Does anyone take SAM/SAMe? Do you find any benefits from taking it?
A SAMe study abstract is below, with a link to it at the bottom.
Abstract
Background: The most critical point in the treatment of prostate cancer is the progression towards a hormone-refractory tumour, making research on alternative therapies necessary. This study focused on the methyl donor S-adenosylmethionine (SAM), which is known to act as an antitumourigenic in several cancer cell lines. Though a genome-wide downregulation of proto-oncogenes in prostate cancer cell lines treated with SAM is obvious, the anticancer effects remain elusive. Thus, in this study, the impact of SAM treatment on the cell cycle, apoptosis and cancer-related pathways was investigated.
Methods and results: After performing SAM treatment on prostate cancer cell lines (PC-3 and DU145), a cell-cycle arrest during the S-phase, a downregulation of cyclin A protein levels and an upregulation of p21 cell cycle inhibitor were observed. The proapoptotic Bax/Bcl-2 ratio and the caspase-3 activity were elevated; additionally, the apoptosis rate of SAM treated cells increased significantly in a time-dependent manner. Moreover, immunoblots displayed a downregulation of Erk1/2 and STAT3 phosphorylation accompanied by a reduced expression of the STAT3 protein.
Conclusion: SAM caused changes in cancer-related pathways, probably leading to the effects on the cell cycle and apoptosis rate. These results provide deeper insights into the anticancer effects of SAM on prostate cancer cells.
Ok thanks. I’m not doing bat on my own. I might try it if it is made available at the hospitals but for some reason that doesn’t seem to be materializing. I write to the jhu doc a free years ago but he didn’t reply.
I took a pretty deep dive into all the supps. SAM-E did come up but I didn't see enough evidence it was just going to make my urine worth more. Problem with all these supps is they are in vitro (test tube) studies, or in vivo with mice. Even if both show positive results, typically there's no long-term, well designed studies to show if it does good, does nothing or does harm in human patients. In other cases, equivalent dose to make any sort of difference in us humans is toxic. (But one could say, so is chemotherapy.)
Low doses of supplements are actually most effective. There odd s paradox that occurs when people take high doses of some supplements, that makes the disease worse. In a small amount of supplements, its the opposite. There are alot of studies on humans but most of them are from other countries. To each their own. Some supplements are useful because it’s next to impossible to get those ingredients from food.
"Increasingly effective therapies targeting the androgen receptor have paradoxically promoted the incidence of neuroendocrine prostate cancer (NEPC), the most lethal subtype of castration-resistant prostate cancer (PCa), for which there is no effective therapy. Here we report that protein kinase C (PKC)λ/ι is downregulated in de novo and during therapy-induced NEPC, which results in the upregulation of serine biosynthesis through an mTORC1/ATF4-driven pathway.
This metabolic reprogramming supports cell proliferation and increases intracellular S-adenosyl methionine (SAM) levels to feed epigenetic changes that favor the development of NEPC characteristics.
Altogether, we have uncovered a metabolic vulnerability triggered by PKCλ/ι deficiency in NEPC, which offers potentially actionable targets to prevent therapy resistance in PCa." [1]
Good observation. Why avoid a small predator to get eaten by a big one. Have endocrine cancer deaths increased since the use of 2d line AR drugs? Sometimes I wonder if the AR drugs almost guarantee and extra 2 years of life, but take away the possibility of an extra 5-10. This topic is rarely discussed but one of my oncologist and I had a good discussion about it.
It puzzles me that doctors & patients are so keen to use really aggressive protocols, when the drugs are merely palliative. Not only do they not cure advanced PCa, but they fail in a relatively short period of time. When I started out, there were really few otions: Lupron for 2 years followed by Taxotere. Nowadays, the feeling seems to be that something new will turn up.
I feel that it is a mistake to follow one protocol until it fails. The cancer simply becomes harder to manage. From a 2014 paper: "Neuroendocrine prostate cancers (NEPCs) are rare." Not so rare these days, unfortunately.
One question I've always pondered is, do all roads (currently) lead to the same destination arriving at times that are not that much different in the context of the BIG picture? If that's the case, do you want to take the more bumpy road with the rougher ride to get to the destination marginally later?
The bumpy road is higher stress sometimes. Qol is a consideration. I’m not entrenched in fighting for one side but i try to look at both sides in an unbiased way. I think the treatment decisions should come down to the patient getting the data and deciding what they want to do.
I hear ya. I’m amazed at some of the doctors that just want to plow forward with one treatment on top of another even when the cancer volume is low. I can understand if there is a chance with chemo but later on down the road is different. There seems to be no consideration of trying to prevent adaptation of the cancer. I guess their are two schools of thought - cancer is dumb or cancer is smart/adaptive. I heard a doctor say this today, “good doctors treat the illness, great doctors treat the patient with the illness.” I would change the word “good” to “subpar”
Sorry no response so far. I'm still trying to figure what in the hell is "S-Adenosylmethionine"... is it something you add to your car's engine to make keep the engine in sync with your windshield wipers?.......
SAM is a part of the larger consideration of methyl donors and relationships to micronutrients, including B12 and folate etc on the one hand, and epigenetic mechanisms mediated by DNA methylation. Here is a good review of the topic for those desiring a deeper understanding.
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