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hair loss is not the same as MALE PATTERN hair loss.... no drug can actually cause MPB
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It is a fact that it causes hair loss, but their hypothesis's for why it happens are rubbish, according to what i know. Plus that looks like a typical snake oil site. They are exploiting a fact by providing a guess-level explanation and selling random products.
It is also a fact that dietary cholesterol doesn't generally raise your cholesterol.
I am currently eating liberal amounts of meat and butter every day and my cholesterol is lower than it was when i was avoiding it like the plague.
Therefore, there is no "paradox", as they tout. Low cholesterol levels diminish the production of the upstream metabolites (cortisol and prog), while specialized tissues like hair follicles and the prostate convert all the T they can get into DHT without brakes, despite the increasing amounts of serum E2 the organism releases to compensate. (The imbalance comes from the difference between serum molecules (cortisol and preg) and locally produced DHT. Low cholesterol reduces serum hormones more than the locally produced ones.)Comment
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im aware the body produces its own cholesterol, and any dietery cholesterol would result in lower amounts of the bodies own endegonous production of cholesterol to maintain the balance.It is a fact that it causes hair loss, but their hypothesis's for why it happens are rubbish, according to what i know. Plus that looks like a typical snake oil site. They are exploiting a fact by providing a guess-level explanation and selling random products.
It is also a fact that dietary cholesterol doesn't generally raise your cholesterol.
I am currently eating liberal amounts of meat and butter every day and my cholesterol is lower than it was when i was avoiding it like the plague.
Therefore, there is no "paradox", as they tout. Low cholesterol levels diminish the production of the upstream metabolites (cortisol and prog), while specialized tissues like hair follicles and the prostate convert all the T they can get into DHT without brakes, despite the increasing amounts of serum E2 the organism releases to compensate. (The imbalance comes from the difference between serum molecules (cortisol and preg) and locally produced DHT. Low cholesterol reduces serum hormones more than the locally produced ones.)
However, beta sitosterol/niacin is another drug that is used to lower cholesterol also.
When i was on them both i experienced hair loss in the mpb regions and the typical mpb itch. This is fact. Im thinking 5 alpha reductase enzymic activity was very high for some reason.
cholesterol lowering drugs - statins, also have a side effect of hair loss.Comment
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Human Skin is a Steroidogenic Tissue: Steroidogenic Enzymes and Cofactors Are Expressed in Epidermis, Normal Sebocytes, and an Immortalized Sebocyte Cell Line (SEB-1)
Although the human sebaceous gland can synthesize cholesterol from acetate and can further metabolize steroids such as dehydroepiandrosterone into potent androgens, the de novo production of steroids from cholesterol has not been demonstrated in human skin. The goal of this study was to delineate the steroidogenic pathway upstream from dehydroepiandrosterone by documenting the presence of members of the P450 side chain cleavage system (P450scc). This system catalyzes the initial step in steroid hormone synthesis following translocation of cholesterol to the inner mitochondrial membrane. In concert with its cofactors, adrenodoxin and adrenodoxin reductase, and the transcription factor steroidogenic factor 1, P450scc converts cholesterol to pregnenolone. An SV40 immortalized human sebaceous gland cell line (SEB-1) was established in order to facilitate investigation of the P450scc system. The sebaceous phenotype of SEB-1 sebocytes was confirmed using immunohistochemistry, Oil Red O staining, and gene array expression analysis. Presence of P450scc, adrenodoxin reductase, cytochrome P450 17-hydroxylase (P450c17), and steroidogenic factor 1 was documented in human facial skin, human sebocytes, and SEB-1 sebocytes. Using immunohistochemistry, antibodies to the above proteins localized to epidermis, hair follicles, sebaceous ducts, and sebaceous glands in sections of facial skin. Results of immunohistochemistry were confirmed with Western blotting. Biochemical activity of cytochrome P450scc and P450c17 was demonstrated in SEB-1 sebocytes using radioimmunoassay. The relative abundance of mRNA for P450scc, P450c17, and steroidogenic factor 1 in SEB-1 sebocytes and sebaceous glands was compared to mRNA levels in ovarian theca and granulosa cells using real-time quantitative polymerase chain reaction. Gene array expression analysis and quantitative polymerase chain reaction indicated that mRNA for P450scc is more abundant than mRNA for both P450c17 and steroidogenic factor 1 in sebaceous glands and SEB-1 cells. These data demonstrate that the skin is in fact a steroidogenic tissue. The clinical significance of this finding in mediating androgenic skin disorders such as acne, hirsutism, or androgenetic alopecia remains to be established.Comment
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The activity of HMG-CoA reductase and acetyl-CoA carboxylase in human apocrine sweat glands, sebaceous glands, and hair follicles is regulated by phosphorylation and by exogenous cholesterol.
Smythe CD, Greenall M, Kealey T.
Department of Clinical Biochemistry, University of Cambridge, Addenbrooke's Hospital, UK.
Human apocrine and sebaceous glands function to secrete lipids, predominantly triglycerides, fatty acids, cholesterol and its esters, and, in the sebaceous gland, squalene. The enzymes that catalyze the important regulatory steps in cholesterol and fatty acid biosyntheses, 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase and acetyl-CoA carboxylase, respectively, were therefore studied in isolated human skin appendages, and their relevant kinetic parameters determined. The enzyme activities that were observed can account for previously described rates of incorporation of radiolabeled substrates into the appropriate lipids by glands in vitro. Reduced enzyme activities following homogenization in the presence of fluoride indicated that both of these enzymes in skin appendages are inactivated by phosphorylation. The activity of the enzyme known to catalyze this phosphorylation, the AMP-activated protein kinase, was also measured. Compactin was shown to inhibit HMG-CoA reductase in homogenates of these appendages. Conversely, incubation of whole sebaceous glands with compactin resulted in the stimulation of enzyme activity, which suggests that these appendages can respond to diminishing cholesterol levels. The effect of exogenous low density lipoprotein and 25-hydroxycholesterol on HMG-CoA reductase activity from skin appendages was investigated. HMG-CoA reductase activity in both apocrine and sebaceous glands was reduced following incubation with either low density lipoprotein or 25-hydroxycholesterol. Low density lipoprotein receptor and lipoprotein lipase mRNA expression was also detected in skin appendages. These results indicate that apocrine and sebaceous glands have the capacity to sequester dietary cholesterol and fatty acids that may have important implications for the understanding of both acne and axillary odor.
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Fascinating, but it's difficult for me to make any conclusion from that, other than that dietary cholesterol is clearly a factor in hair follicle health, which we already know.
We also know that the hair follicle makes DHT prevalently from serum T, so the function of the steroidogenesis must have some other use. In that case low serum cholesterol would cause a prevalence of DHT metabolism in the follicles because while serum T is mantained (and thus DHT can be made), so isn't for the different steroid the follicle needs to make endogenously. I'm just throwing a wild guess, though.
I wonder how it ties in with the overproduction of sebum in hair follicles in MPB.Comment
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Androgenetic alopecia in children: report of 20 cases.
Androgenetic alopecia (AGA) is the most common type of hair loss in adults. Although there are differences in the age at onset, the disease starts after puberty when enough testosterone is available to be transformed into dihydrotestosterone. We report 20 prepubertal children with AGA, 12 girls and eight boys, age range 6-10 years, observed over the last 4 years. All had normal physical development. Clinical examination showed hair loss with thinning and widening of the central parting of the scalp, both in boys and girls. In eight cases frontal accentuation and breach of frontal hairline were also present. The clinical diagnosis was confirmed by pull test, trichogram and dermoscopy in all cases, and by scalp biopsy performed in six cases. There was a strong family history of AGA in all patients. The onset of AGA is not expected to be seen in prepubertal patients without abnormal androgen levels. A common feature observed in our series of children with AGA was a strong genetic predisposition to the disease. Although the pathogenesis remains speculative, endocrine evaluation and a strict follow-up are strongly recommended.Comment
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Not sure if I mentioned this but I would guess that the PGD2 influence is downstream of the DHT influence in the cascade. I actually don't know if DHT is the trigger or they both contribute but I'd guess they are one and the same pathway. We know that upon observing miniturising follicles under high power magnification there are signs of inflammation. That's got to be important right?Comment
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Albeit DHT is produced in the follicle tissue itself, as well a systemically, it is still technically a systemic hormone. PGD is a local transmitter, so the assumption it is downstream of DHT is fairly solid.
Everything points to hair loss being a chronic inflammatory process.
@2020:
Wikipedia's AGA page has been updated a little:
Sex hormone-binding globulin (SHBG), which is responsible for binding testosterone and preventing its bioavailability and conversion to DHT, is typically lower in individuals with high DHT. SHBG is downregulated by insulin.
Increased levels of Insulin Growth Factor-1 (IGF-1) have been correlated to vertex balding.[18]
High insulin levels seem the likely link between metabolic syndrome and baldness. Low levels of SHBG in men and non-pregnant women are also correlated with glucose intolerance and diabetes risk, though this correlation disappears during pregnancy.[19]Comment
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it can be good and bad.
its probably good for hair growth but bad because of the seb gland overgrowth
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its highley likley and in my opinion, pgd2 is being, locally upregulated for a tottally different reason. Not becuase of dht.
Something else is causing the inflammation, because of the increases in dht.
The increase in pgd2 is your immune system reacting against something.
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PGD2 isn't necessarily an inflammatory agent, though. It's just a message transmitter. Then again, in balding men hair follicles do undergo inflammation, so it matters little.Comment
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then explain how DHT blockers stop that "inflammation" if DHT isn't that important in MPBComment
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