We’ve got 15 year old “Peaters” who call you retarded for using EVOO
Because FUPAs…POOFAs? No, PUFAs, that’s the one
The ~10% PUFA that comes packed with vitamin E, phenolic and polyphenol compounds, etc. is really gonna be the end of muh tabolism
Corporate science loves manufacturing uncertainty in the scientific literature.
If independent research shows consistent harm, funding a bunch of inconclusive or null-result studies shifts the narrative from "evidence clearly showing that X is bad" to "experts disagree"
Instead of disproving harm, they just produce enough noise in the literature to make the science inconclusive.
This is enormously effective because regulatory bodies and consumers often require near-unanimous consensus.
The tobacco industry did this for decades. They funded research that muddied smoking's link to cancer even when independent literature was already damning.
Even worse, if results start looking bad, they pull funding before it completes or gets published so negative evidence never surfaces.
Tobacco was the original blueprint. Pharma does this with drugs, Agrochemical does this with pesticides, Telecom does this with EMF. This happens over and over.
Studies only prove so much.
@anymanfitness@ScottyOptimal Here’s a good review, not much clinical data yet. Certainly more than enough for me to avoid it personally
https://t.co/K8UiQ5aMF2
The world is so cooked man, can’t even have a chair in your room without someone saying
“OMG is that the cuck chair 😲”
Vault porn, slaughter everyone involved
Simple
How exactly do people square away the undeniable benefits of DHA and EPA from seafood, especially in relation to UV light exposure, when they insist that all polyunsaturated fatty acids are a net negative for health and metabolism?
@NoahRyanCo@nordman__ Is this the study you’re talking about? If the only data for this is this prostate model then I disagree, unless I’ve missed something else https://t.co/Vrtqm6e0SU
The rats were castrated and then given testosterone to induce BPH. DHT likely increased in the prostate tissue due to its anti inflammatory and protective effects, and then was reduced when the tissue was given an exogenous source of a strong antioxidant (astaxanthin).
I don’t think this indicates that astaxanthin is a direct systemic 5ar inhibitor. It seems to down regulate DHT production in the prostate by resolving some of the oxidative and inflammatory stress that signaled the need for local androgenic protection.
From my understanding it seems that the reduction of DHT in this tissue is a downstream effect of improved cellular redox, and not a pharmacological inhibition of the androgen metabolism.
I’m currently blasting astaxanthin for sun protection and don’t notice any anti-androgenic effects.