Okay, but how do you know what is attributable to the environmental factors vs natural cellular aging? Cellular aging happens differently among different people because everyone is so different genetically. There might be gene combinations that cause certain processes to happen slower or faster that are at play in male pattern baldness. Its not contradictory to say environmental factors play a minor role because cellular aging is not proven to be from environmental factors like your suggesting. Old people die from cellular aging regardless of clean air or more veggies. It doesnt stop cellular aging.
DHT is concrete now. You need to prove that environmental factors change androgen levels significantly or AR significantly to change male pattern baldness. I dont think they do. Your immune systems reaction to DHT, or your sensitivity is not under your influence anymore than you can change your diet, and prevent allergies.
"the genetic component is how we respond to inflammation. It is no coincidence that Androgenetic Alopecia is correlated with metabolic syndrome and cardiovascular disease."
Correlation does not equal causation. Many many studies suggest things that were mere coincidences, and later turned out to be not true. If you cant explain why male pattern baldness directly causes higher cardiovascular disease than I have a hard time believing it does even if some stats draw some vague correlation. Not good enough
"cytokines, hormones, and transcription factors involved with Androgenetic Alopecia and AR"
We know everything involved with this?
Anyways im not going to argue anymore on this because I am not that knowledgeable on biology or medicine to be able to make a scientific argument for my case. I just dont believe some things small studies suggest are always true.
Of course there are genetic differences in cellular aging. Like I said before, cellular aging is heavily influenced by the environment. Did you know metabolism is one of the main causes of cellular aging? You can adjust your metabolism via calorie intake. Caloric deficits are proven to extend life. At the same time, chronic caloric surplus decreases lifespan by increasing cell division and also increasing metabolism byproducts. Reactive oxygen species are a byproduct of metabolism, which can lead to increased oxidative stress. Intake of antioxidants via diet can help alleviate this. Of course, the natural base antioxidant capacity differs from people to people, but it is also heavily influenced by diet.
Inflammation and toxins will also result in premature cellular aging. Again, this is environmental. Of course nothing will stop the natural aging process, but to say environmental factors have an insignificant impact is erroneous.
There is increasing evidence that gut flora imbalance and western diets play a large role in the increase in autoimmune diseases and allergies. Again, this is environmental. Your gut health is heavily related to mental health and also the immune system. Gut flora is all environmental, and not genetic.
In addition, the evidence for the correlation between metabolic syndrome, CVD, and Androgenetic Alopecia is undeniable now. It is not some small studies drawing vague correlations. You can look up the large amount of studies from accredited journals yourself.
If there is a problem to be solved, then you ask questions; you don't keep denying things or you will get nowhere. The DHT theory is in no way complete; that is why you have keep investigating. Going back to the CVD relation, your can either say "correlation not causation" and abandon the research right there and just wait for an answer, or you can continue investigating.
What if I told you there are studies showing those with Androgenetic Alopecia are more likely to have hypertension? Just a correlation? What if I tell you that studies show those with hypertension have higher serum IL-6 and inflammation, and that IL-6 is the main inflammatory cytokine involved in the hair loss cascade? What if I also tell you that in vitro studies show that IL-6 upregulates androgen receptors? Still just an insignificant correlation?
How about in vitro study demonstrating a greater sensitivity to oxidative stress in balding scalp derma papilla cells vs nonbalding cells? No significance? How about an in vitro study demonstrating that oxidative stress can upregulate TGF-beta, the cytokine responsible for fibrosis? TGF-beta is also part of the androgen cascade, and suppresses hair growth.
If you look into the biochemical implications of this blood flow study, then you will see why this is significant. Optionally, you can continue to dismiss it.
