Several studies have come out recently showing that those who are overweight have a different gut microbiome composition than those who are lean. There have also been interesting mouse studies showing that transplanting feces from obese mice into lean mice causes the lean mice to become obese. A 2010 study that found that supplementation with the probiotic Lactobacillus gasseri SBT2055 decreased abdominal fat and body weight. The case for our microbes helping to shape our weight is fairly strong.
But why do some people have higher gut microbe populations of certain beneficial species than others? Genetics! Along with diet and environment, of course!
I find it fascinating that genetics plays a big role in the types of microbes that can live in our bodies. Specific genetic variants can promote or discourage microbes in our guts. For example, a FUT2 polymorphism causes some people to be immune to the Norovirus and the rotavirus (sometimes called the stomach flu).
Here are a few of the genes that play a role in determining which microbes inhabit the gut microbiome:
This gene affects plasma lipoprotein levels including triglyceride levels as well as levels of certain gut bacteria. Several SNPs in this gene have been associated with triglyceride levels and obesity risk.
An April 2016 twin study looked at metabolic syndrome (including weight) and found that rs651821 was associated with metabolic syndrome (MetS). The study results found that metabolic syndrome was more common in those with the C allele and, for each C allele, there was an average increase in triglycerides of 24.65 mg/dL. In looking at the gut microbiome, the study found that those with the minor allele (C) had fewer Bifidobacterium regardless of their MetS status. Bifidobacterium species have been linked (in this study and in others) to lower BMI and better overall health.[ref]
Several MYD88 variants have been found to reduce levels of MYD88 (most are not covered by 23andMe data). These are just reduced levels, though, not a complete ‘knockout’, so the results of the mouse studies may not be completely applicable.
Nucleotide-binding oligomerization domain containing 1 (or NOD1)
Mice deficient in Nod1 have increased susceptibility to H. pylori. Other studies have shown that NOD1 variants lead to increased risk of inflammatory bowel diseases in some population. One study concluded, “Taken together, these data may suggest that NOD1 plays a variable role in different populations that could depend upon environmental and dietary factors.” [ref]
Toll-like receptor 4 (TLR4) plays an important role in our innate immunity and is especially active against gram-negative bacterial infections. TLR4 variants have been investigated in conjunction with cancer risk, vaccine response, and transplant rejection among other things.
From Genetics Home Reference: “This gene encodes a member of the SLC39 family of solute-carrier genes, which show structural characteristics of zinc transporters. The encoded protein is glycosylated and found in the plasma membrane and mitochondria, and functions in the cellular import of zinc at the onset of inflammation. It is also thought to be the primary transporter of the toxic cation cadmium, which is found in cigarette smoke.”
There are probiotics available containing multiple strains of bifidobacteria.
More to read:
A recent study did extensive analysis on the microbes associated with visceral fat, BMI, and other obesity markers. The study also found several genes correlated with specific bacteria that are associated with obesity. The SNPs (none of which are included in 23andMe results) were in the FHIT, TDRGI, and ELAVL4 genes. The full study is open to read and worth checking out.