response to an oral glucose tolerance test in normal adults. J Clin Endocrinol Metab. 2000 Dec;85(12):4515-9. http://pmid.us/11134101.

Is There a Perfect Diet?

Posted by on January 18, 2012 54 comments

We’ve begun blogging at Psychology Today, and I figured I’d start with an introduction to our diet. This is a slightly altered version of our first post there. — Paul

“All healthy persons are alike; each unhealthy person is unhealthy in his own way.”

If Tolstoy were a diet-and-health blogger, this might be how he would begin.

All healthy persons are alike

The composition of cells hasn’t changed much since the origin of complex multi-cellular life about 500 million years. Apart from water, the major components are fatty membranes and proteins. More than half the proteins are glycosylated – bonded to glucose-derived carbohydrates. These compounds – fats, proteins, and glucose – are the basic “macronutrients” needed by cells. In organisms, these cells are supported by an extracellular matrix composed of glycans and proteins; this matrix is mineralized in bones and teeth.

Why do animal species differ in their nutritional needs? Actually, nutrient needs differ remarkably little across the animal kingdom. This is why animals comprise “food” for one another: the ingredients of all animals are the same, so one animal nourishes another.

It is also why breast milk varies little across all mammalian species: the composition of cow’s milk is not much different from the composition of lion milk, for instance – or human milk for that matter.

Human nutrient needs differ from those of other mammals chiefly by virtue of our larger brains, which are rich in omega-3 fats and require extra glucose for energy. But large brains only modestly tweak the needed macronutrients: compared to other mammals, an extra 10-15% of calories as glucose, and an extra 1% of calories as omega-3 fats, are more than sufficient to nourish a human.

If all animals are alike in their nutrient needs, why are diets so different? Why don’t lions sup with lambs?

It turns out that what differs among the animals is the composition of the digestive tract. Animals have evolved digestive tracts and livers to transform diverse food inputs into the uniform set of nutrients that all need. Herbivores have foregut organs such as rumens or hindgut chambers for fermenting carbohydrates, turning them into fats and volatile acids that can be used to manufacture fats. Carnivores have livers capable of turning protein into glucose and fat.

When we look past the digestive tract at what nutrients are actually delivered to the body, all mammals obtain a remarkably similar set of nutrients. By calories, mammalian diets are always composed of a majority, typically 50-75%, of saturated and monounsaturated fats (including the short-chain fatty acids produced by fermentation of fiber); a mix of carbohydrates and protein, usually totaling around 25-40%; and a modest amount of polyunsaturated fat, typically less than 10%.

If diets differ because of digestive tract differences, we should expect the same pattern to recur in humans. All humans have the same nutrient needs, but our optimal food intake may vary if our digestive tracts differ.

In fact there is evidence for variations in digestive tract structure among human populations. Melissa McEwen has summarized evidence that Africans have slightly larger colons, suggesting a slightly more plant-focused evolutionary diet, and Europeans have slightly smaller colons, suggesting a more animal-focused evolutionary diet [1, 2].

Longer colons allow more fermentation of plant fiber, but they don’t dramatically change macronutrient ratios of the diet. Across human populations, the optimal human diet probably doesn’t vary in any macronutrient by more than 5% of energy or so.

So there is little support for a “blood type diet” or “metabolic type” with significantly different food needs. All healthy people can and should eat a similar diet – one that approximates to our body’s nutrient needs.

Each Unhealthy Person is Unhealthy in his Own Way

What are the causes of ill health? We believe there are three fundamental causes of ill health: malnutrition, toxins, and infectious pathogens.

There are dozens of elemental nutrients – vitamins, minerals, and biological compounds – whose absence in the diet can impair health. Many thousands of toxins, totaling several grams in weight daily, enter the human body; as Bruce Ames and Lois Gold have shown [3], plants make a host of natural food toxins, and food storage and cooking create more. Finally, we are continually exposed to microbes; there are probably hundreds of pathogens capable of establishing human infections.

It doesn’t take a mathematician to see that there myriad possible combinations of malnutrition, poisoning, and infection. The causes of disease are legion; it’s no surprise that the manifestations are so various. The number of possible combinations of disease causes is more than the number of humans. To a first approximation, every disease is unique.

Each combination of causes will affect the optimal diet in a different way. People who are malnourished will benefit from getting more of the things they are malnourished in, and perhaps less of others which balance those – as reducing zinc may help someone who is copper deficient, or reducing omega-6 fats may help someone who is omega-3 deficient. People exposed to toxins may benefit from an extra dose of toxin-metabolizing nutrients. People with infections may benefit from diets which starve pathogens of needed nutrients, or which support immune function. People with gut dysbioses may benefit from removing or reducing whole classes of foods – starches, fructose, FODMAPs, fiber, even protein.

Infections can make a big difference in the optimal diet. Ketogenic diets, which starve the brain of glucose but feed it with small molecules derived from fats, are highly effective against bacterial infections of the central nervous system, since bacteria depend on glucose metabolism. But hepatitis B and C viruses can utilize the process of gluconeogenesis – manufacture of glucose from protein – for their own benefit, so people with hepatitis benefit from higher carb diets.

Other pathologies disrupt the ability to handle certain nutrients. Diabetes is characterized by an inability to secrete insulin, and diabetics usually benefit from low-carb diets. Migraines, like epilepsy, may be caused by genetic or other impairments to brain glucose metabolism, and can often be cured by ketogenic diets, as several of our readers have discovered.

With ill health, the optimal diet often changes. Sick people often have to tweak their diet, and the nature of the change varies with the nature of the pathology.

Diet Can Be a Diagnostic and Therapeutic Tool

Precisely for this reason, diet and nutrition have a valuable place in the healer’s arsenal. A sick person’s response to dietary changes can be informative about the nature of his pathology.

For instance, ketogenic diets are therapeutic for bacterial and viral infections, but can feed protozoa, fungi, and worms (which have mitochondria and can metabolize ketones). Response to a ketogenic diet can help expose the nature of an infectious pathogen.

Because neurons are dependent on glucose or ketones for energy, any pathology which disrupts glucose utilization will cause neuronal starvation, and neurological and psychological distress, which can be relieved by provision of ketones. A well-designed, nourishing ketogenic diet may often ameliorate psychiatric and neurologic disorders.

Dietary tactics can help prevent as well as treat disease. For instance, fasting upregulates autophagy (“self-eating”), the cellular mechanism for recycling damaged or unnecessary components. But autophagy is a central part of the innate immune system; it is how cells destroy invading microbes. Intermittent fasting as a regular practice helps keep the body infection-free, and during intracellular infections refraining from food is often a helpful strategy.

For some pathogens, on the other hand, providing the immune system with plenty of food is usually a better strategy. “Feed a cold, starve a fever” – or is it the other way around? Your body will usually tell you what to do, suppressing or promoting hunger as needed.

Conclusion

There is no one diet that is perfect for everyone, but that is mainly because not everyone is healthy.

Fortunately, healthy people are generally alike in their dietary requirements. We can identify a diet that is very good for nearly everyone, and can tweak that diet in various ways to help diagnose and heal diseases. That is the goal of our book, Perfect Health Diet, and of this blog.

References

[1] Katsarski M, Singh U. [Anatomical characteristics of the sigmoid intestine and their relationship to sigmoid volvulus among the population of Uganda and the city of Plovdiv, Bulgaria]. Khirurgiia (Sofiia). 1977;30(2):159-63. http://pmid.us/916568.

[2] Madiba TE, Haffajee MR. Sigmoid colon morphology in the population groups of Durban, South Africa, with special reference to sigmoid volvulus. Clin Anat. 2011 May;24(4):441-53. http://pmid.us/21480385.

[3] Ames BN, Gold LS. Paracelsus to parascience: the environmental cancer distraction. Mutation Research 2000 Jan 17; 447(1):3-13. http://pmid.us/10686303.