Having SNP In the MTHFR gene or the methylation pathway can contribute to SIBO. But what is the connection between poor methylation, a sluggish gallbladder, MTHFR and SIBO?
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The MTHFR gene and Methylation cycle need to be functioning optimally so that a methyl donor called SAMe (s-adenosylmethionine) is produced in sufficient quantities. The methyl donor SAMe is required for over 200 other functions in the body by giving methyl groups to molecules or genes in need of SAMe such as the COMT gene and PEMT gene.
The connection between MTHFR and SIBO
MTHFR is a gene in the methylation pathway that is responsible for converting folate into methylfolate. Methylfolate is the active form of folate, which then goes on to support the production of SAMe.
Methylation is the addition of a methyl group to a molecule that activates the receiving molecule. The “activated” molecule can then go on to support other functions in the body. SAMe is one of your body’s primary methyl donors required for other genes to function by donating methyl groups.
One gene that requires and uses up the most SAMe in the body is the PEMT gene. The PEMT gene requires SAMe as a co-factor to produce phosphatidylcholine. According to Dr. Ben Lynch, approximately 70% of SAMe is used up by the PEMT gene to make phosphatidylcholine.
Phosphatidylcholine is essential for:
- helping to prevent fatty liver
- preventing the formation of gallstones in the gallbladder
- keeping the bile flowing smoothly out of the gallbladder
Having a gallbladder that functions well with optimal smooth bile flow is crucial to preventing SIBO. Bile is antimicrobial and helps sterilize the small intestine and prevent SIBO. A deficiency in phosphatidylcholine causes bile to become too thick and sludgy.
If your methylation cycle isn’t optimal, this can cause a sluggish gallbladder that doesn’t release enough bile. As a result of insufficient bile flow from the gallbladder, SIBO can develop.
Is SIBO genetic
The genetic connection of SIBO lies in understanding the various interconnections between MTHFR, the production of SAMe, and the PEMT gene and bile flow.
I have several SNP’S in the methylation pathway and a PEMT SNP. As a result, I had a reduced ability to make SAMe and phosphatidylcholine. Someone is likely to develop SIBO if there is a folate deficiency, B12 deficiency, or choline deficiency in addition to SNPs in these genes.
SNPs and possible unknown nutritional deficiencies in these nutrients were why I had a sluggish gallbladder and developed SIBO. Supporting my dirty MTHFR gene and PEMT gene played a huge role in healing my SIBO.
Having oxidative stress also inhibits the methylation pathway and the production of SAMe. Identifying the cause of inflammation in the body and getting inflammation down is necessary to optimize your methylation cycle. I had elevated inflammation and SNP’s in my methylation pathway along with a PEMT gene SNP which created a perfect recipe for SIBO to develop.
How to support the PEMT gene to prevent SIBO
One of the best ways to support your methylation cycle and sluggish gallbladder to prevent SIBO overgrowth is by supplementing with phosphatidylcholine (optimal pc). Phosphatidylcholine can help to promote bile flow which is your body’s natural antimicrobial defense against SIBO.
Supplementing with phosphatidylcholine will also indirectly support your methylation cycle by freeing up the methyl donor SAMe to work elsewhere in the body. There will no longer be such a demand by the body to make SAMe for the PEMT gene. Two hundred other processes will be happy to have SAMe as a co-factor so these other genes can now do the work they need to do.
As you can see, everything is interconnected in the body. Understanding your unique biochemistry and underlying genetic susceptibility to SIBO can massively help to improve your health and digestive symptoms.
If you are interested in doing genetic testing, you can do an at-home saliva test using the Strategene DNA Test Kit. You will also receive your strategene report and additional education to help you understand your unique genetics.