Shoot me! Shoot me now!

 

In the previous two posts I wrote about the different types of gut flora and their physiological functions. In this post, I want to write about what can go terribly wrong when our commensal gut flora are unhappy.

Let’s first define the term dysbiosis or disordered flora. I find that this term is thrown around a lot on the web without truly understanding what it really means. Dysbiosis does not only affect the gastrointestinal tract. Dysbiosis can occur in the mouth, lungs, sinuses, your skin or anywhere there are commensal bacterial populations.

Gut dysbiosis is a subtype of dysbiosis that specifically affects your GI tract. It gets most of the attention because symptoms can be truly awful! I know because I’ve had most of them and have felt like that poor woman in the picture above.

Gut dysbiosis usually involves the stomach, small intestine and bowel. However, there is no doubt that mouth and upper respiratory dysbiosis can precipitate gut dysbiosis through the swallowing of bacterial-laden mucus in combination with stomach acid that is not as acidic as it should be.

And on that note, here’s a heads up to those of you out there popping antacids and proton-pump inhibitors like your favorite candy to treat gastroesophageal reflux disease or GERD. That stomach acid you’re trying to tame is there for a reason. Strange but true. It’s not only there to properly begin protein digestion from the food you eat, but also to kill any harmful bacteria you swallow that might be contained in your food or mouth. And you thought mother nature had screwed up some how.

Anyway, back to gut dysbiosis. Let me be clear that not all stomach or GI upset is due to gut dysbiosis. For example, you may be lactose intolerant and get gassy from drinking milk because you don’t make the enzyme lactase.

Or perhaps you get gassy from eating too much soluble and indigestible fiber. That’s normal because these fibers are not digested in your small intestine so they end up in your colon where colonic bacteria ferments them. In the process, lots of gas is produced.

If these foods make you too gassy then you just may need to take it easy on the fruits, veggies, legumes and whole grains to get some relief. If this solves your problem then you probably don’t have gut dybiosis.

However, gut dysbiosis isn’t transient like these examples. Gut dysbiosis results in long-standing symptoms that usually affect the functions of the small and large intestine. Here’s a very partial list of signs that you may have gut dysbiosis. I say partial because entire books have been written about the many side effects of nutrient malabsorption and deficiency:

  • If you have gas and bloating regardless of what you eat.
  • If you have fat in your stool also known as steatorrhea. This is an indication of fat malabsorption. This can be determined with a stool test although if lots of feces sticks to the side of your toilet bowl after you flush then that’s a pretty good sign that you have steatorrhea.
  • Unusually dry skin. This too can be an indicator of fat malabsorption.
  • Stool that always floats indicating the presence of trapped gas.
  • A stool test that detects undigested protein.
  • Anemia in the absence of any proven bleeding or deficiency of iron in the diet. If after a thorough examination by your doctor, tests show no obvious cause, then suspect that pathogenic bacteria are either stealing iron from the food you eat or that the cells lining your small intestine are too damaged to absorb it.
  • Any vitamin or mineral deficiency in the presence of a well-rounded, nutrient-dense diet.
  • Recurring constipation or diarrhea or both.
  • Painful bloating and stomach distension caused by being unable to pass gas.
  • Recurring genital yeast infections. For women that means vaginal yeast infections and for men jock itch. Thrush or a yeasty film on your tongue in the absence of compromised immunity is also an indicator.
  • Feeling excessively tired as if you’re fighting an infection.
  • Chronic insomnia in the absence of undue stress or other obvious cause.
  • Ongoing anxiety or depression or mood swings with no obvious triggers.
  • Skin rashes or dermatitis herpetifomis, a sure sign of celiac disease or gluten intolerance.

As I said, this list is very partial. Note that many of these same symptoms are seen in people who have yet to be diagnosed with celiac disease or those who are gluten intolerant. It’s not at all unusual for both groups to have small intestinal bacterial overgrowth (SIBO) as a result of wheat ingestion.

SIBO is just that, an overgrowth of pathogenic bacteria (and yeast) in the small intestine. SIBO is a form of gut dybiosis that specifically affects the upper GI tract and has both dietary and non-dietary causes. I’ll have more to say about SIBO in an upcoming post.

It should be glaringly obvious by now that any of the functions attributed to gut flora in the previous post will be compromised in the presence of disordered gut flora. If your beneficial bacteria are overwhelmed by harmful yeast and pathogenic bacteria, the chance of them functioning properly are pretty nil.

If you’re “lucky” (lucky as in getting slapped upside the head lucky) you’ll soon get the message from your gut. Although for many of us thick-headed types, myself included, the warning signs may be either ignored or suppressed by drugs or “health” supplements. It was only after my symptoms got much worse and were labeled as Irritable Bowel Syndrome that I started looking for the cause rather than concentrate on symptom relief. If you’re not “lucky,” as are many undiagnosed celiacs who suffer no gastrointestinal discomfort, damage is still occurring but you’re oblivious to it until something much worse grabs your attention.

Gut dysbiosis will always negatively impact nutritional status when it occurs in the small intestine. Both the ability to properly digest fat, protein and carbohydrate, not to mention vitamins and minerals, will be impaired. I don’t care how nutrient-dense and organic your diet is. If you can’t properly digest the food you eat, it’s not going to do you much good.

Sure, it’s better to eat a good diet than a bad one. I’ll never, ever dispute that. Throwing large quantities of nutrient-dense food against an impaired digestive system is bound to be better than throwing large quantities of junk food at it. However impaired your digestive functions may be, at least you’ll absorb more in the former case than the latter.

Nevertheless, at the end of the day if eating all those organic veggies and fruit or sprouted grains or grass-fed beef or wild-caught salmon still leaves you feeling relatively or actually malnourished, then it’s time to investigate why. Chances are your digestive tract and gut flora, for whatever reason, are not functioning as they should.

This was certainly the case for me. Anyone who knows me personally knows I take my food seriously but no matter what nutrient-dense meal I ate, the gut dysbiosis remained. Eating well doesn’t always translate into being nourished, a concept that escapes quite a few health “gurus,” doctors and nutritionists.

So what else besides digestion is affected? Well, the ability to produce B vitamins and vitamin K. Recall that these vitamins are produced by commensal gut flora and are necessary to regulate inflammation, blood clotting and bone health.

Many of the important physiological end products of healthy gut flora fermentation such as acetate, propionate, butyrate and conjugated linoleic acid will be greatly reduced or non-existent.

Gut dysbiosis by definition means that pathogenic bacteria and yeast are no longer being kept in check by friendly gut flora. Because of this, increased intestinal permeability or leaky gut is all but a foregone conclusion. The constant inflammation these organisms and their toxic metabolites cause at the level of the gut wall will compromise the barrier function that protects you from the contents of your intestines.

Immune function will be compromised both within the intestine and elsewhere as your body fights harmful bacterial and yeast overgrowth. Given the role of commensal gut flora in the development of both immune B and T cells, first-line immune defense mechanisms are also impacted by gut dysbiosis.

Mood and sleep will be negatively affected as well. Either directly via pathogens migrating along the vagus nerve to the brain or by decreased production of gut serotonin or by increased inflammatory stress or sheer exhaustion caused by fighting a chronic low-grade infection or all the above.

Causes of gut dysbiosis

There are many, many causes of gut dysbiosis and no doubt more will be discovered in the coming years: excessive antibiotic intake, stress, low stomach acid, inflammation, bacterial and viral infections, yeast overgrowth, opioids, decreased intestinal movement or motility, radiation, chemotherapy and surgery–all can all be non-dietary causes of dysbiosis.

As for dietary causes, the two I consider to be the biggest culprits are gluten grains and excess alcohol consumption. I’ll have more to say in future posts about why I believe gluten grains, and in particular, wheat is a food best avoided even in those who are not genetically predisposed to celiac disease. I’ll also post on the digestive hazards involved when overindulging in alcohol.

Following is a list of medical conditions that are associated with disordered gut flora. By no means is this list exhaustive. I just want to give you an inkling of the many conditions associated with gut dysbiosis.

Please note the words “associated with.” An association never implies causation. Saying “this” is associated with “that” never should be read to mean that “this” caused “that.” Confusing association with causation is a common mistake. You’ll run across it often when health or nutritional studies are reported on in the media.

In the medical conditions discussed below, it’s not at all clear whether the disordered gut flora is causing the disorder or the disorder is causing the gut dysbiosis. I suspect a bit of both. It’s easy to imagine a scenario where a pathogen attaches itself to the gut wall causing inflammation and this inflammation in turn attracts other pathogens in a positive (although for you negative) feedback loop. Or conversely inflammation caused by a dietary substance encourages the adhesion and growth of harmful bacteria and yeast which in turn increases inflammation.

So with that as introduction, let’s look at some common diseases and see what research has learned about the bacterial populations associated with them. I’m indebted to the authors of the excellent overview research paper: Gut Microbiota: next frontier in understanding human health and development of biotherapeutics. (1)

Diseases associated with gut dysbiosis

Autoimmune diseases show a high correlation with gut dysbiosis. This shouldn’t come as much of a surprise. In an autoimmune disorder, the immune system is mistakenly attacking the tissue of its own host.

The initial immune response was likely precipitated by some antigen that crossed or continues to cross the intestinal wall. This should not be happening in a healthy GI tract. If the protein or antigen that crosses into systemic circulation resembles any tissue structure within the body, the antibody produced will attack those tissues as well.

One example would be gluten ataxia, an autoimmune disease that negatively impacts balance and coordination so that an afflicted person is quite unsteady when they stand or walk. Because the amino acid sequence of gluten is similar to the Purkinje cells that control balance in the cerebellum, the immune system of those afflicted is tricked into attacking and destroying the balance regions of the brain. (2)

Celiac disease is another devastating disease caused by an autoimmune reaction to gluten that cross reacts with tissues in the small intestine resulting in damage to the intestinal brush border. In celiacs, fecal samples have revealed a decrease in Bifidobacterium, Clostridium histolyticum, Clostridium lituseburense, Faecalibacterium prausnitzii, and increased counts of Bacteroides/Prevotella as well as Gram-negative bacteria. (3)

As I said earlier, it’s not unusual for celiacs and those like myself who are gluten intolerant, to have bacterial and yeast infections even after we give up eating gluten. Since inflammation and reduced intestinal motility (two byproducts of gluten consumption) predisposes to small intestinal bacterial and yeast overgrowth, many who give up eating gluten will likely need to address these issues to make a full recovery.

In type I diabetes, another autoimmune disease, mice studies have revealed alterations in gut flora with those having higher proportions of Lactobacillus and Bifidobacterium species resistant to developing the disease. (4 – 6)

Inflammatory bowel diseases like ulcerative colitis and Crohn’s disease also reveals disordered gut flora. In those experiencing inflammatory bowel disease reduced gut flora diversity is seen as well as increased levels of Bacteroidetes and Enterobacteriaceae along with reduced Firmicutes. (7)

In those suffering from Crohn’s disease the following bacterial strains were 5 to 10 times less prevalent than in controls: Eubacterium rectale, B. fragilis, Bacteroides vulgatus, Ruminococcus albus, R. callidus, R. bromii, and F. prausnitzii. Conversely, the following stains were most prevalent: Enterococus, C. difficile, E. coli, Shigella flexneri and Listeria. (8)

Those with irritable bowel syndrome have fewer Bifidobacteria, Collinsella cocleatum and increases in Veillonella and Enterobacteriaeae. (9 – 11)

In colon cancer patients, decreased populations of E. rectale and F. prausnitizii and increased levels of E. faecalis have been reported. Colon cancer patients have also been shown to have significantly elevated populations of Bacteroides and Prevotella. (12) (13)

Allergy sufferers also show altered gut microbiota displaying decreased Bifodobacteria and increased populations of B. fragilis, Staphylococus and E. coli. (14 – 16)

Obesity in both children and adults is also associated with gut dysbiosis. (17 – 21) I think a real case can be made that obesity is the body’s attempt to prevent a malnourished state caused by malabsorption by increasing hunger signals and decreasing resting metabolism and the desire or energy to move.

And in type 2 diabetics, increases are seen in Bacteriodes and Parabacteroides bacteria while decreases in Firmicutes, Clostridia, Bifidobacterium and Bacteroides are common. (22) (23)

***

I have no doubt that many more diseases will show associations with disordered gut flora in the future given its many important functions in maintaining our health. What should be clear from this post is that whatever harms your commensal gut flora harms your health. So be kind to your gut flora or else!

 

References:

  1. Prakash S., Rodes L., et al., (2011). Gut microbiota: next frontier in understanding human health and development of biotherapeutics. Biologics: Targets and Therapy 5: 71-86.
  2. Nanri K., Shibuya M., Taguchi T., Hasegawa A., Tanaka N., 2011. Selective loss of Purkinje cells in a patient with anti-gliadin antibody-positive autoimmune cerebellar ataxia. Diagnostic Pathology PMCID: PMC3042899.
  3. De P.G., Nadal I., Medina M., et al., 2010.  Intestinal dysbiosis and reduced immunoglobulin-coated bacteria associated with coeliac disease in children. BMC Microbiolology 10:63.
  4. Brugman S., Klatter F.A., Visser J.T., et al., 2006. Antibiotic treatment partially protects against type 1 diabetes in the bio-breeding diabetes-prone rat. Is the gut flora involved in the development of type 1 diabetes? Diabetologia. 49:2105–2108.
  5. Schwartz R.F., Neu J., Schatz D., Atkinson M.A., Wasserfall C., 2007. Antibiotic treatment partially protects against type 1 diabetes in the bio-breeding diabetes-prone rat. Is the gut flora involved in the development of type 1 diabetes? Diabetologia 50:220–221.
  6. Roesch L.F., Lorca G.L., Casella G., et al., 2009. Culture-independent identification of gut bacteria correlated with the onset of diabetes in a rat model. ISME Journal 3:536–548.
  7. Walker A.W., Sanderson J.D., Churcher C., et al., 2011. High-throughput clone library analysis of the mucosa-associated microbiota reveals dysbiosis and differences between inflamed and non-inflamed regions of the 
intestine in inflammatory bowel disease. BMC Microbiology 11:7.
  8. Kang S., Denman S.E., Morrison M., et al., 2010.  Dysbiosis of fecal microbiota in Crohn’s disease patients as revealed by a custom phylogenetic 
microarray. Inflammatory Bowel Disease 16:2034–2042.
  9. Si J.M., Yu Y.C., Fan Y.J., Chen S.J., 2004. Intestinal microecology and quality of life in irritable bowel syndrome patients. World Journal of Gastroenterology 10:1802–1805.
  10. Kassinen A., Krogius-Kurikka L., Makivuokko H., et al., 2007. The fecal 
microbiota of irritable bowel syndrome patients differs signifi- cantly from that of healthy subjects. Gastroenterology 133: 24–33.
  11. Tana C., Umesaki Y., Imaoka A., Handa T., Kanazawa M., Fukudo S., 2010. Altered profiles of intestinal microbiota and organic acids may be the origin of symptoms in irritable bowel syndrome. Neurogastroenterology & Motility 22:512–515.
  12. Balamurugan R., Rajendiran E., George S., Samuel G.V., Ramakrishna B.S., 2008). Real-time polymerase chain reaction quantification of specific butyrate- producing bacteria, Desulfovibrio and Enterococcus faecalis in the feces of patients with colorectal cancer. Journal of Gastroenterology and Hepatology 23:1298–1303.
  13. Sobhani I., Tap J., Roudot-Thoraval F., et al., 2011. Microbial dysbiosis in colorectal cancer (CRC) patients. PLoS One 6:e16393.
  14. Penders J., Stobberingh E.E., Thijs C., et al., 2006. Molecular fingerprinting of the intestinal microbiota of infants in whom atopic eczema was or was 
not developing. Clinical and Experimental Allergy 36:1602–1608.
  15. Vael C., Nelen V., Verhulst S.L., Goossens H., Desager K.N., 2008. Early intestinal Bacteroides fragilis colonisation and development of asthma. BMC Pulmonary Medicine 8:19.
  16. Watanabe S., Narisawa Y., Arase S., et al., 2003. Differences in fecal microflora 
between patients with atopic dermatitis and healthy control subjects. 
Journal of Allergy Clinical Immunology 111:587–591.
  17. Ley R.E., Backhed F., Turnbaugh P., Lozupone C.A,. Knight R.D., Gordon J.I., 2005. Obesity alters gut microbial ecology. Proceedings of the National Academies of Science U S A. 102:11070–11075.
  18. Turnbaugh P.J., Hamady M., Yatsunenko T., et al., 2009. A core gut microbiome in obese and lean twins. Nature 457:480–484.
  19. Turnbaugh P.J., Ley R.E., Mahowald M.A., Magrini V., Mardis E.R., Gordon J.I., 2006. An obesity-associated gut microbiome with increased capacity for energy harvest. Nature 444:1027–1031.
  20. Turnbaugh P.J., Backhed F., Fulton L., Gordon J.I., 2008. Diet-induced obesity is linked to marked but reversible alterations in the mouse distal gut microbiome. Cell Host & Microbe 3:213–223.
  21. Kalliomaki M., Collado M.C., Salminen S., Isolauri E., 2008. Early differences in fecal microbiota composition in children may predict overweight. American Journal of Clinical Nutrition 87:534–538.
  22. Larsen N., Vogensen F.K., van den Berg F.W., et al., 2010. Gut microbiota in human adults with type 2 diabetes differs from non-diabetic adults. PLoS One 5:e9085.
  23. Wu X., Ma C., Han L., et al., 2010. Molecular characterisation of the faecal microbiota in patients with type II diabetes. Current Microbiology 61(1): 69–78.

 

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