A Completely New View On Hairloss Genetics, Structure And Hormones

enki369

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Oct 24, 2020
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hey everyone l am new to this forum and would love to share my hypothesis on what l believe to cause hair loss sorry if my english is not the best or if this gets long winded, l am 27 and noticed that l was losing my hair at about 22 really fast I was eating terribly at the time but once I started my trade (plumbing) it slowed down massively I think now I'm maybe a norwood 1-1.5 and believe being active and getting more sun has contributed to the slowing down of my hair loss, I've done all the bull**** diets keto, primal and paleo and been trying to peat for about 2 years now and now have a much better understanding of how environment and metabolism ties in with hair loss but as with many people here I always still wondered why some people despite there crap eating never lose there hair while I was being soooo strict and slowly seeing it fall out and going through all the forums and groups like hair guard and danny roddy have hypothesized as to what it might be, I believe there is a genetic occurrence that is strongly influenced by an environmental and nutritional impact let me explain.


l believe now especially on this forum we have a very good understanding of the hormonal implications of hair loss and now people are starting to look int0 the structural aspects like skull expansion and scalp tightness which I believe is a bit of crap as it doesn't explain the full picture, I believe that people that lose there hair have a larger sebaceous area and the follicle bulge and actually holds more sebum than people who don't have hair loss and that the is a relationship between the sebum pressure in the follicle itself and that this increased pressure and retention of sebum is what is causing the inflammation I believe that the bacteria is feeding on this sebum within the follicle and excreting fatty acids filled with estrogens and other destructive inflammatory substances locally in the follicle bulge itself I believe that there is a biofilm making it hard to clean and expel the sebum and bacteria that occurs within the follicle and this causes fibrosis and calcification of the follicle bulge shrinking the follicle space, I believe that areas that have more pressure on the sebaceous gland and hair bulge i.e. the vertex and temples make those follicles subset able to this phenomenon this explains the shape and pattern of baldness along with histamine reactions from the immune system and this very reason it why some people can get away with eating large amount of pufa but still have amazing heads of hair because weather it be genetic or something else they just have smaller sebaceous area in there follicle bulge and this is why women don't lose their hair because men have increased size and density of there sebaceous glands compared to women and not purely dht itself I think people like danny roddy have done an incredible job of explaining the paradoxes with relation to dht, thyroid and steroid hormones which all have a massive impact on the sebaceous glands it also explains why things like Botox have increased hair counts by 18% over 24 weeks similar to finasteride because they blunt the activity of the sebaceous glands and this action and not to what its believed to do stopping scalp tension by relaxing scalp muscles is why it works, l believe tension is a part of it but only because 'gravity' increasing the pressure of the sebum within the follicle bulge itself, unfortunately danny is too invested in peat and his idea that its all to do with metabolism that he has failed to see and connect the structure of the follicle itself with hormones a lot ofpeople say to him why do homeless people have hair and all the eat is the occasional 7eleven pie and drugs to which he only answers its probably because they have less stress COME ON MATE!!! don't get me wrong everything that roddy implies is very important because people with the predisposition of having a larger sebaceous area will lose their hair more quickly if they don't adhere to his protocols because things like thyroid progesterone have links with the activities of sebum production we have to make connections and link all these anomalies together lets take a look at things we know but don't fully understand why
-hamiltons unects had less oily sebaceous secretions
-there is a 4 fold increase in mast cells in the scalps of balding men (l believe is immune reaction from the inflammation from the bacteria within the sebum)
-men have more and larger sebaceous glands and area than women
-it is a observation that men with pattern baldness have bigger sebaceous glands than those without pattern baldness
-yeasts like malassezia that feed on sebum eat the saturated fats and excrete unsaturated fatty acids which end up over the skin causing dandruff and scalp itchiness which is very common in people with pattern baldness
-hormones like dht and progesterone have a big impact on sebum production more dht more sebum, low progesterone more sebum and less control of sebum activity
-there is an increase in dht and pdg2 in the scalps of balding men this l don't know weather its because the bacteria eat the sebum which has a feedback loop of producing more sebum like when you wash your hair too much it increases sebum production so the need for more dht locally in the hair follicle of if the bacteria excretes fatty acids (prolactin's and prostaglandins) which have been shown to antagonize the androgen receptors in the hair follicle
-antifungals have a positive impact on hair growth
-some people slow or stop there hair loss with methods like scalp massage that surposesly removes sebum, but honestly if you ask me your only getting a portion of the sebum out within 10-20mins in a 24 hour day hence why a lot of people calm no positive effects from things like detumescene therapy but hey also remember the guy that did this study as bull$@#tas it is that study he did that study because he observed that the follicles of people with baldness had a thick oily substances cloaked around them.
-treatments like fin and even zix(zinc sulphate and b6) seem to work zinc being used to treat acne and b6 for prolactin
sorry if this is long winded or scattered l have really bad adhd and struggle to clearly express my arguments in clear order this topic has bothered me a lot l will sit with the fact that its because of androgen sensitivity everyone knows that's crap and not logical and l also feel that if its just metabolism, estrogen and prolactin then why do barely any women lose there hair there has to be a link with structure that is influenced by the hormones i still have some more arguments on the idea but like a said it was very hard for me to even write this but l feel this is the most open forum on the idea and the only forum where people can somewhat think clearly as compared with idiots on hair loss forums , still this leaves me with the question though if I am right about this then why some peoples sebaceous area grow larger than others I guess you could say genetics but i really believe there has to be changes locally within the bulge itself and that the whole system is important but it can't really be accurately explained with this alone really think about how some people eat in a way here to keep metabolism high and are sooooo strict and still are losing there hair but some old man in his 60's eats nothing else than grains pufa and smoke but still has his hair danny cant really answer this himself his argument of its all just stress is as easy a statement to say as 'its all just genetics I am sensitive to dht' I also believe the the hair follicle bulge has to be looked at like the gut and that the bacteria and environment within the bulge will also leak out the excreted unsaturated fatty acids into the surrounding tissues and capillaries unfortunately l dont know really what could possibly remedy this condition other than try to eat and live healthy maybe botox could be a possible solution and may conduct a experiment and get 150units injected into my scalp to see the what comes of it in these studies they had a 80% success rate so it couldn't hurt if l do such a thing trust me THERE WILL BE PHOTO'S!!!!!!

whats everyones opinions on this hypothesis?
 

baccheion

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One sign of progesterone (from the testes) deficiency is male pattern balding. Melatonin, a hormone associated with progesterone, peaks just before puberty and then falls until death.

Will it reverse? Unsure. Doubt it. Is it and associated progesterone suppression/decline the source of prevention? Sure.

Many things lead to such progesterone decline. Most commonly adrenal strain/hyperplasia, stress, poor thyroid, broken sleep cycle, etc.
 

Pablo Cruise

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You bit off a lot here mate. Test your hypothesis. I don't know if there are studies comparing sebaceous gland size and scalp bioderm. Hair loss is all about hormones and little of anything else, IMHO. Inflammation, mast cells, sebum, diet, Biotin, etc have little role in AGA. Consider DHT stimulates transforming growth factor beta 1 (TGFß1) which leads to miniaturization of the hair follicle. Inflammation, sebum is symptomatic so SGBH, DHT, Progesterone or whatever else is where the answer is......I feel. When I read studies I see how some have affected a hair growth pathway with chemical or effort. I do not believe WNT agonist or PGE1 is a solution. The genius researchers are following a mechanism but not real causation. Of course I don't have any real answers, just believe the process is corrupted.
 
OP
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enki369

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Changes in the sebaceous gland in patients with male pattern hair loss (androgenic alopecia) - PubMed
there is one study about the increase in size in people with pattern baldness the thing is l cannot answer is why do not 1 but 2 studies have been conducted and via the use of botox injections had a pretty much similar result as finasteride with an 18% increase over 24 weeks and as you can clearly see with the photographs there is regrowth if you try and link together finasteride with botox and maybe see if these two totally different substances and see how they affect the body and their mechanisms of action then l think we have a major piece of the puzzle.

now the people reading this study on botox say "its scalp tension" that's why they had such as increase in hair density and that the increase in oxygen which stops dht which upregulates fibrosis this could be very well true but too me seems hmmmm not the case look at though the other action that botox has on numbing oil production now think about dht's role in the skin oil production because lets not think the skin and hair are not connected dht has a major role in your oil production now that we have the link between botox and finaseride as possibly stopping baldness because of the stimulation of the oils in our skin well now we can start correlating oil production with baldness didn't hamliton observe in the eunuchs they had dramatically less oily secretions? no one has a definite answer on hair loss I have still to this day seen no major photographic evidence of people using pro metabolic protocls and saying they fixed there hair loss I'm sure they exist but they NEVER take to many photos, to think its all hormones imbalance from bad eating lower metabolism, of course!! metabolism is important but that doesn't explain to me why one two of best friends have prediabetes eat a ***t ton of soy are overweight have all sorts of blood pressure problems but wait they have perfect hair!!! the one thing i have noticed and from reading the internet is that they never have dandruff they never get a scalp itch like me and many other people get I really wonder because they is a massive correlation with lower thyroid function and hair loss then whats the difference in people that have low thyroid and have hair? is this not like maybe the most important question of all "what about the people with hormones imbalances prediabetes, smokers that have hair" what makes these people different "Oh there hair is more ressitant to stress come on we have been trying to explain hairloss with hormones forever and what do we have to show for it 2 fda approved mediacations that chemically castrate us or destroy our cardiovascular system

I love the conversation people have here but i feel although maybe that people on this forum are just like the others on hair loss forums and try to explain everything through bloodwork and l really don't think with hair loss that bloodwork like its absolutely everything i think is really important because it influences the structure but the structure of the follicle is really being forgotten and we have all these clues but cant relate them together because its all dht, prolactin, prostaglandins, tfg beta and 1 mmp-9 come on and structure has nothing to do with it? then answer why male patterns baldness happens in a pattern? there has to be some sort of structural element that links things together its obvious just look at how there is a pattern? I really believe that mites living in the hair follicle may have something to do with it too just like having lots of gut bacteria excreting bowel endotoxin I believe that possibly has to do a lot with perifollicular inflammation thats largely ignored and where do these mites live on sebum food for thought what do you think
 

Kenny

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Apr 13, 2020
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wouldnt accutane be the cure then? it dries up your sebaceous glands.

its main side effect is hair loss...
 

czecha

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Nov 8, 2020
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Changes in the sebaceous gland in patients with male pattern hair loss (androgenic alopecia) - PubMed
there is one study about the increase in size in people with pattern baldness the thing is l cannot answer is why do not 1 but 2 studies have been conducted and via the use of botox injections had a pretty much similar result as finasteride with an 18% increase over 24 weeks and as you can clearly see with the photographs there is regrowth if you try and link together finasteride with botox and maybe see if these two totally different substances and see how they affect the body and their mechanisms of action then l think we have a major piece of the puzzle.

now the people reading this study on botox say "its scalp tension" that's why they had such as increase in hair density and that the increase in oxygen which stops dht which upregulates fibrosis this could be very well true but too me seems hmmmm not the case look at though the other action that botox has on numbing oil production now think about dht's role in the skin oil production because lets not think the skin and hair are not connected dht has a major role in your oil production now that we have the link between botox and finaseride as possibly stopping baldness because of the stimulation of the oils in our skin well now we can start correlating oil production with baldness didn't hamliton observe in the eunuchs they had dramatically less oily secretions? no one has a definite answer on hair loss I have still to this day seen no major photographic evidence of people using pro metabolic protocls and saying they fixed there hair loss I'm sure they exist but they NEVER take to many photos, to think its all hormones imbalance from bad eating lower metabolism, of course!! metabolism is important but that doesn't explain to me why one two of best friends have prediabetes eat a ***t ton of soy are overweight have all sorts of blood pressure problems but wait they have perfect hair!!! the one thing i have noticed and from reading the internet is that they never have dandruff they never get a scalp itch like me and many other people get I really wonder because they is a massive correlation with lower thyroid function and hair loss then whats the difference in people that have low thyroid and have hair? is this not like maybe the most important question of all "what about the people with hormones imbalances prediabetes, smokers that have hair" what makes these people different "Oh there hair is more ressitant to stress come on we have been trying to explain hairloss with hormones forever and what do we have to show for it 2 fda approved mediacations that chemically castrate us or destroy our cardiovascular system

I love the conversation people have here but i feel although maybe that people on this forum are just like the others on hair loss forums and try to explain everything through bloodwork and l really don't think with hair loss that bloodwork like its absolutely everything i think is really important because it influences the structure but the structure of the follicle is really being forgotten and we have all these clues but cant relate them together because its all dht, prolactin, prostaglandins, tfg beta and 1 mmp-9 come on and structure has nothing to do with it? then answer why male patterns baldness happens in a pattern? there has to be some sort of structural element that links things together its obvious just look at how there is a pattern? I really believe that mites living in the hair follicle may have something to do with it too just like having lots of gut bacteria excreting bowel endotoxin I believe that possibly has to do a lot with perifollicular inflammation thats largely ignored and where do these mites live on sebum food for thought what do you think
People who are low thyroid and have hair are not masculine, thats the main difference.
How often do you see skinny fat men who are low in hormones have hair loss?
If you want to dry up your sebaceous glands all you need to do is eat extremely low fat. This will also lower all your hormones as fat is an important precursor. I have tried it for a while. Nonexistent sebum suddenly. Low T. Low libido. No hairloss. Zero itch. Depression. Dry skin. Zero acne. Many bowel movements. Loss of beard and body hair. Zero inflammation. Maybe pufa depletion has something do with it as well. It’s an interesting experiment. I wonder if zero fat plus exogenous androgens would make us superhuman but I’m not planning on taking roids
 
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LLight

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The Missing Blood Lipid Excretory System

"In Japan, people started to consume soybean salad oil in 1933. In 5 years these people began to experience lots of abnormal hair loss. Same thing happened in Taiwan: the products entered the market in 1966, and population with excessive hair shedding was increased noticeably around 5 years later. In China, less than 40% of men had baldness before 1984. Salad oil became popular since 1985; now more than 80% of men has baldness, and baldness has become more prevalent among female in China than in Taiwan and Japan. Although overconsumption of high-fat food is the main cause, the destructiveness of sticky plant oil cannot be ignored. The stickiness of these oils becomes more prominent during the process of frying and stir-frying (the two very common Chinese cooking styles), and once getting into human body the oils become a kind of stubborn blood lipid that can’t be cleaned easily.

The fact that the scalp is usually observed to be excessively oily during the initial stage of abnormal hair loss indicates that hair loss is highly related to high level of lipids. Patients diagnosed with cardiovascular diseases have abnormal hair loss sooner or later, and all patients suffering ischemic stroke are bald. In other words, hair loss is the warning sign of high level of blood lipids and cardiovascular diseases.

If one intakes excessive amount of fats and for some reason there is no sufficient pressure on the scalp, blood lipid vesicles will be full of lipids and hair follicles will be choked as well, then blood f low towards the follicles will stop. Without blood supply the hair follicles will atrophy and hair shedding will occur."​
 

LLight

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Activating the FXR and the LXR might have effects on blood lipids.

FXR Activation Increases Reverse Cholesterol Transport by Modulating Bile Acid Composition and Cholesterol Absorption
"Our data indicate that activation of FXR inhibits intestinal cholesterol absorption via modulation of bile acid pool size and composition, thus leading to increased RCT. Targeting hepatic FXR and/or bile acids may be useful for boosting RCT and preventing the development of atherosclerosis."
4β-Hydroxycholesterol Signals From the Liver to Regulate Peripheral Cholesterol Transporters
"The hepatic PXR–circulating 4βHC–peripheral LXR pathway could have important implications for lipid homeostasis. Circulating 4βHC might serve as a signaling molecule informing the extrahepatic tissues about the cholesterol concentration in liver. This notion is supported by the finding in swine that a high-cholesterol diet resulting in doubling of the hepatic cholesterol concentration increased 4βHC 18-fold in serum and 21-fold in cardiac left ventricle (Shimabukuro et al., 2016). LXR agonists are known to activate reverse cholesterol transport (RCT), a beneficial pathway transporting cholesterol from periphery to the liver and intestine for excretion (Temel and Brown, 2015). The activation of LXR and enhanced RCT protects against lipid deposition in vascular endothelium (Lee and Tontonoz, 2015). Therefore, as LXR agonist, the increased 4βHC concentration could be hypothesized to result in the activation of RCT and attenuation of pro-atherogenic actions associated with PXR activation in liver and intestine (Zhou, 2016). Although in vitro experiments indicate that PXR may regulate 25HC and 27HC production, the circulating levels of these oxysterols with important immunologic actions were not increased by rifampicin in vivo.

Although PXR activation by short-term rifampicin dosing did not affect cholesterol levels to a significant degree in our study, the treatment with PXR agonists such as carbamazepine, phenobarbital, and phenytoin is associated with increased HDL while total cholesterol remains constant (Nikkila et al., 1978; O’neill et al., 1982). CYP content of liver biopsy samples correlates with HDL in patients with epilepsy (Luoma et al., 1980), and in psychiatric patients CYP3A activity correlates strongly with HDL (Choong et al., 2013). Phenytoin increased HDL and especially HDL2 but not HDL3, total cholesterol, or LDL in a placebo-controlled parallel trial in patients with low HDL (Miller et al., 1995). Occupational exposure to pesticide lindane, a potent PXR agonist (Kojima et al., 2011), associates with remarkably high HDL concentrations (Carlson and Kolmodin-Hedman, 1972). Thus, there are indirect evidence in humans for the significance of CYP3A activity in cholesterol, and especially HDL, metabolism suggesting that 4βHC may have a role in activating reverse cholesterol transport in vivo. As the half-life of HDL is a few days (Blum et al., 1977), one-week dosing of rifampicin, as in our study, is too short a time period for the full effect of 4βHC elevation on HDL level to be manifested. Of note, 4βHC levels are low in conditions associated with low HDL levels such as metabolic syndrome, obesity, and nonalcoholic fatty liver disease (Tremblay-Franco et al., 2015; Woolsey et al., 2015). Furthermore, women are known to have higher 4βHC and HDL compared with 4βHC and HDL levels in men (Diczfalusy et al., 2011; Wang et al., 2011)."​
 

LLight

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Water restriction could induce the upregulation of the CYP3A4 enzyme in the liver.
This enzyme seems to be able to convert cholesterols into oxysterols (25-hydroxycholesterol and 4β-hydroxycholesterol).

Moreover, these oxysterols are known to be ligands for the Liver X Receptor (LXR).

Farnesoid X receptor is essential for the survival of renal medullary collecting duct cells under hypertonic stress

"Given a ubiquitous distribution pattern of both FXR and TonEBP, they may act in concert in regulating many other biological processes than those involved in the response to hypertonicity in renal medulla.

Similar to TonEBP, FXR may also represent a hypertonicity-responsive gene."
The FXR is hypothesized to be triggered by hyperosmolarity like TonEBP/NFAT5.
 

redsun

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People who are low thyroid and have hair are not masculine, thats the main difference.
How often do you see skinny fat men who are low in hormones have hair loss?
If you want to dry up your sebaceous glands all you need to do is eat extremely low fat. This will also lower all your hormones as fat is an important precursor. I have tried it for a while. Nonexistent sebum suddenly. Low T. Low libido. No hairloss. Zero itch. Depression. Dry skin. Zero acne. Many bowel movements. Loss of beard and body hair. Zero inflammation. Maybe pufa depletion has something do with it as well. It’s an interesting experiment. I wonder if zero fat plus exogenous androgens would make us superhuman but I’m not planning on taking roids

Your hormones are made from cholesterol, not fat. Animal fats can contain cholesterol. Vitamin A dries them out pretty good, too good if you take too much but thats a good thing if you are one of those people with very oily skin and/or acne due to excessive oil. Vitamin B1, B3, B6, zinc, and iron will increase oiliness of the face usually. Maybe for whatever reason when you eat too low fat, more B1 is lost (extra carbs) or you have less intake of certain nutrients such as what I mentioned making it more dry. You likely lack precursors for hormone synthesis and for whatever reasoning reduced fat intake (and thus more carb intake) worsens it and thus low libido, depression, dry skin, etc...
 

baccheion

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People who are low thyroid and have hair are not masculine, thats the main difference.
How often do you see skinny fat men who are low in hormones have hair loss?
If you want to dry up your sebaceous glands all you need to do is eat extremely low fat. This will also lower all your hormones as fat is an important precursor. I have tried it for a while. Nonexistent sebum suddenly. Low T. Low libido. No hairloss. Zero itch. Depression. Dry skin. Zero acne. Many bowel movements. Loss of beard and body hair. Zero inflammation. Maybe pufa depletion has something do with it as well. It’s an interesting experiment. I wonder if zero fat plus exogenous androgens would make us superhuman but I’m not planning on taking roids
Did you ensure sufficient fat-soluble vitamin intake? Were you consuming fruit/fructose for a majority of carbs? Fructose is made into cholesterol.
 

MitchMitchell

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Oct 26, 2020
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wouldnt accutane be the cure then? it dries up your sebaceous glands.

its main side effect is hair loss...

it’s possible that accutane dries it out so much that hair becomes thin and brittle. You still need SOME sebum.

OP’s idea that baldness is consistent with exaggerated in people with high sebum makes sense. Story of my life. When I’m extra careful about avoiding whatever makes my skin oily, hair gets better.

also explains why many guys respond to Dutasteride better than finasteride. Dut blocks 5ar type 1 not just 2&3 like fin. Testosterone (not DHT) binding to receptors should yield less sebum. But not zero like accutane.
 

Ras

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It should be possible for an algorithm to predict hairloss. Put it into an adequate computer and give it enough data on correlations, and it should find what produces common alopecia. If we knew everything knowable, we would see a line connecting the dots: if this, then that. Ancient man knew when to harvest the best wood. Correlation is not always causation, but there can be no causation without correlation. Under God, cause and effect is all in all.
 
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Kenny

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It should be possible for an algorithm to predict hairloss. Put it into an adequate computer and give it enough data on correlations, and it should find what produces common alopecia. If we knew everything knowable, we would see a line connecting the dots: if this, then that. Ancient man knew when to harvest the best wood. Correlation is not always causation, but there can be no causation without correlation. Under God, cause and effect is all in all.
Reminds me of this:
Artificial Intelligence Finds New Drug To Treat Hair Loss

I wouldn't hold my breath on this though.
 
OP
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enki369

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l think lack of sebum could expose you to dry skin and fungus but too much will also be the case, but lately l am starting to read up about demodex and am starting to think that these could be a massive player there is little understanding on these little suckers they are suspected for host of skin issues, they feed on the sebum, there usually start to occur on people from the ages of 20-30, they occur more in men than women, they live in the sebaceous gland and around the follicle, there lifespan is 2 weeks and some make a month in which they die and "melt" in your follicle or sebaceous gland up to 25 can live in one follicle!!! and we are talking about hormones how big is a demodex mite to even the size of a cell? and this thing is living in your follicle, eating your sebum, excreting in your follicle (l wonder how much of the $h1t turns to mold and fungus), laying eggs in your follicle hell even shagging in your follicle!!!! and to die and melt in your follicle. Demodex is seen to be as relatively harmless but we live in a society where finasteride is safe, sugar is poison, omega 3 is healthy is it that simple yet that complicated that baldness could be a long term mange demodex are very hard to permanently control, what if finasteride was just slowly control there populations by controlling sebaceous secretions cutting short there food supplies, that's why when people get off finasteride they lose their hair quick because of the androgen receptor becoming more sensitive and gives and explosion of sebum which in turn feeds the demodex, people with larger pores in their scalp are more susceptible because of the area for the mites to live and also to feed as the pore is a larger storage for sebum and through people with a predisposition of having larger pores through the lack of quality nutrition have the constant attack of free radical damage from unsaturated fats create moments of oily explosions in which the mites come and take host this could also explain how they say you find a buildup of dht around the follicle of balding men the mites constantly eating your sebum is like when you wash your hair of all the oils you create a feed back loop causing your hair to be more oily maybe dht is getting buildup in this area because the need keep enough sebum to stop your skin from going dry think about this how does your body know that it has mites? it now it needs so much sebum for keep your skin in some balance but is producing excess in a feedback loop just to feed these mites in which that sebum turns to excrement!!! and this constant attack is what ultimately causing fibrosis of the follicle l have read of some peoples accounts of clearing demodex from there scalp and having their hair grow back and the explosions of when they die are in the exact shape of their hairline and how they tried in vain to tell there friends I could only find two accounts and you also have to wonder about the legitimacy of anything on the internet but l wonder if its been something this simple yet complicated, demodex cause a lot of immune responses as well maybe this could also explain the accumulation of mast cells in the scalps of balding men. All accounts l have read of people getting rid of their demodex said that it took months they had bad eruptions in the skin probably the mites dying off in the follicle but once it cleared there hair (eyelashes, eyebrows and beard normally because no one really does the scalp) grow back much thicker and stronger faster and it all ties in and makes some sense why would it not you would be taking major inflammation out of the ACTUALL FOLLICLE!!! so l am going to try to really rev up my metabolism get co2 up and try get rid of what possible mites l have and see my results I will share whatever photos I have
 

lvysaur

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l am 27 and noticed that l was losing my hair at about 22 really fast I was eating terribly at the time but once I started my trade (plumbing) it slowed down massively I think now I'm maybe a norwood 1-1.5 and believe being active and getting more sun has contributed to the slowing
Same thing happened to me

Exercise improves endotoxin elimination. Might have something to do with it.
 

Orion

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Oct 23, 2015
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I killed those bastards (on my face) with zz cream. Looks like they sell a shampoo too. Might be worth a try

Nice. Most would probably like something with less ingredients, but zinc oxide looks like the best safe option. Too bad it is insoluble in water, making a spray would be best. But it is soluble in oils, maybe coconut oil/ZnO cream.
 

MitchMitchell

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Honestly the more I think of what’s causing hair loss the more I’m blaming a host of factors that ultimately send androgen and/or estrogen receptors sensitivity through the roof, or over activation of those receptors. Could be xenoestrogens (SERMs common side effect = hair loss...), could be whatever increases prolactin which increases androgen receptor density locally, could be local inflammation that triggers more E2*DHT, and so on.

Looking at who’s got perfect hair pretty much always... children. No cortisol, no androgens, no estrogens, prepuberty (=castrate) levels. Extremely rare hypothyroidism. Very strong antioxidant system. Nearly impossible to recreate?

Thyroid to slow down the pituitary and adrenals + topical solutions?
 
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