Search Results for: Helicobacter pylori

Shou-Ching’s Mom’s Kimchi

Posted by on March 21, 2013 93 comments

We previously offered a recipe for Homemade Kimchi (June 26, 2011). It is an excellent recipe, but Shou-Ching wanted to continue experimenting until she reproduced the flavor and texture of her mother’s kimchi that she loved as a child growing up in Korea.

She thinks she’s got it.

Health Benefits of Kimchi

But before we share the recipe, a few reasons to make kimchi. Kimchi has been reported to:

  • Reduce body weight and blood pressure in the overweight and obese. [1]
  • Inhibit autoimmune diseases such as atopic dermatitis [2]
  • Inhibit development of allergy. [3]
  • Have anticancer effects. [4]
  • Inhibit development of atherosclerosis. [5]
  • Have antimicrobial effects on some of the most common gut pathogens, including Listeria, Staphylococcus, Salmonella, Vibrio, and Enterobacter. [6]

Against those benefits, kimchi consumption has been associated with higher rates of stomach cancer [7], perhaps due to its high content of salt [8] or N-nitroso compounds [9].

Homemade kimchi is far superior to store-bought kimchi. To accelerate fermentation, commercial kimchis usually contain sugar, but this means they will go bad soon after exposure to oxygen. Homemade kimchi, without added sugar, can retain its freshness up to several weeks after it is first exposed to air. The mix of bacteria in homemade kimchi may be far more healthful.

Preparing the Kimchi

This version starts with one large head of Chinese or Napa cabbage and the following vegetables:

  • A daikon radish
  • An equal volume of carrots
  • Green onion
  • Garlic
  • Ginger

Set aside the cabbage for a bit. Shred the radish and carrots in a grater; mince the green onion, garlic, and ginger in a food processor. Add 3 tbsp chili powder:

Mix the vegetables thoroughly and add salt and fish sauce (optional, but we use 1 tbsp of a light fish sauce) to taste:

Cover these vegetables in plastic wrap, to start the fermentation off in the right direction, for a few hours while preparing the cabbage.

Cut the head of cabbage lengthwise in half, and then each half in quarters, all lengthwise:

Then chop along the other direction until the whole cabbage is reduced to bite size pieces.

Transfer the chopped cabbage to a bowl a handful at a time – a handful of cabbage, a teaspoon of salt; a handful of cabbage, a teaspoon of salt; continue transferring cabbage and salt until all the cabbage is in the bowl:

Put a weight on top of the cabbage to compress it and release water:

Wait two hours. Over this time the cabbage will shrink as it loses water:

After two hours, rinse the cabbage in fresh water and put it in a strainer. Take the cabbage in your hands and squeeze water out; then transfer the dehydrated cabbage to the other bowl with the mixed vegetables. Continue until all the cabbage has been transferred.

Mix the cabbage and the other vegetables thoroughly:

Taste the mixture to see if it needs more salt. Transfer everything to a container that can make an airtight seal for the fermentation process.

It is important to create an anaerobic environment, similar to that in the gut. This pyrex bowl with a plastic lid makes an airtight seal:

In case pressure should build up and break the seal, we enclosed the container in a plastic bag:

Leave the sealed container at room temperature in a dark place for four to seven days before opening. It should have a mildly sour (acidic) taste; that signifies the presence of lactic acid from lactic acid generating bacteria.

Serve:

Conclusion

Depending on how much water was squeezed out of the cabbage, the kimchi may be more or less watery. There’s nothing wrong with a watery ferment, but when more water is present, more salt may be needed to achieve an appropriately acidic ferment.

As time goes on, the kimchi will become increasingly sour. When the taste starts to become unpleasant, Koreans cook the kimchi into a soup, killing the bacteria. Some of the benefits of kimchi are retained if the kimchi is cooked. [3]

Although with live cultures anything is possible and a few people may experience digestive disturbances from eating kimchi, many more find that kimchi improves their digestive function. It is an excellent probiotic.

References

[1] Kim EK et al. Fermented kimchi reduces body weight and improves metabolic parameters in overweight and obese patients. Nutr Res. 2011 Jun;31(6):436-43. http://pmid.us/21745625.

[2] Won TJ et al. Therapeutic potential of Lactobacillus plantarum CJLP133 for house-dust mite-induced dermatitis in NC/Nga mice. Cell Immunol. 2012 May-Jun;277(1-2):49-57. http://pmid.us/22726349. Won TJ et al. Oral administration of Lactobacillus strains from Kimchi inhibits atopic dermatitis in NC/Nga mice. J Appl Microbiol. 2011 May;110(5):1195-202. http://pmid.us/21338447.

[3] Hong HJ et al. Differential suppression of heat-killed lactobacilli isolated from kimchi, a Korean traditional food, on airway hyper-responsiveness in mice. J Clin Immunol. 2010 May;30(3):449-58. http://pmid.us/20204477.

[4] Park KY et al. Kimchi and an active component, beta-sitosterol, reduce oncogenic H-Ras(v12)-induced DNA synthesis. J Med Food. 2003 Fall;6(3):151-6. http://pmid.us/14585179.

[5] Kim HJ et al. 3-(4′-hydroxyl-3′,5′-dimethoxyphenyl)propionic acid, an active principle of kimchi, inhibits development of atherosclerosis in rabbits. J Agric Food Chem. 2007 Dec 12;55(25):10486-92. http://pmid.us/18004805.

[6] Kim YS et al. Growth inhibitory effects of kimchi (Korean traditional fermented vegetable product) against Bacillus cereus, Listeria monocytogenes, and Staphylococcus aureus. J Food Prot. 2008 Feb;71(2):325-32. http://pmid.us/18326182. Sheo HJ, Seo YS. The antibacterial action of Chinese cabbage kimchi juice on Staphylococcus aureus, Salmonella enteritidis, Vibrio parahaemolyticus and Enterobacter cloacae. J Korean Soc Food Sci Nutr 2003, 32:1351-1356.  Hat tip Rafael Borneo, http://dietasaludperfecta.blogspot.com.ar/2013/03/kimchi-un-superalimento.html.

[7] Zhang YW et al. Effects of dietary factors and the NAT2 acetylator status on gastric cancer in Koreans. Int J Cancer. 2009 Jul 1;125(1):139-45. http://pmid.us/19350634. Nan HM et al. Kimchi and soybean pastes are risk factors of gastric cancer. World J Gastroenterol. 2005 Jun 7;11(21):3175-81. http://pmid.us/15929164.

[8] Lee SA et al. Effect of diet and Helicobacter pylori infection to the risk of early gastric cancer. J Epidemiol. 2003 May;13(3):162-8. http://pmid.us/12749604.

[9] Seel DJ et al. N-nitroso compounds in two nitrosated food products in southwest Korea. Food Chem Toxicol. 1994 Dec;32(12):1117-23. http://pmid.us/7813983.

How Common Are Chronic Infections?

Posted by on June 24, 2010 10 comments

Very common.

One way of assessing the rate of infections is by looking for antibodies. This underestimates the rate of infection, because infections do not always generate antibodies, and antibodies can be lost during a persistent infection. However, antibodies can be detected in a simple blood test, making them the most useful measure of prevalence.

So what fraction of the population has antibodies to pathogens that produce chronic disease?

One representative study [1], conducted among Alaskan Eskimos, found that:

  • 94% were infected with cytomegalovirus (CMV), 90% with herpes simplex 1 (HSV1), 38% with herpes simplex 2 (HSV2), 80% to H. pylori, and 42% to C. pneumoniae.
  • Over 70% had antibodies to at least 3 of the five pathogens tested.
  • Seropositivity increased with age: a majority had antibodies to HSV2 and C. pneumoniae by age 45.

Infection rates are similar in other populations. Let’s look just at C. pneumoniae:

  • Among Japanese, 59% to 73% have antibodies. [2] Dr. Naoyuki Miyashita notes that “C. pneumoniae is widely distributed and that nearly everybody is infected with the agent at some time.” [3]
  • Among Finns, the prevalence of antibodies rises sharply through childhood, reaching 70% in 15-19 year olds. In elderly Finnish men, prevalence is 100%. [4]
  • Among Israelis, 31% of children and 74% of adults are antibody-positive. [5]
  • Among Italian schoolchildren, 29% have antibodies, and the prevalence increases steadily with age. [6]
  • In Singapore, antibody prevalence is 75% in men and 65% in women. By age group, it is 46.5% at ages 18-29 and 78.9% above age 40. [7]

Keeping in mind that C. pneumoniae infections often do not trigger antibody production, it seems certain that by age 40 nearly everyone has been infected.

Likewise there is no avoiding infection with other chronic pathogens. Likely agents include bacteria like Mycoplasma and viruses like cytomegalovirus, Epstein-Barr, and HSV1.

These infections cause few symptoms in the young. Over time, however, pathogens reproduce within the body and increase their numbers. The immune system is gradually overpowered. In the elderly, symptoms of chronic infection become increasingly common.

A thesis of this blog is that most of what we consider “aging” is not a natural degeneration of the human body, but increasing debilitation from chronic infections. Cardiovascular disease, dementia and memory loss, neuropathy and lost balance and falls, “grouchy old man” syndrome, cold intolerance, inflamed and arthritic joints – these are all symptoms of chronic infection.

But this is good news. Through diet, nutrition, and antibiotics, we can cure chronic infections. By doing so, nearly everyone can hope to maintain vitality and good health to a ripe old age – 100, or older.

[1] Zhu J et al. Prevalence and persistence of antibodies to herpes viruses, Chlamydia pneumoniae and Helicobacter pylori in Alaskan Eskimos: the GOCADAN Study. Clin Microbiol Infect. 2006 Feb;12(2):118-22. http://pmid.us/16441448.
[2] Miyashita N et al. Seroepidemiology of Chlamydia pneumoniae in Japan between 1991 and 2000. J Clin Pathol. 2002 Feb;55(2):115-7. http://pmid.us/11865005.
[3] Miyashita N. [Chlamydia pneumoniae infections]. Kekkaku. 2006 Sep;81(9):581-8. http://pmid.us/17037392.
[4] Tuuminen T et al. Prevalence of Chlamydia pneumoniae and Mycoplasma pneumoniae immunoglobulin G and A antibodies in a healthy Finnish population as analyzed by quantitative enzyme immunoassays. Clin Diagn Lab Immunol. 2000 Sep;7(5):734-8. http://pmid.us/10973446.
[5] Ben-Yaakov M et al. Prevalence of antibodies to Chlamydia pneumoniae in an Israeli population without clinical evidence of respiratory infection. J Clin Pathol. 2002 May;55(5):355-8. http://pmid.us/11986341.
[6] Dal Molin G et al. A population based seroepidemiological survey of Chlamydia pneumoniae infections in schoolchildren. J Clin Pathol. 2005 Jun;58(6):617-20. http://pmid.us/15917413.
[7] Koh WP et al. Seroprevalence of IgG antibodies against Chlamydia pneumoniae in Chinese, Malays and Asian Indians in Singapore. Int J Epidemiol. 2002 Oct;31(5):1001-7. http://pmid.us/12435775.

What Telomeres Tell Us About Human Disease

Posted by on April 7, 2011 18 comments

We believe that almost all diseases are caused by food toxins, malnutrition, and infections. Toxic and malnourishing diets depress immunity and make infections worse.

Once you have this point of view in mind, supporting evidence is everywhere.

Take, for example, a story today in ScienceDaily about depression. Depression is not just a mental illness, but a whole body illness:

Previously considered a mental illness affecting only the brain, major depressive disorder, or MDD, now is believed to be tied to significant physical damage outside the brain, explained Wolkowitz. For example, depressed individuals are more likely to develop the diseases of advanced age, including diabetes, heart disease, osteoporosis, stroke and dementia. [1]

The ScienceDaily article summarizes new research showing a link between depression and telomere length in white blood cells. Telomeres are the end-caps on chromosomes. If telomeres become too short, DNA becomes unstable, genetic integrity is lost during cell division, and cells become senescent (crippled beyond hope of recovery) or commit apoptosis (suicide).

An enzyme called telomerase lengthen telomeres. Normally, most cell types maintain a balance between telomerase levels and replication so that telomeres are maintained at healthy lengths throughout normal cell life.

It turns out that in depressed people, white blood cell telomeres are shorter than in normal people, even though telomerase is more active. [2] Moreover, for a given telomere length, the more telomerase activity, the more depressed the patient. [3] Finally, telomerase activity predicts which patients will recover: patients who recovered from depression had the highest telomerase activity along with their short telomeres. [3]

This suggests that some exogenous factor, not part of normal human biology, is shortening telomeres in the depressed; and that the body’s capacity to resist this factor determines its ability to recover from depression. If the body can overcome the exogenous factor, eliminating its ability to shorten telomeres, then the depression goes away.

What could this exogenous factor be?

Telomeres and Viral Infections

Well, it happens that a number of viruses shorten telomeres in white blood cells.

Cytomegalovirus reduces telomere length in T cells:

After primary CMV infection, we observed … a steep drop in telomere length. Moreover, we found in a cohort of 159 healthy individuals that telomere shortening was more rapid in CMV-seropositive individuals and correlated with the amount of differentiated T cells in both CD4(+) T cells and CD8(+) T cells. [4]

The Epstein-Barr virus (EBV) is carried by more than 90% of the adult world population and has been implicated in several human cancers. [5]  EBV disrupts the caps of telomeres, creating dysfunctional telomeres: “The telomere capping protein TRF2 was partially displaced from telomeres in EBV-infected cells, suggesting an EBV-mediated uncapping problem.” [5]

HIV also shortens telomeres: “Analysis of telomere length in HIV-1 exposed U373 showed a statistically significant telomere shortening” [6]. Interestingly, telomere shortening by HIV was reversed by providing N-acetylcysteine, suggesting that NAC should be beneficial for AIDS and possibly other chronic viral infections.

Connections between viruses and telomere loss run deep. In fact, it has been proposed that cellular senescence, the usual outcome of telomere loss, evolved as an anti-viral defense mechanism. [7]

If viruses cause major depression, then they probably also cause the diseases associated with depression. After all, they have to infect the rest of the body before they can infiltrate the brain. So we should look at viruses and other systemic diseases, and see if the connection with telomere shortening holds in those diseases.

Cancer and Blood Cell Telomeres

There is steadily increasing evidence implicating viruses as causes of cancers. Wikipedia (“Infectious causes of cancer”) has a summary:

Worldwide approximately 18% of cancers are related to infectious diseases…. Viruses are usual infectious agents that cause cancer but bacteria and parasites may also have an effect.

A virus that can cause cancer is called an oncovirus. These include human papillomavirus (cervical carcinoma), Epstein-Barr virus (B-cell lymphoproliferative disease and nasopharyngeal carcinoma), Kaposi’s sarcoma herpesvirus (Kaposi’s Sarcoma and primary effusion lymphomas), hepatitis B and hepatitis C viruses (hepatocellular carcinoma), and Human T-cell leukemia virus-1 (T-cell leukemias). Bacterial infection may also increase the risk of cancer, as seen in Helicobacter pylori-induced gastric carcinoma.[2] Parasitic infections strongly associated with cancer include Schistosoma haematobium (squamous cell carcinoma of the bladder) and the liver flukes, Opisthorchis viverrini and Clonorchis sinensis (cholangiocarcinoma).[3]

According to some authors, viruses are one of the most important risks factor for cancer development in humans, second only to tobacco use.[4]

This summary overlooks some known associations (such as that between XMRV and prostate cancer, see our post Retroviruses and Chronic Fatigue Syndrome, Aug 24, 2010) and evidence that tobacco use raises cancer risk primarily in people with a high viral infectious burden (see ref. [10] below). Although only 18% of cancers may yet have been confidently linked to infectious pathogens, it is not impossible that 100% of cancers are caused by as-yet-mostly-unidentified infectious pathogens, probably mainly viruses.

If viruses cause cancers, and if viruses shorten white blood cell telomeres, then we would expect cancer patients to have shortened telomeres.

Well, gastric cancer patients have shorter white blood cell telomeres, and being in the bottom half of telomere length doubles gastric cancer risk:

GC patients had significantly shorter average telomere length than matched controls (mean +/- SD 0.89 +/- 0.19 vs 1.06 +/- 0.25, P < 0.001)…. We found that short telomere length was associated with a significantly increased GC risk (adjusted odds ratio = 2.14, 95% confidence interval = 1.52-2.93)…. Collectively, our findings provide the first evidence linking the short telomere length in peripheral blood lymphocytes to elevated GC risk. [8]

Lung cancer patients have shorter white blood cell telomeres, and being in the bottom half of telomere length triples lung cancer risk:

Telomere length was significantly shorter in lung cancer patients than in controls (mean +/- standard deviation: 1.59 +/- 0.75 versus 2.16 +/- 1.10, P < 0.0001). When the subjects were categorized into quartiles based on telomere length, the risk of lung cancer was found to increase as telomere length shortened (P(trend) < 0.0001)…. [I]ndividuals with short telomeres were at a significantly higher risk of lung cancer than those with long telomeres (adjusted odds ratio = 3.15, 95% confidence interval = 2.12-4.67, P < 0.0001). [9]

Bladder cancer patients also had short white blood cell telomeres. Being in the bottom quarter of telomere length increases risk 4.5-fold, 6.3-fold for smokers:

Patients with bladder cancer displayed significantly shorter telomeres than control subjects (P = 0.001). Median telomere length ratio was 0.95 (range 0.53-3.2) for cases and 1.1 (0.51-2.4) for controls. Moreover, the adjusted odds ratio (OR) for bladder cancer was significantly increased in the quartile with the shortest telomere length OR = 4.5 [95% confidence interval (CI) 1.7-12]. [10]

Same story with head and neck cancer [11], renal cancer [12], breast cancer [13], and probably also thyroid cancer [14].

Cardiovascular Disease

A weakness of those cancer studies is that they only looked at blood cell telomeres and the presence of cancer; they didn’t also measure viral burden, for instance by looking for antibody seropositivity.

So I was pleased to find a study that did that in coronary heart disease. Again, white blood cell telomeres were shorter in heart disease patients:

Telomere length (TL) was approximately 0.5 kilobases (kb) shorter in leukocytes from patients with CHD than in their age-matched control subjects….

TL shortening was particularly pronounced in CD8+CD28(-) T cells obtained from cytomegalovirus-seropositive CHD patients. [15]

So cytomegalovirus may be involved in coronary heart disease.

The reason all these studies have looked at white blood cells is because it is easy to get blood samples. But sometimes it is possible to get samples from diseased and normal tissues and do a direct comparison.

That was done in this study of atherosclerotic plaques:

Arterial segments which did not develop atherosclerosis such as the saphenous vein and internal mammary artery, had longer telomere length than aortic segments. On the other hand, telomere length was shorter in aortic tissues which presented atherosclerotic lesions compared to corresponding tissues without atherosclerotic lesions. These results also suggest tissue regulation of telomere size by local factors likely related to oxidative stress responses.

So the normal vessels have long telomeres, indicating an absence of viral infections, but the atherosclerotic plaques have short telomeres, suggesting of high infectious burden.

Conclusion

Telomere shortening is probably a marker of infectious burden, especially of viral infections. Telomere shortening in blood cells is associated with major depression, cancer, heart disease, and probably nearly every other disease.

Diseases probably result from a combination of factors, but a heavy burden of chronic infectious pathogens is probably almost always one of them. These pathogens are usually little more than parasites, sapping nutrients from human cells and disabling their immune defenses. But combined with toxic and malnourishing diets, they cripple the body and shorten lifespan.

The association of shortened telomeres with shortened lifespan may be due to the life-shortening effects of infections.

This is why the immunity-enhancing dietary steps discussed in Step Four of our book are so central to a long and healthy life. We cannot avoid exposure to these pathogens. But we can keep their numbers down, so that they do minimal harm to us throughout life.

References

[1] University of California – San Francisco (2011, April 6). Link between chronic depression and accelerated immune cell aging. ScienceDaily. Retrieved April 7, 2011, from http://www.sciencedaily.com/releases/2011/04/110405151223.htm.

[2] Wolkowitz OM et al. Leukocyte telomere length in major depression: correlations with chronicity, inflammation and oxidative stress – preliminary findings. PLoS One. 2011 Mar 23;6(3):e17837. http://pmid.us/21448457.

[3] Wolkowitz OM et al. Resting leukocyte telomerase activity is elevated in major depression and predicts treatment response. Mol Psychiatry. 2011 Jan 18. [Epub ahead of print] http://pmid.us/21242992.

[4] van de Berg PJ et al. Cytomegalovirus infection reduces telomere length of the circulating T cell pool. J Immunol. 2010 Apr 1;184(7):3417-23. http://pmid.us/20176738.

[5] Lacoste S et al. Chromosomal rearrangements after ex vivo Epstein-Barr virus (EBV) infection of human B cells. Oncogene. 2010 Jan 28;29(4):503-15. http://pmid.us/19881539.

[6] Pollicita M et al. Apoptosis and telomeres shortening related to HIV-1 induced oxidative stress in an astrocytoma cell line. BMC Neurosci. 2009 May 22;10:51. http://pmid.us/19463156.

[7] Reddel RR. Senescence: an antiviral defense that is tumor suppressive? Carcinogenesis. 2010 Jan;31(1):19-26. http://pmid.us/19887513.

[8] Liu X et al. Constitutive telomere length and gastric cancer risk: case-control analysis in Chinese Han population. Cancer Sci. 2009 Jul;100(7):1300-5. http://pmid.us/19432888.

[9] Jang JS et al. Telomere length and the risk of lung cancer. Cancer Sci. 2008 Jul;99(7):1385-9. http://pmid.us/18452563.

[10] Broberg K et al. Constitutional short telomeres are strong genetic susceptibility markers for bladder cancer. Carcinogenesis. 2005 Jul;26(7):1263-71.  http://pmid.us/15746160.

[11] Wu X et al. Telomere dysfunction: a potential cancer predisposition factor. J Natl Cancer Inst. 2003 Aug 20;95(16):1211-8. http://pmid.us/12928346.

[12] Shao L et al. Telomere dysfunction in peripheral lymphocytes as a potential predisposition factor for renal cancer. J Urol. 2007 Oct;178(4 Pt 1):1492-6. http://pmid.us/17707063.

[13] Shen J et al. Short telomere length and breast cancer risk: a study in sister sets. Cancer Res. 2007 Jun 1;67(11):5538-44. http://pmid.us/17545637.

[14] Capezzone M et al. Telomeres and thyroid cancer. Curr Genomics. 2009 Dec;10(8):526-33. http://pmid.us/20514214.

[15] Spyridopoulos I et al. Accelerated telomere shortening in leukocyte subpopulations of patients with coronary heart disease: role of cytomegalovirus seropositivity. Circulation. 2009 Oct 6;120(14):1364-72. http://pmid.us/19770396.

[16] Nzietchueng R et al. Telomere length in vascular tissues from patients with atherosclerotic disease. J Nutr Health Aging. 2011;15(2):153-6. http://pmid.us/21365170.

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

Posted by on November 15, 2010 307 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

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[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.