The Big Picture

Intestinal Microbiome: In Sickness and in Health

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Since the time you are born, you carry intestinal bacteria with you. Your intestinal microbiome is with you all the time—in sickness and in health. My previous post on Understanding Intestinal Bacteria explained what the intestinal microbiome is, how it impacts your health, and whether certain types of bacteria are “good” or “bad.” Important points to remember include: 1) intestinal bacteria has a huge impact on health; 2) there’s no such thing as “good” bacteria, though some are less harmful than others; and 3) a healthy balance of intestinal bacteria is what’s most important when it comes to your health. Now, let’s look at three key differences between the intestinal microbiome of a generally healthy person versus that of an unhealthy person.

1. A healthy person’s intestinal microbiome contains a more optimal balance of bacteria.

Individuals who suffer from asthma, eczema, allergies, irritable bowel syndrome, colitis, heart disease, diabetes, obesity, depression, anxiety, and autism all share the common feature of a bacterial imbalance in the intestine.1-7 This imbalance can be seen in the ratio of the two most common phylum in the human intestinal microbiome: Firmicutes and Bacteroidetes. Firmicutes and Bacteroidetes are two large groupings of germs which contain a tremendous number of families and species within them. It has been shown repeatedly that the balance of these two groups is more equal in healthy individuals. In unhealthy and obese individuals, on the other hand, the microbial population significantly favors the Firmicutes phylum.4 One problem with viewing the Bacteroidetes as “good” is that the diseases which are present in the individuals with the classic imbalance have elevated levels of endotoxin, a toxic byproduct of the Bacteroidetes germs. Autism is different in that it favors a higher ratio of the Bacteroidetes phylum.8 This supports the concept that it is not as simple as good and bad; the general specific germs and their effects do not fit into broad categories.

2. Healthy individuals have lower levels of total bacteria.

In healthy individuals, the whole population of the intestinal microbiome is lower, and the intestinal cells are better-functioning. This means that the bacterial toxic load is less, and the intestinal barrier provides a greater resistance to toxic exposure. To put it more simply, healthy people have lower levels of intestinal bacteria. Period. The less bacteria living in your digestive system, the better. In a perfect world, we would all live in a totally germ-free (i.e. bacteria-free) environment. Studies have shown that if this were possible, we would live longer, healthier lives.9 But, of course, this is not possible in the real world.

The most important thing is to reduce the overall amount of bacteria in the gut.

One way to do this is to limit the presence and growth of intestinal bacteria in the first place by eating an optimal diet (see Foundation for Human Nutrition: Part IV). Another possibility may be to reduce bacterial overgrowth by using bacterial therapy—which has been shown to work in some cases, such as in the treatment and cure of C. diff. This brings me to my next point…

3. Unhealthy individuals may benefit from bacterial therapy.

The implications of recent studies on bacterial therapy are very inspiring. Fecal transplants have been used to cure C. diff with 98% reliability. Similar therapies have been used to treat malnutrition in starving children. And many more studies and clinical trials are in the works. However, there is still a lot of research that needs to be done in this area. The relationship between individual bacteria species is so complex that it is nowhere close to being fully understood. Even at the cutting edge of science, we still cannot pick individual bacteria to put in a pill and have a predictable positive influence. The good news? Research projects such as the Human Microbiome Project are currently working to develop reliable bacterial therapies.

Interested in learning more? Stay tuned for more blog posts related to this subject. For even more info on the latest topics in health and nutrition, sign up for my newsletter.

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References

  1. Cani PD, Amar J, Iglesias MA, et al. Metabolic endotoxemia initiates obesity and insulin resistance. Diabetes 56, No. 7 (July 2007): 1761-1772. http://diabetes.diabetesjournals.org/content/56/7/1761.full
  2. Ferrer M, Ruiz A, Lanza F, et al. Microbiota from the distal guts of lean and obese adolescents exhibit partial functional redundancy besides clear differences in community structure. Environ Microbiol 15, No. 1 (Jan 2013): 211-226. http://www.ncbi.nlm.nih.gov/pubmed/22891823
  3. Bäckhed F, Manchester JK, Semenkovich CF, et al. Mechanisms underlying the resistance to diet-induced obesity in germ-free mice. Proc Natl Acad Sci U S A 104, No. 3 (Jan 2007): 979-984. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1764762/
  4. Valiquette L, Sirard S, Laupland K. A microbiological explanation for the obesity pandemic? Can J Infect Dis Med Microbiol 25, No. 6 (Nov-Dec 2014): 294-295. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4277155/
  5. Marri PR, Stern DA, Wright AL, et al. Asthma-associated differences in microbial composition of induced sputum. J Allergy Clin Immunol 131, No. 2 (Feb 2013): 346-352. http://www.ncbi.nlm.nih.gov/pubmed/23265859
  6. McIntyre CW, Harrison LEA, Eldehni MT, et al. Circulating endotoxemia: a novel factor in systemic inflammation and cardiovascular disease in chronic kidney disease. CJASN 6, No. 1 (Jan 2011): 133-141. http://cjasn.asnjournals.org/content/6/1/133.full
  7. Sandek A, Bjarnason I, Volk HD, et al. Studies on bacterial endotoxin and intestinal absorption function in patients with chronic heart failure. Int J Cardiol 157, No. 1 (May 2012): 80-85. http://www.ncbi.nlm.nih.gov/pubmed/21190739
  8. De Angelis M, Piccolo M, Vannini L, et al. Fecal microbiota and metabolome of children with autism and pervasive developmental disorder not otherwise specified. PLoS One 8, No. 10 (Oct 2013). http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0076993
  9. Jones JM, Wilson R, Bealmear PM. Mortality and gross pathology of secondary disease in germfree mouse radiation chimeras. Radiation Research 45, No. 3 (Mar 1971): 577-588. http://www.jstor.org/stable/3573066?seq=1#page_scan_tab_contents

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