- Joined
- Jan 19, 2009
- Messages
- 1,839
Not even going to bother getting into this discussion AGAIN on this forum. This is one of the most tried and true medications on the planet. It has stood the test of time in an enormous patient population.
I've posted this here before, biochemistry of many drugs that bb use as well as anti aging etc . Great resources..
https://www.pharmgkb.org/pathway/PA165948566
And if your curious about the biochemistry of the aforementioned pathways
https://themedicalbiochemistrypage.org
Or the genes that govern these pathways
**broken link removed**
Great sites there brother thanks.
I'm interested in this as I use met but man all this crazy shit we do to our bodies and we're worried about this one supp POSSIBLY having a drawback?
If it actually helps for our purposes, that should be the debate....
Well metformin is a year round thing. The rest are just in limited time cycles. The two things that really made me nervous were the claims that the effect of exercise becomes useless along with decreased aerobic performance (as a guy who does a lot of HIIT, that's serious to me). I'm pleased to see the counter studies posted in this thread though.
This article is complete horse shit. I would take anything this woman has to say with a grain of salt. Actually I would completely ignore anything she has to say. Some NoCal libertard with an agenda. Really it borders on a complete fabrication.
https://www.ncbi.nlm.nih.gov/pubmed/20071560
"In addition, 12-h postprandial blood glucose was measured in all three trials. Insulin sensitivity was similar between MET and EX but was 43 % higher than both MET and EX after MET + EX. Our data suggest that habitual metformin treatment in insulin-resistant patients does not blunt the acute insulin-sensitizing effects of a single bout of exercise that on the contrary, tends to enhance it."
Rex.
This is the problem with reading single studies as a determinate of efficacy. Here is a similar study, performed on a similar patient population except with steady use of the drug. https://www.ncbi.nlm.nih.gov/m/pubmed/24682492/?i=2&from=/20071560/related
And the results show the opposite, improved insulin sensitivity.
When sample sizes are small there are so many counter arguments.. it is statistically probable with an n=9 sample to select the 9 individuals ( in case of first study ) who are not able to achieve any effects from metformin over a 2-3 week trial, and have predisposition to slow metabolism of drugs.
The way ampk-a is measured as a determinate of efficacy is also flawed. AMPKalpha Antibody detects endogenous levels of AMPKα protein. The antibody detects both the α1 and α2 isoforms, but not the B or Y subunits.
Patients could be lacking the substrate needed for phosphorylation of ampk, so many variables exist. Peer review is utilized for this reason. I've submitted work on ncbi, among other journals, and found some peer review to be quite vicious in pointing out potential variables..albeit necessary to direct future research.