Guest Blog by: Dr. Arland Hill (D.C.)
Homocysteine continues to gain acceptance as a risk factor in a number of conditions. Once thought to be associated with mostly cardiovascular disease, homocysteine is now recognized as a contributor to numerous states of dysfunction, including arthritis, cognitive decline, osteoporosis and many more. Given the vast reaching effects of homocysteine, having an ideal treatment protocol in place to address elevations seems necessary, if not even absolutely crucial.
Examination of the literature to lower homocysteine can be confusing at times, with some studies showing lack of efficacy of B vitamins. However, these studies were not without criticism and ultimately a return to the basics of physiology has shown B vitamins to be an efficacious intervention. When looking at the methionine cycle and delving deeper into the biochemistry of homocysteine, it becomes rather clear that without methyl donors, homocysteine conversion to methionine gets stalled and homocysteine begins to build up. As such, the methyl donors B12 and folate have become the primary interventions for homocysteine lowering therapy.
For some however, B12 and folate therapy are not enough. Most of these individuals fall under the category of having a variant for the methyltetrahydrofolate reductase enzyme, commonly abbreviated MTHFR. Variants in this enzyme impair the ability to reduce folate, thus making the conversion of homocysteine to methionine inefficient and promoting accumulation. This is seemingly overcome fairly easily in elevated cases by the use of L 5-methyltetrahydrofolate. Upon normalization of homocysteine in this manner, levels can generally be kept in an ideal range by the use of folate, a non-synthetic, as compared to folic acid.
As relatively straightforward as this all seems, the story does not end here. A deeper look at the influences on our genes shows the complexity of modulating homocysteine. There must exist a constant balance between homocysteine and methionine. If the objective is to lower homocysteine, downregulating the enzymes that lead to its conversion and upregulating those that convert it to methionine would appear ideal. To do this very thing, one should look no further than omega 3’s. The polyunsaturated omega 3’s, known to most of us as fish oils, can directly affect the expression of the genes that control the enzymes linked to homocysteine metabolism. Since the omega 3’s do not directly insert into the biochemical pathway of the methionine cycle, their actions clearly have to be based on another mechanism of action, one we now recognize as genetic.
Consider the therapeutic potential here for a number of patients. Let’s take the aforementioned conditions for which homocysteine is known to affect. Equally validated in the literature to support cardiovascular disease, arthritis, cognitive decline, and osteoporosis, omega 3’s will not only reduce inflammation but will also modify genetic expression of those enzymes metabolizing homocysteine. This makes testing and adding omega 3’s to any clinical protocol at minimum a consideration given the considerable effects of homocysteine and the therapeutic potential of omega 3’s.
Please review the website below for more information: http://www.ncbi.nlm.nih.gov/pubmed/22260268
