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Male Pattern Baldness
Unlike the epidermis, which regenerates continually, hair follicles anchored in the subcutis periodically regenerate by spontaneous repetitive cycles of growth (anagen), degeneration (catagen), and rest (telogen). The loss of hair follicles in response to injuries or pathologies such as alopecia endangers certain inherent functions of the skin. Thus, it is of interest to understand mechanisms underlying follicular regeneration in adults. In this work, a phytochemical rich in the natural vitamin E tocotrienol (TRF) served as a productive tool to unveil a novel epidermal pathway of hair follicular regeneration. Topical TRF application markedly induced epidermal hair follicle development akin to that during fetal skin development. This was observed in the skin of healthy as well as diabetic mice, which are known to be resistant to anagen hair cycling. TRF suppressed epidermal E-cadherin followed by 4-fold induction of β-catenin and its nuclear translocation. Nuclear β-catenin interacted with Tcf3. Such sequestration of Tcf3 from its otherwise known function to repress pluripotent factors induced the plasticity factors Oct4, Sox9, Klf4, c-Myc, and Nanog. Pharmacological inhibition of β-catenin arrested anagen hair cycling by TRF. This work reports epidermal E-cadherin/β-catenin as a novel pathway capable of inducing developmental folliculogenesis in the adult skin.
"While doctors are slowly being educated about the value of gamma-tocopherol, Life Extension has discovered a method to increase the antioxidant and anti-inflammatory properties of gamma-tocopherol. It turns out that when sesame seed lignans are added to gamma tocopherol in controlled laboratory studies, lipid peroxidation rates are lowered by 50% compared to gamma-tocopherol alone.18-20
Equally important are studies showing that sesame lignans increase tissue levels of gamma- tocopherol as much as 833% compared to no sesame.21 The significance of this finding is that while gamma-tocopherol in the blood can help protect against LDL-induced oxidation in the arterial wall, free-radical damage can still run rampant in the brain, kidneys, and other organs. Increasing tissue levels of gamma tocopherol is critical to neutralizing destructive free radicals generated in cells outside the vascular system. Sesame lignans have been shown to specifically increase tissue levels of gamma-tocopherol.
In a brief, two-week study on human subjects, Life Extension measured various indicators of free radical and inflammatory damage. Gamma-tocopherol plus sesame lignans was shown to be 25% more effective on average than the same amount of gamma-tocopherol combined with toco-trienols. The significance of this finding is that tocotrienols are one of nature’s most potent antioxidants, yet low-cost sesame was found to work even better." AMA Discovers Gamma Tocopherol - page 1 - Life Extension
I've only been taking tocotrienols for about a month. It sounds like the best bet for hair follicle regeneration from tocotrienols would be to rub them directly into your scalp as well as take them. I've only been taking them.
I believe I arrested further hair loss years ago. Folliculogenesis, hair follicle regeneration is obviously much harder.
Quote from tim on November 15, 2023, 7:02 pmJaw and scalp tension affecting the galea aponeurotica and blood supply to the scalp, hypothyroidism, insulin resistance, liver disease, heavy metal toxicity, Hypervitaminosis A, micronutrient deficiencies and more can all be present in a woman and they will still be unlikely to experience MPB. Why? The same reason eunuchs don't go bald. Lack of DHT. Only if you inject testosterone into a eunuch can they go bald.
This is relevant to the post about beta catenin that @orion recently linked to:
Dihydrotestosterone (DHT) is the most potent androgen that regulates hair cycling. Hair cycling involves cross-talk between the androgen and Wnt/β-catenin pathways. However, how DHT regulates hair follicle (HF) growth through the Wnt/β-catenin pathway has not been well investigated. This study aimed to investigate the roles of DHT in hair growth in vivo and in vitro. Human scalp HFs were treated with different concentrations of DHT (10-5, 10-6, 10-7, 10-8, and 10-9 mol/L) for 10 days. The effects of DHT on hair shaft elongation, the proliferation of hair matrix cells, and the levels of β-catenin, GSK-3β, and phosphorylated GSK-3β (ser9) were evaluated in the cultured HFs. The effects of DHT were further investigated in C57BL/6 mice. Moreover, the growth of cultured human HFs was observed after interfering with the β-catenin pathway through inhibitors or activators in the presence or absence of DHT. We found that different concentrations of DHT had different effects on human HFs in vitro and C57BL/6 mice. At 10-6 mol/L, DHT inhibited HF growth and β-catenin/p-GSK-3β expression, whereas 10-7 mol/L DHT induced HF growth and β-catenin/p-GSK-3β expression. In addition, a β-catenin inhibitor (21H7) inhibited HF growth in vitro, while a β-catenin activator (IM12) promoted HF growth in vitro and antagonized the inhibition of HFs by high levels of DHT. These results suggest that DHT plays a pivotal role in region-specific hair growth, which may be related to the Wnt/β-catenin pathway.
Hair development involves crosstalk between the epidermal and dermal compartments in the hair follicle [17,25]. The Wnt/β-catenin signaling pathway is a master regulator of hair cells, including outer root sheath cells (ORS), hair matrix cells, and derma papilla cells during hair morphogenesis and the regeneration of hair follicles. Furthermore, Wnt/β-catenin signaling induces the onset of anagen and regulates the hair cycle [10,21,26]. The Wnt/β-catenin signaling pathway also plays an important role in hair morphogenesis and the regeneration of hair follicles [26]. Huelsken et al. demonstrated that genetic ablation of β-catenin failed to cause placode morphogenesis in mouse epidermis [27], implying that Wnt signals are important in hair development. Thus, the Wnt/β-catenin signaling pathway is a potential factor in treating hair loss.
In addition, many studies have demonstrated that various natural products effectively activate the Wnt/β-catenin signaling pathway against hair loss [94,95,96,97,98,99,100,101,102,103,104]. Tocotrienol, a vitamin E analog, has antioxidant properties. Ahmed et al. demonstrated that topical treatment with a tocotrienol-rich formulation (TRF) significantly stimulated epidermal hair follicle development and the onset of early anagen in the depilated dorsal skin of mice [94]. In addition, TRF suppressed the expression level of E-cadherin and stimulated the nuclear localization of β-catenin [94].
Hi Tim - massively disagree RE: DHT and testosterone.
In fact, women *do* experience hair loss. It is typically not in as specific a pattern as men, and is more likely to be diffuse thinning. However, in scans, it has been shown that women's scalp tension (in individuals with hair loss) is drastically lower and drastically different to a man's. See the pictures attached. This could be the reason for the differences in "amounts" of hair loss and the patterns. The high scalp tension areas on men's heads are where we lose the most hair - the front temple parts, the vertex etc. - women's scalp tension in these areas is much lower relatively speaking. As mentioned in my other comment - this may be due to skull shape differences, muscle strength difference of the frontalis and occipitalis muscles - or could be something else entirely. Why this happens, I do not know. But the scalp tension theory / blood flow theory is certainly relevant as to the cause.
Whilst I am not on the Peat band-wagon, and don't agree with all of the advice, I think Danny Roddy's video series on male pattern baldness successfully dispells the DHT theory. Open to being wrong though ...
It has also been shown that progesterone drastically increases hair counts. And prolactin drastically lowers it. Pregnant women typically experience a noticeable thickening of their hair (and often beautifying of their aura) - the "glow". Whereas lots of women complain of shedding post-pregnancy, which is often attributed to stress, but also is due to a huge surge in prolactin for milk production. Prolactin is the hormone that mammals who shed during the summer months produce to start the molt.
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https://ggenereux.blog/discussion/topic/suzanne-somers/#postid-25846
Gosh hormones are so sticky and tricky. I don't doubt that they explain the difference between how males and females experience allopecia. Even the smallest amounts of hormones change everything. At the pointer above I have posted an anecdote about how a small fecal transfer between a menopausal woman and adult male caused him to have menopausal symptoms. As a guy with Crohns, perhaps he had some VA problems? Perhaps VA toxicity causes sluggish movement/detox of hormones? My migraines (which I now think of as cranial pressure) were always influenced by hormonal days, and getting moving helped more than anything else. I suppose sluggish lymph might explain why sedentary-ness is bad (besides just loss of muscle).
I posted that little meme of the character "Les Grossman" of Tropic Thunder dancing. I wonder if there is some sort of "truth we all recognize" in his type-A leadership and his balding head. As I remember, though, the guy got things done, LOL.
haha that being said my husband is pretty sedentary and type A and has hair. I suppose he may just not be pre-disposed to this particular symptom, and he isn't doing some sort of magic lifestyle thing. FWIW, another thing that I thought of is he has always used dandruff shampoo, for all of our 35-year marriage.
Hi Andrew,
In fact, women *do* experience hair loss. It is typically not in as specific a pattern as men, and is more likely to be diffuse thinning. However, in scans, it has been shown that women's scalp tension (in individuals with hair loss) is drastically lower and drastically different to a man's. See the pictures attached. This could be the reason for the differences in "amounts" of hair loss and the patterns.
Yes they do. I'm talking specifically about pattern baldness not other forms and premenopausal women rarely experience pattern hair loss to the degree that men often do.
The high scalp tension areas on men's heads are where we lose the most hair - the front temple parts, the vertex etc. - women's scalp tension in these areas is much lower relatively speaking. As mentioned in my other comment - this may be due to skull shape differences, muscle strength difference of the frontalis and occipitalis muscles - or could be something else entirely. Why this happens, I do not know. But the scalp tension theory / blood flow theory is certainly relevant as to the cause.
Yes I don't disagree with that. Reduced blood flow could have many effects on a hair follicle including via affecting DHT levels.
Examples of scalp tension correlating with hairloss isn't strong evidence for it playing a primary role though. Do you know of any evidence of a strong correlation among a random sample of men and women with and without hairloss?
Whilst I am not on the Peat band-wagon, and don't agree with all of the advice, I think Danny Roddy's video series on male pattern baldness successfully dispells the DHT theory. Open to being wrong though ...
DHT is central to MPB. Just because many other hormones (estradiol, progesterone, prolactin, T3, T4, melatonin, CRH, ACTH, cortisol, TRH, galanin) have effects on hair follicles does not mean DHT is not a central actor in MPB. Just because DHT causes vellus body hair follicles to become terminal hair follicles doesn't mean that it can't cause the opposite with scalp hair follicles, it does.
This is from a recent post of mine on this thread:
We found that different concentrations of DHT had different effects on human HFs in vitro and C57BL/6 mice. At 10-6 mol/L, DHT inhibited HF growth and β-catenin/p-GSK-3β expression, whereas 10-7 mol/L DHT induced HF growth and β-catenin/p-GSK-3β expression.
Higher DHT levels inhibited hair follicle growth and lower levels induced hair follicle growth. How it affects hair follicles across different parts of the body is even more nuanced.
It has also been shown that progesterone drastically increases hair counts. And prolactin drastically lowers it. Pregnant women typically experience a noticeable thickening of their hair (and often beautifying of their aura) - the "glow". Whereas lots of women complain of shedding post-pregnancy, which is often attributed to stress, but also is due to a huge surge in prolactin for milk production. Prolactin is the hormone that mammals who shed during the summer months produce to start the molt.
Progesterone acts as a DHT inhibitor at hair follicles, that is one of the main ways that it influences hair follicles.
@tim - it's a big ask, but I'd love to know what you think of this video series:
A tid-bit quote from the end of part 1: "Failed Theory: It is hardly mentioned, but Dr James B Hamilton, who's research serves as the foundation of all current pattern hair loss research, left the door open for more coherent theories on the genesis of baldness.
A piece of evidence he mentioned that ran counter to the genetic androgen hypothesis was post-natal pattern baldness. Soon after birth, marked hair loss is seen in newborn infants in both sexes. Baldness is seen in the same areas that hair is lost from grown men and women.
"Male" pattern baldness is also common in menopausal women, post-partum "male" pattern baldness, "male" pattern baldness among women who use contraceptives [my neighbour's daughter, age 21 - a beautiful young woman, has pretty significant hairline / temple recession]. And additionally, vertex baldness can be used as a marker for coronary heart disease, myocardial infarction, arterial stiffness, insulin resistance, metabolic syndrome, inflammation, obesity and even cancer.
The genetic androgen hypothesis of pattern baldness has failed."
I would highly recommend listening to the series. I am not saying he is right about everything, but I do think it could give you some fresh perspectives - looking at the same problem from a different lens. I am not saying you are wrong, but I do think that the focus on DHT is a dead-end.