You're making too many generalizations, which is exactly why no one gets anywhere in the hair loss industry. Water making the hair shaft thicker is absolutely not bonkers unless you're also willing to say that water doesn't cause plumper skin in women as well as bloating due to water retention. What you're saying is non-sense. You'd essentially be denying that women (or really anyone) don't experience water retention in the skin.. and if water retention can happen in the skin (and it does), then it is certainly capable of happening in the hair. Women experience variations in water retention every month due to their menstrual cycle. In addition, I've literally experienced this phenomenon in my own hair multiple times... like literally during 5 independent experiments I did using finasteride. So, by saying that it's not possible that the hair shaft can change in volume and texture in a very short time span, as I've said it does (and as OP apparently experienced), you're directly contradicting my own experience and essentially calling me a liar.Water going up into the hair shaft and making it thicker is an absolutely bonkers proposition.
Aldosterone does not "shred" hair and you should be more specific and qualify statements when you want to use vague language like that. Aldosterone, on it's own does not have negative effects on hair. It's only aldosterone binding the mineralocorticoid receptor which has negative effects in both the body in general, and hair growth. However, aldosterone has physiological effects which are mineralocorticoid receptor-independent and rely on c-Src induced phosphorylation of the IGF-1 receptor which promotes the PI3 kinase/Akt signaling pathway... which ties in nicely with the long-held notion that IGF-1 plays a role in hair growth. So, the reason that spironolactone likely has positive effects on hair loss is due to the fact that:Besides that, aldosterone shreds hair. It's not good for it, and it's upregulated in bald scalp. Mr antagonists have been shown to promote hair growth. Aldosterone and the MR promote collagen synthesis and fibrosis, and that's probably why spironolactone works so well, because it's an MR antagonist.
1. aldosterone can't bind the mineralocorticoid receptor and cause its negative effects on not only hair, but also vascular, cardiac, and other tissues.
2. the lack of mineralocorticoid receptor activation will cause a reflexive upregulation in aldosterone synthesis, which means increased induction of IGF-1 phosphorylation.
So, in short, aldosterone induced fibrosis of many different types of tissues via mineralcorticoid receptor activation = bad. Aldosterone induced phosphorylation of the IGF-1 receptor can be a good thing. This is why specificity is important. You can't just go around making blanket statements like "aldosterone is bad" or it shreds hair or whatever. It's not aldosterone itself. It's cascade of events that occur as a direct result of aldosterone overactivating the mineralocorticoid receptor either due to overexpression of the receptor, overproduction of aldosterone, or both.
I never claimed fibrosis is the cause of hair loss. It's just another piece in the same puzzle. My stance on the true cause of hair loss has been consistent and it's littered all over this thread, this forum, and other forums. Here's a quote from a post I made like an hour ago:However, fibrosis isn't the cause of hair loss, it's just inhibits regrowth.
ALL forms of hair loss (with the exception of alopecia universalis), whether male pattern, female pattern, accutane induced, or most other drug-induced forms of loss, are caused by insufficient intrafollicular estrogen synthesis. They're all just slight variations in what causes the lack of intrafollicular estrogenic activity.
In male pattern, the primary cause is the high intrafollicular expression of 5AR which draws away the follicle's entire supply of androgens and leaves insufficient levels behind for aromatization. The male pattern is simply due to the variation in both 5AR and aromatase expression in different areas of the scalp.
In female pattern, the primary cause is low aromatase expression and/or low estrogen receptor expression. The female scalp usually has quite low expression of 5AR, so it generally plays very little role in the "female pattern" you see in their hair loss. Females that experience diffuse "female" pattern hair loss have uniformly (or globally) lower levels of aromatase and/or estrogen receptor expression than normal, which leads to insufficient intrafollicular estrogenic activity. This manifests in an evenly distributed pattern of loss across the entire scalp.
In accutane-induced loss, there is an impairment of the aromatase pathway which leads to a linear increase in hair loss on top of any other condition (like male pattern hair loss), if there is any. Accutane-induced loss on its own (with no underlying male pattern loss) will manifest the same as female pattern loss because accutane affects the aromatase pathway uniformly.. not just in the scalp, but the entire body.
This is easily false. If it were the case, finasteride or any other 5AR antagonist would be the cure. Case closed. None of us would be on here if DHT were the cause of hair loss because we already have a very effective way of completely wiping out the body's synthesis of DHT.Sorry, but there's no getting around the fact that DHT is the cause.