I commented on this when it was initially posted a few months back.
***After reading over the full text- the only really conclusive, usable and replicated clinical data I found from this study reinforces that those with fatty liver disease should avoid excess fat in their diet. The rest of the...
Not sure why you would be concerned about your liver- but there is no interactions with either Milk Thistle or N-acetyl cysteine.
Silymarin, the active constituent in Milk Thistle, does not have sufficient bioavailability to pose any sort interaction risk with your antibiotics or ostarine...
A pharmacokinetic interaction with ostarine which would hinder elimination of amoxicillin or the clavulanate would be the major problem of the combination- however this would seem highly unlikely given ostarines primary eliminated route is (unchanged) via feces, contrasting...
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There are a few papers on this- but these are probably the most deeming.
As far I understand the theory behind the potential ergogenic/anabolic action of supplemental ARA is to influence the hormetic response of muscle inflammation. As such I'm not...
I'm not too sure you comprehended the information you have read. As far as I understand- PGE2 is actually desired metabolite and you certain wouldn't want to restrict the AA metabolism to it. Most of the preliminary research that assessed inflammatory cascades as a mediator of muscle cell...
Propranolol is a less than desirable med for that purpose for a few reasons. It's a non-selective beta blocker- meaning it will inhibit sympathetic input into heart as well as the bronchioles. The former can reduce exercise capacity- essentially by placing a governor on your heart rate when you...
Clozapine is actually an atypical antipsychotic (newish generation)- and is least likely to produce undesirable D2 antagonist adverse effects (extrapyramidal kinesic effects , elevated prolactin).
Lurasidone is more than likely the reason for the elevated prolactin.
In any case I wouldn't...
What antipsychotic are you taking?
There may well be a direct contraindication to taking a pro-dopamine supplement with your medication.
A primary mechanism of antipsychotic meds is inhibiting dopamine transmission- some of the older generation meds are indiscriminate in dopamine antagonism (so...
The data on the Mucuna increasing LH and T (actually found decrease in FSH) was tested in hypogonadic/hyperprolactinaemic men- so the increase in LH and T is without a doubt consequential of prolactin inhibition.
Unless I'm mistaken there isn't any evidence that Mucuna can increase LH/T in...
This is a point of contention in the literature. Research demonstrating a decrease in gonadotrophin levels use either absurdly high oral doses of non-polar constituent rich extracts or high doses via intravenous administration. My opinion is that the drop of FSH observed in this research may be...
It was once believed that the dose of aspirin dictated the the enzyme affinity (COX-1 vs COX-2), however it seems the selectivity is substrate concentration dependent- as evidence by very low dose aspirin inhibiting COX-2 in cancer cells lines.
For the purposes of maximizing effects of ArA...
What you've described sounds very much like advanced sleep phase syndrome (ASPS). It very unusual that GFXT would have anything to do with it. Being a syndrome there is really no recognized pathology that would serve for accurate diagnoses- and therefore as your clinical picture seems somewhat...
Ursolic acid is actually quite comprehensively studied.
In regards to your question-the most deeming evidence suggests that in a calorie deficit ursolic acid can down regulate the normal production of key atrophic enzymes (specifically E3 ubiquitin ligases: atrogin-1 and Muscle Ring Finger-1)...
The affects of Vitex on dopamine transmission at lactotrophs are specific to extract constituents and are polarized by the dose (low dose--> D2 antagonist, high dose --> D2 agonist activity). This suggests either the most likely active dopamingeric constituents have partial agonist activity or...
Those numbers look consistent with normal male fluctuations in sex hormones and gonadotrophins.
Given the fact that endogenous production 7alpha/beta OH-DHEA occurs as result of an irreversible metabolism of DHEA- there isn't a chance that it could be converted to anything suppressive.
At the level of absorption it is the same as lithium carbonate (and chloride). The difference seems to be in the volume of and tissue distributions.
Irregardless of this it will be ionic lithium (dissociated from the mineral/salt carrier) that will cause the manifestations of toxicity.
Geez, I would be extremely hesitant in recommending lithium for self-medicating. Not only is the dose response idiosyncratic but it has a narrow therapeutic range whereby doses are often established via blood level monitoring.
An organic nitrate or even a nitrate donor should never and would never be used as a sole agent to control BP. It is far too unreliable- especially with chronic dosing.
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