I just read a summary of an abstract by European Journal of Surgical Oncology (Volume 34, Issue 7, July 2008, Pages 805 -810) titled: Association between polymorphisms of folate-metabolizing enzymes and risk of prostate cancer
I have been reading up on the MTHFR gene mutation as I see a link with my health. I have high homocysteine. There is also a strong history of heart disease in my family. I was also reading that methyl groups bind to histamine and break it down. I have had allergy problems for years. And now the link to prostate cancer.
My oncologist wants me to take a B6/B12/Folate supplement for the high homocysteine. I am trying to understand methylation, but i have not gotten a good grasp on the concept.
I read that 23andMe testing can determine if someone has MTHFR mutation. Has anyone done this? Anyone have experience with MTHFR? Or trying to fix methylation? Any input is appreciated as I am trying read up on this subject and how it applies to us.
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Captain_Dave
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Yes, I too have the genetic mutation and have had high homocysteine for a while. I am trying to address this with my primary care physician through use of methylated b-complex (adenosyl/hydroxy b12). Pure encapsulations and Thorne Research have the highest quality OTC versions. If you plug your 23 & me info into the "Genetic Genie" website it will give you your genetic information that you can share with your doctor. You will need on e that practice integrative care. Thank you for sharing the article. It is a connection I was unaware of. BTW- my PC is aggressive (Gleason score of 9) and Stage IV post prostatectomy diagnosis. Is yours an aggressive type?
I was diagnosed at age 50 in 2011 with PSA of 16 and Gleason score of 7 (3+4 I think). I had RP surgery and they told they got it all, margins were negative and nothing in the lymph nodes. Year and a half later PSA started going up. I went for radiation. After, PSA was <0.01 for a year and a half. Now rising again. Last test it was 0.1. I am going to an integrative oncologist. He wants me on a clean diet, exercise and supplements. He is going to take my PSA every 2 months.
It must be 9 years since my bad experience with B12. My blood work from an annual medical showed elevated homocysteine. My integrative medicine doctor thought I might be B12-deficient. In support of that, my hair analysis showed zero cobalt. I told him that I was using a multi-B vitamin. He said that I was probably not absorbing B12 well.
He was against sublingual products. For $24, I received a small bottle of B12 liquid & enough syringes for 6 months. I was shown how to inject into belly fat.
I had been testing PSA monthly. The previous 6 readings were identical. Suddenly, my PSA was rising at an alarming rate. After 4 months, I searched PubMed for <B12 prostate>. Surprisingly, there was a connection. B12 was associated with aggressive PCa; homocysteine with protection.
The reason is that PCa wants to become hypermethylated. In particular, the DNA promoter region for tumor suppressor genes is methylated (silenced) in PCa.
In humans, methyl normally comes from folate - via foliage (greens).
When SAM drops off its methyl load, we are left with homocysteine.
Folic acid - a synthetic - partially converts to folate. Grains products are fortified with it in the U.S., Canada & many other countries - but none in the E.U. Deficiency is rare in bread/rice eaters in the U.S. Why supplement with folic acid if you are getting plenty?
Studies that have used B6-B9-B12 to lower homocysteine have not lowered cardiovascular events.
Be very wary of repairing the SAM cycle. You might find that as homocysteine goes down, PSA goes up. And once PCa is hypermethylated, they are not readily demethylated.
I neglected to discuss MTHFR polymorphisms (now numbering 24? variations).
From ny perspective, there are all sorts of reasons why methyl-related factors increase PCa risk. Once PCa occurs, it may not make sense to address those problems.
With low methylaton (hypomethylation) there will be DNA instability & cancer risk.
When the cancer has happened, hypomethylation is our friend. Increasing methylation will help prevent other cancers, but will lead to hypermethylation of the CpG islands related to PCa tumor suppressor genes.
Here is an old paper (2002), but I think it clearly deals with the issue:
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