Why haven’t one of you High-Functioning autists solved hair loss?
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Depends on how you understand it. The reason is not, but the process speeds up.
@Te1963 I think that indeed demodex are responsible of acne.
Every time I see a person with hairloss in front or temples they have a shiny forehead - excess of sebum. So it could be either something in sebum or demodex. But I've also seen claims that DHT caused hair cells apoptosis in vitro. Would be interesting to know if people with high DHT but low sebum secretion lose hair.
To avoid misunderstanding, my body's response in rosacea, i.e increased blood flow to face was actually benefiting to hair. It's when rosacea started to improve that hairloss worsened.
Every time I see a person with hairloss in front or temples they have a shiny forehead - excess of sebum. So it could be either something in sebum or demodex. But I've also seen claims that DHT caused hair cells apoptosis in vitro. Would be interesting to know if people with high DHT but low sebum secretion lose hair.
To avoid misunderstanding, my body's response in rosacea, i.e increased blood flow to face was actually benefiting to hair. It's when rosacea started to improve that hairloss worsened.
I was actually investigating the factors involved in hair cell apoptosis early on, when I started posting on this thread. It was a whole pattern of biochemical signaling leading from allergy, mast cell activation, prostaglandin D2, bone demineralisation, bone marrow stromal cell differentiation (involving production of fibroblasts and keratinocytes used in the scalp), DHT, etc. The various caspase enzymes which eventuated in the process generally trigger the apoptosis in hair cells. That was why I generally view alopecia as one of the many alternatives the body has to preventing the development of cancer. Given that various treatments have different responses in each case it strikes me that not all cases involve precisely the same pattern of factors. One person can fix a single issue and completely restore their hair while another fixes the same issue and nothing happens. Whether this involves allergy, blood flow, bone marrow (and stem cell differentiation), or something else, seems to depend upon each case I have read about.
As for the rosacea; I understood that curing it appeared to induce the alopecia. However, since demodex actually feed on our hormones I think that it might be possible that a large enough 'colony' of them, wherever your rosacea was, might have been able to reduce your hormone levels to the point where it wasn't feeding demodex in your scalp. Of course, it's still possible that there might not have been demodex in your scalp and that the raised hormones might be inducing another series of biochemical reactions such is generally speculated on. I assume that the hormones trigger growth and sexual replication of the mites, leading to demodicosis if they are in a host with high enough hormone levels. The fact that people experiencing alopecia tend to have higher percentages of androgen receptors than other people raises some questions though. NR3C4 'receptors' bind to hormones which enter cells and carry them into the nucleus of cells. Assuming that demodex were responsible for hair loss it might be possible that they aren't just feeding upon the hormones but also the receptor peptides. In theory, the more peptides they absorb the greater the effect of any hormones they feed on. I will try to look into whether there are natural agonists for these peptides; there usually are.
None of this is simple. I've read that not oils will clog the pores. One oil which gets my attention though is coconut oil. Even though demodex doesn't seem to feed on the various fatty acids which comprise it the oil can still clog the pores of the skin, leading to similar issues as we experience. This indicates to me that demodex mites don't have to be involved in every case of oily/shiny scalp. I have also been trying to correlate various treatments for alopecia with the possibility of demodex. Some can be very hard to connect. Baking soda has been used, successfully, to treat both alopecia and demodex. Apparently, it weakens their protective shells. Tea tree oil has been used, successfully, to treat both things; it kills demodex in just minutes though is best mixed with another oil to prevent inflammation or damage.
poppinz, I had to go into google scholar to find the right research to explain your loss of hair after treatment of the rosacea/demodex. Demodex induces vascular endothelial growth factor (VEGF). You will find this under the heading Rosacea: an inflammatory continuum in this article. https://link.springer.com/article/10.1007/s13555-020-00458-9 VEGF is already being sold, under the name Anastim, for hair growth. https://www.gourmetstylewellness.com/news/treatments/vegf-now-available-hair-loss-treatment/ Curing the demodex infection probably eliminated the stimulation of that inflammatory pathway. On the plus side you should be aware that ending the VEGF signaling has likely reduced your risks of developing cancer. VEGF signals for the development of new blood vessels (angiogenesis). Another name for this, once it becomes too prolific, is cancer. https://pubmed.ncbi.nlm.nih.gov/16301830/
@Te1963 I think you go a little fast in conclusions. The improvement of my rosacea had nothing to do with treating demodex. I'm inclined to believe that demodex are not the cause of rosacea (as of now there is no consensus on what causes this disorder). Also I wouldn't think angiogenesis leads to cancer, I've lived with increased angiogenesis for more than 10 years with no sign of cancer. It is a hard to live condition, however as a side effect it protected me from hairloss.
Apparently demodex get their steroids from people (probably by eating our sebum?) I doubt however that this could have some effect on people's hormone levels. But than that would make sense that their population must be much greater in men than in women.
Apparently demodex get their steroids from people (probably by eating our sebum?) I doubt however that this could have some effect on people's hormone levels. But than that would make sense that their population must be much greater in men than in women.
poppinz, I learned a long time ago that the older an expert is, in any profession, the more likely they are to have entrenched idea's on their speciality. This isn't a set pattern, and there are exceptions, but it's enough to mean that it can take ten to twenty years before new products or idea's go from development to mainstream use. This also occurs in medical practice and many concepts which have already become accepted among mainstream medical researchers can take decades before they are accepted by practicing physicians.
Before I decided whether demodex was the most likely cause of rosacea I did the search on google scholar, typing in 'rosacea demodex 2022'. There are actually a surprising number of results and they all seemed to be operating along the same conclusion; that the same products treating rosacea also appear to be effective in treating demodex, eg; https://www.tandfonline.com/doi/abs/10.1080/09546634.2020.1770168 This isn't conclusive evidence but things which are generally accepted as science fact in one decade are often discredited in the next. Science operates along the principle of treating currently accepted idea's as the facts until proven otherwise. It often requires a new generation to become experts in their fields for those facts to change. I don't know about you but I would rather find my answers on hair growth and health a little faster than a decade or two. That generally means forming a hypothesis based upon the best available information; best guesses!
I understand what you mean about angiogenesis. In response to hypoxemia, the cells in my body have produced an enzyme called threonyl tRNA synthetase for nearly ten years. It induces angiogenesis. However, my body has also produced PL-7 antibodies, which destroy that enzyme in order to try to prevent it from resulting in cancer. If I hadn't been tested for a form of autoimmune myopathy I would never have known this was happening. Nothing is ever simple when it comes to how the body works.
As for where the demodex obtain the hormones from, I have read accounts detailing feasting on live skin cells, hair, and sebum. https://my.clevelandclinic.org/health/diseases/22775-demodex-face-mites I found one study, of a single case of sebaceous filament (the kind of hardened sebum which you might be able to squeeze from pores at the end of the nose) where the analysis of the sebum included evidence of demodex tails. I'm uncertain how many studies have actually investigated the composition of such filaments to this level of attention. Since demodex die and decompose in the pores, becoming part of the sebum, it might indicate that this plays a role in that hardening and clogging of pores in many cases. Demodex do not excrete anything they eat during their two week lifespan. This means that, when they die, there are a lot of unknowns regarding their potential toxicity within our pores, particularly if skin cells continue to be damaged by other demodex. I am still convinced that the hardening of sebum, alopecia, bone demineralisation, and issues with bone marrow stromal cell differentiation, are all part of the same picture. What I also believe is that many different causes can contribute to resulting in the same disease picture, whatever that happens to be. Since you suggested that demodex might have an involvement I have tried to understand which toxins they might contribute to the picture but, unfortunately, there is still a huge amount which isn't known about them despite it being over a hundred and fifty years since their discovery. I have found very little about their biochemical makeup and have been forced to assume that they might be similar to dust mites, which are well researched. This allows speculation on what toxicity they might have to cells but it really is just guesswork; the reason that I haven't posted it.
Before I decided whether demodex was the most likely cause of rosacea I did the search on google scholar, typing in 'rosacea demodex 2022'. There are actually a surprising number of results and they all seemed to be operating along the same conclusion; that the same products treating rosacea also appear to be effective in treating demodex, eg; https://www.tandfonline.com/doi/abs/10.1080/09546634.2020.1770168 This isn't conclusive evidence but things which are generally accepted as science fact in one decade are often discredited in the next. Science operates along the principle of treating currently accepted idea's as the facts until proven otherwise. It often requires a new generation to become experts in their fields for those facts to change. I don't know about you but I would rather find my answers on hair growth and health a little faster than a decade or two. That generally means forming a hypothesis based upon the best available information; best guesses!
I understand what you mean about angiogenesis. In response to hypoxemia, the cells in my body have produced an enzyme called threonyl tRNA synthetase for nearly ten years. It induces angiogenesis. However, my body has also produced PL-7 antibodies, which destroy that enzyme in order to try to prevent it from resulting in cancer. If I hadn't been tested for a form of autoimmune myopathy I would never have known this was happening. Nothing is ever simple when it comes to how the body works.
As for where the demodex obtain the hormones from, I have read accounts detailing feasting on live skin cells, hair, and sebum. https://my.clevelandclinic.org/health/diseases/22775-demodex-face-mites I found one study, of a single case of sebaceous filament (the kind of hardened sebum which you might be able to squeeze from pores at the end of the nose) where the analysis of the sebum included evidence of demodex tails. I'm uncertain how many studies have actually investigated the composition of such filaments to this level of attention. Since demodex die and decompose in the pores, becoming part of the sebum, it might indicate that this plays a role in that hardening and clogging of pores in many cases. Demodex do not excrete anything they eat during their two week lifespan. This means that, when they die, there are a lot of unknowns regarding their potential toxicity within our pores, particularly if skin cells continue to be damaged by other demodex. I am still convinced that the hardening of sebum, alopecia, bone demineralisation, and issues with bone marrow stromal cell differentiation, are all part of the same picture. What I also believe is that many different causes can contribute to resulting in the same disease picture, whatever that happens to be. Since you suggested that demodex might have an involvement I have tried to understand which toxins they might contribute to the picture but, unfortunately, there is still a huge amount which isn't known about them despite it being over a hundred and fifty years since their discovery. I have found very little about their biochemical makeup and have been forced to assume that they might be similar to dust mites, which are well researched. This allows speculation on what toxicity they might have to cells but it really is just guesswork; the reason that I haven't posted it.
VEGF is already a treatment option for alopecia, with Minoxidil inducing it's expression and Anastim containing it. What I have been looking at is how it induces stromal cell differentiation into blood vessel cells; https://pubmed.ncbi.nlm.nih.gov/28352314/ This is likely to be the connection between the bone marrow/bone demineralisation issues, which I mentioned early on, and the development of alopecia. There is a fine balance in VEGF signaling, inducing healthy blood flow on one side and inducing cancer development (angiogenesis) on the other. Our bodies have a number of methods to try to maintain this balance but it can get the balance wrong, leading to other diseases, including alopecia; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5562355/ VEGF signaling doesn't just work to induce the development of blood vessels but also induces vasodilation, bringing blood flow to under-nourished tissues. https://pubmed.ncbi.nlm.nih.gov/25310988/ Phosphatases modulate this VEGF signaling; https://pubmed.ncbi.nlm.nih.gov/27888154/ This is how ceramide appears to affect VEGF signaling; https://pubmed.ncbi.nlm.nih.gov/24606881/ Synthetic ceramide is also being investigated for increasing sphingosine and sphinganine levels in hair; https://pubmed.ncbi.nlm.nih.gov/28711498/ However, it appears as though ceramide synthase 4 is going to be the really interesting product which could really help us. It not only affects stromal cell differentiation but also modulates hair follicle cycling. https://pubmed.ncbi.nlm.nih.gov/25705848/
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Vegf? Veganfuck?
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Well you better get in the mood BOYO
IGF-1 (insulin growth factor-1) is another signaling molecule which affects all of the factors which I have discussed. Bone demineralisation, stromal cell differentiation, hair loss, VEGF (vascular endothelial growth factor) levels, etc. In conditions such as coeliac disease both IGF-1 and VEGF levels decrease, due to lack of available nutrients. There are actually quite a lot of dietary and lifestyle factors which can affect IGF-1 levels. https://www.optimallivingdynamics.com/blog/increase-insulin-like-growth-factor-igf-1-levels Similar for VEGF; https://youarethehealer.org/mold-an...d-illness/vascular-endothelial-growth-factor/
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Hello Janey
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Why haven't one of you high-functioning autists solved hair loss?
That is another puzzling fact which is explained by my alternative theory of hair loss:
If hair loss is actually a form of autism, curing hair loss might also cure all of autism. The high-functioning autists don't want that because they don't want their kind to go extinct.
That is another puzzling fact which is explained by my alternative theory of hair loss:
My theory: Hair loss is actually a form of autism.
Evidence: Whenever I see one of those hair transformations on YouTube, be it hair systems or hair transplants or whatever, before I always think "This dude looks like he has severe autism.", while after I think "There's a handsome young chap" .
I expect that the human brain is good at spotting patterns and that our intuitions are truth-tracking. (Otherwise, we are left with philosophical skepticism.) Therefore, based on my pattern-recognition and intuition, I conclude that hair loss and autism are actually the same thing, somehow.
Change my mind.
If hair loss is actually a form of autism, curing hair loss might also cure all of autism. The high-functioning autists don't want that because they don't want their kind to go extinct.
Regan, That might correlate in many cases. I lost my hair early, decades ago in my late teens, and have long described myself as being low on the autism spectrum. Functional enough that I can fit in without problems but dysfunctional enough not to remain connected to people; just can't work them out. In my case it was likely to have been coeliac disease. However, it can't explain some cases. I'm fairly sure that some people, who develop full body hair loss, simply lack a sufficient number of some type of receptors. That makes it a genetic condition which doesn't relate to VEGF and IGF-1 levels. I don't know how much you know about genetic mutations but a lot of different toxic exposures can induce mutations. The body can only try to repair these mutations at a set pace so the exposures can be overwhelming for the body and they can become the norm, rather than the exception. So late onset of a mutation could result in alopecia simply due to the bodies inability to detect certain signaling.
On the other hand; coeliac disease might be an example of a mutation which has developed in an ancestor and been inherited. Coeliac disease has been connected, by researchers, to autism. https://pubmed.ncbi.nlm.nih.gov/19564647/ Since coeliac connects VEGF and IGF-1, along with other signaling, it might relate to your speculation.
However, I am currently wondering whether dairy may be a major factor as well. 6-sialyllactose is a compound found in both human and cow milk. It has been found to suppress VEGF-mediated angiogenesis; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6774418/ A link between dairy and autism has posited by a huge number of people and yet there appears to have been no research performed to try to prove or disprove the idea. That might be due to potential dairy industry backlash against such research. As for a connection between dairy and IGF-1 it could be recombinant bovine somatotropin. This is injected into cows, in order to increase milk production. However, it greatly increases IGF-1 levels in the milk. https://www.veganlifestylecoach.com/news/2017/5/27/dairy-igf-1-insulin-like-growth-factor-1 This is purported to relate to excessive angiogenic effect and the development of cancer. Alopecia relates to low levels of both VEGF and IGF-1 so the body might respond to excessive intake of IGF-1 by producing antibodies to it. Of course this is just speculation. However it might help to explain the adaptive response which occurs to many of the treatments for alopecia. Strangely, although IGF-1 antibodies are sold by companies as treatments for cancer there appears to be almost no medical research available to the public upon them.
On the other hand; coeliac disease might be an example of a mutation which has developed in an ancestor and been inherited. Coeliac disease has been connected, by researchers, to autism. https://pubmed.ncbi.nlm.nih.gov/19564647/ Since coeliac connects VEGF and IGF-1, along with other signaling, it might relate to your speculation.
However, I am currently wondering whether dairy may be a major factor as well. 6-sialyllactose is a compound found in both human and cow milk. It has been found to suppress VEGF-mediated angiogenesis; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6774418/ A link between dairy and autism has posited by a huge number of people and yet there appears to have been no research performed to try to prove or disprove the idea. That might be due to potential dairy industry backlash against such research. As for a connection between dairy and IGF-1 it could be recombinant bovine somatotropin. This is injected into cows, in order to increase milk production. However, it greatly increases IGF-1 levels in the milk. https://www.veganlifestylecoach.com/news/2017/5/27/dairy-igf-1-insulin-like-growth-factor-1 This is purported to relate to excessive angiogenic effect and the development of cancer. Alopecia relates to low levels of both VEGF and IGF-1 so the body might respond to excessive intake of IGF-1 by producing antibodies to it. Of course this is just speculation. However it might help to explain the adaptive response which occurs to many of the treatments for alopecia. Strangely, although IGF-1 antibodies are sold by companies as treatments for cancer there appears to be almost no medical research available to the public upon them.
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Janey
I tracked the connection between bone marrow stromal cell differentiation, angiogenesis, fibroblasts, and keratinocytes, etc, down to GHK-cu (glycyl-L-histidyl-L-lysine). Again, it is already marketed as a hair loss product. Truly an amazing copper dependent peptide with all of its effects on the body; http://skinbiology.com/copper-peptides-stem-cells.html https://www.peptidesciences.com/blog/what-is-ghk-cu-and-how https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4180391/
It's possible that the reason that excess copper relates to cancer might involve GHK-Cu due to the angiogenic effect of the peptide.
The way that this appears to work, aside from proliferation of blood vessels, is that anything which damages the skin induces TGF-beta (transforming growth factor) signaling in order to repair the tissues. This is the reason that conditions such as dermatitis are involved in hair loss. Anyway, the TGF-beta signaling turns off keratinocyte activity and affects the growth of hair; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7072438/ There are actually quite a fair few natural ways to inhibit TGF-beta and ceramide turns out to be one of them. https://www.frontiersin.org/articles/10.3389/fphar.2019.00715/full
It's possible that the reason that excess copper relates to cancer might involve GHK-Cu due to the angiogenic effect of the peptide.
The way that this appears to work, aside from proliferation of blood vessels, is that anything which damages the skin induces TGF-beta (transforming growth factor) signaling in order to repair the tissues. This is the reason that conditions such as dermatitis are involved in hair loss. Anyway, the TGF-beta signaling turns off keratinocyte activity and affects the growth of hair; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7072438/ There are actually quite a fair few natural ways to inhibit TGF-beta and ceramide turns out to be one of them. https://www.frontiersin.org/articles/10.3389/fphar.2019.00715/full
It turns out that the connection between TGF-1 and hair loss is likely to involve the fact that fibroblasts and keratinocytes commence as bone marrow stromal cells (stem cells). TGF-1 signaling can instruct such cells to return to being stem cells in order to repair tissue damage in the region; https://pubmed.ncbi.nlm.nih.gov/19153598/ https://www.researchgate.net/public...nchymal_transition_in_epidermal_keratinocytes One of the treatments for alopecia involves injection of fibroblast cells into the scalp. This appears to indicate that the experts understand that the signaling induces loss of these cells from the scalp, induced by their reversion to stem cells. Sonic hedgehog signaling regulates this conversion, for better or worse. Many past treatments for hair loss would never have worked because they lacked the fibroblast or keratinocyte cells required for producing hair. It's likely that the degree of reversion of these cells affects the level of difficulty we experience in trying to restore hair growth. My own focus, at the moment, is upon a range of topical or dietary factors which can reduce/inhibit TGF-1 signaling.
Since I can't find any articles on this on this forum it is worth knowing that an article, published several years ago, documented a 13 year old girl suffering from alopecia totalis since the age of 2 who experienced complete hair regrowth after taking a medication called dupilumab as treatment for eczema. https://www.webmd.com/skin-problems...uld-eczema-drug-restore-hair-lost-to-alopecia A quick check of this medication informed me that it inhibits interleukin-4 and interleukin-13 in the body. Another quick check led me to finding that both of these are involved with osteoblasts (bone forming cells) and stimulating their production of interleukin-6. https://pubmed.ncbi.nlm.nih.gov/11248656/ Surprisingly, interleukin-6 is supposed to trigger hair growth phase; https://pubmed.ncbi.nlm.nih.gov/16757150/ However, it is known to inhibit elongation of hair follicles; https://pubmed.ncbi.nlm.nih.gov/21881585/ Prostaglandin D2 signaling, involved in allergic reactions, is known to induce interleukin-6 expression, so resulting in hair loss.
I strongly suspect that alopecia areata is the result of a poor signaling mechanism between osteoblasts and fibroblasts. Both of these types of cells express interleukin-6. In osteoblasts this signaling is suspected of inducing bone formation; https://pubmed.ncbi.nlm.nih.gov/16112634/ Interleukin-6 is actually integral to function of bone marrow; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6333051/ In fibroblasts it appears to induce a range of different effects, including stimulation of hair growth phase. As my own focus is currently upon attempting to induce hair growth using a cheap ceramide cream I have been researching a lot of different articles on how or why this might occur. What I have been finding is that ceramide appears to inhibit interleukin-6 expression in osteoblasts, https://pubmed.ncbi.nlm.nih.gov/10400316/ while inducing interleukin-6 expression in fibroblasts, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2192147/ Research has been focusing upon specific ceramides, which tend to be expensive, yet I suspect that the form of ceramide may not be as essential as is being posited.
I strongly suspect that alopecia areata is the result of a poor signaling mechanism between osteoblasts and fibroblasts. Both of these types of cells express interleukin-6. In osteoblasts this signaling is suspected of inducing bone formation; https://pubmed.ncbi.nlm.nih.gov/16112634/ Interleukin-6 is actually integral to function of bone marrow; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6333051/ In fibroblasts it appears to induce a range of different effects, including stimulation of hair growth phase. As my own focus is currently upon attempting to induce hair growth using a cheap ceramide cream I have been researching a lot of different articles on how or why this might occur. What I have been finding is that ceramide appears to inhibit interleukin-6 expression in osteoblasts, https://pubmed.ncbi.nlm.nih.gov/10400316/ while inducing interleukin-6 expression in fibroblasts, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2192147/ Research has been focusing upon specific ceramides, which tend to be expensive, yet I suspect that the form of ceramide may not be as essential as is being posited.
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its been 30 years since the last hair loss cure came to market and it was found on accident. 30 YEARS