The pathogenesis of male-pattern-baldness (MPB) is the same as acne. The first step in acne is a condition called follicular-hyperkeratinization or hyperkeratosis. Simply put, this means excess skin production inside and around the hair-follicle. The next step is caused by excess sebum production, followed by P.Acnes infestation of the pilosebaceous-follicle, with subsequent inflammation. So to summarize, MPB, just like acne, is caused by four main factors: (1) follicular-hyperkeratinization, (2) excess sebum production, (3) P.Acnes, and (4) inflammation .
Free-IGF-1 (insulin-like-growth-factor-1) stimulates the proliferation of keratinocytes (skin cells below the scalp). As the keratinocytes mature, they migrate to the top of the scalp and become what is known as corneocytes. If all goes well, the corneocytes are supposed to be shed off the scalp in a process called apoptosis. The shedding of corneocytes or the apoptosis of corneocytes, is under the influence of IGFBP-3 (insulin-like-growth-factor-binding-protein-3) and endogenous retinoids. In men with male-pattern-baldness, they have excess free-IGF-1 and not enough IGFBP-3 . The result of this is hyperkeratinization; too much skin production, and not enough skin exfoliation. This causes the hair-follicle to be blocked by excess skin. Free-IGF-1 is required for keratinocyte proliferation in humans  and too much IGF-1 results in hyperkeratosis .
Free-testosterone stimulates sebum production by converting into DHT (dihydrotestosterone) within the sebaceous-glands. Both insulin and free-IGF-1 can not only stimulate the synthesis of androgens from testicular-tissue  , but high levels of both insulin and free-IGF-1 also inhibit the livers production of SHBG (sex-hormone-binding globulin)  . SHBG is shown to be lower in men and woman with androgenic-alopecia (MPB) [9-13]. As SHBG goes up, free-testosterone goes down. As free-testosterone goes down, less is available to be converted into DHT. With less DHT comes less sebaceous-activity.
So far I have shown that a lack of IGFBP-3 (and excess free-IGF-1) causes hyperkeratinization of hair-follicles. And that low levels of SHBG promote excess sebum production. Next, after combining these two scenarios, we get P.Acnes infiltration. You see, the excess skin is now blocking not only the hair-follicle from sprouting out of the scalp, but now, also the flow or excretion of sebum. As a consequence, the sebum builds-up within the pilosebaceous-follicle. With this anaerobic-environment caused by the hyperkeratosis and with all this trapped excess sebum, the situation becomes the perfect breeding ground for a bacterium named P.Acnes, which feeds off the trapped sebum. The body is smart and the immune-system detects these nasty critters and attacks them with inflammation . This explains why Nizoral-shampoo seems to be effective in controlling the symptoms of MPB . The active ingredient in Nizoral-shampoo is ketoconazole, which has been shown to kill P.Acnes .
The solution to this cascade of events, would be to obviously lower your free-IGF-1 activity. Lowering free-IGF-1 would, (1) decrease the IGF-1:IGFBP-3 ratio, and (2) increase SHBG, thus preventing hyperkeratinization of the hair-follicles and excess sebum production. Preventing hyperkeratosis and sebum production would prevent P.acnes infestation and the subsequent inflammation that follows.
So how does one lower free-IGF-1 levels? Studies are consistent in showing that a vegan-diet causes both a decrease in IGF-1 and an increase in SHBG [17-31]. Many of these studies indicate that vegans have higher SHBG and lower IGF-1 despite the fact they are consuming high-fat diets, like eating lots of nuts or avocados. I personally believe that an extremely-low-fat vegan diet is optimal, due to the fact that dietary-fat causes insulin-resistance. Insulin-resistance causes high-insulin and IGF-1 in the blood. I also believe that fructose should be limited as much as possible. Fructose readily converts into fat in the liver, in a process called de-novo-lipogenesis and once again, fat paralyzes insulin-action, thus keeping it in the blood for extended periods of time, instead of driving glucose into the cells. Animal-protein, especially protein from dairy-products, rich in methionine, casein, and essential amino-acids seems to be the best stimulator of IGF-1. This explains why vegan-diets, low in "high-quality" protein increase SHBG and decrease IGF-1 regardless of fat content. With that stated I personally believe with all of my heart, that you would get the best results with a diet consisting only of beans, whole-grains and vegetables. Nuts and fruit (fat and sugar) should be eaten rarely.
Avoiding dairy-products is of huge importance! Nothing increases free-IGF-1 more than dairy-products; this has been consistently shown over and over again in the scientific-literature. And this should come as no surprise, considering the purpose of milk is to stimulate rapid-growth, development and maturity of the newborn. Dairy-products also contain DHT precursors   and potent estrogens [34-36].
After over 30 years of nutritional dogma barking over and over again that "diet has nothing to do with acne". Recent research has proven beyond a doubt, that diet does affect acne and that dairy-products and high-fat, sugar-laden processed-food are the largest culprits [37-45]. And since the pathology of MPB and acne are identical, any type of diet that promotes acne has the potential to promote MPB in genetically-predisposed people.
Eating a low-fat, low-fructose, high-fiber vegan-diet high in complex-carbohydrates should stop the progression of MPB hormonally. However this is unlikely to get rid of all the follicular-hyperkeratinization that has already occurred over time. To reverse hyperkeratosis, exfoliate the scalp and regrow "lost" hair, I highly suggest using glycolic-acid topically. Glycolic-acid is what's called an alpha-hydroxy-acid. Alpha-hydroxy-acids are shown to diminish corneocyte cohesion, induce exfoliation and reverse hyperkeratosis . This should promote regrowth. I've been using glycolic-acid since the beginning of the year (along with my complex-carbohydrate-vegan-diet), I have removed a copious amount of dead-skin-cell "build-up" from my scalp. Nearly three-grams of dead-skin so far! And my hair has drastically thickened! I'm completely convinced this is the correct way to combat MPB.
So to rehash or recap everything said here: a high level of free-IGF-1 (caused by eating a high-fat, high-protein, rich western-diet) causes follicular-hyperkeratinization and down-regulation of SHBG. Low SHBG correlates with the metabolic-syndrome [47-51] and promotes excess sebum production. Excess sebum is trapped, along with the hair-follicle, beneath the excess skin (produced by over-expression of IGF-1), this gives rise to P.Acnes; a bacterium that feeds off sebum and generates inflammation from the immune-system. Eating a diet consisting of beans, whole-grains and vegetables will drastically decrease IGF-1 and increase SHBG, preventing any further progression of MPB. Glycolic-acid used topically will reverse the hyperkeratosis already present and promote regrowth.
I would also like to close by saying that the effects of the complex-carbohydrate-vegan-diet can be magnified by practicing intermediate-fasting, exercise, getting plenty of sunshine exposure on the body and drinking nothing but water and organic-green-tea.
 Implications for the role of diet in acne.
 Vertex balding, plasma insulin-like growth factor 1, and insulin-like growth factor binding protein 3.
 The role of IGF-I in human skin and its appendages: morphogen as well as mitogen?
 Overexpression of insulin-like growth factor-1 induces hyperplasia, dermal abnormalities, and spontaneous tumor formation in transgenic mice.
 Short-term exposure to insulin-like growth factors stimulates testosterone production by testicular interstitial cells.
 Regulation of testicular function by insulin and transforming growth factor-beta.
 Effect of insulin-like growth factor-type 1 (IGF-1) and insulin on the secretion of sex hormone binding globulin and IGF-1-binding protein (IBP-1) by human hepatoma cells.
 Differential effects of insulin and insulin-like growth factor 1 on the production of plasma steroid-binding globulins by human hepatoblastoma-derived (Hep G2) cells.
 Hormonal profile of men with premature balding.
 Hormonal profile in men with premature androgenic alopecia.
 Serum testosterone and sex hormone binding globulin levels in women with androgenetic alopecia.
 Sex hormone-binding globulin and saliva testosterone levels in men with androgenetic alopecia.
 Low sex-hormone binding globulin levels in young women with diffuse hair loss.
 Induction of proinflammatory cytokines by a soluble factor of Propionibacterium acnes: implications for chronic inflammatory acne.
 Ketoconazole shampoo: effect of long-term use in androgenic alopecia.
 In vitro activities of azole antifungal agents against Propionibacterium acnes isolated from patients with acne vulgaris.
 Diet and Sex Hormone-Binding Globulin.
 Effects of replacing meat with soyabean in the diet on sex hormone concentrations in healthy adult males.
 The effects of low-protein diet and testosterone on sex hormone-binding globulin capacity in male rabbits.
 Long-term low-protein, low-calorie diet and endurance exercise modulate metabolic factors associated with cancer risk.
 Effects of dietary protein content on IGF-I, testosterone, and body composition during 8 days of severe energy deficit and arduous physical activity.
 The effects of dietary protein on serum IGF-1 levels in adult humans.
 Dietary correlates of plasma insulin-like growth factor I and insulin-like growth factor binding protein 3 concentrations.
 Determinants of circulating insulin-like growth factor I and insulin-like growth factor binding protein 3 concentrations in a cohort of Singapore men and women.
 The influence of dietary intake on the insulin - like growth factor (IGF) system across three ethnic groups: a population - based study.
 The associations of diet with serum insulin - like growth factor I and its main binding proteins in 292 women meat - eaters, vegetarians, and vegans.
 Relationship of Dietary Protein and Soy Isoflavones to Serum IGF-1 and IGF Binding Proteins in the Prostate Cancer Lifestyle Trial.
 Long-term effects of calorie or protein restriction on serum IGF-1 and IGFBP-3 concentration in humans.
 The low-methionine content of vegan diets may make methionine restriction feasible as a life extension strategy.
 A low-fat, whole-food vegan diet, as well as other strategies that down-regulate IGF-I activity, may slow the human aging process.
 Hormones and diet: low insulin-like growth factor-I but normal bioavailable androgens in vegan men.
 Acne, dairy and cancer: The 5alpha-P link.
 A survey of the steroids in cows' milk.
 Estrone and 17beta-estradiol concentrations in pasteurized-homogenized milk and commercial dairy products.
 Concentrations of 17beta-estradiol in Holstein whole milk.
 Exposure to exogenous estrogen through intake of commercial milk produced from pregnant cows.
 Acne vulgaris: a disease of Western civilization.
 Does diet really affect acne?
 The association of acne vulgaris with diet.
 High school dietary dairy intake and teenage acne.
 Evidence for acne-promoting effects of milk and other insulinotropic dairy products.
 Role of insulin, insulin-like growth factor-1, hyperglycaemic food and milk consumption in the pathogenesis of acne vulgaris.
 Permanent impairment of insulin resistance from pregnancy to adulthood: the primary basic risk factor of chronic Western diseases.
 Milk--the promoter of chronic Western diseases.
 Nutrition and acne.
 Hyperkeratinization, corneocyte cohesion, and alpha hydroxy acids.
 Relationships of circulating sex-hormone-binding globulin with metabolic traits in humans.
 Testosterone and sex hormone-binding globulin predict the metabolic syndrome and diabetes in middle-aged men.
 Lower sex hormone-binding globulin is more strongly associated with metabolic syndrome than lower total testosterone in older men: the health in men study.
 The triad of erectile dysfunction, hypogonadism and the metabolic syndrome.
 Association of testosterone and sex hormone-binding globulin with metabolic syndrome and insulin resistance in men.
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