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Reversing Diabetes by achieving a healthy gut microbiota

Let’s look at yet another way to treat type 2 diabetes without the use of prescription medications. As I previously wrote, nearly the entire focus of type 2 diabetes management in mainstream medicine is prescription medications. Now we know that diabetes can be effectively treated without a doctor.

In this article I’ll share the relationship between gut microbiota and diabetes. Further, let’s look at how restoring optimal gut microbiota using phages and probiotics treats or even reverses diabetes.   

Gut health–diabetes relationship

I previously shared how diabetes can be reversed in just 30 days using a strict nutrient-rich raw food diet. One predominant effect of raw food consumption is the “clean up” effect this has on intestinal microbiota. Raw food is a powerful promoter of health intestinal bacteria.

Is there a relationship between healthy intestinal microbiota and diabetes, you ask? Let me share what I’ve learned.

Science on this subject took a leap forward in October 2014 at a research symposium in Chicago, IL, titled “Diabetes and the Microbiome” sponsored by the American Diabetes Association and the JDRF (Juvenile Diabetes Research Foundation).[i]  Relationships between diabetes and the microbiome, how gut microbes program the immune system, and microbiome’s effect on energy balance (sugar metabolism & obesity) were presented by more than 100 scientists and doctors.

They agreed that:

•  The rise in the prevalence of type 2 diabetes (about 95% of diabetes cases in the U.S.) is coincident with increases in obesity, and microbiome-host interactions are one key environmental factor that influences type 2 diabetes risk and progression; several studies have linked the intestinal bacterial environment to metabolic health.

•  People with type 1 diabetes have a lower microbial diversity compared with healthy subjects

•  Our gut microbiome, and more specifically probiotic treatment modifies the development of type 1 diabetes

•  Diabetes incidence increases and age of onset is younger in animals with lower microbiota diversity 

•  The transfer of a single healthy gut bacteria species (e.g. Lactobacillus johnsonii) from diabetes-resistant animals protects recipient animals from getting type 1 diabetes

•  Prebiotics and probiotics to develop and maintain beneficial microbes favors weight loss and weight maintenance could be effective in reversing the metabolic abnormalities of diabetes

Since then, more research has been done that clearly demonstrates that your gut microbiome can be modified through genetic and environmental circumstances. In fact, seventy to 90% of all the cells occupying your body are microbial (bacteria) with a large genetic variation (40%), while only 10-30% of your cells are human cells with a very low genetic variation (0.5%). This means that microbial genes are about 1,000 times more abundant than your own human genes, which means microbe-host interactions have a critical role in your human health and disease. 

Improvements in deoxyribonucleic acid (DNA) sequencing and mass spectrometry technologies have allowed the comprehensive collection of information on our unique gut ecosystem.[i]  Largely because of this, gut microbiota have emerged recently as an essential player in the development of type 1 diabetes, type 2 diabetes, and obesity.[ii]

Another likely mechanism for gut microbiota to directly influence diabetes progression is by inflammation from microbes, bacterial products and metabolites, and antibiotics by promoting permeability of the gut lining, which leads to chronic low-grade inflammation including autoimmune destruction of pancreatic β-cells (known cause of type 1 diabetes).

For example, studies using bovine milk oligosaccharides (BMOs) and other pre-biotics increased Bifidobacteria and other healthy microbiota, reversed gut permeability, and reduced inflammation. The effect is to help prevent the onset of diet-induced obesity and diabetes.

What’s more, specific microbes are associated with insulin resistance, metabolic syndrome, and type 2 diabetes.[i]  Crazy as this may sound, in randomized controlled clinical trials of fecal transplantation into male subjects with insulin resistance and metabolic syndrome, some subjects showed enhanced insulin sensitivity (key way to treat type 2 diabetes) and increased levels of fecal short-chain fatty acids (SCFA), which is a known to heal the gut lining.

Even more recently, study[i] data in rodents and human longitudinal studies have linked gut microbiome composition and function to anti-pancreatic immunity, insulin-resistance, and obesity. Through their metabolites and enzymatic activity, the gut bacteria shape human (host) metabolism, energy extracted from your diet and even contribute to healthy immune system and reduced tissue inflammation. Accumulating evidence suggests that gut microbiota contribute to the pathogenesis of diabetes[ii] and that targeting gut microbiota is one main future treatment for diabetes.[iii]

Treatment using phages

The drawback to the all raw foods approach I explained earlier is that very few people can actually sustain such a stringent dietary intervention. However, diabetics who consume only half of their foods as raw food (a more practical scenario) and achieve a healthy gut microbiota from supplementation, can still enjoy a profound diabetes-reversing effect. I can’t think of a better way to heal the gut lining and optimize the microbes there than the combination of pre-biotics, probiotics and phages. Phages? The most effective way to rapidly clear out harmful gut wall bacteria so pre- and pro-biotics can do their work in healing the gut microbiota balance is by consuming phages (bacteriophages). Phages only attack bacterial cells, but not human cells. 

Prior to the discovery of antibiotics, phages were the main cure for bacterial infections. d’Herelle’s first experimental phage therapy used an oral phage solution to effectively treat dysentery.[i]  However, pharmaceutical companies subsequently developed and widely promoted antibiotics and phages became largely forgotten. More recently phages have again come to the forefront as a way to target harmful intestinal bacteria. If you put “diabetes, phages” into the Pubmed search bar you’ll come up with 2220 search results. Obviously the research on this is quite active.

I am excited to share more details of the power of phage therapy for gut health and disease reversal, along with its compelling peer-reviewed science in my next blog.  


To feeling well,


Michael Cutler, M.D.

[1] Semenkovich CF, Danska J, Darsow T, Dunne JL, Huttenhower C, Insel RA, McElvaine AT, Ratner RE, Shuldiner AR, Blaser MJ. American Diabetes Association and JDRF Research Symposium: Diabetes and the Microbiome. Diabetes. 2015 Dec;64(12):3967-77. PMID: 26420863. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4876761/


[1] Aw W, Fukuda S. Understanding the role of the gut ecosystem in diabetes mellitus. J Diabetes Investig. 2018;9(1):5-12. https://pubmed.ncbi.nlm.nih.gov/28390093/


[1] Tai N, Wong FS, Wen L. The role of gut microbiota in the development of type 1, type 2 diabetes mellitus and obesity. Rev Endocr Metab Disord. 2015;16(1):55-65. doi:10.1007/s11154-015-9309-0. https://pubmed.ncbi.nlm.nih.gov/25619480/


[1] Khan MT, Nieuwdorp M, Bäckhed F. Microbial modulation of insulin sensitivity. Cell Metab 2014;20:753–760. https://pubmed.ncbi.nlm.nih.gov/25176147/


[1] Paun A, Danska JS. Modulation of type 1 and type 2 diabetes risk by the intestinal microbiome. Pediatr Diabetes. 2016;17(7):469-477. doi:10.1111/pedi.12424. https://pubmed.ncbi.nlm.nih.gov/27484959/


[1] He C, Shan Y, Song W. Targeting gut microbiota as a possible therapy for diabetes. Nutr Res. 2015;35(5):361-367. doi:10.1016/j.nutres.2015.03.002. https://pubmed.ncbi.nlm.nih.gov/25818484/.


[1] He C, Shan Y, Song W. Targeting gut microbiota as a possible therapy for diabetes. Nutr Res. 2015;35(5):361-367. doi:10.1016/j.nutres.2015.03.002. https://pubmed.ncbi.nlm.nih.gov/25818484/.


[1] d’Herelle F. Sur Le rôle Du microbe filtrant bactériophage dans La dysentérie bacillaire. Comptes Rendus Académie Sci. 1918;167:970–972.


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