Category Archives: Disease - Page 29

Love’s Labors Lost

One of my favorite writers is Elizabeth Scalia, “The Anchoress,” now a blogger for First Things. She has long suffered from a condition diagnosed as lupus, an autoimmune disease, but now after many years has been discovered to have Lyme disease. Lyme is a treatable infectious condition. Elizabeth writes:

A too-long-undiagnosed bout with Lyme Disease has left me challenged with arthritis and some neurological damage. The arthritis has its uses: I can predict rain, and the pain gives me something to offer up in prayer, or as penance.

Not so the neurological issues. At the peak of my illness I was unable to figure out how to do the dishes; my organizational skills have never fully recovered, and verbally I sometimes wander into strange lands, referring to cereal as cookies, or to hats as helmets.

Regular readers of this blog will know that I am not surprised that an “autoimmune” disease has turned out to be an infectious disease. Autoimmunity (where it genuinely exists – chronic infections are often misdiagnosed as autoimmune conditions even where no autoimmunity is present) seems to be mainly a side effect of chronic infections – collateral damage in a guerilla war with pathogens that conceal themselves behind human “cellular shields.”

Antibodies against the thyroid and gut engendered by gluten disappear within six months after cessation of wheat eating. [1, 2] I suspect that most autoantibodies engendered by pathogens will disappear on similar time scales once the underlying infection is cured.

I have previously written of my conviction that Alzheimer’s is an infectious disease. This conviction that grew out of my own experience: I had a 17-year chronic illness characterized by increasingly severe and embarrassing memory loss. At its worst I could not remember a friend with whom I had shared a small office for a year, and could not write (because I could not remember the previous paragraph when starting a new one, nor recall illustrative examples). The whole illness was cured by diet and antibiotics, and my memory is back to normal. I suspect that nearly all cases of Alzheimer’s can be cured by the same methods (the most important of which can be found here).

Elizabeth writes of the effect these diseases can have on a marriage:

CBS News correspondent Barry Petersen recently filed a report on the early-onset Alzheimer’s that began affecting his wife, Jan Chorlton, at the age of forty. It is an undeniably moving story; after introducing the viewer to images of the beautiful and lively Chorlton, the report shows us Petersen’s sixty-year old, still-beautiful wife, now living in what appears to be a top-notch assisted-living facility. She is unable to sustain simple conversation or to recognize her husband. Chorlton talks of a man she will always love, while Petersen openly weeps. When he asks his wife if she can name that man, she giggles, “Mr. Happy.”

Medical experts are introduced and they declare that there is no treatment for Alzheimer’s Disease, and no way to prevent it. In the near-future, we are told, sixteen million Americans will be diagnosed with Alzheimer’s Disease.

Petersen reveals that he is now in a relationship with a widow; they live together, and they both love Jan in what one of them calls “this very peculiar new American family.” The piece closes challenging anyone to gainsay them, who has not walked in their shoes.

But, was it not precisely for such situations that marriage vows were designed? “For better, for worse, for richer, for poorer, in sickness and in health, together or apart.” Love, which is limitless, is supposed to be strong enough – even if we do not think we are – to survive these challenges.

One of the saddest aspects of chronic illness is the damage it can do to marriages. A perusal of chronic disease message boards, like the one I followed at cpnhelp.org, can easily turn up tales of disease sufferers abandoned by their spouses.

It terrifies me to consider where I would be had I not had the persistent support of a loving wife. It is hard to believe I could have recovered without her.

Our motive for writing The Perfect Health Diet is to help people regain and maintain good health – to create healthy centenarians. But perhaps one side effect will be to save a few marriages – to encourage “Mr Happy” to be “Mr Persistent-In-Love.”

Caring for a chronically ill spouse is a labor of love. The laborer deserves his wage, and love deserves its reward. If there is one bit of advice that is more important than any other, in marriage and in disease, it is this: Don’t give up! Don’t ever give up!

References

[1] Berti I et al. Usefulness of screening program for celiac disease in autoimmune thyroiditis. Dig Dis Sci. 2000 Feb;45(2):403-6. http://pmid.us/10711459.

[2] Mainardi E et al. Thyroid-related autoantibodies and celiac disease: a role for a gluten-free diet? J Clin Gastroenterol. 2002 Sep;35(3):245-8. http://pmid.us/12192201.

Thyroid: More Evidence That “Normal” is Unhealthy

Two inexpensive blood tests should be done routinely, but often aren’t: Vitamin D levels (by serum 25-hydroxyvitamin D) and thyroid stimulating hormone levels (TSH). There are few easier ways to substantially improve health than to normalize levels of these hormones.

One difficulty, however, is disagreement over what “normal” levels are. The standard “normal” range for TSH on lab tests is about 0.5 to 4.6 mIU/L. This range originally encompassed two standard deviations about the US mean, meaning that 95% of the population fell in the “normal” range. Unfortunately, evidence that TSH values in this range were healthy has always been lacking.  In fact, many people with “normal” TSH live with symptoms of hypothyroidism.

As awareness has grown of the biological significance of thyroid hormone, researchers have looked more closely into the correlation of TSH levels with health.  This research is revealing is that many people are thyroid-deficient and that improving thyroid status can dramatically improve health.

The best research has been conducted in Europe:

  • The HUNT study of 25,000 healthy Norwegians found that their prospects were substantially affected by thyroid function. Those with a TSH level of 1.5 to 2.4 were 41% more likely to die over the next 8 years than those with TSH below 1.5; those with TSH 2.5-3.4 were 69% more likely to die. [1]
  • An Italian study showed that pregnant women with TSH between 2.5 and 5.0 had a miscarriage rate 70% higher than women with TSH below 2.5. [2]

Now, a Dutch study shows that the likelihood of breech birth rises monotonically with the mother’s TSH levels at gestational week 36. [3] Breech birth is a significant hazard:  it commonly requires a Caesarean section delivery, and both mother and infant are more likely to die or otherwise suffer damaged health if the baby presents in the breech position. The Dutch study found that:

  • Pregnant women with a TSH of 0.5 or less had NO breech births at all, and those between 0.51 and 0.71 had only a 1% chance of a breech birth.
  • Pregnant women with a TSH between 0.71 and 2.49 had about a 5% chance of breech birth.
  • Pregnant women with TSH of 2.50 to 2.89 had an 11% chance of breech birth, while those with TSH above 2.89 had a 14% chance of breech birth.

The authors didn’t provide a detailed breakdown of breech rates for TSH levels in the middle range, but it is a safe bet that TSH levels of 1.5 to 2.49 were much more dangerous than TSH levels of 0.72 to 1.0.

What these studies are telling us is that:

  1. People with the healthiest thyroid status have very low TSH. A TSH level below 0.5 can indicate either hyperthyroidism (too much thyroid hormone) or perfect health. Any TSH above 0.5 is suggestive of, at a minimum, a slight deficiency of either iodine or selenium.
  2. You can have impaired thyroid status with normal free T4 hormone levels. This study and others have found that TSH levels, not free thyroid hormone levels, are the best indicator of health.
  3. Health becomes significantly impaired above TSH levels of about 1.5. Any TSH above 1.5 should be addressed, if only through iodine and selenium supplementation (or abundant seaweed consumption with ~3 Brazil nuts per day.) Since a TSH of 1.5 is about the population mean, it’s a fair inference that most Americans are needlessly suffering impaired health due to impaired thyroid status.
  4. Especially during pregnancy, thyroid and iodine status are critical. Breech birth and miscarriage are far from the only negative consequences of impaired thyroid status. An elevated TSH usually indicates an iodine deficiency, and “even a mild iodine deficiency during pregnancy and during the first years of life adversely affects brain development.” [4] Iodine deficiency is the most common worldwide cause of mental retardation (cretinism), and elevated TSH during pregnancy can be expected to reduce the IQ of the child by up to 10 points and to produce other neurological deficits, including “visuomotor, memory, attention and posture” deficits. [5]

So, if your doctor doesn’t do it routinely, ask for TSH and vitamin D measurements at your next physical. There are few easier ways to improve your health than fixing thyroid and vitamin D status.

[1] Asvold BO et al. Thyrotropin levels and risk of fatal coronary heart disease: the HUNT study. Arch Intern Med. 2008 Apr 28;168(8):855-60. http://pmid.us/18443261.

[2] Negro R et al. Increased Pregnancy Loss Rate in Thyroid Antibody Negative Women with TSH Levels between 2.5 and 5.0 in the First Trimester of Pregnancy. J Clin Endocrinol Metab. 2010 Jun 9. [Epub ahead of print] http://pmid.us/20534758.

[3] Kuppens SM et al. Maternal thyroid function during gestation is related to breech presentation at term. Clin Endocrinol (Oxf). 2010 Jun;72(6):820-4. http://pmid.us/19832853.

[4] Remer T et al. Iodine deficiency in infancy – a risk for cognitive development. Dtsch Med Wochenschr. 2010 Aug;135(31/32):1551-1556. http://pmid.us/20665419.

[5] Joseph R. Neuro-developmental deficits in early-treated congenital hypothyroidism. Ann Acad Med Singapore. 2008 Dec;37(12 Suppl):42-3. http://pmid.us/19904446.

Bowel Disease, Part IV: Restoring Healthful Gut Flora

A healthy gut is a multi-species society: it is the cooperative product of the human body with trillions of bacterial cells from a thousand or more species.

An unhealthy gut is, more often than not, the product of a breakdown in this collaboration. Often, it is triggered by displacement of cooperative, commensal species of bacteria by pathogenic bacteria, fungi, viruses, and protozoa. This is why a long course of antibiotics, killing commensal bacteria, is often the prelude to bowel ailments.

It is difficult for the immune system to defeat gut infections without the help of commensal bacteria. Think about what the immune system has to deal with. The ulcers in ulcerative colitis are essentially the equivalent of infected skin abscesses, but in the colon. Here is a description of a bowel lesion in Crohn’s disease:

Ileal lesions in Crohn’s disease (CD) patients are colonized by pathogenic adherent-invasive Escherichia coli (AIEC) able to invade and to replicate within intestinal epithelial cells. [1]

Now imagine an infected skin abscess, but with feces spread over it three times a day, or stomach acid and digestive enzymes.  How quickly would you expect it to heal?

Commensal “probiotic” bacteria are like a mercenary army fighting on behalf of the digestive tract.  By occupying the interior lining of the digestive tract, they deprive pathogens of a “home base” that is sheltered from immune attack. If commensal bacteria dominate the gut, the immune system can usually quickly defeat infections.

This suggests that introduction of probiotic bacteria to the gut should be therapeutic for bowel disease.

Probiotic Supplements Are Inadequate

Most supermarket probiotics contain Lactobacillus or Bifidobacterium species. These species are specialized for digesting milk; they populate the guts of infants as they start breastfeeding, and are used by the dairy industry to ferment cheeses and yogurt.

These supplements are very effective at fighting acute diarrhea from most food-borne infections.  A fistful of probiotic capsules taken every hour will usually quickly supplant the pathogens and end diarrhea.

However, against more severe bowel diseases caused by chronic infections and featuring damaged intestinal mucosa, these species are usually not helpful.  One issue is that they provide only a tiny part of a healthful adult microbiome.  A recent study surveyed the bacterial species in the human gut, and found these species to be most abundant [2]:

Figure: Abundant gut bacterial species

As this figure shows, Bacteroides spp. are the most common commensal bacteria, with Bacteroides uniformis alone providing almost 10% of all bacterial genes in the gut. Lactobacillus and Bifidobacterium do not appear among the 57 most abundant species.

This study showed, by the way, that patients with irritable bowel syndrome have 25% fewer types of bacterial gene in their gut than healthy people, and that the composition of bacterial genes in feces clearly distinguishes ulcerative colitis, Crohn’s disease, and healthy patients.  In other words, in the bowel diseases a few pathogenic species have colonized the gut and entirely denuded it of about 25% of the commensal species that normally populate the gut. This finding supports the idea that restoring those missing species might be therapeutic for IBS.

Bacterial Replacement Therapies Work

So if IBS patients are missing 25% of the thousand or so species that should populate the gut, or 250 species, and if common probiotics provide only 8 or so species and not the ones that are missing, how are the missing species to be restored?

The answer is simple but icky. Recall that half the dry weight of stool consists of bacteria. A healthy person daily provides a sample of billions of bacteria from every one of the thousand species in his gut. They are in his stool.

So a “fecal transplant” of a healthy person’s stool into the gut of another person will replenish the missing species.

Scientists have known for a long time that this was likely to be an effective therapy, but it is only now entering clinical practice. The New York Times recently made a stir by telling this story:

In 2008, Dr. Khoruts, a gastroenterologist at the University of Minnesota, took on a patient suffering from a vicious gut infection of Clostridium difficile. She was crippled by constant diarrhea, which had left her in a wheelchair wearing diapers. Dr. Khoruts treated her with an assortment of antibiotics, but nothing could stop the bacteria. His patient was wasting away, losing 60 pounds over the course of eight months. “She was just dwindling down the drain, and she probably would have died,” Dr. Khoruts said.

Dr. Khoruts decided his patient needed a transplant. But he didn’t give her a piece of someone else’s intestines, or a stomach, or any other organ. Instead, he gave her some of her husband’s bacteria.

Dr. Khoruts mixed a small sample of her husband’s stool with saline solution and delivered it into her colon. Writing in the Journal of Clinical Gastroenterology last month, Dr. Khoruts and his colleagues reported that her diarrhea vanished in a day. Her Clostridium difficile infection disappeared as well and has not returned since.

The procedure — known as bacteriotherapy or fecal transplantation — had been carried out a few times over the past few decades. But Dr. Khoruts and his colleagues were able to do something previous doctors could not: they took a genetic survey of the bacteria in her intestines before and after the transplant.

Before the transplant, they found, her gut flora was in a desperate state. “The normal bacteria just didn’t exist in her,” said Dr. Khoruts. “She was colonized by all sorts of misfits.”

Two weeks after the transplant, the scientists analyzed the microbes again. Her husband’s microbes had taken over. “That community was able to function and cure her disease in a matter of days,” said Janet Jansson, a microbial ecologist at Lawrence Berkeley National Laboratory and a co-author of the paper. “I didn’t expect it to work. The project blew me away.” [3]

Fecal transplants can be done without a doctor’s help:  someone else’s stool can be swallowed or inserted in the rectum. If taking feces orally, swallow a great deal of water afterward to help wash the bacteria through the stomach and its acid barrier.

Dogs and young children sometimes swallow feces.  It is unpleasant to consider, but desperate diseases call for desperate measures. Perhaps one day, healthy stools will be available in pleasant-tasting capsules, and sold on supermarket shelves.  Not yet.

Attacking Pathogenic Biofilms

Most bacterial species will build fortresses for themselves, called biofilms.  These are polysaccharide and protein meshworks that, like bone, become mineralized with calcium and other minerals. These mineralized meshworks are built on bodily surfaces, like the gut lining, and protect bacteria from the immune system, antibiotics, and other bacterial species. 

Pathogenic species known to generate biofilms include Legionella pneumophila, S. aureus, Listeria monocytogenes, Campylobacter spp., E. coli O157:H7, Salmonella typhimurium, Vibrio cholerae, and Helicobacter pylori. [4]

Biofilms favor the species that constructed them. So, once pathogens have constructed biofilms, it is hard for commensal species to displace them.

Therapies that dissolve pathogenic biofilms can improve the likelihood of success of probiotic and fecal transplant therapies. Strategies include enzyme supplements, chelation therapies, and avoidance of biofilm-promoting minerals like calcium.  Specifically:

  • Polysaccharide and protease digesting enzymes. Human digestive enzymes generally do not digest biofilm polysaccharides, but bacterial enzymes that can are available as supplements. Potentially helpful enzymes include hemicellulase, cellulase, glucoamylase, chitosanase, and beta-glucanase. Non-human protease enzymes, such as nattokinase and papain, might also help. [5]
  • Chelation therapy.  Since biofilms collect metals, compounds that “chelate” or bind metals will tend to gather in biofilms. Some chelators – notably EDTA – are toxic to bacteria.  So EDTA supplementation tends to poison the biofilm, driving bacteria out of their fortress-shelter. This prevents them from maintaining it and makes the biofilm more vulnerable to digestion by enzymes and commensal bacteria. It also tends to reduce the population of pathogenic bacteria.
  • Mineral avoidance. The supply of minerals, especially calcium, iron, and magnesium, can be a rate-limiting factor in biofilm formation. Removal of calcium can cause destruction of biofilms. [6] We recommend limiting calcium intake while bowel disease is being fought, since the body can meet its own calcium needs for an extended period by pulling from the reservoir in bone. Upon recovery, bone calcium can be replenished with supplements. Iron is another mineral which promotes biofilms and might be beneficially restricted. We do not recommend restricting magnesium.

Some commercial products are available which can help implement these strategies. For instance, Klaire Labs’ InterFase (http://www.klaire.com/images/InterFase_Update_Article.pdf) is a popular enzyme supplement which helps digest biofilms, and a version containing EDTA is available (InterFase Plus).

Attacking Biofilms With Berries, Herbs, Spices, Vinegar, and Whey

Plants manufacture a rich array of anti-microbial compounds for defense against bacteria.

There is reason to believe that traditional herbs and spices, which entered the human diet during the Paleolithic and have been passed down through the generations for tens of thousands of years, were selected by our hunter-gatherer ancestors as much for their ability to promote gut health as for their taste. Dr. Art Ayers notes that:

Plants are adept at producing a wide array of chemicals with refined abilities to block bacterial functions. So when researchers sought chemicals to solve the problem of pathogens forming biofilms, it was natural to test plant extracts for inhibiting compounds. In a recent article [7], D.A. Vattem et al. added extracts from dietary berries, herbs and spices to bacterial pathogens, including the toxin producing Escherichia coli (EC) O157:H7, and checked for the ability to produce a chemical that signals the formation of a biofilm. The effective phytochemicals inhibited the bacteria from recognizing a critical density of bacteria, i.e. quorum sensing, and responding with the production of the biofilm-triggering chemical.

Blueberry, raspberry, cranberry, blackberry and strawberry extracts were effective as quorum sensing inhibitors (QSIs). Common herbs such as oregano, basil, rosemary and thyme were also effective. Turmeric, ginger and kale were also tested and found to contain QSIs. [8]

A few other remedies can weaken biofilms:

  • Acetic acid in vinegar can solubilize the calcium, iron, and magnesium in biofilms, removing these minerals and weakening the biofilm; citric acid binds calcium and can disrupt biofilms. [9]
  • Lactoferrin, a molecule in milk whey, binds iron and inhibits biofilm formation and growth. [10]
  • N-acetylcysteine can destroy or inhibit biofilms. [11]

Conclusion

Fecal transplants are the best probiotic. Tactics to disrupt pathogenic biofilms can assist probiotics in bringing about re-colonization of the digestive tract by commensal bacteria.

Along with a non-toxic diet (discussed in Part II) and nutritional support for the immune system and gut (discussed in Part III), these steps to improve gut flora make up a natural program for recovery from bowel disease.

UPDATE: Please read the cautions by two health professionals, annie and Jesse, about potential dangers of self-treatment with fecal transplants and EDTA. It is always better to pursue these therapies with a doctor’s assistance and monitoring.

Related Posts

Other posts in this series:

  1. Bowel Disorders, Part I: About Gut Disease July 14, 2010
  2. Bowel Disease, Part II: Healing the Gut By Eliminating Food Toxins m July 19, 2010
  3. Bowel Disease, Part III: Healing Through Nutrition July 22, 2010

References

[1] Lapaquette P, Darfeuille-Michaud A. Abnormalities in the Handling of Intracellular Bacteria in Crohn’s Disease. J Clin Gastroenterol. 2010 Jul 7. [Epub ahead of print]. http://pmid.us/20616747.

[2] Qin J et al. A human gut microbial gene catalogue established by metagenomic sequencing. Nature. 2010 Mar 4;464(7285):59-65. http://pmid.us/20203603.

[3] Carl Zimmer, “How Microbes Defend and Define Us,” New York Times, July 12, 2010,  http://www.nytimes.com/2010/07/13/science/13micro.html.

[4] Donlan RM. Biofilms: microbial life on surfaces. Emerg Infect Dis. 2002 Sep;8(9):881-90. http://pmid.us/12194761.

[5] Tets VV et al. [Impact of exogenic proteolytic enzymes on bacteria]. Antibiot Khimioter. 2004;49(12):9-13. http://pmid.us/16050494.

[6] Kierek K, Watnick PI. The Vibrio cholerae O139 O-antigen polysaccharide is essential for Ca2+-dependent biofilm development in sea water. Proc Natl Acad Sci U S A. 2003 Nov 25;100(24):14357-62. http://pmid.us/14614140.  Geesey GG et al. Influence of calcium and other cations on surface adhesion of bacteria and diatoms: a review. Biofouling 2000; 15:195–205.

[7] Vattem DA et al. Dietary phytochemicals as quorum sensing inhibitors. Fitoterapia. 2007 Jun;78(4):302-10. http://pmid.us/17499938.

[8] Art Ayers, “Spices are Antimicrobial and Inhibit Biofilms,” Dec. 7, 2008, http://herbal-properties.suite101.com/article.cfm/spices_are_antimicrobial_and_inhibit_biofilms.

[9] Art Ayers, “Cure for Inflammatory Diseases,” Sept. 2, 2009, http://coolinginflammation.blogspot.com/2009/09/cure-for-inflammatory-diseases.html. Desrosiers M et al. Methods for removing bacterial biofilms: in vitro study using clinical chronic rhinosinusitis specimens. Am J Rhinol. 2007 Sep-Oct;21(5):527-32. http://pmid.us/17883887.

[10] O’May CY et al. Iron-binding compounds impair Pseudomonas aeruginosa biofilm formation, especially under anaerobic conditions. J Med Microbiol. 2009 Jun;58(Pt 6):765-73. http://pmid.us/19429753.

[11] Cammarota G et al. Biofilm demolition and antibiotic treatment to eradicate resistant Helicobacter pylori: A clinical trial. Clin Gastroenterol Hepatol. 2010 May 14. [Epub ahead of print] http://pmid.us/20478402. Zhao T, Liu Y. N-acetylcysteine inhibit biofilms produced by Pseudomonas aeruginosa. BMC Microbiol. 2010 May 12;10:140. http://pmid.us/20462423.

Lactose Intolerance: Often A Result of ‘Silent’ Wheat-Derived Bowel Disease

In the comments to last week’s post on food toxins and bowel disease, I stated that, “People with bowel problems will usually do well to avoid dairy proteins, but my belief is that people with healthy bowels can usually manage dairy.”

Today, Peter links to some evidence for that proposition.

In 2005 a group led by Antonio Gasbarrini at Catholic University in Rome studied patients who experienced diarrhea and bloating after dairy consumption. They gave all patients an H2-lactose breath test, which tests the ability of the small intestine to digest the milk sugar lactose, and tests for celiac disease antibodies.

The found that 24% of those with lactose malabsorption, but only 2% of those who could digest lactose, tested positive for celiac disease antibodies. [1] It appears that destruction of the small intestine by wheat is a leading cause of inability to digest lactose – the prerequisite for lactose intolerance.

A 2008 follow-up study showed that when these patients gave up wheat and other gluten-containing grains, they recovered the ability to digest lactose:

The present study shows that a large proportion of CD patients experience a regression of lactose malabsorption after receiving a gluten-free diet. This may be related to normalization of the brush border with an improvement of lactase enzyme activity. LBT should be performed after 12 months in CD patients on a gluten-free diet in order to assess the persistence/disappearance of lactose malabsorption, thus avoiding an unnecessary lactose-free diet. [2]

Now these papers deal only with lactose malabsorption, not problems with partially digested cow casein peptides, which are the most important cause of difficulties from dairy.  So they don’t prove that dairy is safe for those who don’t eat grains and have healthy bowels.

However, they do give a bit of encouragement to those of us who are loathe to follow Loren Cordain’s advice to give up dairy.  

[1] Ojetti V et al. High prevalence of celiac disease in patients with lactose intolerance. Digestion. 2005;71(2):106-10. http://pmid.us/15775678.

[2] Ojetti V et al. Regression of lactose malabsorption in coeliac patients after receiving a gluten-free diet. Scand J Gastroenterol. 2008;43(2):174-7. http://pmid.us/17917999.