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Male Pattern Baldness
Quote from tim on June 28, 2020, 4:58 amThanks for responding.
Be careful not to confuse vA with Hypervitaminosis A which I was discussing. Hypervitaminosis A definitely causes balding, it's an established symptom. I'm just trying to understand why not if.
What I meant was that possibly there could be other underlying conditions that can cause vitaminosis A with less vitamin A consumption than the average. I’m just thinking we can’t have all the same tolerances and that other factors may be involved.
I was losing my hair since high school, hair line fading and follicle hurting.
I think that there are many factors in it, with different people having different proportions of them. For me it has started definitely from Accutane - so compatible with hypervitaminosis A. Blood thickness plays a big role in my opinion in it too. As for muscle tension mentioned in the article I think it comes not from bone expansion, but from losing of scalp/skull adipose tissue, and as they say probably androgens and stress tend to keep muscles tight. Right gut bacteria is important too (maybe for producing vitamins or lowering inflammation) Sorry for being gross, when I have well formed stools (most of time I don't) I have less hair loss (or some regrow) .
I have many of those conditions, Mold and bacteria gut issues, probably thick blood from high iron(?), and lots of stress all my life as well as many other conditions - many if not all of symptoms of mercury toxicity - i really want to include hyper vitaminosis A as a symptom as well 😁 but it’s all my speculation
Blood thickness plays a big role in my opinion in it too.
Viscosity and/or coagulation? What do you think are the causes behind this?
Leech therapy has a lot of promise here. Perhaps scalp massages to loosen the galea as well as using leeches on the scalp could help a lot while one implements all the dietary and lifestyle factors one can to reduce inflammation in the scalp and get blood back to normal.
Having a low VA diet long term along with sufficient Vit K should help reduce calcification too.
When I look back at my baby photos it appears that I've always had a MPB hairline, LOL. And, the little girl that I used to know who had mysterious migraines like my own... She seemed to have it as well. Her case went on to alopecia at one point, although it went into remission, thankfully.
I wonder if blood "thickness" has something to do with the raynaud's syndrome that I sometimes get. (ie, white and blue areas in the extremeties) (example from the interwebs: not my photo, not my hands). It is a thing that often accompanies diseases like lupus that I like to think of as being caused by VA overload.
Quote from tim on June 28, 2020, 6:07 pmBlood thickness plays a big role in my opinion in it too.
Viscosity and/or coagulation? What do you think are the causes behind this?
I'd say viscosity, but it's just a layman opinion. The last time I gave blood sample, it didn't want to come out, the nurse had to give little taps on the vein. Maybe too much iron from all that beef?
I also watch a youtube channel (in russian) where a guy observes his blood on microscope after different things , and there are quite a few that affect viscosity negatively (as he says erythrocytes glue to each other and form chains) , like sugar, coffee, don't remember everything. Another interesting (not related to topic) thing he noticed is that no matter conditions, what he thinks is blood bacteria disappears at 3 a.m.
@lil-chick , I had raynaud (not that bad as on the photo) diagnosed even before taking Accutane, looks like raynaud and rosacea go together often.
Some more thoughts on MPB and vA:
As men age testosterone lowers and estrogen (produced by aromatase from testosterone) and DHT (produced by 5-alpha-reductase from testosterone) go up. This is likely as a result of developing Hypervitaminosis A as we age. Excess retinoic acid increases aromatase activity. It possibly also increases 5-alpha-reductase activity in the skin. Excess retinoic acid depletes riboflavin which is a 5-ar inhibitor. Excess retinoic acid depletes zinc which is a 5-ar inhibitor.
Excess retinoic acid depletes K2, K2 deficiency causes calcification of skull foramens and in the scalp. K2 deficiency causes atherosclerosis too which can affect scalp microvasculature thus reducing hair follicle blood supply.
Very promising...
2.3 Retinoids in the hair follicle
Studies with transgenic mice support a role for RA in the hair follicle. Both a reduction in RA signaling (Krt14 & Krt5 Cre Rxratm4Ipc null mice) and an excess of retinol and atRA (Krt14 Dgat1tm2Far null mice) within the basal epidermis and outer root sheath led to progressive alopecia [6, 86, 87]. Blocking RA signalling (Rxratm4Ipc null mice) delayed anagen initiation, while increasing retinol and atRA (Dgat1tm2Far null mice) accelerated the transition from telogen to anagen. This increased anagen induction and alopecia could be reduced in Dgat1tm2Far null mice by severely reducing dietary vitamin A intake. RXR partners with many nuclear receptors and these effects were originally attributed to its partnering with the vitamin D receptor (VDR), as Vdrtm1Mbd null mice have similar progressive alopecia and anagen inhibition [88, 89]. While it is unlikely that the effects of reduced DGAT1 lead directly to altered vitamin D metabolism or signalling, as they could be reversed by altering dietary vitamin A, an indirect effect of excess vitamin A on vitamin D metabolism or signalling in the hair is possible as interactions between these two vitamins have been seen [90–92]. These Rxratm4Ipc null mice also have elevated proliferation and defective differentiation in IFE and increased inflammation, which were not seen in Vdrtm1Mbd null mice [93], suggesting other RXR partners are involved. Exogenous atRA also induced catagen in cultured hair follicles [94]. In addition, exogenous atRA with BMP directed the differentiation of embryonic [95] and induced pluripotent stem cells into keratinocytes that when grafted into nude mice produced normal epidermis, hair follicles, and sebaceous glands [96]. Transgenic mice that overexpress a dominant negative Rara targeted to the epidermis have aberrant skin, no hair or wrinkles and die shortly after birth [97, 98]. These mice have reduced epidermal barrier function due to defects in lipid metabolism [98, 99]. These effects were not seen in mice that overexpress a dominant negative thyroid receptor [97] or Rxr [100] in the epidermis. In addition, VDR responses were not altered by dominant negative Rara expression, suggesting that these effects are specific to RAR and RA signaling and not other partners of RXR. A similar defect in lipid metabolism and epidermal barrier function was seen in epidermal (Krt14CreERT2) and suprabasal (CMV-CreERT) targeted Rargtm3Ipc null mice [47], although an initial report of epidermal (Krt5) targeted Raratm3Ipc and Rargtm3Ipc double null mice failed to see this effect [101]. No studies have examined epidermal or hair follicle specific Rarb null mice or triple Rar null mice as it was assumed that RARB was not important in the epidermis, as it was not expressed in the nucleus [101] and no skin or hair defects were seen in the original Rarbtm1Ipc null mice [102]. Yet weak expression of RARB was seen in the follicle keratinocytes [103] and we saw cytoplasmic only localization of RARB in the basal epidermis, sebaceous gland, outer root sheath, and hair follicle bulge [24]. In addition, RARs may be important in other cells within the PSU that do not express Krt14 or Krt5. Combined, the results from these studies suggest that atRA alters stem cells to regulate the hair cycle at both the telogen to anagen and anagen to catagen transitions, as well as regulate lipid metabolism in the IFE to maintain epidermal barrier function, but not all of the receptors responsible or specific mechanisms have been elucidated.
Several reports have localized components of RA synthesis and signaling to the hair follicle in various or unknown stages of the hair cycle [23, 103–106]. To obtain a more complete picture, we localized a whole system of retinoic acid synthesis and signaling proteins to the hair follicle, including all seven stem cell regions (Figure 3, [24, 107]). This localization pattern changed throughout the hair cycle with a peak occurring during mid-anagen through early catagen. We have confirmed this pattern of RA synthesis during mid-anagen using RA reporter mice (Tg(RARE-Hspa1b/lacz)12Jrt/J made by [108]; Figure 3c). RA synthesis was present in the cells of the sebaceous gland duct, the site of BLIMP1+ stem cells, and throughout the whole isthmus, site of MTS24, LRIG+, UI, and LGR6+ stem cells, during mid-anagen (Figure 3b, Red). Topical atRA induced LRIG+ cells to expand and give rise to cells in the sebaceous gland, infundibulum, and IFE [77]. Thus, endogenous RA synthesized within the isthmus may be important for the maintenance of the sebaceous gland, infundibulum, and IFE. In addition, wounds heal faster when hair follicles are in anagen [109], thus the peak of RA synthesis within the isthmus during anagen may also contribute to better wound healing. RA synthesis also localized to the bulge region during mid-anagen (Fig 3c) and some RA synthesis enzymes and binding proteins remained in the bulge throughout the hair cycle ([24], Fig 3a,b). RA synthesis enzymes (DHRS9 and ALDH1A2) and RARA, B, and G localized to proliferating keratinocytes as they migrated downward during early anagen, and RA synthesis was seen in the outer and lower cells of the bulb, where LGR5+ stem cells also localized [24, 81]. During late anagen/early catagen there was a drop in the expression of RARs within the bulb and an increase in CRBP, suggesting a role in catagen induction. These localization patterns suggest that RA may also play a role in the maintenance of hair follicles and its cycle. Together, the results from these studies suggest that endogenous RA may be important for all of the stem cells in the hair follicle and the maintenance of the hair follicle, sebaceous gland, and IFE, although the specific mechanisms of these effects are yet to be determined.
Figure 3
Retinoic acid synthesis in the hair follicle
Telogen (a) and anagen (b) hair follicles are color coded with retinoic acid synthesis components: DHRS9 plus RARs (yellow), DHRS9 alone (pink), RARs alone (purple), CRABP2 (blue), CRBP (green), ALDH1A1, 2, or 3 (orange), a complete system with DHRS9, ALDH1A1, 2, or 3, CRABP2, and RARa, b,or g (red). Stem cell locations are marked in relation to this localization pattern of RA synthesis components. (c) RA synthesis as determined by immunohistochemistry with an antibody against beta-galactosidase in RA reporter mice (Tg(RARE-Hspa1b/lacz)12Jrt/J). Modified from Everts et al [24].
Excess RA was found to reduce the number and length of hair follicles in vitro [110]. Feather specification and dermal condensations were also inhibited by excess RA, which altered the pattern of Hox gene expression and NCAM in the developing feather, a structure similar to the mammalian hair follicle [111]. In addition, Dgat1tm2FarTg(KRT14-cre)1AMC null mice have cyclical hair loss that is restored by reducing dietary vitamin A, as discussed above [6]. We found increased expression of RA synthesis enzymes and binding proteins in biopsies from patients with several hair loss diseases and skin from their mouse models, including central centrifugal cicatricial alopecia (CCCA) and alopecia areata (AA; HB Everts, LE King Jr, unpublished observation). Flowers et al [112] also found increased retinol, atRA, retinyl esters and mRNA of retinoid binding proteins and target genes in one of these animal models. Primary cicatricial alopecias are a collection of scarring hair loss diseases that result in inflammatory attack of the hair follicle, their stem cells, and permanent hair loss [113]. The cause of this disease is unknown but theories include altered sebaceous gland function with reduced sebum [114], reduced PPARG [115], structural defects in the hair follicle [114], and loss of immune privilege in the hair follicle [116]. Alopecia areata is an autoimmune non-scarring hair loss disease that is mediated by CD8+ T cell attack on the lower cycling hair follicle [117–119] and a loss of immune privilege in the hair follicle [120–122]. We also found that reducing dietary vitamin A prevented cicatricial alopecia and delayed the onset of alopecia areata in mouse models (HB Everts, JP Sundberg, unpublished observation). Future studies are needed to better understand the mechanisms of RA’s function within the hair follicle to produce better treatments for these hair loss diseases.
Very interesting @tim-2!
From birth I have a small area (about 1 inch diameter) on the left side of my head, two three inches over my ear, which has been completely bald, kind of shiny scar tissue. I was told that this was the case in other areas of my body but that subsequently the skin became normal. This happened when I was too small to remember;
That area on my head has not changed for the last 68 years
BUT
now some hair , very fine and only a few, is growing on it. In fact it kind of tickles a bit from time to time.