SAM-e (S-adenosyl-methionine) has been shown to be efficacious in several health conditions. Although SAM-e, as a methyl donor, participates in a wide variety of biochemical reactions, it can provide important support for the healthy functioning of joints, neurological processes and the liver.
SAM-e’s joint support lies not only in its ability to help regulate the body’s normal inflammatory processes, but also on its putative participation in proteoglycan synthesis and joint cartilage synthesis. SAM-e is thought to function physiologically as a signal of sulfur availability. Some suggest that supplemental S-adenosyl-methionine may compensate for the decreased SAM-e levels in chondrocytes induced by the inflammatory cytokine interleukin-1, and thus upregulate the chondrocyte’s synthesis of joint proteoglycans.
As a major source of methyl groups in the brain, SAM-e, in conjunction with other methyl donor metabolites such as betaine, choline, or folate, may optimize the synthetic/degradative rate of neurotransmitters, i.e. serotonin and dopamine, and the brain’s sensitivity to them. With few side effects SAM-e has been shown in meta analysis of multiple studies to offer tangible support for healthy mental functioning.
As a hepato-protective compound, SAM-e has been shown to be useful to support the body’s response to adverse biochemical alterations induced by lead and/or alcohol exposure. This characteristic of SAM-e’s activity is also effective in protecting the central nervous system. SAM-e can be an integral part of a hepatoprotective therapeutic regimen. Other studies have indicated that SAM-e may decrease cholestasis by optimizing a healthy flow of bile to the gastrointestinal tract.
SAM-e tablets may be a useful nutritional supplement for individuals looking for support of joints, mental health, or liver health.
* These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.
This product was added to our catalog on Wednesday 04 June, 2014.