Melissa’s Recap of the Weston A Price Conference

Posted by on November 18, 2010 10 comments

Melissa McEwen, host of the Hunt.Gather.Love blog and a commenter here, has a recap of the Weston A. Price Foundation’s recent Wise Traditions conference.

A few of her observations with my comments:

Stephan Guyenet and Chris Masterjohn are gentlemen as well as scholars. None of us will be surprised to hear this.

The Inuit eat a lot of plants. This was a finding by researcher Anore Jones, who has a book out called Plants that We Eat. (Thanks, Gary.) If you would like a flavor of Anore’s writing, check out an earlier report Anore did for the U.S. Fish and Wildlife Service in 2006 called Fish that We Eat, available here. It has interesting information, like the fact that freezing fish for 2 weeks kills the parasites that infect humans. Maybe we should eat frozen fish instead of fresh fish!

A lot of healthy cultures used steaming and boiling. This is one of our recommendations in the book:  cook at low temperatures. Very high temperatures generate toxins. It’s never a surprise that traditional cultures developed health-maximizing practices. It is a surprise how quickly we lost their knowledge.

Check out Melissa’s blog for the rest!

Cooking with Rice, I: Chicken Soup

Posted by on November 18, 2010 40 comments

Since many Americans and Europeans are not familiar with how to use rice, we thought it would be nice to offer some ideas, mainly drawn from Asian cooking.

(The zero-carb dangers series is continuing, but as it’s science heavy I thought mixing in a food post would be fun.)

We make a soup every weekend and have a bowl to start dinner most days of the week. Chicken soup is a classic winter dish. We have a brief recipe in the book, but here is a variant. In the book recipe, the chicken is pulled out before it disintegrates, the meat and skin pulled from the bones and returned to the soup. Here, the chicken is left in the soup and cooked much longer to create a thicker and more nutritious broth. The downside is that many small chicken bones are left in the soup.

The Recipe

We like a garlic-salt-and-pepper flavor. Garlic is very important for the flavor of the soup; use at least 12 cloves, I prefer 20. Slice each clove in half so that the flavor seeps into the broth more easily.

Use enough water for the chicken to float but not swim:

For the most nourishing broth, simmer 2-3 hours. Skim off scum that rises to the top, but don’t skim off fat. If you wish a soup with less protein, remove the chicken breast meat after one hour, returning the rest of the chicken to the soup; the breast meat can be used for other dishes, like chicken salad.

Meanwhile, you can pre-soak some uncooked rice in water. This helps the rice open in the soup:

After 30 minutes or more of soaking, pour off this water to remove starch and surface contaminants, then add the rice to the soup. Cook another 1 hour. With shorter cooking, the rice remains intact; with longer cooking the rice releases starch into the broth for a thicker broth.

By this time the chicken should be falling apart. Use a spoon to break it to small pieces. Add salt and pepper and other spices to taste. In the last half hour, you can add any vegetables you wish to cook in the soup.

You can also add vegetables after the soup is finished, for a crunchier texture. In this case we added cilantro, carrots, and scallions:

Finally, after cooking is done and just before eating, you can add fat sources to hot soup for a richer taste. We use egg yolks or heavy cream. I rather like cream with turmeric. Here is how it looks with three egg yolks:

Dangers of Zero-Carb Diets, II: Mucus Deficiency and Gastrointestinal Cancers

Posted by on November 15, 2010 308 comments

Jan Kwasniewski developed his Optimal Diet something like 40 years ago and it has become extremely popular in Poland.

Kwasniewski recommended that adults should eat in the ratio

60 g protein – 180 g fat – 30 g carbohydrate
(Source).

In terms of calories this is roughly 240 calories protein / 1640 calories fat / 120 calories carbohydrate on a 2000 calorie diet.

The Perfect Health Diet proportions are more like 300 calories protein / 1300 calories fat / 400 calories carbohydrate.  So the diets would be similar if about 300 calories, or 15% of energy, were moved from fat to carbohydrate in the form of glucose/starch (not fructose/sugar!).

Note that we recommend obtaining at least 600 calories per day from protein and carbs combined. This ensures adequate protein for manufacture of glucose and ketones in the liver. But the Optimal Diet prescribes only 360 calories total (less in women), suggesting that gluconeogenesis cannot, over any long-term period, fully make up for the dietary glucose deficiency.

In the book, we note that a healthy body typically utilizes and needs about 600 glucose calories per day. On the Bellevue All-Meat Trial in 1928 Vilhjalmur Stefansson ate 550 protein calories per day, which is probably a good estimate for the minimum intake needed to prevent lean tissue loss on a zero-carb diet.

With only 360 carb plus protein calories per day, the Optimal Diet forces ketosis if lean tissue is to be preserved. Since at most 200 to 300 calories per day of the glucose requirement can be displaced by ketones, the Optimal Diet is living right on the margin of glucose deficiency.

Gastrointestinal Cancers in Optimal Dieters

I learned over on Peter’s blog that Optimal Dieters have been dying of gastrointestinal cancers at a disturbing rate. Recently Adam Jany, president of the OSBO (the Polish Optimal Dieters’ association), died of stomach cancer at 64 after 17 years on the Optimal Diet. Earlier Karol Braniek, another leader of the OSBO, died at 68 from duodenal cancer.

A Polish former Optimal Dieter who has now switched to something closer to the Perfect Health Diet noted that gastrointestinal cancers seem to be common among Optimal Dieters:

The impression we get is that there’s rather high occurrence of gut cancer, including stomach, duodenum, colon … [source]

I want to talk about why I think that is, since the danger that the Optimal Dieters are discovering was one of the key factors leading us to formulate and publish the Perfect Health Diet.

Zero-Carb Diets Can Induce Mucus Deficiency

I ate a high-vegetable but extremely low-carb diet from December 2005 to January 2008. At the time I thought I was getting about 300 carb calories a day, but I now consider this to have been a zero-carb diet, since I don’t believe carb calories are available from most vegetables. Vegetable carbs are mostly consumed by gut bacteria, whose assistance we need to break down vegetable matter, or by intestinal cells which consume glucose during digestion.

Throughout my 2 years on this zero-carb diet, I had dry eyes and dry mouth. My eyes were bloodshot and irritated, and I had to give up wearing contact lenses. Through repeated experiments, I established that two factors contributed to the dry eyes – vitamin C deficiency and glucose deficiency. After I solved the vitamin C issue, I did perhaps 50 experiments over the following few years, increasing carbs which made the dry eyes go away and reducing them which made them immediately come back. This established unequivocally that it was a glucose deficiency alone that caused the dry eyes.

Rebecca reports similar symptoms in herself and her low carb friends.

This is also a well-known symptom during starvation. As a review cited by LynMarie Daye (and referenced by CarbSane in the comments) notes,

Since hepatic glycogen stores are depleted within 24 h of fasting, blood glucose concentrations are maintained thereafter entirely through gluconeogenesis. Gluconeogenesis is mainly dependent on protein breakdown (a small amount comes from the glycerol released during lipolysis) and it thus results in protein wasting. It is the effects of protein malnutrition that lead to the eventual lack of ability to cough properly and keep the airways clear, in turn leading to pneumonia and death during prolonged starvation; hypoglycaemia does not occur. [1]

Another common symptom of very low carb diets is constipation. This is often attributed to lack of fiber, but I am skeptical. I will get to the various possible causes of constipation in a future post, but for now I’ll just point out that a deficiency of gastrointestinal mucus would create a dry colon and cause constipation.

What connects a zero-carb diet to dry eyes, dry mouth, dry airways, and dry gastrointestinal tract?

Tears, saliva, and mucus of the sinuses, airways, and gastrointestinal tract are all comprised substantially of glycoproteins called mucins. Mucins are primarily composed of sugar; they typically have a number of large sugar chains bound to a protein backbone.

For instance, the main mucin of the gastrointestinal tract, MUC2, is composed of a dimerized protein – each protein weighing 600,000 Daltons individually, so 1.2 million Daltons for the pair – plus about 4 million Daltons of sugar, for a total mass of 5 million Daltons. In the mucus, these large molecules become cross-linked to form “enormous net-like covalent polymers.” (source)

If, for whatever reason, mucin production were halted for lack of glucose, we would have no tears, no saliva and no gastrointestinal or airway mucus.

Mucin Deficiency Causes Cancer

There is a strong association between mucus deficiency and gastrointestinal cancers.

H. pylori is the strongest known risk factor for stomach cancer. [2] H. pylori infection is found in about 80% of gastric cancers. [3] One reason H. pylori promotes stomach cancer so strongly may be that it diminishes mucus in the stomach, as this photo shows:

Top: Normal stomach mucosa. Bottom: Stomach mucosa in an H. pylori infected person.

Scientists have created mice who lack genes for the main digestive tract mucins. These give us direct evidence for the effects on cancer of mucin deficiency.

Experiments in Muc1 knockout mice and mice with Muc1 knockdown have shown that under Helicobacter infection, mice deficient in Muc1 develop far more cancer-promoting inflammation than normal mice. [4]

The main mucin of the intestine is Muc2. The group of Leonard Augenlicht of the Albert Einstein Cancer Center in New York has studied mice lacking Muc2. They develop colorectal cancer. [5]

Tracing backward one step toward the source of mucin deficiency, the sugars in mucin are built from smaller pieces called O-glycans. It has been shown that mice that are deficient in O-glycans are prone to colorectal cancer: “C3GnT-deficient mice displayed a discrete, colon-specific reduction in Muc2 protein and increased permeability of the intestinal barrier. Moreover, these mice were highly susceptible to experimental triggers of colitis and colorectal adenocarcinoma.” [6]

Nutrient Deficiencies Can Also Play a Role

Some micronutrients are required for mucin production – notably vitamin D. [7, 8] Poland is fairly far north, and many of the Optimal Dieters could have been low in vitamin D.

Other important micronutrients for cancer prevention are iodine and selenium. Poland in particular had the lowest iodine intake and among the highest stomach cancer death rates in Europe. After Poland in 1996 began a program of mandatory iodine prophylaxis, stomach cancer rates fell:

In Krakow the standardized incidence ratio of stomach cancer for men decreased from 19.1 per 100,000 to 15.7 per 100,000, and for women from 8.3 per 100,000 to 5.9 per 100,000 in the years 1992-2004. A significant decline of average rate of decrease was observed in men and women (2.3% and 4.0% per year respectively). [9]

So among the Polish Optimal Dieters, the elevated gastrointestinal cancer risk caused by mucin deficiency may have been aggravated by iodine and sunlight deficiencies.

Conclusion

A healthy diet should be robust to faults. The Optimal Diet is not robust to glucose deficiency.

There’s good reason to suspect that at least some of the Optimal Dieters developed mucin deficiencies as a result of the body’s effort to conserve glucose and protein. This would have substantially elevated risk of gastrointestinal cancers. Thus, it’s not a great surprise that many Optimal Dieters have been coming down with GI cancers after 15-20 years on the diet.

We recommend a carb plus protein intake of at least 600 calories per day to avoid possible glucose deficiency. It’s plausible that a zero-carb diet that included at least 600 calories per day protein for gluconeogenesis would not elevate gastrointestinal cancer risks as much as the Optimal Diet. But why be the guinea pig who tests this idea?  Your body needs some glucose, and it’s surely less stressful on the body to supply some glucose, rather than forcing the body to manufacture glucose from protein.

Fasting and low-carb ketogenic diets are therapeutic for various conditions. But anyone on a fast or ketogenic diet should carefully monitor eyes and mouth for signs of decreased saliva or tear production. If there is a sign of dry eyes or dry mouth, the fast should be interrupted to eat some glucose/starch. Rice is a good source. The concern is not only cancer in 15 years; a healthy mucosal barrier is also essential to protect the gut and airways against pathogens.

Related Posts

Other posts in this series:

  1. Dangers of Zero-Carb Diets, I: Can There Be a Carbohydrate Deficiency? Nov 10, 2010.
  2. Danger of Zero-Carb Diets III: Scurvy Nov 20, 2010.
  3. Dangers of Zero-Carb Diets, IV: Kidney Stones Nov 23, 2010.

References

[1] Sonksen P, Sonksen J. Insulin: understanding its action in health and disease. Br J Anaesth. 2000 Jul;85(1):69-79. http://pmid.us/10927996.

[2] Peek RM Jr, Crabtree JE. Helicobacter infection and gastric neoplasia. J Pathol. 2006 Jan;208(2):233-48. http://pmid.us/16362989.

[3] Bornschein J et al. H. pylori Infection Is a Key Risk Factor for Proximal Gastric Cancer. Dig Dis Sci. 2010 Jul 29. [Epub ahead of print] http://pmid.us/20668939.

[4] Guang W et al. Muc1 cell surface mucin attenuates epithelial inflammation in response to a common mucosal pathogen. J Biol Chem. 2010 Jul 2;285(27):20547-57.  http://pmid.us/20430889.

[5] Velcich A et al. Colorectal cancer in mice genetically deficient in the mucin Muc2. Science. 2002 Mar 1;295(5560):1726-9. http://pmid.us/11872843.

 [6] An G et al. Increased susceptibility to colitis and colorectal tumors in mice lacking core 3-derived O-glycans. J Exp Med. 2007 Jun 11;204(6):1417-29.  http://pmid.us/17517967.

 [7] Paz HB et al. The role of calcium in mucin packaging within goblet cells. Exp Eye Res. 2003 Jul;77(1):69-75. http://pmid.us/12823989.

[8] Schmidt DR, Mangelsdorf DJ. Nuclear receptors of the enteric tract: guarding the frontier.  Nutr Rev. 2008 Oct;66(10 Suppl 2):S88-97. http://pmid.us/18844851.

[9] Go?kowski F et al. Iodine prophylaxis–the protective factor against stomach cancer in iodine deficient areas. Eur J Nutr. 2007 Aug;46(5):251-6. http://pmid.us/17497074.

Choline Deficiency and Plant Oil Induced Diabetes

Posted by on November 12, 2010 70 comments

I’m going to deviate from my original plan for the “Dangers of a Zero-Carb Diet” series to discuss a topic that came up in the comments to the first post.

Leonie’s Diabetes and the Rose Corn Oil Trial

What prompted this diversion is Leonie’s interesting comment from Wednesday’s post:

I developed diabetes several years after being on a low carb diet. Continuing low carb to manage the diabetes did not halt its progress. It has taken about 18 months of adding more carbs (60 – 100 gr/day) to my diet to bring my fasting glucose down by a couple of mmol and eating more carbs has also lowered my Hba1c and post meal spikes significantly. I wonder if the liver is another organ that may be affected by carbohydrate deficiency.

I had not heard of such cases before, or so I thought, but Dr. Deans in the comments reminded us that Peter at Hyperlipid had noticed two similar cases in the Rose Corn Oil trial. [1] (The Rose Corn Oil trial, of course, figures prominently in our book’s discussion of PUFA toxicity.)

In the Rose Corn Oil trial, there were three arms – a normal diet arm, a high corn oil arm, and a high olive oil arm. The normal dieters were expected to eat “fried foods, fatty meat, sausages, … ice cream, cheese, … milk, eggs, and butter” while the oil arms were supposed to restrict these foods and replace them with corn or olive oil.

Here’s what happened:

Four patients were removed from the trial for other reasons. Two developed non-cardiac thromboembolism and were given anticoagulant therapy. The other two were removed because of diabetes mellitus. One of them already had mild diabetes, but glycosuria increased considerably soon after he started oil. Oil was stopped and glycosuria disappeared. Oil was restarted, but was stopped a month later because heavy glycosuria recurred. The other patient, not a previously recognized diabetic, developed glycosuria with a diabetic glucose-tolerance test a few weeks after starting oil. [1]

The patients who developed diabetes came one from the corn oil arm and one from the olive oil arm. Likewise, the patients who developed thromboembolisms came one from the corn oil arm and one from the olive oil arm. No such disasters occurred on the “fatty meat” arm.

Since all three diets were similarly fatty, it doesn’t appear to be the quantity of fat that was the issue. Rather it was the type of lipid, or some micronutrient that was present in the animal and dairy foods but lacking in the plant oils.

For insight into what the problem might be, let’s look at how scientists poison lab animals.

Insights from Diet Animal Poisoning Research

You have to pity diet researchers. It takes 60 years for bad diets to poison humans enough to significantly raise mortality rates. Yet a diet researcher is supposed to gain a Ph.D. in 4 years (or in 5 while simultaneously obtaining an MD!), do a postdoc in 2 years, win a grant in the first years of an entry-level position with PI status, and then demonstrate productive results within the term of a 2-to-5 year grant. Deadlines are pressing: A study needs to start rats or mice on two diets, and have one diet produce much better health than the other, in considerably less than a two-year time frame.

Just comparing McDonald’s fast food with a Mediterranean diet won’t do. Two years later both sets of mice will die happily of old age, with no significant differences between groups. Peer reviewers judge you to have discovered no new results. No new results means no paper, no grant, no job.

So “diet” researchers first have to become experts at quickly inducing disease in rats and mice. Find a diet that poisons animals in a few months, compare it to another diet that doesn’t, and you have a paper. Look for variations that slow or hasten the poisoning, and you have more papers. To be a highly productive scientist, one must be a skilled animal poisoner.

Various techniques have been developed for this purpose, including: knocking out some crucial gene; breeding a mutant strain that naturally develops disease; giving the animals poison with their food; or depriving them of crucial nutrients. Almost every study of diet in mice or rats uses one of these techniques.

If a missing nutrient can cause diabetes within a few years for Leonie and 12 to 18 months for the Rose Corn Oil trial volunteers, it’s likely to be pretty good at inducing disease in animals too. There’s a good chance diet animal poisoning researchers have already stumbled upon it in rats or mice.

Choline Deficiency Diseases

One of the most popular deficiency diets among researchers is the choline-deficient diet. A useful paper by Dutch scientists [2] gives a nice look at the impact of choline deficiency on rats.

Choline deficiency (CD) by itself induces metabolic syndrome (indicated by insulin resistance and elevated serum triglycerides and cholesterol) and obesity.

A combined methionine and choline deficiency (MCD) actually causes weight loss and reduces serum triglycerides and cholesterol, but induces more severe liver damage. The MCD diet prevents the body from manufacturing choline from methionine, vitamin B12, and folate, so MCD diets severely reduce choline levels; and without choline VLDL particles are not produced. Without VLDL particles, fats and cholesterol are trapped in the liver and never reach the blood and adipose cells.

Here is a measure of insulin resistance on the two diets:

The induction of insulin resistance by the CD diet is very rapid, requiring less than a week.

Induction of insulin resistance is thought to be mediated by elevated TNF-alpha production by adipose cells and by hypertriglyceridemia. Since the MCD diet neither raised serum triglycerides nor caused obesity which induces TNF-alpha production in adipose cells, it did not cause insulin resistance.

What Does This Have to Do With Diabetes?

Insulin resistance is a key step in the development of diabetes:

  • Insulin resistance in the liver causes the liver to release more glucose into the blood (since insulin inhibits glucose release by the liver). This is discussed in a nice paper [3] found by LynMarie Daye and cited in the comments by CarbSane.
  • Peripheral insulin resistance means that the rest of the body is less sensitive to insulin. The pancreas has to produce more insulin to dispose of the excess glucose that the liver is releasing.

This elevation of insulin and glucose levels is a crucial step toward diabetes; it is “pre-diabetes.”

Persistently elevated glucose levels can then poison the beta cells of the pancreas, diminishing insulin secretion capability and causing diabetes. [4]

The Rose Corn Oil trial was not a low-carb diet, so postprandial glucose levels could easily have risen to toxic levels.

If a CD diet can cause insulin resistance in a week, it’s plausible that it might cause diabetes in 12 to 18 months, which is when the Rose Corn Oil trial patients developed it.

What About the Thromboembolism Cases?

MCD diets induce fibrinogenesis. In the blood, excess fibrin formation leads to clotting, and clots can block vessels to cause thromboembolisms. It may be that the thromboembolism cases in the Rose Corn Oil trial had methionine, folate, or B12 deficiencies to go with their choline deficiency.

Why Do Plant Oils Induce Diabetes But Not Animal Fats?

So why did diabetes develop in the corn and olive oil arms of the Rose Corn Oil trial but not the “fatty meat and dairy” arm?

Well, look at the choline content of these foods:

Choline content of one cup (~200 g) oil or fat or 227 g (1/2 lb) meat

Beef liver 968.0 mg
Cube steak (beef) 290.0 mg
Beef tallow 164.0 mg
Butter 42.7 mg
Olive oil 0.6 mg
Corn oil 0.4 mg

Source: http://nutritiondata.com.

Take away meat and dairy and replace them with plant oils, and it’s very easy to have a choline deficiency.

What Does This Have to Do With Zero-Carb Diets?

Maybe nothing … without carb consumption, postprandial glucose levels are not as high, and beta cell poisoning is less likely … but it may be that a zero-carb diet aggravates a choline deficiency in some fashion. I will leave this as a topic for further research.

UPDATE: Leonie in a new comment gives us more information: she has PCOS, goiter with nodules, and auto-antibodies. This suggests autoimmunity as a more likely explanation for her zero-carb diabetes.

Conclusion

In the book, we recommend the use of animal fats such as beef tallow for cooking, and recommend that pregnant women and vegetarians supplement with choline. We thought seriously about recommending that everyone supplement choline, but were reluctant to recommend too many supplements.

In retrospect, we should have recommended choline supplements for everyone who is overweight, has elevated blood glucose or lipids, or has elevated liver enzymes.

We have been using beef tallow as our cooking oil for several months now. It might be good practice for everyone to favor animal fats like beef tallow over plant oils for cooking.

References

[1] Rose GA et al. Corn oil in the treatment of ischaemic heart disease.  Br Med J. 1965 Jun 12;1(5449):1531-3. http://pmid.us/14288105.

[2] Veteläinen R et al. Essential pathogenic and metabolic differences in steatosis induced by choline or methione-choline deficient diets in a rat model. J Gastroenterol Hepatol. 2007 Sep;22(9):1526-33. http://pmid.us/17716355.

[3] Sonksen P, Sonksen J. Insulin: understanding its action in health and disease. Br J Anaesth. 2000 Jul;85(1):69-79. http://pmid.us/10927996.

[4] Leibowitz G et al. Glucose regulation of ?-cell stress in type 2 diabetes. Diabetes Obes Metab. 2010 Oct;12 Suppl 2:66-75. http://pmid.us/21029302.