The Microbiota and Mitochondria: How They Work Together To Protect or Damage Your Health

The human body is interconnected in many ways. Conventional medicine often works in a fragmented manner, where doctors specialize in different parts of the body. Integrative and functional medicine doctors, on the other hand, take a more global view where they look at how a dysfunction in one part of your body may affect another. It’s this broader approach to treating disease that is often the most successful in the long- term. That’s why today I’d like to discuss the interplay between two aspects of health: the microbiome and the mitochondria. Dysfunctions in both the microbiome and mitochondria can make a patient more susceptible to many health concerns such as cancer and autism or worsen the symptoms of a given disease.

Microbial communities reside in many places within your body. This population of microbial communities is known as the microbiota or microbiome. In fact, there are an estimated 100 trillion of these microbes—10 times more than there are cells in the human body. The microbiome also is estimated to include at least 100-fold more genes than the human genome. Among many other benefits, supplementing the microbiota in your body by taking various forms of probiotics may decrease total and low-density lipoprotein (LDL) cholesterol levels,1 reduce the amount of time that flu symptoms last,2 reduce eczema symptoms,3 and maintain the body’s ability to use insulin effectively even after overeating a high-fat meal.4

The gut microbiome is highly enriched for genes that play an important role in energy production and metabolism. Mitochondria are involved in cellular function and metabolism by producing ATP, the energy molecule that serves as fuel to your body.

cell phone with low battery warningI like to compare the mitochondria to batteries in a flashlight or cell phone. If those batteries are underpowered, the device won’t work properly. It’s the same with the cells in the human body. They need energy to function and ATP provides that energy.

Mitochondrial dysfunction—when the mitochondria aren’t producing enough ATP to properly fuel cells—is associated with many diseases including chronic fatigue syndrome,5 diabetes,6,7 Alzheimer’s5 and Parkinson’s disease,8 cancer,5 heart disease,9 fibromyalgia,10 and autoimmune disorders.5

When the mitochondria produce too many reactive oxygen species—otherwise known as free radicals—this affects the microbiota’s ability to regulate the gut epithelial barrier.11 The gut epithelial barrier is the lining of the intestinal wall that prevents undigested food particles, toxins, and other substances from entering into the systemic circulation and causing allergies and disease. Researchers also have found that microbiota release metabolites that can directly interfere with ATP production in the mitochondria.11

Microbiota can influence the activity of mitochondria by regulating the production of free radicals through interactions with toxins, proteins, or other metabolites released by gut microbiota.12 This interaction can be harmful or beneficial, depending on the microbiota strain quality and diversity. Researchers now believe that the microbiota by way of their ability to regulate the mitochondria can influence the health of cells.12

According to one group of scientists, “All these data suggest that microbiota target mitochondria to regulate its interaction with the host. Imbalance of this targeting may result in pathogenic state as observed in numerous studies.”11

There’s more evidence that the mitochondria and microbiota work together.  Short-chain fatty acids are produced by the microbiota during fermentation of dietary carbohydrates and some proteins and present to some extent in the diet.  These short-chain fatty acids may have both beneficial and harmful effects on mitochondrial activity.13

If the interplay between the microbiome and the mitochondria isn’t working properly it can also lead to the development of cancer and other signs of cellular dysfunction. When an individual consumes a poor diet filled with excess sugar and refined carbohydrates and fruits and vegetables covered in pesticides it can change the gut microbiome, which in turn changes cellular metabolism and affects the mitochondria in such a way as to increase susceptibility of cells to becoming susceptible to a diseased state.14

The Autism Connection

More evidence linking the mitochondria and the gut microbiota comes from studies on autism. A large number of people who have autism spectrum disorder (ASD)

have both mitochondrial dysfunction and gastrointestinal (GI) problems.15 It’s estimated that the prevalence of mitochondrial dysfunction in people who have ASD is 5%, much higher than in people who don’t have ASD.16 In addition, one study found that 80% of children with ASD demonstrated below normal function of the electron transport chain in blood cells known as lymphocytes.17 The electron transport chain is an important part of the mitochondrial process that generates ATP.

Gastrointestinal problems are common in people who have mitochondrial disorders and are also common in people who have mitochondrial disorders coinciding with autism, which offers further support that the gut microbiota may undergo changes in mitochondrial disorders.15

Because mitochondria are known for their role in producing cellular energy, the most affected body organs and systems in people who have mitochondrial dysfunction are those that have the highest energy demand, including the GI tract and the microbiota that reside there. These are some of the same organs and systems commonly affected in children with ASD.15

Additionally, rodents given high intravenous doses of propionic acid, a short-chain fatty acid produced by the gut microbiota Clostridia, Bacteriodetes, and Desulfovibrio, develop symptoms similar to ASD.18 The brain tissue of rats treated intravenously with propionic acid exhibits many neurochemical changes similar to those seen in ASD, including neuroinflammation, increased oxidative stress (free radical damage), and depletion of the antioxidant glutathione.18 These changes directly or indirectly are involved in mitochondrial dysfunction by way of interfering with processes that are dependent on the amino acid carnitine- dependent pathways. Antibiotics also are known to damage these carnitine-dependent pathways in part by changing the gut flora so that it favors bacteria that produce propionic acid.18

The fact that these excessive levels of propionic acid are associated with mitochondrial dysfunction, lends further support to the idea that the microbiota works together with the mitochondria.19

Supporting Your Microbiota and Mitochondria

Taking a good probiotic is the best way to ensure that your body is populated with enough healthy microbes to counteract the pathogenic varieties. To support the mitochondria, I recommend my patients supplement with a few foundational supplements including coenzyme Q10, creatine monohydrate, and alpha-lipoic acid. Resveratrol can also be added to this regimen. In cells from early-onset Parkinson’s disease, resveratrol enhanced mitochondrial function and ATP production.20 It also halted the development of diabetic cardiomyopathy in diabetic rats, in part by its favorable effects on the mitochondria.20

References:
1. Cho YA, Kim J. Medicine (Baltimore). 2015;94:e1714.
2. Jespersen L, et al. Am J Clin Nutr. 2015;101:1188-96.
3. Inoue Y, et al. Int Arch Allergy Immunol. 2014;165:247-54.
4. Hulston CJ, et al. Br J Nutr. 2015;113:596-602.
5. Pagano G, et al. Oxid Med Cell Longev. May 4, 2014;2014:541230.
6. Amer MA, et al. 2011;10:3722-30.
7. Khan S, et al. Translational Research. 2011;158:344-59.
8. Di Monte DA, et al. Ann Neurol. 1992;32 Suppl:S111-5. 9. Yu E. Heart. 2014;100 Suppl 3:A128-9.
10. Cordero MD, et al. Arthritis Res Ther. January 28, 2010;12:R17.
11. Saint Georges Chaumet Y, Edeas M. Pathog Dis. 2015 Oct 23. pii: ftv096. [Epub ahead of print.]
12. Saint Georges Chaumet Y, et al. Cell Mol Biol (Noisy le grand). 2015;61:121-4.
13. MacFabe DF. Microb Ecol Health Dis. 2015;26:28177.
14. Hagland HR, Søreide K. Cancer Lett. 2015;356:273-80.
15. Frye RE, et al. Microb Ecol Health Dis. 2015;26:27458.
16. Rossignol DA, Frye RE. Mol Psychiatry. 2012;17:290-314. 17. Giulivi C, et al. JAMA. 2010;304:2389-96.
18. MacFabe DF. Microb Ecol Health Dis. 2012;23:10.3402/ mehd.v23i0.19260.
19. Frye RE, et al. Microb Ecol Health Dis. 2015;26:26878.
20. Ferretta A, et al. Biochim Biophys Acta. 2014;1842:902-15.

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