Category Archives: Diets - Page 11

Pictures from the Paleolithic

Posted by on May 5, 2011 38 comments

After two weeks of science-heavy posts, I thought I’d do something light: a picture show.

Paleolithic Body Shapes

It’s often said that Paleolithic men were large-boned and very muscular. For instance:

The limb bones of the early Upper Palaeolithic Gravettian people are not only large but also have massive muscle attachments.

This is true of some Paleolithic skeletons, including Neanderthals and Eastern Gravettians, but it is far from generally true. (Gravettian is the name for a European toolkit used between about 28,000 and 22,000 BC.)

In fact, the Paleolithic population that expanded through Europe in the Upper Paleolithic was notably tall and slender. Here is a Gravettian skeleton from Grottes des Enfants 4 in Grimaldi, Italy [1]:

Note the narrow hips, narrow rib cage, and slender bones. The body shape is not dissimilar to some tall, slender East African populations today.

Of course, you can be small-boned and slender and strong. Still, it’s likely this population fought with poison-tipped throwing weapons like the atlatl, not with spears like the Neanderthals, and consequently needed much less strength. Also, they were fishermen and horticulturists, not big game hunters; their nitrogen isotope ratios prove that much of their protein came from fish.

What about obesity? Don Matesz had an interesting post this week, in which he argued that the Venus of Willendorf proves that Paleolithic Europeans were familiar with the shape of obese women:

Source: Wikipedia.

Indeed, it appears that post-menopausal weight gain may have been a problem on Paleolithic diets. As were sagging breasts:

Source: Wikipedia.

Paleolithic Art

The Gravettians were major producers of cave art. A few years ago, Friedrich Blowhard of 2blowhards.com did a great review of a book by anthropologist J. David Lewis-Williams, The Mind in the Cave: Consciousness and the Origins of Art, which sought to explain the origins of Paleolithic cave art.

Lewis-William’s idea is that is that the art was the product of shamanistic religious rituals involving hallucinations. The art was placed in the darkest and most inaccessible corners of caves because those were the best places to have a private hallucination.

Here is the Mammoth from Rouffignac:

To be sure, some of the cave art was in more accessible locations. Here is the Hall of the Bulls at Lascaux:

One thing I learned from Friedrich’s review is that animals were often painted as if they were floating in air – either lacking hooves, or with the bottoms of the hooves visible. Here is a bison at Altamira:

If Paleolithic art was created in an hallucinogenic state, it might explain The Sorcerer from Les Trois Freres:

Paintings of humans were rare until the latest stages of the Upper Paleolithic. Via DonsMaps.com, here are some Paleolithic Frenchmen from La Marche, Vienne, France about 12,000 BC:

Paleolithic artists did sometimes represent the fish that made up so much of their diet. Here is a Paleolithic salmon:

Here is a sculpture of a bird:

Conclusion

I’m happy to appropriate their diet, and I admire their art, but I must say, I’m quite pleased to be living now rather than then.

And now — that duck is making me hungry. It must be time for dinner!

References

[1] Holt & Formicola (2008) “Hunters of the Ice Age: The Biology of Upper Paleolithic People,” Yearbook of Physical Anthropology 51:70–99.

How to Raise HDL

Posted by on April 20, 2011 167 comments

In the earlier two posts of this series (HDL and Immunity, April 12; HDL: Higher is Good, But is Highest Best?, April 14), we established that HDL is central to the immunity and toxin clearance, and that it’s probably desirable to have more of it than our body’s natural levels, since we are in a more pathogen-and-toxin-rich environment than the Paleolithic and evolution hasn’t caught up to the situation.

The question is: how?

Disease Can Upregulate HDL

Chris Kresser left two great comments (here and here):

I tend to view HDL >85 or 90 in the presence of other inflammatory or immunological markers as a potential sign of infection or immune dysregulation.

I don’t have the reference handy, but I came across a study associating elevated HDL and CRP (occurring together) with INCREASED risk of heart disease….

I frequently see HDL >100 in patients with several other markers of inflammation, such as elevated CRP, ferritin, WBC, monocytes, etc.

Yes, indeed; as one review of HDL and heart attacks states, “many patients who experience a clinical event have normal, or even high, levels of HDL cholesterol.” [1]

Heart attacks result from a high burden of infected atherosclerotic lesions. When the body is fighting infections, it upregulates its defense mechanisms, including HDL.

Mario added a great comment along this line:

This could explain why runners have higher levels of HDL: to fight infections that abound among them!

And, the fact that pathogen-fighting HDL particles do not go back to the liver can explain why the half-life of HDL in runners is much higher than in sedentaries http://www.ncbi.nlm.nih.gov/pubmed/6748208.

These facts lead us toward one possible strategy for raising HDL: swallow a lot of pathogens!

Our Strategy: Benign Hormetic Stress

But this isn’t likely be desirable. Higher HDL may do some good, but the pathogens are likely to do a lot more harm.

So we have to look at tactics for raising HDL that do more good than harm. I think it’s useful to classify tactics in three groups:

  • Beneficial Methods. These methods have no known toxicity, but cause the body to increase HDL levels – perhaps because of an association with danger in our evolutionary past.
  • Mildly Toxic, Plausibly Beneficial Methods. These methods have some toxicity, but there is a plausible case to be made that the toxicity is innocuous or insignificant, so that the benefits of higher HDL will outweigh the harms.
  • Damaging Methods. Intentionally swallowing HDL-increasing pathogens or toxins is probably a bad strategy most of the time, and should be avoided.

I’ll look at tactics one by one.

Coconut Oil-Induced Ketosis

One of the most powerful, and probably also benign, ways to raise HDL is intermittent fasting or ketogenic dieting, with ketosis enhanced by the use of coconut oil or MCT (medium-chain triglyceride) oil.

Ketosis stimulates the ketone receptor GPR109A, which strongly induces HDL synthesis. GPR109A is better known as the receptor on which niacin acts to raise HDL, but its physiological ligand was not known until recently when it was found to be the ketone beta-hydroxy-butyrate. [2] It looks like any time a human goes into ketosis, HDL is upregulated.

Why we evolved a mechanism to increase HDL during ketosis is not known. However, it’s easy to imagine plausible stories. Ketosis would have been a frequent event in the Paleolithic, since most hunter-gatherers probably ate low-carb diets. However, ketosis would have been associated with times of stress:

  • Ketosis occurs during fasting, and involuntary fasting is a threat to health that forces eating of marginal foods from which infection risks are high.
  • Ketosis can also be induced by a lack of carb-containing plant foods; this would naturally lead to a shortage of animal foods, and famine, soon after. Famine depresses immunity and increases risk of infection.
  • Drought was probably a common cause of both lack of carb-rich foods and famine. Drought would tend to force reliance on marginal, polluted or infected water sources.

In the modern world, we control our food intake and can generate ketosis safely without ever reaching a famine state that significantly depresses immunity. There are safe ways to activate GPR109A via intermittent ketogenic dieting with minimal risk of ill effects.

I believe the chief risks from ketogenic dieting are:

1.      Promotion of protozoal and fungal infections. While ketogenic dieting is helpful against bacterial and viral infections, fungi and protozoa are eukaryotes who can metabolize ketones in their mitochondria. In fact, because ketones are water-soluble small molecules and diffuse into pathogen mitochondria, while glucose and fatty acids are chaperoned through the human body by transport molecules, ketones are a uniquely available energy substrate for parasitic fungi and protozoa. Moreover, glucose is a major resource for the immune defense against these pathogens, and induction of ketosis by carb restriction can diminish immunity against protozoa and fungi. Since protozoal infections such as Toxoplasma gondii and fungal infections such as Candida are now common, each afflicting perhaps 30% of the population or more, this is a major concern.

2.      Ketosis induced through severe carb and protein restriction may trigger the dangers of zero-carb dieting. I’ve done a series on this (it started here).

The solution is to achieve ketosis intermittently, through tactics like daily intermittent fasting, and to induce it positively through the consumption of short-chain fats such as are found in coconut oil or MCTs, or through leucine supplementation. A healthy diet, ketogenic or not, should meet our recommendations of at least 200 carb calories from starches and at least 600 calories from carbs plus protein.

Physical Activity

Exercise is another method for raising HDL that seems entirely healthful.

In the evolutionary environment, continuous exertion probably signaled danger: either a difficult hunt or, more likely, some form of warfare with other humans. In either case, injury and a need for wound repair was a likely prospect. Breaching of the skin barrier by wounds mean infections. Since HDL plays a role in wound repair and infection resistance, it would make sense to upregulate HDL production during exertion.

In one 12-week trial, HDL was raised by 24.8% on a moderate-intensity walking program and by 20.9% on a high-intensity walking program. [3]

In the evolutionary milieu, sitting for 16 hours a day would have indicated a lack of danger and little need for HDL. It turns out that daily sitting time strong predicts low HDL – and it only takes a day for HDL levels to adjust. In rats, 16 hours of daily inactivity caused a 20-25% drop in HDL levels by the end of the first day [4]:

The same phenomenon occurs in humans: 20 days of bed rest leads to a 20% reduction in HDL [5].

Resistance training also helps, but perhaps not as much as reduced sitting time. Obese sedentary women raised HDL by 15% following a 9-week, 3 times per week resistance training protocol. [6]

Overall, the most effective way to raise is HDL through activity is simply to reduce the daily time spent sitting and increase the time spent standing or walking.

Sitting is also a major risk factor for obesity, diabetes, and cardiovascular disease. [7] So it looks like high activity levels are strongly health-improving.

Until recently I was sitting or sleeping about 23 hours a day, which can’t be healthful. To repair that I recently built a standing desk. Now I stand, kneel (on a padded bench), or half-kneel half-stand throughout my working hours. I strongly recommend a standing desk as an effective way to increase HDL.

High-Fat Diets and Dairy Fat Consumption

When long-chain fats are eaten, they are transported from the intestine by particles called chylomicrons. Researchers injected radiolabeled chylomicrons into rats to determine the fate of the components. They found that chylomicrons frequently turn into HDL:

Catabolism of chylomicrons is associated with a rapid transfer of phospholipid, apoA-I, and possibly apoA-IV into HDL. Chylomicron phospholipid appears to give rise to vesicles which are probably incorporated into preexisting HDL. Chylomicron surface components may be an important source of plasma HDL. [8] (Hat tip CarbSane.)

Which long-chain fats are best? A case can be made for dairy fats.

There is a clear association between eating dairy fats and having high HDL. Blood levels of trans-palmitoleic acid, an omega-7 trans-fat obtainable only by eating milk products from ruminants, is strongly associated in prospective cohort studies with higher HDL. [9b] Feeding experiments in guinea pigs confirm that butter oil increases HDL. [9]

Seth Roberts cut his coronary artery calcification score by 24% by eating a half-stick of butter per day; perhaps butter’s HDL-raising property deserves the credit. High dairy fat consumption is associated with improved health in prospective cohort studies, for instance much lower rates of diabetes and lower CRP levels. [9b]

The reason dairy fats work is uncertain. The mechanism could be via chylomicron breakdown, and other fats might work nearly as well. People who eat the most dairy fats probably eat high-fat diets that are low in omega-6 fats, and omega-6 fats reduce HDL; so the dairy fats could just be a marker for high-fat low-omega-6 diets. However, it’s possible that the ruminant trans-fat CLA is especially beneficial. It might not hurt to copy Seth, and eat a lot of butter.

Alcohol

Interestingly, drinking alcohol may be a healthful way to raise HDL. We’ve previously discussed epidemiological evidence for health benefits from drinking and the matter of how to drink safely (Is It Smart to Drink?, Sep 9, 2010), but didn’t discuss alcohol’s effect on HDL.

Well, it’s significant. Alcohol increases HDL-C level, with higher doses of ethanol leading to higher HDL levels and lower rates of coronary artery disease. This works as long as there is no liver damage. Once liver damage begins, alcohol lowers HDL. [10]

This is good news because alcohol alone does not damage the liver – only the combination of alcohol with polyunsaturated fats – either omega-6 or omega-3 will do. As long as alcohol is consumed only with saturated fats, it is likely to be beneficial to health.

Here’s some numbers relating alcohol dose to HDL increase:

  • One beer per day raised HDL by 4.4% without affecting other lipid parameters. [11]
  • A half-bottle of wine per day (containing 39 g ethanol) raised HDL by 17% without affecting other lipid parameters. [12]

It is possible that red wine is particularly beneficial for HDL due to certain plant compounds that accompany the alcohol. [13]

In an analysis of the MRFIT trial, alcohol’s HDL-raising effect was found to be responsible for half of its benefits for mortality from coronary heart disease. [14] It appears that alcohol’s other health benefits, from its glucose-lowering effect to its stress-relieving effect, are less important for health than its HDL-raising effect.

Niacin

Niacin supplementation is the most common doctor-prescribed way to raise HDL. Dr. William Davis of Track Your Plaque fame is an ardent advocate of niacin, as are many other cardiologists.

Niacin increases HDL the same way ketones do, by activating the ketone receptor GPR109A. Gram doses of niacin are roughly equally effective with tablespoon doses of coconut oil in raising HDL. For instance, four grams of niacin per day for 6 weeks raised HDL levels by 50%. [15]

However, there are two key differences:

1.      Niacin is toxic whereas ketones are not.

2.      Ketones diffuse throughout the body whereas niacin binds certain cells, notably fat cells, preferentially and this concentrates its toxicity.

The localization of niacin to fatty tissues is clear in this radiogram taken 5 minutes after injection of radioactive-labeled niacin to a mouse [16]:

Major sites of niacin binding are the skin, the liver, and the fat surrounding the kidney. This is why these are sites of niacin toxicity: the toxins from niacin conversion are localized here.

Skin flushing is the most obvious sign of niacin toxicity, but organs can also be damaged. As one review states, “Unfortunately, when used as a pharmaceutical, niacin has more than its share of drug toxicities, including hepatotoxicity, gastric toxicity, glucotoxicity, and, most commonly, skin toxicity.” [17]

Niacin toxicity results from the manner in which it is converted to the active forms of vitamin B3, NAD and NADP. Niacinamide, an alternative form of vitamin B3, is converted to NAD and NADP without toxicity, but does not stimulate the GPR109A receptor and does not raise HDL levels.

Time-release niacin is especially prone to poisoning the liver. [18] The liver’s main niacin disposal pathway can only metabolize a small amount of niacin at a time. Time-release niacin causes more niacin to pass through this high-toxicity liver pathway.

Another issue with niacin is that NAD is the rate-limiting vitamin for bacterial metabolism. Excess vitamin B3 intake, therefore, promotes bacterial infections.

In general, I consider niacin to be an alternative to coconut oil-driven ketosis rather than a complement to it. Both niacin and ketones act on the same receptor, and the HDL increases from coconut oil alone are so large (commonly to 120 mg/dl or higher) that adding niacin on top would be gilding the lily.

Since benefits from niacin against atherosclerosis probably come either from HDL increases or from other effects of activating GPR109A [19], it is likely that coconut oil delivers all or nearly all the benefits of niacin.

In most cases, due to its lack of toxicity, coconut oil should be preferred. The exception would be people who have significant protozoal or fungal infections but not bacterial infections. Since ketones feed the former while niacin feeds the latter, such people may benefit from niacin instead of coconut oil.

Some other HDL-raising factors

In general, good nutritional status supports high HDL levels. In some populations, multivitamin and multimineral supplements have been shown to raise HDL. [20]

Micronutrients that are beneficial may include vitamin C, taurine, and glycine. Bile acids are made from cholesterol using vitamin C and are then conjugated with taurine and glycine. Bile duct blockage tends to lower HDL and providing bile-supporting nutrients like vitamin C [21] and taurine [22, 23] can under some circumstances raise HDL. Glycine is richly present in gelatin (cooked collagen), and taurine in uncooked or rare meats.

Plant fiber and polyphenols have been reported to raise HDL. For instance, a polyphenol-rich carob fiber was found to raise HDL by 7% while lowering LDL [24], and psyllium has been reported to raise HDL [25]. It is unclear to me whether this is a beneficial pathway or not. On the one hand, butyrate and other volatile fatty acids from gut flora may stimulate the ketone receptor. On the other hand, many of these polyphenols are directly toxic, and fiber increases gut bacterial populations and endotoxin flux into the body. HDL may be upregulated because it has more toxins to clear.

Higher potassium excretion is associated with higher HDL, suggesting that high intake of potassium-rich foods like potatoes, bananas, and vegetables might raise HDL. [26] Since potassium-rich foods are also usually fiber-rich, this association may be mediated by short-chain fats from fermentation of fiber by gut bacteria. But potassium is a nutrient low-carb dieters can easily become deficient in, so it may be worth tending to.

Some Things to Avoid

Dietary components that promote lipid peroxidation, including fructose, omega-6 fats, and trans-fats, lower HDL levels. Smoking also lowers HDL. [27]

A Japanese study found that “Concerning dietary habits, total cholesterol was lower by a mean of 13 mg/dl (0.34 mmol/L), triglycerides lower by 40 mg/dl (0.45 mmol/L), and HDL-cholesterol higher by 5 mg/dl (0.13 mmol/L) in the group who ate 7 or more Japanese-style meals in the 9 meals during 3 days than in the group who ate 3 or less Japanese-style meals in the 9 meals.” [27]

Japanese-style meals are low-toxicity and essentially Perfect Health Diet compliant. The alternative is probably western style food high in wheat, vegetable oils, and sugar.

Conclusion

HDL can be raised in destructive ways – such as ingestion of toxins or pathogens – but there are healthy ways to raise HDL.

I believe the following four ways are healthiest, and are sufficient to optimize HDL levels:

  • Eat a nourishing diet rich in saturated and monounsaturated fat, especially dairy fat, but low in omega-6 fats, fructose, and other toxins. In short: eat the Perfect Health Diet.
  • Be physically active. Be on your feet as much as possible; favor a standing desk over sitting. Do resistance exercise or other intense exercise occasionally.
  • Engage in intermittent fasting, and consume a lot of coconut oil, coconut milk, or MCTs to stimulate the ketone receptor.
  • Drink alcoholic beverages – but only when consuming meals low in polyunsaturated fats. Drink up when you eat beef, but be cautious when the entrée is salmon.

Niacin, the most effective pharmaceutical for raising HDL, has some toxicity and is probably inferior to coconut oil and intermittent fasting except in people with protozoal or fungal infections.

Our best wishes for high HDL!

Related posts:

References

[1] Navab M et al. HDL and cardiovascular disease: atherogenic and atheroprotective mechanisms. Nat Rev Cardiol. 2011 Apr;8(4):222-32. http://pmid.us/21304474.

[2] Ahmed K et al. GPR109A, GPR109B and GPR81, a family of hydroxy-carboxylic acid receptors. Trends Pharmacol Sci. 2009 Nov;30(11):557-62. http://pmid.us/19837462.

[3] Spate-Douglas T, Keyser RE. Exercise intensity: its effect on the high-density lipoprotein profile. Arch Phys Med Rehabil. 1999 Jun;80(6):691-5. http://pmid.us/10378497.

[4] Bey L, Hamilton MT. Suppression of skeletal muscle lipoprotein lipase activity during physical inactivity: a molecular reason to maintain daily low-intensity activity. J Physiol. 2003 Sep 1;551(Pt 2):673-82. http://pmid.us/12815182.

[5] Yanagibori R et al. The effects of 20 days bed rest on serum lipids and lipoprotein concentrations in healthy young subjects. J Gravit Physiol. 1997 Jan;4(1):S82-90. http://pmid.us/11541183.

[6] Costa RR et al. Effects of resistance training on the lipid profile in obese women. J Sports Med Phys Fitness. 2011 Mar;51(1):169-77. http://pmid.us/21297577.

[7] Hamilton MT et al. Role of low energy expenditure and sitting in obesity, metabolic syndrome, type 2 diabetes, and cardiovascular disease. Diabetes. 2007 Nov;56(11):2655-67. http://pmid.us/17827399.

[8] Tall AR et al. Metabolic fate of chylomicron phospholipids and apoproteins in the rat. J Clin Invest. 1979 Oct;64(4):977-89. http://pmid.us/225354.

[9] Rice BH et al. Ruminant-produced trans-fatty acids raise plasma total and small HDL particle concentrations in male Hartley guinea pigs. J Nutr. 2010 Dec;140(12):2173-9. http://pmid.us/20980644.

[9b] Mozaffarian D et al. Trans-palmitoleic acid, metabolic risk factors, and new-onset diabetes in U.S. adults: a cohort study. Ann Intern Med. 2010 Dec 21;153(12):790-9. http://pmid.us/21173413.

[10] Lakshman R et al. Is alcohol beneficial or harmful for cardioprotection? Genes Nutr. [Epub ahead of print] http://pmid.us/20012900.

[11] Thornton J et al. Moderate alcohol intake reduces bile cholesterol saturation and raises HDL cholesterol. Lancet. 1983 Oct 8;2(8354):819-22. http://pmid.us/6137650.

[12] McConnell MV et al. Effects of a single, daily alcoholic beverage on lipid and hemostatic markers of cardiovascular risk. Am J Cardiol. 1997 Nov 1;80(9):1226-8. http://pmid.us/9359559.

[13] Brien SE et al. Effect of alcohol consumption on biological markers associated with risk of coronary heart disease: systematic review and meta-analysis of interventional studies. BMJ. 2011 Feb 22;342:d636. http://pmid.us/21343206.

[14] Suh I et al. Alcohol use and mortality from coronary heart disease: the role of high-density lipoprotein cholesterol. The Multiple Risk Factor Intervention Trial Research Group. Ann Intern Med. 1992 Jun 1;116(11):881-7. http://pmid.us/1580443.

[15] Carlson LA, Hamsten A, Asplund A. Pronounced lowering of serum levels of lipoprotein Lp(a) in hyperlipidaemic subjects treated with nicotinic acid. J Intern Med 1989; 226: 271–6.

[16] Carlson LA. Nicotinic acid: the broad-spectrum lipid drug. A 50th anniversary review. J Intern Med. 2005 Aug;258(2):94-114. http://pmid.us/16018787.

[17] Dunbar RL, Gelfand JM. Seeing red: flushing out instigators of niacin-associated skin toxicity. J Clin Invest. 2010 Aug 2;120(8):2651-5. http://pmid.us/20664168.

[18] Bassan M. A case for immediate-release niacin. Heart Lung. 2011 Mar 15. [Epub ahead of print] http://pmid.us/21414665.

[19] Lukasova M et al. Nicotinic acid inhibits progression of atherosclerosis in mice through its receptor GPR109A expressed by immune cells. J Clin Invest. 2011 Mar 1;121(3):1163-73. http://pmid.us/21317532.

[20] Li Y et al. Effects of multivitamin and mineral supplementation on adiposity, energy expenditure and lipid profiles in obese Chinese women. Int J Obes (Lond). 2010 Jun;34(6):1070-7. http://pmid.us/20142823.

[21] Yanai H, Morimoto M. Effect of ascorbate on serum lipids and urate metabolism during exhaustive training. Clin Sci (Lond). 2004 Jan;106(1):107-9. http://pmid.us/12927020.

[22] Choi MJ. Effects of dietary taurine supplementation on plasma and liver lipids in OVX rats fed calcium-deficient diet. Nutr Res Pract. 2008 Spring;2(1):13-6. http://pmid.us/20126359.

[23] Elvevoll EO et al. Seafood diets: hypolipidemic and antiatherogenic effects of taurine and n-3 fatty acids. Atherosclerosis. 2008 Oct;200(2):396-402. http://pmid.us/18242615.

[24] Ruiz-Roso B et al. Insoluble carob fiber rich in polyphenols lowers total and LDL cholesterol in hypercholesterolemic sujects. Plant Foods Hum Nutr. 2010 Mar;65(1):50-6. http://pmid.us/20094802.

[25] Giacosa A, Rondanelli M. The right fiber for the right disease: an update on the psyllium seed husk and the metabolic syndrome. J Clin Gastroenterol. 2010 Sep;44 Suppl 1:S58-60. http://pmid.us/20616745.

[26] Ishikawa M et al. Taurine’s health influence on Japanese high school girls. J Biomed Sci. 2010 Aug 24;17 Suppl 1:S47. http://pmid.us/20804624.

[27] Hata Y, Nakajima K. Life-style and serum lipids and lipoproteins. J Atheroscler Thromb. 2000;7(4):177-97. http://pmid.us/11521681.

A Cure for Migraines?:

Posted by on March 29, 2011 104 comments

The weekend was happy for us, because a number of readers left word of health improvements.

Raynaud’s Syndrome, Constipation, and Other Problems Relieved

Becky reported that her Raynaud’s was better:

Hat tip and thank you: After I started reading your blog, and adding in “safe starches”, my Reynaud’s largely cleared up with temperatures over 20F. This wasn’t the intention, but a wonderful side-effect. Last month, when the sun came out and the temps got over 25, I enjoyed a successful 2-mile snow hike for the first time in three years. =)

Kate reported the same:

I too have had Raynaud’s all my life … In the past two months, I have modified my diet in line with Paul’s suggestions for Migraine. I now eat 200 calories worth of safe starch, all the recommended supplements, and as much coconut oil as I can stomach. I am also doing the 16/8 fast. My Raynaud’s has further improved, as measured by the fact I sometimes forget to turn the heat up in the morning, and cold extremities don’t always alert me to my forgetfulness!

Bill, who last October reported a variety of health complaints which persisted after he adopted a Primal Diet in May 2009, has experienced a big improvement:

I definitely feel 100% better with a more appropriate caloric intake and some starch.

Betty reported her constipation was gone:

You have blessed my life. I had one final symptom that was chronic all my life. Constipation. I e-mailed you last week and you offered up some suggestions. PRAISE THE LORD! I have had NO IBS, or constipation since following your advice. I am, and will be forever grateful.

I’ll discuss my constipation advice in Thursday’s post. Today I want to discuss migraines.

Migraines

You may recall that reader Rob Sacks cured his migraines through ketogenic dieting. I asked Kate if her migraines had responded. Here was her reply:

Thanks for asking about the Migraines. They are in fact vastly improved, which I attribute solely to your recommendations. I can say that, because I have tried virtually everything else in the past.

Kate sent me a full account of her experiences by email. It is fascinating and she has given me permission to share it. The next section was written entirely by Kate.

Kate’s Story

Thanks for asking about the migraines.  They are in fact vastly improved!  Since they have been so intractable in the past, I guess I was waiting to make sure the effect was stable before I reported my results. But clearly something remarkable is happening, thanks to your recommendations!

A little history.  I started getting these headaches in my late 30s.  (I am now 52).  In the beginning I thought I had the stomach flu, because in addition to the headache I would always throw up or have dry heaves.  The worst headaches would keep me immobilized in bed for up to two days.  My brother-in-law, a neurologist, convinced me they were migraines. I finally consulted a doctor, who put me on midrin, which did not help, and a few months later I started on imitrex, which did help, at least at first.  Eventually, my headache pattern evolved, and I had at least a mild headache every day, punctuated by the occasional doozy.  Apparently, this is a pretty common progression, especially with women my age.  I always suspected there was something wrong with my lifestyle or diet, and over the years I have tried numerous experiments, but nothing ever worked.  Here is a summary of what I have tried, more or less in order. Unless noted, these were all for three months.

What I tried The inspiration The results
Chelated Magnesium and riboflavin Mauskop’s book What Your Doctor May Not Tell Your about Migraines nada
Expensive German butterbur preparation Magnum website (www.migraine.org) nada
Forever Well Gut Brain Therapy (a mix of probiotics, peptides, and a state of the art supplement to support the organs of elimination) Magnum website I think I slept a little better.  No help with headaches.  Was surprised that the president of the company called me to see if the supplements were helping
Amitriptyline, a tricyclic anti depressant—my first foray into pharmaceutical prophylactics My doctor insisted I consult a neurologist Tried for 4 months. Slept like a zombie, and acted like one.  No help with headaches.
45 minutes of low intensity aerobics 6 days a week Inspired by Crowley and Lodge’s Younger Next Year—Never mind I had been exercising regularly all my life. Got a heart rate monitor and got after it.  No help for headaches.
No caffeine, alcohol, triptans, or over the counter analgesics Buchholz  Heal Your Headache. I love my coffee, so this was a big step for me. Did this for four months.  Very sleepy for first few days.  Did NOT help with headaches.  However, I felt I could rule out medicine overuse headaches.
Cerapamil—A calcium channel blocker My primary care manager thought it would be worth a try. Tried for four months, and upped dose after a few weeks.  Extreme constipation and painful cramps.  No help with headaches.
Low carb diet Found a reference to a german website of someone who had cured his headaches with a low carb diet.  I had always though low carb diets were ridiculous, but decided to give it a try Immediate improvement within a few days!  Also cured insomnia and acid stomach within a week. Headaches were less severe by about 50%.  Frequency was unchanged however.  Remained on low carb diet and manipulated the variables, but did not find further headache improvement.
Vitex Always felt there was a hormonal connection nada
Natural progesterone cream Same Didn’t help my headaches, but did weird things to my period
Nortriptyline–another tricyclic antidepressant My brother-in-law, a neurologist thought I should try it. Did seem to help a little.  Had to stop in less than a month because it gave me high blood pressure.
Birth Control-Yaz PCM sent me to gynecologist for heavy menstrual bleeding.  Benign fibroids found.  Doc was sure Yaz (without placebo pills) would help heavy bleeding and headaches.  I didn’t care about the bleeding, but I rose to the headache relief bait. Tried for five months. Spotted every day, but got no headache relief.
Inderal-a beta blocker Neurologist Seemed to help, but my blood pressure went too low.
Fish oil, vitamin D, coenzyme Q10, and various other supplements Grasping at straws Tried these at various times. No noticeable effects
Acupuncture same No noticeable effects, but I didn’t really believe
Self analysis, meditation Sarno The Mind Body Prescription I think there is something to this, but no headache relief for me.  Do feel more at peace with myself.
Topamax-epilepsy drug Neurologist Low dose did not help.  Worked up to 100mg over four months. Did not help headaches.  Gave me extreme anxiety about driving on limited access roads.  I didn’t notice the connection, but my college age daughter did.  I immediately tapered off.

Got off the Topamax last summer, and forswore further pharmaceutical prophylactics at that point.  In the meantime I stumbled upon the profusion of “primal” material that is now out.  I had not read any low carb stuff for a couple years, and I enjoyed reading Sisson, Wolf, Cordain, et al.  I started eating more saturated fat. I also read Fallon’s Nourishing Traditions, and started eating liver again, which I had loved as a child.  Her book inspired me to order some kelp tablets for iodine, and I took one here and there when I thought of it.  In January, in my blog travels, I stumbled on your site.  I ordered the book and was intrigued by your and Shou-Ching’s ideas about disease and chronic conditions.  I was already familiar with the idea of a ketogenic diet for epilepsy, so I was immediately interested in trying a more ketogenic diet for myself.

I ordered all your basic supplements, and immediately upped my kelp to two capsules.  I had been using coconut oil for curries, so I started using it habitually.  Started eating 200 calories of starches that you recommended—this was a little scary, after studiously avoiding them for four years!  I was afraid I they might keep me awake at night, but I am sleeping like a log. Started fasting 16/8, which was easy once you absolved me for having cream in my morning coffee!

Within a week of starting this regimen my chronic headache started to disappear! Some days I would only have a headache for part of the day, and occasionally I would have no headache at all!  I read somewhere on your site that NAC is good on a ketogenic diet, so I ordered it too.  I had never heard of this supplement before.  It seems to have made a further positive difference.  I have started taking it twice a day.  Once before bed, and once in the late afternoon, when the headache sometimes starts coming back.  Since I added NAC, I have been nearly headache free.

Another amazing development concerns anxiety.  Over the years I have become somewhat anxious when I drive on highways. I grip the steering wheel tightly, sit forward in the seat, and am generally hyper vigilant. I always chided myself for my lack of nerves, but that didn’t help.  As mentioned above, this was magnified by the Topomax.  I never had this issue when I was younger; indeed I used to fly helicopters in the army.  Two weeks ago I drove up to New Jersey to pick up my daughter, a 3.5 hour trip from where I live in Northern Virginia.  I stopped two hours into the trip to make a pit stop, and I suddenly realized I was totally relaxed, and had been for the entire trip!  The PHD is strong brain medicine indeed!

Thanks for all your research, insights, and ideas.  I think the Perfect Health Diet is going to be a game changer for many people.  Hopefully it is the start of a sea change at how we approach the chronic maladies of our times.

Mechanisms

Thank you, Kate! That’s a fantastic chronicle of your history.

This is already a long blog post, so I won’t go into an analysis of why and how the ketogenic variant of the Perfect Health Diet can cure migraines, reduce anxiety, and improve sleep. I’ll only add a few things.

First, there is a case report in the literature of a ketogenic diet helping migraines. [1]

Second, the diet helps in part by getting around mitochondrial dysfunction. Some other nutritional supplements that support mitochondrial function have a chance to help:

  • carnitine [2]
  • riboflavin [3,5]
  • CoQ10 [4,5]
  • alpha lipoic acid [4]
  • magnesium [4, 5]

I realize that you’ve already tried those, Kate, and didn’t notice an effect, but you may notice a benefit now that your diet is better. If in the past they reduced headache severity from 100% to 99%, you wouldn’t have noticed a change. If now they reduce severity from 2% to 1%, or 1% to 0%, the improvement might be obvious. So you might re-consider them now.

Finally, in the interests of full disclosure I should note that some doctors expect improvements from diet and nutrition to be short-lived: “high-dose vitamin and cofactor treatment and, where applicable, high-fat diet, are well tolerated and possibly effective in the short term, but ineffective in the longer term” against mitochondrial disorders. [6]

I believe that fading benefits are likely a result of eating the wrong diet, and that on the ketogenic version of the Perfect Health Diet the good effects will prove permanent. But time will tell.

Conclusion

We believe that diseases are generally caused by food toxins, malnutrition, and pathogens. The Four Steps of the Perfect Health Diet eliminate food toxins, optimize nutrition, and enhance immunity; therefore they remove most of the causes of disease and should render most diseases curable.

But we had no idea, last October when our book was released, which cures would appear first.

It’s interesting that migraines are appearing so early as a curable disease. I think this says a lot about the discipline, and eagerness for a cure, of Rob and Kate. Rob was willing to fast for 30 days (!); Kate read the book in January and was able immediately to make substantial diet, lifestyle, and supplement changes.

It seems that a painful but non-debilitating disease will create the most dedicated, venturesome patients.

I’m very grateful to Kate for trying the diet and sharing her story. Hopefully we can bring the good news to others, and gather more evidence to prove that diet is the best therapy – for migraines, and for many other diseases as well.

References

[1] Strahlman RS. Can ketosis help migraine sufferers? A case report. Headache. 2006 Jan;46(1):182. http://pmid.us/16412174.

[2] Kabbouche MA et al. Carnitine palmityltransferase II (CPT2) deficiency and migraine headache: two case reports. Headache. 2003 May;43(5):490-5. http://pmid.us/12752755.

[3] Triggs WJ et al. Neuropsychiatric manifestations of defect in mitochondrial beta oxidation response to riboflavin. J Neurol Neurosurg Psychiatry. 1992 Mar;55(3):209-11. http://pmid.us/1564483.

[4] Sun-Edelstein C, Mauskop A. Foods and supplements in the management of migraine headaches. Clin J Pain. 2009 Jun;25(5):446-52. http://pmid.us/19454881.

[5] Taylor FR. Nutraceuticals and headache: the biological basis. Headache. 2011 Mar;51(3):484-501. http://pmid.us/21352223.

[6] Panetta J et al. Effect of high-dose vitamins, coenzyme Q and high-fat diet in paediatric patients with mitochondrial diseases. J Inherit Metab Dis. 2004;27(4):487-98. http://pmid.us/15303006.

Protein for Athletes

Posted by on March 15, 2011 103 comments

How much protein should athletes consume?

Bodybuilders have long known that consuming extra protein makes it easier to add muscle. Yet low protein dieting can enhance immunity against viruses and bacteria, and extends lifespan in animals.

The Perfect Health Diet, because we’re positive toward saturated fats and starches, will often lead to lower protein consumption than other Paleo diets that restrict fatty or starchy foods. So it’s natural that some athletes and bodybuilders have asked how to optimize protein intake.

Robert recently asked about this, but let’s look specifically at the case of Advocatus Avocado:

I believe my performance improved (albeit marginally–the differences aren’t large) when I allowed my protein/carb/fat ratios to remain consistent despite my high caloric intake, which is ~3,600 calories/day. In other words, I had a sense of better performance when I lowered my fat% to around 65 and allowed around 200g/day of protein (I work out 2-3x a week for an hour).

At 3,600 calories per day, 65% fat is 2340 calories; 200 g protein is 800 calories; that leaves 460 calories carbs. How do these compare with Perfect Health Diet recommendations for athletes?

Nitrogen Balance, Exhaustion of Benefits, and Toxicity

There are a few magic numbers for protein intake that we want to be aware of:

  • Nitrogen balance. Nitrogen comes into the body in dietary protein and leaves the body in urine as ammonia, urea, and uric acid after proteins are metabolized. So when a person is in nitrogen balance, the amount of dietary protein matches the amount of metabolized protein, and the protein content of the body is unchanged. Very likely, the muscle content is unchanged too.
  • Exhaustion of benefits. We want to find the “plateau region” for nutrients. Athletes want to know: at what level of protein intake does protein no longer help build muscle?
  • Toxicity. At what level of protein intake does protein begin to damage health?

Luckily Ned Kock of the superb Health Correlator blog has done much of the work for us in his post “How much protein does one need to be in nitrogen balance?.”

He presents this chart, from a book on Exercise Physiology [1]:

There’s a great deal of variability across persons. Some people are in nitrogen balance at protein intake of 0.9 g/kg/day; others need as much as 1.5 g/kg/day. At 1.2 g/kg/day, half the sample was in nitrogen balance.

Various factors influence the interpretation of this data:

  • The sample was of endurance athletes. Endurance exercise increases protein needs, so most people would reach nitrogen balance at lower protein intakes. Resistance exercise doesn’t require as much protein: Experienced bodybuilders are typically in nitrogen balance at 1.2 g/kg/day. [2]
  • Most of the sample probably ate a high-carb diet. Glucose needs were met from dietary carbohydrates. Low-carb dieters would need additional protein for glucose manufacture.
  • As Ned states, in caloric deficit, protein needs are increased; in caloric surplus, protein needs are decreased. If you’re restricting calories for weight loss, expect to need a bit more protein to avoid muscle loss.
  • Supplementing leucine “increased protein synthesis and decreased protein breakdown” [2], thus leading to nitrogen balance at lower protein intakes.
  • The point of nitrogen balance is dynamic: if everyone in the sample ate 0.9 g/kg/day, then they’d eventually get into nitrogen balance at 0.9 g/kg/day. The body adjusts to conserve muscle at given food availability.

The average person needs much less protein to be in nitrogen balance. The US RDA for protein, 0.8 g/kg/day, was set so that 97.5% of Americans would be in nitrogen balance. [2] But just to be conservative, and because we’re developing advice for athletes, let’s consider 1.5 g/kg/day as the protein intake that brings our athletes into nitrogen balance.

What about the protein intake that exhausts benefits?  At what intake is muscle synthesis no longer promoted?

Ned, citing a review paper [2], offers the following answer: “[P]rotein intake beyond 25 percent of what is necessary to achieve a nitrogen balance of zero would have no effect on muscle gain.”

On my reading it’s not so easy to infer a clear answer, but let’s go with this. If so, then muscle gains would be exhausted at 1.25*1.5 = 1.875 g/kg/day even for the most strenuous athletes.

What about toxicity?

We deal with this in our book (p 25). At a protein intake of 230 g/day (920 calories), the body’s ability to convert ammonia to urea is saturated. [3] This means the nitrogen from every additional gram of protein lingers in the body as ammonia, a toxin.

Clearly marginal dietary protein is toxic, via ammonia poisoning, at this intake level. A reasonable estimate for where toxicity begins is between 150 to 200 g/day.

Putting it together: A prescription for athletes

Let’s say our athlete is an 80 kg man. Then maximum muscle gain will be achieved at a protein intake of 1.875*80 = 150 g/day. Toxicity will begin somewhere between 150 to 200 g/day. So the “plateau region” where all the benefits, and none of the toxicity, are achieved is between 150 g/day and some protein intake not much above 150 g/day.

The plateau region is quite narrow! What this tells us is that athletes should consume about 150 g/day protein.

This assumes a high-carb diet, so that no protein is needed for gluconeogenesis. The body utilizes about 600 calories/day of glucose, plus another 100 calories per hour of intense training.

With carb intakes below 600 calories/day, additional dietary protein would be needed, because protein would be consumed nearly 1-for-1 with the missing carbs.

So we can summarize these results as follows:

  • On a high-carb diet (>600 calories/day), 600 protein calories/day maximizes muscle gain.
  • On a low-carb diet (<600 calories/day), 1200 carb+protein calories/day maximizes muscle gain.

Looking back at Advocatus Avocado’s personal experience, he eats a low-carb diet with 460 carb calories per day. We predict therefore that he would need 740 protein calories a day to maximize his muscle gain (plus up to another 100 calories per hour of training, to replace lost glycogen).

Advocatus says he needs 800 protein calories/day to maximize muscle gain. Close enough for blog work!

At these protein intake levels, Advocatus is probably experiencing mild ammonia toxicity. He might slightly improve his health by eating a few more carbs, and cutting his protein intake a bit.

He might also find that leucine supplementation would reduce his protein needs a bit.

Overall, however, I think his experiences are consistent with our framework for understanding nutritional needs. Those who are content with maintaining an ordinary person’s muscle mass can get by with relatively low protein intakes of 0.8 g/kg/day or less. But muscle-building athletes need high protein intakes, around 1.9 g/kg/day, to maximize the rate of muscle gain. If they eat low-carb, they may need even more protein. Such high protein intakes are likely to exceed the threshold of toxicity.

References

[1] Brooks, G.A., Fahey, T.D., & Baldwin, K.M. (2005). Exercise physiology: Human bioenergetics and its applications. Boston, MA: McGraw-Hill.

[2] Wilson, J., & Wilson, G.J. (2006). Contemporary issues in protein requirements and consumption for resistance trained athletes. Journal of the International Society of Sports Nutrition, 3(1), 7-27.

[3] Rudman D et al. Maximal rates of excretion and synthesis of urea in normal and cirrhotic subjects. J Clin Invest. 1973 Sep;52(9):2241-9. http://pmid.us/4727456.