Carbon Dioxide: The "Cure" for Male Pattern Baldness?

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Since producing 'Explaining The "Horseshoe" Shape of Male Pattern Baldness' I've been receiving a lot of questions about scalp massage and microneedling as potential therapies to increase blood flow and the delivery of oxygen and nutrients to balding hair follicles. While I don't think a relaxing massage would hurt, I'm extremely skeptical of microneedling as it seems to fall under the cut, burn, poison model of modern medicine. This video is an attempt at shifting the conversation away from methods that are as old as baldness itself, and towards a bioenergetic view of pattern hair loss with an emphasis on carbon dioxide.

Explaining The "Horseshoe" Shape of Male Pattern Baldness

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“The role of mast cells in male-pattern baldness is unknown, but the large numbers often present is a striking feature.”[1] 

"We postulate that because of the underlying anatomy, there is a relative microvascular insufficiency to regions of the scalp that lose hair in male pattern baldness and that is associated with local tissue hypoxia in those regions. The vascular supply of the scalp is derived from branches of the internal carotid artery and branches of the external carotid artery. The frontal region of the scalp, which loses hair in male pattern baldness, is supplied by the supraorbital and the supratrochlear arteries. These are relatively small branches of the internal carotid artery system. The temporal [sides] and occipital [back of head] regions of the scalp, which do not lose hair in male pattern baldness, are supplied by larger branches of the external carotid artery. Specifically, these are the superficial temporal, posterior auricular, and occipital arteries. Further, the frontal and vertex regions of the scalp overlie the galea aponeurotica, which is relatively avascular. The temporal and occipital regions of the scalp overlie the temporalis and occipitalis muscles, which provide a rich network of musculocutaneous perforator blood vessels. These anatomic differences contribute to the tenuous nature of the dermal blood supply to the frontal and crown regions of the scalp."[2]

"We hypothesized that this difference in pattern of prostaglandin D-synthase expression may constitute a developmental pattern inherent to normal as well as alopecic scalp skin, thus defining a ‘field’ vulnerable to acquired hair loss." “These data indicate that scalp is spatially programmed via mast cell prostaglandin D-synthase distribution in a manner reminiscent of the pattern seen in androgenetic alopecia.” "In a prior study of male pattern alopecia, increased numbers of mast cells have been seen in balding vertices compared to non-balding occipital scalp and, in fact, this pattern was also observed in five control subjects studied, though there were greater numbers of mast cells in the patients with alopecia.” "In the 1990’s mast cells were found to be actively degranulating in the inflammatory infiltrates of scalp with male pattern alopecia and this was proposed to contribute to perifollicular fibrosis.”[3] 

"Mast cells express the high-affinity estrogen receptor and studies have shown that estrogens augment their activities: in the presence of high levels of estrogens, mast cell responses to compound 48/80 are increased, leading to more substantial degranulation and release of histamine and serotonin.” "Progesterone is necessary for the maintenance of pregnancy and plays a key role in maintaining cervical integrity prior to labour induction. Progesterone can prevent the migration of mast cells in response to chemokines and down-regulate surface chemokine receptor expression. In addition, mast cell function can be altered by the presence of high concentrations of progesterone. For example, progesterone inhibits the secretion of histamine from mast cells. Notably, these observations would suggest that mast cells present within the uterus during pregnancy are quiescent and inhibited by high levels of progesterone, and also that recruitment of mast cell progenitors from the circulation may be limited.” "At present the prevalence of allergies, including allergic rhinitis, hayfever, eczema, food allergies and urticaria, is rising." [4]

"Results from this study provide the first evidence of a unique regulatory mechanism by which CO2 inhibits mast cell degranulation and histamine release by repressing stimulated increases in intracellular calcium. Thus, our data provide a plausible explanation for the reported therapeutic benefit of noninhaled intranasal delivery of 100% CO2 to treat allergic rhinitis." [5]

1. Male pattern alopecia a histopathologic and histochemical study (1975) 
2. Transcutaneous PO2 of the scalp in male pattern baldness: a new piece to the puzzle (1996)
3. A prostaglandin D-synthase-positive mast cell gradient characterizes scalp patterning (2014) 
4. The role of mast cells and their mediators in reproduction, pregnancy and labour (2010) 
5. Treatment of mast cells with carbon dioxide suppresses degranulation via a novel mechanism involving repression of increased intracellular calcium levels (2011)

Male Pattern Baldness: Hypothyroidism in Disguise?

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Do The "Essential Fatty Acids" Cause Pattern Hair Loss?

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“All members of this group [prostaglandins] are synthesized from ‘polyunsaturated’ fatty acids that must be supplied by the diet. From a quantitative standpoint, arachidonic acid is the major precursor.” “Meats and peanuts contain small amounts [of arachidonic acid], but the liver forms most of it from linoleic acid. Arachidonic acid is the precursor of the prostaglandins with two double bonds, and of the several other biologically potent substances."[1] 

"These results define PGD2 as an inhibitor of hair growth in male-pattern baldness and suggest the PGD2-GPR44 pathway as a potential target for treatment.”[2] 

"EFA deficiency has been shown to exert an anti­inflammatory effect."[3] 

"In summary, the anti-inflammatory effect of EFA deficiency was more marked that that of dietary (n-3) fatty acid supplementation in acute inflammation."[4]

1. Endocrine Physiology by Constance R. Martin (1985)
2. Prostaglandin d2 inhibits hair growth and is elevated in bald scalp of men with androgenetic alopecia (2012)
3. Essential fatty acid deficiency: a new look at an old problem (1986)
4. Manipulation of the acute inflammatory response by dietary polyunsaturated fatty acid modulation (1990)

Higher Prolactin in Pattern Baldness?

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"A conclusion has been made that one of the most important mechanisms of the adaptive effect of prolactin is its ability to suppress thyroid function, thus decreasing the metabolism level, which results in reduction of oxygen consumption…"[1]

"Subsequent actions of prolactin may involve the following: a) an increased intracellular concentration of potassium and a reduced level of sodium, b) an increased level of cGMP and a reduced level of cAMP, c) an enhanced rate of prostaglandin biosynthesis mediated by a stimulation of phospholipase A2 activity, and d) a stimulation of polyamine synthesis."[2]

"...serum prolactin concentrations reflect endogenous serotonin..." "...aromatase activity correlated significantly with prolactin..."[3]
 
"After glucose load the hyperprolactinaemic patients showed a decrease in glucose tolerance and a hyperinsulinaemia." "These findings suggest a diabetogenic effect of prolactin."[4]

"These observations indicate that cutaneous symptoms such as seborrhea, acne, hypertrichosis/hirsutism, alopecia may evidently occur in hyperprolactinemia, representing or mimicking androgen-induced skin symptoms. In such cases, therefore, evaluation of prolactin levels together with androgen blood levels and thyroid gland function tests should be performed to exclude underlying endocrinopathy."[5]

1. Metabolism of thyroid gland cells as affected by prolactin and emotional-physical stress (1991)
2. Mechanism of prolactin action (1980)
3. Effects of aromatase inhibition and androgen activity on serotonin and behavior in male macaques (2013)
4. Prolactin: a diabetogenic hormone (1977)
5. Disorder of hair growth in hyperprolactinemia (1988)

Generative Energy #28: Talking with Ray Peat: The Origins of Authoritarianism

 
 

I’m incredibly excited to share my third interview with Ray about the origins of authoritarianism. The conversation covers a wide range of topics including Ray’s philosophical influences, former CIA director Allen Dulles, Wilhelm Reich, authoritarianism as a sickness, Nicole Foss’s idea of degrowth, and Ray’s thoughts on an “optimal” society. The conversation was originally recorded on June 24th, 2016. Special thanks to Ray for providing me with his time and my Patrons for making this content possible.

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“The Anarchists are right in everything; in the negation of the existing order, and in the assertion that, without authority, there could not be worse violence than that of authority under existing conditions. They are mistaken only in thinking that Anarchy can be instituted by a revolution. "To establish Anarchy." "Anarchy will be instituted." But it will be instituted only by there being more and more people who do not require protection from governmental power, and by there being more and more people who will be ashamed of applying this power.” — Leo Tolstoy (1899)
“‘When ignorance reigns in society and disorder in the minds of men, laws are multiplied, legislation is expected to do everything, and each fresh law being a fresh miscalculation, men are continually led to demand form it what can proceed only from themselves, from their own education and their own morality.’ It is no revolutionist who says this, nor even a reformer. It is the jurist, Dalloy, author of the Collection of French law known as ‘Repertoire de la Legislation.’ And yet, though these lines were written by a man who was himself a maker and admirer of law, they perfectly represent the abnormal condition of our society. 
In existing States a fresh law is looked upon as a remedy for evil. Instead of themselves altering what is bad, people begin by demanding a law to alter it. If the road between two villages is impassable, the peasant says: -‘There should be a law about parish roads.’ If a park-keeper takes advantage of the want of spirit in those who follow him with servile observance and insults one of them, the insulted man says: -- ‘There should be a law to enjoin more politeness upon park-keepers.’ If there is stagnation in agriculture or commerce, the husbandman, cattle-breeder, or corn speculator argues, ‘It is protective legislation that we require.” Down to the old clothesman there is not one who does not demand a law to protect his own little trade. If the employer lowers wages or increases the hours of labour, the politician in embryo exclaims, “We must have a law to put all that to rights,’ instead of telling the workers that there are other, and much more effectual means of settling these things straight; namely, recovering from the employer the wealth of which he has been despoiling the workmen for generations. In short, a law everywhere and for everything! A law about fashions, a law about mad dogs, a law about virtue, a law to put a stop to all the vices and all the evils which result from human indolence and cowardice.” — Peter Kropotkin (1886)
“Probably about 20 to 25 percent of the adult American population is so authoritarian, so scared, so self-righteous, so ill-informed, and so dogmatic that nothing you can say or do will change their minds.” “Dogmatism is by far the best fall-back defense, the most impregnable castle, that ignorance can find. It’s also a dead give-away that the person doesn’t know why he believes what he believes.” — Bob Altemeyer (2006)

01:10 - Chatting about Ray’s 2003 Newsletter
01:59 - Defining authoritarianism and Ray’s experience
09:45 - Where did authoritarianism originate from? (Parmenides, Zeno, Plato, Aristotle, and Heraclitus)
12:41 - “The principle of forgiveness was presented as the appropriate response to a world which is always new. The desire for vengeance comes from a delusive commitment to the world of memory. Virginity is constantly renewed in the world of imaginative life. While Blake said that you can’t forgive someone until they stop hurting you, the desire to be forgiven indicates that there is an opportunity to resolve the problem.” (http://raypeat.com/articles/articles/william-blake.shtml)
16:41 - “In 1933 Reich published The Mass Psychology of Fascism, and the next year Freud expelled him from psychoanalysis; that was the year that Andre Breton excommunicated Dali from surrealism. Both Reich and Dali had important (but dangerous) insights into the effects of the authoritarian culture on consciousness—the destruction of reality by the imposition of an “essentialist” attitude. Dali’s Persistence of Memory, 1931, described the fluidity of reality and consciousness. Later, Dali aligned himself with the fascist side, and his 1954 Decomposition of the Persistence of Memory shows the quantized consciousness. Starting in 1945, the fascist culture blossomed in the US, so people who speak English now have constant contact with the dead essences, and very little incentive to evaluate them. Business/government marketing techniques adjust the meaning-units periodically, so that they are always available to provide the needed frame for the discourse of the moment. A lot of work goes into it.” —Raymond Peat
16:54 - The Dulles brothers (The Devil’s Chessboard by David Talbott)
18:04 - Is authoritarianism a disease?
20:38 - Is the environment bracketing our current progress?
21:08 - Nicole Foss on degrowth (https://www.youtube.com/watch?v=lDr71LHO0Jo)
23:37 - Increasing the people’s knowledge, ability and power
24:31 - Food as way to heighten someone’s awareness
26:19 - The food pyramid as a form of oppression
27:44 - America’s authoritarianism vs. other places
31:29 - “In a speech before the National Alumni Conference at Princeton University on April 10, 1953, newly appointed CIA director Allen Dulles lectured his audience on ‘how sinister the battle for men's minds had become in Soviet hands.’ The human mind, Dulles warned, was a ‘malleable tool,’ and the Red Menace had secretly developed ‘brain perversion techniques.’ Some of these methods were ‘so subtle and so abhorrent to our way of life that we have recoiled from facing up to them.’ Dulles continued, ‘The minds of selected individuals who are subjected to such treatment are deprived of the ability to state their own thoughts. Parrot-like, the individuals so conditioned can merely repeat the thoughts which have been implanted in their minds by suggestion from outside. In effect the brain becomes a phonograph playing a disc put on its spindle by an outside genius over which it has no control.’ Three days after delivering this address Dulles authorized Operation MK-ULTRA, the ClA's major drug and mind control program during the Cold War.” — Acid Dreams (1985)
32:26 - What impact would you like to see your research make on society? Reaching the largest amount of people? or a certain type of person? Or are you completely detached from the outcome? “I’d like to see it lead to the disestablishment of medicine. The same general outcomes Ivan Illich worked for.” —RP (https://raypeatinsight.com/2013/06/06/raypeat-interviews-revisited/)
33:20 - Does Ray think an “optimal” society should include medicine or government?
34:59 - David Alfaro Siqueiros (https://en.wikipedia.org/wiki/David_Alfaro_Siqueiros)

Generative Energy #27: On The Back of a Tiger Interview #2

 
 

“Making an effort to learn how to use techniques of food, hormones, light, activity, etc., is similar to the effort needed to work with a psychologist, and the effort itself is part of the therapy—the particular orientation of the psychotherapist isn’t what’s therapeutic, it’s the ability to participate in meaningful interactions, that is, the ability to provide a situation in which the person can practice being human. When people start thinking about the things in their life that can be changed, they are exercising aspects of their organism that had been atrophied by being in an authoritarian culture. Authoritarians talk about protocols, but the only valid ‘protocol’ would be something like ‘perceive, think, act.’” —Raymond Peat, PhD

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01:17 - Details on the successful Kickstarter
02:04 - A heartened Brad and Jeremy
03:39 - What have you guys been up for the last year?
05:30 - Has the film changed at all?
07:16 - Where are you guys in the filmmaking process?
08:26 - Jeremy and Brad asking big questions
10:25 - Warming up the audience to the cast of Mavericks
11:40 - Uncut audio from the interviews
12:28 - Problems in the establishment
13:31 - Animations and filming experiments
15:16 - Issues in biology and medicine
16:15 - How the script is being written
17:49 - Will consciousness be explored in the film?
18:54 - Will cosmology be explored in the film?
19:07 - How do you empower people without giving recommendations?
20:54 - Will stress and energy be explored in the film?
23:38 - Danny doesn’t understand epigenetics
24:40 - Eugenics is still part of science culture
26:25 - Will politics be explored in the film?
27:48 - Danny thinks the ‘serotonin-makes-you-feel-good’ idea is crumbling
28:34 - Has Brad and Jeremy’s views changed at all since filming the movie?
31:32 - Danny thinks leaving your comfort zone can increase self-awareness
33:01 - ‘Never be in a rush to do anything’
33:25 - Will the film be accessible to lay people?
34:03 - How are Brad and Jeremy stringing the narrative between all the subjects?
34:48 - The passing of Mae-Wan Ho
35:31 - Respecting the life’s work of some of the subjects
35:05 - Keeping up to date with On The Back of a Tiger
40:04 - Next week’s episode with Ray

Generative Energy #26: Talking with Ray Peat: CO2, NAD+/NADH, Antibiotics, Coffee, and More

 
 

“Since the contextuality of communication is always in the foreground when I talk or write, you know that someone is confusing me with an authority when they talk about my ‘protocol’ for something. Context is everything, and it’s individual and empirical.” —Raymond Peat, PhD

“Making an effort to learn how to use techniques of food, hormones, light, activity, etc., is similar to the effort needed to work with a psychologist, and the effort itself is part of the therapy—the particular orientation of the psychotherapist isn’t what’s therapeutic, it’s the ability to participate in meaningful interactions, that is, the ability to provide a situation in which the person can practice being human. When people start thinking about the things in their life that can be changed, they are exercising aspects of their organism that had been atrophied by being in an authoritarian culture. Authoritarians talk about protocols, but the only valid ‘protocol’ would be something like ‘perceive, think, act.’” —Raymond Peat, PhD

01:10 - Show outline
01:40 - The passing of Mae-Wan Ho
03:44 - The organisms as a liquid crystalline
04:55 - Magneto biology
06:59 - Ray’s discovery of Vladimir Vernadsky
09:07 - Background on Ray’s books
10:36 - When Ray became more interested in carbon dioxide
15:10 - Carbon dioxide and evolution
17:11 - Ketosis, Carbon Dioxide, and NAD+/NADH
21:24 - The ketone body ratio and electrode physiology
33:35 - Why wasn’t Albert Szent-Györgyi’s work more accepted?
34:29 - “Old” and “new” hormones and signaling substances
38:53 - The “optimal” metabolic state
40:26 - Ray’s thoughts on antibiotics
43:25 - Ray’s thoughts on thyroid brands
44:52 - Ray’s thoughts on synthetic vs. desiccated
45:07 - How Ray makes his coffee
46:45 - The quality of commercial supplements
48:23 - Ray’s upcoming newsletter

Antihistamines for Pattern Hair Loss?

 
 
 
 

Over the years, a few people have been interested in the ability of antihistamine drugs to completely reverse baldness. For instance, in a small group of ten women with so-called androgenic alopecia an antihistamine called cimetidine showed good to excellent regrowth of hair in seven out of the ten women.[1] In addition to hair regrowth, acne, seborrhea, and hirsutism, which were present in three of the patients, showed significant improvement. Most of the women said that their scalps had become less greasy taking the drug similar to Hamilton's famous immune-to-baldness castrates. 

Around the same time, it was recorded that another antihistamine drug, benoxaprofen, was able to spontaneously reverse baldness in two men. The first case was a 75-year-old man with “hereditary male-pattern baldness” since he was 45. After five months of antihistamine treatment, the gentleman noticed new hairs on previously bald areas of his scalp. The other case, a 45-year-old man who had been balding in a pattern fashion since he was 40, experienced an increased growth of hair over the area of scalp previously lacking hair after nine months of taking benoxaprofen.[2] 

Cetirizine is another antihistamine drug that is currently being explored on various hair loss forums as an antiinflammatory.[3] Unfortunately, similar to cimetidine and benoxaprofen, cetirizine has a host of gnarly side effects that exclude it from being useful in the long-term.

A historical treatment for baldness that hints at a more physiological approach to controlling mast cell degranulation and the subsequent release of histamine is cyproterone acetate.[4] Cyproterone acetate has a semi-successful track record for resolving hair loss orally as well as topically in both men and women.[5] While the drug is commonly referred to as an “antiandrogen” it opposes estrogen (“to castration levels”) and exerts a progesterone-like effect.[6] Estrogen has long been known to activate mast cells while progesterone, working in the opposite direction, quiets them.[7]

Although some of the studies attempting to explain the positive effects of antihistamines on hair regrowth have attributed it to their alleged "anti-androgenic" actions, (specious at best in the case of cimetidine)[8], I have a different take.

I: Histamine and Ordinary Hair Growth

The defining feature of pattern hair loss is a higher ratio of telogen (resting) to anagen (growing) hairs. I think this reframes the conversation away from androgens and "the genes" and helps refocus thinking about the complicated growth cycle of the hair follicle and its interaction with the environment. 

In physiological amounts, histamine appears to play an important role in the cyclical growth of hair. For example, in the energetically expensive early anagen growth phase, the skin content of histamine in mast-cell granules is high promoting quick glycolytic growth. However, when hair follicles reach late anagen, a gradual but radical decrease in histamine begins and the mast cell population diminishes by a third leading to a more differentiated state of growth. During the resting telogen phase of hair growth, the mast cells and histamine increase again and continue to rise in the subsequent anagen preparing the hair for the next growth phase.[9] 

Early Anagen: High Histamine Late Anagen: Low Histamine Telogen: High Histamine

Early Anagen: High Histamine Late Anagen: Low Histamine Telogen: High Histamine

If histamine is tightly regulated during stages of early anagen, turned off during the differentiated period of late anagen, and increased once again during the resting telogen phase, we might expect an excess of histamine (and other mast cell products) to retard normal growth. While I’m not aware of any direct research on the histamine levels of people with pattern baldness, some pieces evidence suggest that the stress substances that promote mast cell accumulation, activation, and histamine release become excessive in pattern baldness.

II: When Energy Fails: Estrogen, Prostaglandins, and Histamine

The accumulation of degranulated mast cells was found to define “the baldness field” or typical horseshoe shape of pattern baldness.[10,11] The migration and activation of mast cells in a tissue are influenced by various hormones and signaling substances. For example, during stress, corticotropin-releasing hormone (CRH) is secreted from the hypothalamus and can induce mast cell degranulation in a dose-dependent manner.[12] CRH also activates the pituitary hormones: luteinizing hormone (LH), follicle stimulating hormone (FSH), thyroid stimulating hormone (TSH), which were found to increase the concentration and degranulation of mast cells. The hormone estrogen, which is increased in stress and age in both sexes, was found to be the most potent activator of mast cells tested.[13]

Image: serotonin, histamine, and mast cells in the hair cycle

Image: serotonin, histamine, and mast cells in the hair cycle

Estrogen inhibits mitochondrial respiration[14.15] reducing carbon dioxide production promoting mast cell degranulation,[16,17] and promoting what has been called "the inherent terminal-to-vellus switch" of the hair growth cycle.[18] Activating mitochondrial uncoupling proteins that dissociate ATP production from carbon dioxide production (generating more carbon dioxide and clearing lactic acid) were found to inhibit mast cell activation.[19] Another way of thinking about it is that the biological functions of estrogen and histamine overlap and reducing either one tends to reduce the other.[20] 

A consequence of the hypoglycemia that an excess of estrogen can create[21,22] is an increased concentration of free fatty acids in the blood. While the saturated fats tend to help terminate the stress reaction,[23] the composition of released fat probably leans towards the polyunsaturated fats that the hormone-like prostaglandins are synthesized from.[24] In 2012, Garza et al. found that a type of prostaglandin, prostaglandin D2, was elevated in the scalps of balding men and inhibited hair growth.[25] Prostaglandin D2 also promotes histamine release from mast cells[26] and is involved in the pathology of many allergenic problems. For instance, asthmatics were found to have 12 to 22 times higher levels of prostaglandin D2 and 4 times higher levels of histamine compared to controls.[27]

Estrogen, free fatty acids, prostaglandins, mast cells, and histamine are involved in the development of fibrosis, or the abnormal progression of the normal formation of fibrous material between cells due to inflammation. In 1992, Jaworsky et al. found that a prominent feature of baldness was mast cell degranulation and the activation of fibroblasts resulting in fibrotic thickening of the hair follicle.[28] In another experiment, 412 people with pattern baldness (193 men and 219 women) confirmed the presence of a significant degree of perifollicular fibrosis in at least 37% of cases. Moreover, balding men with higher levels of inflammation and fibrosis led to worse outcomes using the traditional hair loss remedy minoxidil compared to those with lower levels.[29] 

III: Prolactin, Light, and The Seasonal Variation of Hair Growth

“In birds, prolactin seems to be involved in stimulation of the feather papillae to produce a new plumage. It acts synergistically with estrogen to produce brood patches in birds.” Donnel, C. General Endocrinology (1966)

“In birds, prolactin seems to be involved in stimulation of the feather papillae to produce a new plumage. It acts synergistically with estrogen to produce brood patches in birds.” Donnel, C. General Endocrinology (1966)

Estrogen tends to increase the anti-respiratory pituitary hormone prolactin.[30] In mammals, prolactin has been called the “molting hormone” for its well-known ability to shed old feathers, hair, or skin, to make way for a new growth. Like other mammals, humans appear to be subject to seasonal differences in hair growth, with evidence that both the duration of hair growth and daily growth rates are greater in summer than winter.[31] In fact, an old paper from 1947 explained that one constant feature of hair growth in man was that “summer” hair was more long-lived than “winter” hair.[32] More recently, it was proposed that the hair follicle functioned as a “specialized UV receptor” responding to the nuances of seasonal light input.[33] The marked seasonal effect of hair growth is so remarkable that it has been suggested that any new drug or treatment for baldness should be studied for at least a year to separate any effects from normal seasonal variations.[34] 

Prolactin responds readily to cycles of light and darkness,[35,36] temperature, nutrition, stress, and the feeding rhythm. An excess of prolactin is associated with the development of pattern baldness in both sexes.[37,38] One way prolactin exerts a negative effect on hair is by reducing the intracellular level of cyclic amp (cAMP), a “secondary” regulatory substance that is associated with normal cellular differentiation and function in hair growth. Prolactin also activates the phospholipase A2 enzyme that liberates arachidonic acid from cells for prostaglandin production.[39] Moreover, alterations in mood can sometimes be attributed to higher prolactin levels,[40,41] and might be another aspect of the “balding personality” that I have mentioned previously.

Prolactin tends to rise with another adaptive hormone that activates mast cells, parathyroid hormone.[42] Both parathyroid hormone and prolactin decrease the concentration of carbon dioxide,[43,44] which helps stabilize mast cells.[45] Thyroid hormone is the master regulator of carbon dioxide and in sufficient quantities, carbon dioxide inhibits an excess of both prolactin and parathyroid hormone.[46,47] 

IV: Expand, Extend, Develop, Mature

"It is the urge, which is evident in all organic and human life — to expand, extend, become autonomous, develop, mature — the tendency to express and activate all the capacities of the organism, to the extent that such activation enhances the organism or the self. This tendency may become deeply buried under layer after layer of encrusted psychological defenses; it maybe hidden behind elaborate facades which deny its existence; but it is my belief that it exists in every individual, and awaits only the proper conditions to be released and expressed.” —On Becoming a Person by Carl Rogers (1961)

"It is the urge, which is evident in all organic and human life — to expand, extend, become autonomous, develop, mature — the tendency to express and activate all the capacities of the organism, to the extent that such activation enhances the organism or the self. This tendency may become deeply buried under layer after layer of encrusted psychological defenses; it maybe hidden behind elaborate facades which deny its existence; but it is my belief that it exists in every individual, and awaits only the proper conditions to be released and expressed.” —On Becoming a Person by Carl Rogers (1961)

My perennial argument for the last few years has been that pattern hair loss means that something is wrong. A nontechnical way of viewing the problem might be that the balding person is perpetually experiencing the effects of a “winter metabolism,” or: a chronic light deficiency, lower vitamin D level, higher local levels of estrogen, histamine, cortisol, and prolactin, some degree of insulin resistance, hypertension, higher circulating free fatty acids, higher levels of the inflammatory prostaglandins, deranged calcium metabolism, and a reduced resting pulse rate and body temperature.

Another way of looking at those facts is that red light, thyroid, calcium, vitamins D, K2 and A, sugars, salt, aspirin, caffeine, niacinamide, and maybe even a small dose of an antihistamine drug like cyproheptadine would be simple, cheap, and effective therapies for protection against the inflammation, fibrosis, and maladaptive stress reactions associated with pattern baldness. 

The heavy focus on androgen hormones and “the genes” as causes of baldness have led people to believe that pattern hair loss is a compartmentalized problem rooted in vanity that has nothing to do with their metabolism or lifestyle. Confusion about the role of androgens probably relates to testosterone’s conversion into estrogen during metabolic stress and that dihydrotestosterone (DHT), like DHEA, can increase to buffer the effects of metabolic stress, for example, as an anti-estrogen.[48,49]

References

  1. Aram, H. Treatment of female androgenetic alopecia with cimetidine. Int J Dermatol. 1987 Mar;26(2):128-30. "Ten white women with moderate to severe androgenetic alopecia were treated with cimetidine 300 mg by mouth five times a day. Duration of therapy ranged from 1.59 months, with a median of 5 months. Seven patients (70%) showed good to excellent regrowth of hair.” "The mechanism of cimetidine's action in patients with androgenetic alopecia is presumably due to its antiandrogenic activity, although a placebo effect cannot be discounted.” "Management of androgenetic alopecia in men or endocrinologically normal women has been unrewarding, as there are no consistently successful therapeutic agents available. The possibility of cimetidine offering a useful form of therapy for patients with this disorder prompted the undertaking of the present open study.” "The pattern of hair loss was usually diffuse, most marked on the vertex.” "Acne, seborrhea, and hirsutism, which were present in three of the patients, showed significant improvement. Most patients said that the scalp had become less greasy. No correlation was found between the severity of hair loss and the serum levels of testosterone.” "However, application of 0.025% 17-a-estradiol solution resulted in decrease of the rate of hair loss, but regrowth of hair did not occur."
  2. Fenton, D., et al. Reversal of male-pattern baldness, hypertrichosis, and accelerated hair and nail growth in patients receiving benoxaprofen. Br Med J (Clin Res Ed). 1982 Apr 24; 284(6324): 1228–1229. "Benoxaprofen is a non-steroidal anti-inflammatory drug used to relieve symptoms of rheumatoid arthritis and osteoarthrosis. Reported side effects include photosensitivity, onycholysis, urticarial rashes and pruritus, gastrointestinal ulceration and haemorrhage, and the Stevens-Johnson syndrome. We have reported the development of toxic epidermal necrolysis, leucopenia, and thrombocytopenic purpura in a patient after nine days' treatment with benoxaprofen. We report here on five patients who developed hypertrichosis and accelerated hair and nail growth, two of whom showed reversal of male-pattern baldness." 
  3. Charlesworth, E., et al. Effect of cetirizine on mast cell-mediator release and cellular traffic during the cutaneous late-phase reaction. J Allergy Clin Immunol. 1989 May;83(5):905-12. “Histamine release was not altered by cetirizine treatment, but prostaglandin D2 (PGD2) production, which peaked at 3 to 5 hours, was clearly reduced by cetirizine treatment, being lower at all time points during the reaction…” “The inhibition was most marked during the fifth hour of the reaction when there was a 50% suppression of the PGD2 level by cetirizine.”
  4. Mayo, J., et al. Androgen-dependent mast cell degranulation in the Harderian gland of female Syrian hamsters: in vivo and organ culture evidence. Anat Embryol (Berl). 1997 Aug;196(2):133-40. "The antiandrogen cyproterone acetate prevents the degranulation of mast cells induced by testosterone in both in vivo and in vitro."
  5. Neuman, F., and Graf, K.J. Discovery, development, mode of action and clinical use of cyproterone acetate. "CA has been useful in treating androgen-dependent tumors and "androgenic" diseases such as idiopathic precocious puberty, hirsutism, and male-pattern baldness in adult females, all signs of virilization in females, hypersexuality in adult males, acne and seborrhea, baldness in adult males, and benign prostatic hypertrophy.” "Because of its strong progesterone potency…” "Gynecomastia sometimes develops temporarily in males treated with CA. Serious side effects of CA treatment have not been observed."
  6. Geller, J., et al. Effect of cyproterone acetate on clinical, endocrine and pathological features of benign prostatic hypertrophy. Journal of Steroid Biochemistry, 1975. Vol. 6, pp. 837-843. "Clinical effects of CPA in patients with BPH. In five patients treated with CPA, 250 mg daily by mouth for two-to-four months, all improved clinically (Table 2) by both objective (residual urine and ability to void) and subjective criteria. The resected prostate was surprisingly small compared to the expected values estimated prior to drug treatment.” "The decrease in estrogen to the castration levels demonstrated in two patients during CPA therapy may reflect either a decrease in estrogen secondary to a decrease in testosterone which serves as a precursor for the estrogen, or it may reflect the direct inhibition of estrogen synthesis by Leydig cells. Since estrogen may stimulate squamous metaplasia and fibromuscular growth in the middle and lateral lobes of prostate, the usual anatomic sites of BPH, decreased estrogen production rates with CPA may have relevance to the clinical effects of the drug in BPH."
  7. Menzies, F.M., et al. The role of mast cells and their mediators in reproduction, pregnancy and labour. Human Reproduction Update, 2010, Volume 17, Issue 3, Page 383–396. "MCs express the high-affinity estrogen receptor and studies have shown that estrogens augment their activities: in the presence of high levels of estrogens, MC responses to compound 48/80 are increased, leading to more substantial degranulation and release of histamine and serotonin.” "MCs are found in a diverse range of tissues and have the ability to adapt their function to the microenvironment.” "Interestingly, however, there is an increase in testicular MCs in infertile men through MC activation of fibroblasts and promotion of collagen synthesis, could contribute to testicular fibrosis.” "Progesterone is necessary for the maintenance of pregnancy and plays a key role in maintaining cervical integrity prior to labour induction. Progesterone can prevent the migration of MCs in response to chemokines and down-regulate surface chemokine receptor expression. In addition, MC function can be altered by the presence of high concentrations of progesterone. For example, progesterone inhibits the secretion of histamine from MCs (Vasiadi et al., 2006). Notably, these observations would suggest that MCs present within the uterus during pregnancy are quiescent and inhibited by high levels of progesterone, and also that recruitment of MC progenitors from the circulation may be limited.” "At present the prevalence of allergies, including allergic rhinitis, hayfever, eczema, food allergies and urticaria, is rising."
  8. Orfanos, C., and Happle, R. Hair and Hair Diseases. 1990. “Of the three drugs presently available with antiandrogenic potency, Cimetidine (CI) is the drug which is weakest in this respect, and also that which is the least investigated. Its antiandrogenicity was suspected from side effects which occurred in men during CI treatment for peptic ulcer and other indications, namely gynaecomastia, impotence and reduction in sperm count, despite a rise in plasma testosterone. The antiandrogenic property is not intrinsic to histamine H2-receptor blockade since other histamine H2-receptor antagonists such as ranitidine and tiotidine are devoid of this activity. CI, unlike CPA and SL, is obviously devoid of additional endocrine activities. Thus, common endocrine parameters such as plasma testosterone,free testosterone, DHT, oestradiol, progesterone, FSH, LH and prolactin do not change under the influence of CI.”
  9. Morettie, G., et al. The Hair Cycle Re-Evaluated. International Iournal Of Dermatology (1976). "The skin content of histamine and heparin contained in the mast-cell granules is high at this time [ANA 4].” "The rise in heparin in the first week of anagen probably helps to maintain normal blood fluidity in the simultaneously increased perifollicular vessel networks, which are dilated and made more permeable by histamine.” "When follicles have reached ANA 6, however, a gradual but radical decrease in mast cells, histamine and heparin begins. This continues through the rest of ANA 6 and the whole of catagen. The mast cell population diminishes by a third, when it retreats to the lower dermis and hypodermis."During telogen the mast cells, histamine, and probably heparin, increase again and continue rising in the subsequent anagen, as we know from studies on consecutive hair cycles. The final stage of telogen probably prepares the hair for the next growth phase. This stage and anagen, until the point when the follicles are differentiated and emerge, are characterized by an increase in mast cell population and in their secretory activity.” "During telogen, hair survival is dependent on energy (ATP), mainly produced by anaerobic glycolysis,” "Thyroxine shortens the resting phase, whereas estradiol, adrenal hormones and testosterone prolong telogen."
  10. Lattanand, A. and Johnson, W.C. Male pattern alopecia a histopathologic and histochemical study. J Cutan Pathol. 1975;2(2):58-70. “The role of mast cells in male-pattern baldness is unknown, but the large numbers often present is a striking feature.”
  11. Larson, A.R., et al. A prostaglandin D-synthase-positive mast cell gradient characterizes scalp patterning. J Cutan Pathol. 2014 Apr;41(4):364-9. "We hypothesized that this difference in pattern of prostaglandin D-synthase expression may constitute a developmental pattern inherent to normal as well as alopecic scalp skin, thus defining a ‘field’ vulnerable to acquired hair loss." “These data indicate that scalp is spatially programmed via mast cell prostaglandin D-synthase distribution in a manner reminiscent of the pattern seen in androgenetic alopecia.” "Currently the main successful treatment options for androgenetic alopecia are finasteride, an androgen-based systemic therapy with numerous side effects…” "In a prior study of male pattern alopecia, increased numbers of mast cells have been seen in balding vertices compared to non-balding occipital scalp and, in fact, this pattern was also observed in five control subjects studied, though there were greater numbers of mast cells in the patients with alopecia.” "In the 1990’s mast cells were found to be actively degranulating in the inflammatory infiltrates of scalp with male pattern alopecia and this was proposed to contribute to perifollicular fibrosis.”
  12. Theoharides, T., et al. Corticotropin-releasing hormone induces skin mast cell degranulation and increased vascular permeability, a possible explanation for its proinflammatory effects. Endocrinology. 1998 Jan;139(1):403-13. “Mast cells are involved in atopic disorders, often exacerbated by stress, and are located perivascularly close to sympathetic and sensory nerve endings.” “Moreover, acute psychological stress induces CRH-dependent mast cell degranulation.Intradermal administration of rat/human CRH (0.1-10 microM) in the rat induced mast cell degranulation and increased capillary permeability in a dose-dependent fashion.” “To investigate which vasodilatory molecules might be involved in the increase in vascular permeability, the CRH injection site was pretreated with the H1-receptor antagonist diphenhydramine, which largely inhibited the CRH effect, suggesting that histamine was involved in the CRH-induced vasodilation.” “The present results have implications for the pathophysiology and possible therapy of skin disorders, such as atopic dermatitis, eczema, psoriasis, and urticaria, which are exacerbated or precipitated by stress.”
  13. Jaiswal K., and Krishna, A. Effects of hormones on the number, distribution and degranulation of mast cells in the ovarian complex of mice. Acta Physiol Hung 1996;84(2):183-90. “The changes in the number and degranulation pattern of mast cells varied with the types of hormonal treatment and ovarian compartment. Luteinizing hormone (LH), follicle stimulating hormone (FSH), thyroid stimulating hormone (TSH) and 17-beta estradiol (E2) treatment caused increase (P < 0.05) in the number of mast cells in the hilum as compared with the controls. Increase (P < 0.05) in the number of mast cells in the whole ovarian complex was observed only following FSH and E2 treatment. All the hormones used in the present study increased the percentage degranulation of mast cells in the hilum. However, only LH, FSH and E2 increased the percentage degranulation of mast cells in other compartments of the ovary (medulla, bursa and cortex). TSH and ACTH failed to cause any increase in the percentage degranulation of mast cells in these compartments. The present findings indicate E2 to be the most potent among the hormones tested in causing degranulation of mast cells in all ovarian compartments.” 
  14. Gross. Reproductive cycle biochemistry. Fertility & Sterility 12(3), 245-260, 1961. “The maintenance of an environment conducive to anaerobic metabolism—which may involve the maintenance of an adequate supply of the substances that permit anaerobiosis…seems to depend primarily upon the action of estrogen.” “Glycolytic metabolism gradually increases throughout the proliferative phases of the cycle, reaching a maximum coincident with the ovulation phase, when estrogen is at a peak. Following this, glycolysis decreases, the respiratory mechanisms being more active during the secretory phase. Eschbach and Negelein showed the metabolism of the infantile mouse uterus to be less anaerobic than that of the adult. If estrogen is administered, however, there is a 98 percent increase in glycolytic mechanisms.” “The effect of the progestational steroids may be such as to interfere with the biochemical pattern required for support of this anaerobic environment.”
  15. Nagy, P., and Csaba, I.F. [Action of oestrogens on in vitro metabolism of trophoblast from human early pregnancy]. Zentralbl Gynakol. 1982;104(2):111-6. “Warburg’s manometric method was used to check the action of oestrone, oestradiol, and oestriol on aerobic and anaerobic glycolysis of placental respiration. Oestrogen concentrations of 10(-4) M were found to reduce oxygen consumption and to increase aerobic glycolysis. Such reduction of oxygen consumption was most strongly pronounced in connection with oestradiol, while the strongest rise in aerobic glycolysis took place in the wake of oestradiol and oestrone. Oestrogen action upon anaerobic glycolysis was variable, with the latter remaining unchanged by oestradiol, reduced in response to oestriol, and slightly increased by oestrone.”
  16. Vliagoftis, H., et al. Estradiol augments while tamoxifen inhibits rat mast cell secretion. Int Arch Allergy Immunol. 1992;98(4):398-409. “...17 beta-estradiol augmented secretion of histamine and serotonin, starting at 1 microM and in a dose-dependent manner…” "Tamoxifen, an estrogen receptor antagonist used in the treatment of breast cancer, inhibited serotonin and histamine release from purified rat peritoneal mast cells triggered by compound 48/80 or substance P. Tamoxifen also inhibited the increase in intracellular free Ca2+ originating from an influx of extracellular Ca2+ in response to compound 48/80.” "Tamoxifen may, therefore, have a beneficial effect in other neuroimmunoendocrine disorders both through estrogen receptor blockade and inhibition of mast cell secretion."
  17. Terral, C., et al. [Influence of estrogens on histamines liberation by whole blood induced by allergens in vitro]. Soc Bioi Fil 1981; 175(2):247-52. “A relapse o f bronchial obstruction during women's menstrual cycle in often observed. Incubating blood and rising rates of estrogens produce an increase of histamine-release induced by allergens."
  18. Ohnemus, U., et al. The hair follicle as an estrogen target and source. Endocr Rev. 2006 Oct;27(6):677-706. Epub 2006 Jul 28. “The transformation of terminal to vellus hair follicles in androgenetic alopecia is also associated with a discrete infiltration of perifollicular macrophages and with mast cell activation, which has been proposed to be inherent to the terminal-to-vellus switch itself.”
  19. Theoharides, C., et al. Mast cells and inflammation. Biochim Biophys Acta. 2012 Jan; 1822(1): 21–33. "Recent evidence indicates that mitochondria are involved in the regulation of mast cell degranulation. Mitochondrial uncoupling protein 2 (UCP2) inhibits mast cell activation."
  20. Martin, C. Endocrine Physiology. 1985. “Estrogens stimulate the secretion of growth hormone and prolactin. They also exert localized influences. The most prominent of which is rapidly developing retention of water in the uterus. This is attributed to the release of histamine and prostaglandins.” "Estradiol promotes histamine release, and histamine accelerates endometrial estradiol uptake.” "Subthreshold amounts of estrogen and histamine synergize to invoke a response."
  21. Martin, C. Endocrine Physiology. 1985. "Sustained high estrogen concentrations increase both insulin requirements and insulin secretion."
  22. Goodman, M., et al. Short-term effects of oestradiol benzoate in normal, hypophysectomized and alloxan-diabetic male rats. "In normal rats, OEB decreased plasma glucose, increased plasma immunoreactive insulin, growth hormone and corticosteroid levels, increased pancreatic β-cell granulation, and enhanced glucose stimulation of insulin release in vitro.” "These results suggest that OEB affects experimental diabetes by a direct action on the pancreas, promoting insulin formation, and possibly by an indirect action mediated through hypophysial secretions."
  23. Katoh, K., et al. Saturated fatty acids suppress adrenocorticotropic hormone (ACTH) release from rat anterior pituitary cells in vitro. Comp Biochem Physiol A Mol Integr Physiol. 2004 Feb;137(2):357-64. Addition of saturated fatty acids (butyrate, caprylate, laurate, palmitate and stearate) in a medium at 1 mmol/l, despite effects on the basal release, significantly reduced the ACTH release induced by CRH (1 nmol/l) stimulation. Caprylate suppressed ACTH release in a concentration-dependent manner. However, unsaturated C18 and C20 fatty acids (oleate, linolate, linolenate and arachidonate) at 1 mmol/l significantly increased the basal release, but none of them suppressed CRH (1 nmol/l)-induced ACTH release. In the presence of caprylate (1 mmol/l), CRH (1 nmol/l)-stimulated increase in cellular calcium ion concentration was diminished. From these results we conclude that saturated fatty acids have a suppressing effect on CRH-induced ACTH increase in primary cultured rat anterior pituitary cells.
  24. Speake, B., et al. The preferential mobilisation of C20 and C22 polyunsaturated fatty acids from the adipose tissue of the chick embryo: potential implications regarding the provision of essential fatty acids for neural development. Biochim Biophys Acta. 1997 Apr 21;1345(3):317-26. "The composition of the FFA released into the medium under conditions of basal (i.e., unstimulated) lipolysis was markedly different in several respects from that of the TAG from which it originated. The polyunsaturated fatty acids, 20:4n-6, 20:5n-3, 22:5n-3 and 22:6n-3, were consistently found to be preferentially released into the medium, whereas the major fatty acyl constituents of the tissue, 16:0 and 18:1n-9, were selectively retained in the TAG. For example, at day 18 of development, the proportions (% w/w of fatty acids) of 20:5n-3 and 22:6n-3 released into the incubation medium were respectively 6.5 and 7.5 times higher than in the original tissue TAG.” "Although the regulation of fatty acid mobilisation from adipose tissue TAG has been an area of intensive research for 3 decades, relatively few studies have focussed on the composition of the mobilised fatty acids” "Their observations on the differential release of 52 fatty acids into the medium during the in vitro incubation of rat adipocytes were found to be summarised by the general rule that the Relative Mobilisation of a particular fatty acid is directly proportional to its degree of unsaturation and inversely proportional to its chain length. Thus the proportion of highly polyunsaturated fatty acids such as 20:4n-6 and 20:5n-3 was significantly greater in the medium FFA than in the original cellular TAG.” "A mechanistic explanation for selective mobilisation was proposed based on the differential aqueous solubilities of the various fatty acids. It was suggested that TAG species containing the more polar short and unsaturated fatty acids would be preferentially located at the periphery of the cytoplasmic lipid droplet of the adipocyte and would therefore be more accessible to the hormone sensitive lipase…”
  25. Garza, L.A., et al. Prostaglandin d2 inhibits hair growth and is elevated in bald scalp of men with androgenetic alopecia. Sci Transl Med. 2012 Mar 21;4(126):126ra34. “Given the androgens are aromatized into estrogens, these results may be relevant to hair growth and alopecia in both men and women. Thus, these or similar pathways might be conserved in the skin and suggest that sex hormone regulation of Ptgds may contribute to the pathogenesis of AGA.” “…demonstrates elevated levels of PGD2 in the skin and develops alopecia, follicular miniaturization, and sebaceous gland hyperplasia, which are all hallmarks of human AGA. These results define PGD2 as an inhibitor of hair growth in AGA and suggest the PGD2-GPR44 pathway as a potential target for treatment.”
  26. Peters, S., et al. Effect of prostaglandin D2 in modulating histamine release from human basophils. J Pharmacol Exp Ther. 1984 Feb;228(2):400-6. "Prostaglandin (PG) D2 is the major cyclooxygenase metabolite of arachidonic acid released after immunologic stimulation of mast cells. In this report, we demonstrate that this PG is unlike other PGs previously investigated in that it enhances human basophil histamine release at concentrations of 1 to 100 nM.” "These data suggest that PGD2 may play an important role in allergic and immunologic reactions and suggest a mechanism by which mast cells and basophils can interact during these reactions."
  27. Liu, M., et al. Evidence for elevated levels of histamine, prostaglandin D2, and other bronchoconstricting prostaglandins in the airways of subjects with mild asthma. Am Rev Respir Dis. 1990 Jul;142(1):126-32. "Histamine and certain cyclooxygenase products of arachidonic acid have been implicated as mediators of inflammation and are potent constrictors of human airways.” "Levels of PGD2, 9 alpha,11 beta-PGF2 and PGF2 alpha were 12 to 22 times higher in asthmatic than in normal subjects…” "Levels of PGD2 and 9 alpha,11 beta-PGF2 were increased nearly tenfold in asthmatic subjects compared with those in rhinitic subjects…” "Histamine levels were increased fourfold in asthmatic subjects compared with those in normal subjects (p less than 0.001); however, similar increases were found in rhinitic subjects."
  28. Jaworsky, C., et al. Characterization of inflammatory infiltrates in male pattern alopecia: implications for pathogenesis. Br J Dermatol. 1992 Sep;127(3):239-46. "Ultrastructural studies disclosed measurable thickening of the follicular adventitial sheaths of transitional and alopecic zones compared with those in the non-alopecic zones. This finding was associated with mast cell degranulation and fibroblast activation within the fibrous sheaths.” "The data suggest that progressive fibrosis of the perifollicular sheath occurs in lesions of pattern alopecia, and may begin with T-cell infiltration of follicular stem cell epithelium. Injury to follicular stem cell epithelium and/or thickening of adventitial sheaths may impair normal pilar cycling and result in hair loss.” "Mast cell degranulation was a prominent feature in sheaths of affected follicles, and was associated with ultrastructural evidence of biosynthetic activation of fibroblasts resulting in sheath widening and fibrosis.”
  29. Mahe, Y.F., et al. Androgenetic alopecia and microinflammation. Int J Dermatol. 2000 Aug;39(8):576-84. "Only 55% of male pattern AGA patients with microinflammation had hair regrowth in response to minoxidil treatment, which was less than the 77% of patients with no signs of inflammation, suggesting that, to some extent, perifollicular microinflammation may account for some cases of male pattern AGA which do not respond to minoxidil. Another study on 412 patients (193 men and 219 women) confirmed the presence of a significant degree of inflammation and fibrosis in at least 37% of AGA cases.""Despite such a reduction of circulating 5-DHT levels, however, a number of individuals (60–70%) still remained unresponsive to this treatment, indicating again that simple dysregulation of 5-DHT synthesis levels or a genetic polymorphism of 5α-R genes cannot account for all cases of AGA, and a polygenic etiology should be considered.” "The fact that the success rate of treatment with either antihypertensive agents, or modulators of androgen metabolism, barely exceeds 30% means that other pathways may be envisioned.” "Once aa is released from the cell membrane phospholipids by phospholipase A2 it is metabolized through a complex equilibrium between two families of enzymes, generating either prostaglandins (PGs) (through the activity of PGH synthases, PGHSs) or leukotrienes…” "This upregulation of androgen metabolism by proinflammatory cytokines remains, however, to be established at the pilosebaceous unit level.” "We know now that, at least in about one-third of cases, the tool which causes the lethal damage is a microinflammatory process.” 
  30. Martin, C. Endocrine Physiology. 1985. "Plasma PRL concentrations undergo diurnal variations that include sleep-associated elevations. The levels also rise in response to demanding activity and some forms of stress, and sharp peaks have been observed following food ingestion. Estrogens are potent stimulants that affect DA turnover in the brain. In cycling females. plasma PRL reaches its highesl levels during the times of maximal estrogen secretion."
  31. Montagna, W., et al. Hair Research. 1981. 
  32. Pinkus, F. The story of a hair root. J Invest Dermatol. 1947 Aug;9(2):91-3. "In spite of the differences in generation of hair, one feature is constant. ‘Summer’ hair is more long-lived than ‘winter’ hair in man, a fact established by earlier observations.”
  33. Iyenger, B. The hair follicle: a specialised UV receptor in the human skin? Biol Signals Recept. 1998 May-Jun;7(3):188-94. “From the present study, it appears that light is guided to the hair bulb to activate the melanocytes within the hair follicles. Thus the hair follicles function as specialised UV receptors in the skin responding to nuances of seasonal photic inputs in man. This would explain the coat colour changes seen in animals exposed to large variations in the day-night cycle.”
  34. Trüeb, R., and Tobin, D. Aging Hair. 2010.
  35. Kizer, J., et al. The nyctohemeral rhythm of plasma prolactin: effects of ganglionectomy, pinealectomy, constant light, constant darkness or 6-OH-dopamine administration. Endocrinology. 1975 May;96(5):1230-40. "In addition, there is evidence that environmental lighting in the form of altered length of a photo periods has a profound influence upon the endocrine system.” "Plasma prolactin, on the other hand, is decreased in rats exposed to constant light and increased by constant darkness.""In male rats maintained on a 12 h light-dark schedule (6 AM-6 PM), there is a nyctohemeral cycle of plasma prolactin which consists of a nadir at 11:30 AM and an apogee at approximately 11:30 PM.” "…there is a nyctohemeral rhythm of plasma prolactin, which is reversed by constant light…" “ ...a rhythm of plasma prolactin develops in constant light which is the exact opposite of the normal diurnal variation…”
  36. Relkin, R., et al. Effects Of Pinealectomy And Constant Light And Darkness On Prolactin Levels In The Pituitary And Plasma And On Pituitary Ultrastructure Of The Rat. 1972. "Compared with sham-operated diurnally-illuminated controls, constant darkness caused a decrease in pituitary prolactin content and a rise in plasma prolactin levels. Pinealectomy or constant illumination reversed the effect of constant darkness, resulting in an increase in pituitary prolactin content and a fall in plasma prolactin levels when compared with sham-operated diurnally-illuminated controls."
  37. Schmidt JB. Hormonal basis of male and female androgenic alopecia: clinical relevance. Skin Pharmacol. 1994;7(1-2):61-6. "Our findings showed a significant elevation of F [cortisol] in both male and female AH patients compared to controls, pointing to the suprarenes as a contributing factor in AH. This is confirmed by the observation of exacerbated AH in periods of increased stress.” "The mainly peripheral activity of this hormone and elevated E2 levels in males stress the importance of androgen metabolism especially at the peripheral level.” "Another significant finding was elevated PRL after TRH stimulation. Thus, the androgen-stimulating effect of PRL may also play a role in female AH. Our findings show multilayered hormonal influences in AH."
  38. Foitzik, K., et al. Human scalp hair follicles are both a target and a source of prolactin, which serves as an autocrine and/or paracrine promoter of apoptosis-driven hair follicle regression. Am J Pathol. 2006 Mar;168(3):748-56. "PRL has also been implicated in the pathogenesis of androgenetic alopecia by modulation of androgens, and hyperprolactinemia is associated with an androgenetic alopecia-type hair loss pattern, along with hirsutism (in females)."
  39. Rillema, J. A. Mechanism of prolactin action. Federation Proceedings [1980, 39(8):2593-2598] "Subsequent actions of prolactin may involve the following: a) an increased intracellular concentration of potassium and a reduced level of sodium, b) an increased level of cGMP and a reduced level of cAMP, c) an enhanced rate of prostaglandin biosynthesis mediated by a stimulation of phospholipase A2 activity, and d) a stimulation of polyamine synthesis."
  40. Kellner, R. et al. Hyperprolactinemia, distress, and hostility. Am J Psychiatry. 1984 Jun;141(6):759-63. “Hyperprolactinemic patients were significantly more hostile, depressed, and anxious and had more feelings of inadequacy than family practice patients and non patient employees. The authors recommend measuring the serum prolactin levels of women with depression, hostility, anxiety, and symptoms or signs suggestive of hyperprolactinemia.”
  41. Hollander, E., et al. Prolactin and sodium lactate-induced panic. Psychiatry Res. 1989 May;28(2):181-91. "Sodium lactate infusions reliably induce panic attacks in panic disorder patients but not in normal controls, but the mechanism underlying this response is unknown. We studied the plasma prolactin response to infusion of 0.5 molar sodium lactate in 38 patients with panic disorder or agoraphobia with panic attacks, and 16 normal controls. As expected, baseline plasma prolactin was significantly higher in female subjects than in male subjects. However, the males who experienced lactate-induced panic had significantly elevated baseline prolactin levels compared to male nonpanickers and controls. Prolactin levels increased in all groups during lactate infusion, which may reflect osmotic effects, but were blunted in the late panickers compared to nonpanickers and controls. The elevated baseline prolactin for male panickers supports a relationship between prolactin and anticipatory anxiety. The blunted prolactin response for late panickers suggests a net diminution, rather than a sensitization, of prolactin response in panic anxiety."
  42. Raymond, J., et al. Comparison between the plasma concentrations of prolactin and parathyroid hormone in normal subjects and in patients with hyperparathyroidism or hyperprolactinemia. J Clin Endocrinol Metab. 1982 Dec;55(6):1222-5. "These results show that an excess of plasma PRL is associated with an excess of plasma PTH and vice versa."
  43. Spätling, L., et al. Influence of prolactin on metabolism and energy production in perfused corpus luteum bearing bovine ovaries. "Under the influence of PRL anaerobic glucose metabolism was stimulated by 40.5% and oxidative phosphorylation was inhibited. Energy production from aerobic glucose metabolism rose by only 0.25%.” "This may indicate that PRL is the "older" hormone in phylogenetic terms."
  44. Martin, C. Endocrine Physiology. 1985. “When moderate dosages of PTH are injected into parathyroidectomized animals, the responses include increased urinary excretion of sodium, phosphate, bicarbonate, and amino acids, along with decreased excretion of calcium and hydrogen."
  45. Strider, J.W., et al. Treatment of mast cells with carbon dioxide suppresses degranulation via a novel mechanism involving repression of increased intracellular calcium levels. Allergy. 2011 Mar;66(3):341-50. "Results from this study provide the first evidence of a unique regulatory mechanism by which CO₂ inhibits mast cell degranulation and histamine release by repressing stimulated increases in intracellular calcium. Thus, our data provide a plausible explanation for the reported therapeutic benefit of noninhaled intranasal delivery of 100% CO₂ to treat allergic rhinitis."
  46. Ljunhgall, S., et al. Effects of epinephrine and norepinephrine on serum parathyroid hormone and calcium in normal subjects. Exp Clin Endocrinol. 1984 Dec;84(3):313-8. "During infusion of epinephrine there was a clear rise of the serum parathyroid hormone (PTH) levels already at the lowest concentration. Concomitantly there was a fall in the serum concentrations of calcium. The PTH levels returned to baseline promptly after termination of infusion whereas hypocalcaemia persisted up to 30 minutes, indicating a primary response of PTH to epinephrine.” (Low thyroid people tend to have very high adrenaline.)
  47. Richalet, J.P., et al. Effects of high-altitude hypoxia on the hormonal response to hypothalamic factors. Am J Physiol Regul Integr Comp Physiol. 2010 Dec;299(6):R1685-92. "Thyroid hormones were elevated at altitude (+16 to +21%), while TSH levels were unchanged, and follicle-stimulating hormone and prolactin decreased, while luteinizing hormone was unchanged."
  48. Kunelius, P., et al. The effects of transdermal dihydrotestosterone in the aging male: a prospective, randomized, double blind study. J Clin Endocrinol Metab. 2002 Apr;87(4):1467-72. "The objective of the study was to investigate the effects of dihydrotestosterone (DHT) gel on general well-being, sexual function, and the prostate in aging men. A total of 120 men participated in this randomized, placebo-controlled study (60 DHT and 60 placebo). All subjects had nocturnal penile tumescence once per week or less, andropause symptoms, and a serum T level of 15 nmol/liter or less and/or a serum SHBG level greater than 30 nmol/liter. The mean age was 58 yr (range, 50-70 yr).” "Serum concentrations of LH, FSH, E2, T, and SHBG decreased significantly during DHT treatment. Treatment with DHT did not affect liver function or the lipid profile. Hemoglobin concentrations increased from 146.0 +/- 8.2 to 154.8 +/- 11.4 g/liter, and hematocrit from 43.5 +/- 2.5% to 45.8 +/- 3.4% (P < 0.001). Prostate weight and prostate-specific antigen levels did not change during the treatment. No major adverse events were observed. Transdermal administration of DHT improves sexual function and may be a useful alternative for androgen replacement. As estrogens are thought to play a role in the pathogenesis of prostate hyperplasia, DHT may be beneficial, compared with aromatizing androgens, in the treatment of aging men."
  49. Casey, R., et al. Antiestrogenic action of dihydrotestosterone in mouse breast. Competition with estradiol for binding to the estrogen receptor. J Clin Invest. 1984 Dec;74(6):2272-8. "...Feminization in men occurs when the effective ratio of androgen to estrogen is lowered.” "Administration of estradiol via silastic implants to castrated virgin CBA/J female mice results in a doubling in dry weight and DNA content of the breast. The effect of estradiol can be inhibited by implantation of 17 beta-hydroxy-5 alpha-androstan-3-one (dihydrotestosterone), whereas dihydrotestosterone alone had no effect on breast growth. Estradiol administration also enhances the level of progesterone receptor in mouse breast." "Dihydrotestosterone does not compete for binding to the progesterone receptor, but it does inhibit estrogen-mediated increases of progesterone receptor content of breast tissue cytosol from both control mice and mice with X-linked testicular feminization (tfm)/Y.” "Dihydrotestosterone also promotes the translocation of estrogen receptor from cytoplasm to nucleus; the ratio of cytoplasmic-to-nuclear receptor changes from 3:1 in the castrate to 1:2 in dihydrotestosterone-treated mice. Thus, the antiestrogenic effect of androgen in mouse breast may be the result of effects of dihydrotestosterone on the estrogen receptor. If so, dihydrotestosterone performs one of its major actions independent of the androgen receptor."

Generative Energy #25: A Bioenergetic View of Osteoporosis

 
 

“The true method of knowledge is experiment.” —William Blake

“Experience is, for me, the highest authority. The touchstone of validity is my own experience. No other person’s ideas, and none of my own ideas, are as authoritative as my experience. It is to experience that I must return again and again, to discover a closer approximation to truth as it is in the process of becoming in me. Neither the Bible nor the prophets — neither Freud nor research — neither the revelations of God nor man — can take precedence over my own direct experience. My experience is not authoritative because it is infallible. It is the basis of authority because it can always be checked in new primary ways. In this way its frequent error or fallibility is always open to correction.” —Carl Rogers

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01:18 - Estrogen and bone metabolism
06:12 - Women's Health Initiative
10:30 - Mainstream therapies for osteoporosis
11:45 - Osteopotrosis, carbon dioxide, and lactic acid
15:55 - The hormone-like prostaglandins
18:21 - Thyroid, copper, and cytochrome c oxidase
19:55 - Are there any good iron tests?
26:24 - SSRIs, prolactin, and bone health
31:08 - Is Serotonin and Upper or Downer? (2015)
32:35 - Parathyroid hormone, calcium, and phosphate
36:22 - Clickbait health articles
39:33 - Tetracycline antibiotics for osteoporosis
41:50 - What tests would help with determining bone health?
46:45 - Are lab tests infallible?
49:35 - Georgi, where can we find more of your work this week?

Generative Energy #24: Q&A - Tooth Decay, Supplements vs. Food, Long Walks, and Ray Peat's Work

 
 

“The true method of knowledge is experiment.” —William Blake

“Experience is, for me, the highest authority. The touchstone of validity is my own experience. No other person’s ideas, and none of my own ideas, are as authoritative as my experience. It is to experience that I must return again and again, to discover a closer approximation to truth as it is in the process of becoming in me. Neither the Bible nor the prophets — neither Freud nor research — neither the revelations of God nor man — can take precedence over my own direct experience. My experience is not authoritative because it is infallible. It is the basis of authority because it can always be checked in new primary ways. In this way its frequent error or fallibility is always open to correction.” —Carl Rogers

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01:58 - Thoughts on tooth decay, carbon dioxide, and lactic acid
05:09 - “In the presence of hypothyroidism and magnesium deficiency everything is dangerous, but calcium and sodium are probably among the least dangerous things.” —Raymond Peat, PhD
07:20 - Children with food allergies
11:16 - Is there any reason to treat a child like a small adult?
13:14 - Food or supplements?
20:24 - Can supplements replace liver, oysters, and eggs?
24:35 - Caffeine, aspirin, niacinamide and fatty liver
30:53 - Enriching the environment and day-to-day metabolic enhancing activities
24:16 - Idealabs’ desiccated thyroid product, Tyromax
38:39 - Danny thinks desiccated thyroid should be taken orally
42:55 - Are Danny and Georgi slaves to Ray Peat?
48:24 - What Ray Peat’s work means to Danny
51:36 - Georgi, where can we find more of your work on the Internet this week?
52:30 - Info about next week’s episode

Generative Energy #23: Q&A - Weight Loss, Dating, Red Light, Authorities, Starch Diets

 
 

*I want to clarify at 35:02 that I don’t think that people who disagree with me are authoritarians. Rather, for the second half of the example, I should have emphasized that the people who were intolerant of ideas that collided with their world view were aggressive, inflexible, had an unwarranted level of certitude about what they were saying, and attacked my character when confronted with contrary evidence to their world view. I think those traits are consistent with Bob Altemeyer’s work in the book, The Authoritarians. 

“The true method of knowledge is experiment.” —William Blake

“Experience is, for me, the highest authority. The touchstone of validity is my own experience. No other person’s ideas, and none of my own ideas, are as authoritative as my experience. It is to experience that I must return again and again, to discover a closer approximation to truth as it is in the process of becoming in me. Neither the Bible nor the prophets — neither Freud nor research — neither the revelations of God nor man — can take precedence over my own direct experience. My experience is not authoritative because it is infallible. It is the basis of authority because it can always be checked in new primary ways. In this way its frequent error or fallibility is always open to correction.” —Carl Rogers

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01:18 - Should someone eliminate PUFA as fast as possible?
03:11 - Is the goal to completely inhibit lipolysis?
05:28 - An Overfeeding day when consuming low calories for weight loss?
06:25 - Spread dietary fat intake throughout the day?
07:42 - Georgi’s opinion of commercial shampoos and soaps
11:14 - Taking thyroid but the metabolism is still low
14:17 - Does fructose contribute to “hyperlipidemia”?
18:11 - Thoughts on excess urination—the role of aldosterone
20:13 - Hypothetical scenarios with HF and LF diets
22:28 - Georgi’s thoughts on autism
24:18 - Thoughts on dating from Danny and Georgi
27:59 - Overcoming cold and flu symptoms
30:50 - Thoughts on red light (cytochrome C oxidase)
33:00 - Clarifying our use of the word “authoritarian”—the initiation of force
41:09 - High-starch low-fat diets—how could so many physicians be wrong?
47:39 - Georgi, where can we find more of your work on the internet this week?
48:36 - Details on next week’s episode

Generative Energy #22: A Bioenergetic View of Heart Disease and Stroke

 
 

“The heart’s unique behavior has given cardiologists a particularly mechanical perspective on biology. If a cardiologist and an oncologist have anything to talk about, it’s likely to be about why cancer treatments cause heart failure; a cardiologist and an endocrinologist might share an interest in “cardioprotective estrogen” and “cardiotoxic obesity.” Cell physiology and bioenergetics aren’t likely to be their common interest. Each specialty has its close involvement with the pharmaceutical industry, shaping its thinking. —Heart and hormones by Ray Peat ► http://bit.ly/1p6ZDo8

“Alterations in cardiac energy metabolism can profoundly affect cardiac efficiency. Excessive use of free fatty acids has been shown to be especially important, either by decreasing the efficiency of producing ATP, or by decreasing ATP availability for contractile function.” —Impact of fatty acid oxidation on cardiac efficiency ► http://bit.ly/1p6ZvVC

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01:18 - Rising interest in heart disease and stroke
05:45 - Heart disease begins at a very young age
07:27 - What’s the role of cholesterol in heart disease?
11:13 - The heart and hormones
17:55 - What’s the role of aldosterone “the salt-retaining hormone” in heart disease?
25:38 - Blood volume, sodium, and dietary protein
30:34 - The role of endotoxin in heart disease and stroke
33:09 - Aspirin for heart disease?
38:57 - “Normal” TSH and fatal coronary heart disease
40:20 - Is heart disease a mystery?
42:13 - Where can we find more of your work, Georgi?
42:57 - Do your own research and come to your own conclusions

Generative Energy #21: Are You Listening?

 
 

01:13 - Danny’s teaching experience
03:42 - The folly of solving each other
04:48 - Pain and struggle
06:41 - Struggle leading to creation
07:36 - Carl Rogers’s work
10:35 - ‘Drive in your own lane’
11:29 - ‘Seeking authority to avoid pain’
13:18 - The listening robot
13:58 - Danny’s thinks learning is painful
14:51 - ‘So many people willing to be the final say’
15:33 - Ray’s email responses and learning on your own
18:16 - Karen’s experience with medical professionals
20:25 - What to look for in a listener
22:04 - Acceptance and belonging: ’That’s natural’
23:02 - Danny’s character armor
25:01 - Karen’s experience with rock climbing
26:34 - Therapy led to a higher degree of tolerance for others
29:27 - ‘Your passion as a metaphor for life’
30:57 - A Very Special Genie (http://bit.ly/1ota19m)
32:11 - Anecdote from Danny
36:13 - Percival myth (http://bit.ly/1otazft)

Generative Energy #20: A Bioenergetic View of Dementia

 
 

Generative Energy #20: A Bioenergetic View of Dementia with Danny and Georgi

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01:18 - Please do your own research and come to your own conclusions
04:26 - The mainstream view of dementia
06:12 - Mainstream therapies for dementia
08:27 - Is Alzheimer’s diabetes type III?
09:43 - Is Alzheimer’s an energy problem?
11:56 - Fish oil (EPA and DHA) for brain health?
13:21 - Acrolein—toxic breakdown product of fish oil peroxidation
15:09 - A brief overview of lipid peroxidation from Georgi
17:26 - The pituitary’s role in dementia
20:51 - The role of bacterial endotoxin (lipopolysaccharide) in dementia
23:30 - Danny’s thoughts on penicillin VK and minocycline
26:00 - Strategies for treating dementia
27:15 - Methylene blue for dementia
27:58 - Niacinamide for dementia
29:02 - Pregnenolone, progesterone, and DHEA—for brain health
32:08 - Vitamins A, K, and D for dementia
33:42 - The role of carbon dioxide in dementia and physiology
35:13 - Carbon dioxide protects against advanced glycation end products (AGEs)?
36:24 - Isn’t the Alzheimer brain deficient in omega-3s?
37:58 - How the body disposes of unsaturated fatty acids (glucuronidation)
39:31 - The composition of cardiolipin and Alzheimer’s
42:40 - Georgi touches on Parkinson’s disease
47:26 - Danny’s anecdote about involuntary movement and thyroid hormone
48:21 - Where can we find more of your work on the Internet this week, Georgi?
49:49 - Info on next week’s show

Generative Energy #19: Talking with Ray Peat

 
 

“Since the contextuality of communication is always in the foreground when I talk or write, you know that someone is confusing me with an authority when they talk about my ‘protocol’ for something. Context is everything, and it’s individual and empirical.” —Raymond Peat, PhD

“Making an effort to learn how to use techniques of food, hormones, light, activity, etc., is similar to the effort needed to work with a psychologist, and the effort itself is part of the therapy—the particular orientation of the psychotherapist isn’t what’s therapeutic, it’s the ability to participate in meaningful interactions, that is, the ability to provide a situation in which the person can practice being human. When people start thinking about the things in their life that can be changed, they are exercising aspects of their organism that had been atrophied by being in an authoritarian culture. Authoritarians talk about protocols, but the only valid ‘protocol’ would be something like ‘perceive, think, act.’” —Ray Peat

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01:10 - What Ray did after he graduated (1956)
08:36 - Understanding Ray’s orientation toward radiation
14:16 - Starting Blake College in Mexico City
17:43 - Madalyn Murray’s involvement in Blake College
31:22 - Madalyn Murray takes over Blake College
36:47 - Ray’s own health journey—the lead up to writing his book, Nutrition for Women (1973)
37:52 - Ray’s consistent thesis
42:42 - Ray’s experience with pregnenolone and vitamin E (1983)
45:29 - When Ray began thinking more seriously about unsaturated fats
47:43 - Ray’s “survival diet”
50:18 - Ray’s new newsletter: Mushrooms—observations and interpretations
53:56 - Button mushrooms are anti-aromatase (and anti-nitric oxide)
54:27 - The amount needed for a biological effect and a recipe
55:31 - Some details about Ray’s own diet
56:09 - Does Ray think everyone has to eat like him?
57:03 - Mushrooms and the alt-view of the immune system
1:01:14 - The mushroom sugar, trehalose
1:02:09 - Is lanosterol like cholesterol?
1:03:28 - Can mushrooms replace meat?
1:04:57 - The new availability of Ray’s newsletter: raypeatsnewsletter@gmail ($28 for 12 issues over 2 years)
1:05:20 - What else are you working on Ray?

Recharging The Mosaic Cycle: The Role of G6PDH in Baldness

 
 
 
 

One of my favorite films of 2014 was The Internet’s Own Boy, a film that chronicled the life and death of boy genius and anti-authoritarian activist, Aaron Swartz. Almost immediately after the film was over (you can watch it here on YouTube), I remember reaching out to my friend Karen to tell her how much I enjoyed the film. Half way into our conversation we both noted that Aaron had a great head of hair, and Karen went on to say that she noticed that Aaron’s hair seemed to dim during the times of the film that the documentary discussed Aaron’s digestive ailment, Crohn’s disease. 

The connection between health and hair growth is not fringe and has been widely discussed over the last few decades. As early as 1993, it was known that baldness was associated with developing heart disease[1,2,3,4]. Later, baldness was found to be related to other problems like metabolic syndrome,[5] high cholesterol,[6] reduced bone mineral density,[7] and cancer.[8] 

The evidence that hair growth and health are interconnected doesn’t appear to have penetrated the mainstream, and instead, you’re likely to be blunted over the head with an endless array of pseudo-intellectual blowhards progressing the idea that baldness is simply the result of bad genes and excess masculinity. Their science comprises of rattling off model after model of ever growing complexity that is divorced from the individual and their environment. This compartmentalized anti-science approach to hair loss is often reflected in the phases of the hair growth cycle or the mosaic cycle.

I: The Mosaic Cycle

Hair follicles go through a cyclical growth phase composed of three phases: anagen, the phase of active growth; catagen, the phase of regression; and telogen, the resting period. The proportion of anagen follicles is highest in childhood and lowest in old age, and there are small, relatively constant variations in different regions of the scalp.

When a hormone or drug is said to increase the anagen growth of hair sometimes the substance is deemed good or useful for hair growth. For example, finasteride can increase the anagen growth of hair follicles, but also may be carcinogenic.[9] Similarly, the hormone-like unsaturated fatty acid breakdown product, prostaglandin E2 (PGE2), is said to promote anagen growth and is also associated with cancer.[10,11] Substances that promote growth like finasteride or PGE2 stimulate mitosis, which might appear to have a “positive” effect on hair growth while having a negative systemic effect on the organism. Thus, I think its important to attempt to understand the overall physiology of the balding person and hair growth rather than identifying substances that simply promote anagen growth

Similar to bone marrow, skin, intestine, and other highly proliferative glucose-dependent tissues, the hair follicle is composed of rapidly dividing cells that convert more than 85% of their glucose to lactic acid via glycolysis (fermentation). When the various glucose pathways are studied in growing and resting follicles, the metabolic activities are found to be much higher during the growing anagen phase. For example, in growing follicles glucose utilization increases 200%, glycolysis 200%, the activity of pentose phosphate cycle 800%, metabolism by other pathways 150%, and ATP production via the respiratory chains 270%.[12] 

In the bulb portion of growing follicles, the activity of glucose-6-phosphate dehydrogenase (G6PDH), a key enzyme and rate-limiting factor in the pentose phosphate cycle, increased 350% over that in resting follicles. Clearly, by activating the pentose phosphate cycle, glucose assimilation in growing hair follicles produces not only sufficient energy for itself but also essential substances like the electron carrier, NADPH.

Two important functions of NADPH is to help produce steroids within the hair follicle and to provide “reducing power” to recycle reduced glutathione (GSSG) back to glutathione (GSH), protecting the hair follicle from oxidative damage

II: Glucose-6-Phosphate Dehydrogenase (G6PDH)

A decrease in anagen to telogen hairs (mainly in the frontal-parietal region) is a major symptom of male-pattern baldness. In 1999, Adachi et al. found that G6PDH activity decreases in direct relationship with the decreasing ratio of anagen hairs. In fact, the researchers suggested that “G6PDH could be a suitable marker for diagnosis of alopecia” and that “energy metabolism may be a new strategy to prevent and cure male-pattern alopecia”.[13] 

A decrease in the activity of G6PDH increases the ratio of NADP/NADPH. As the availability of NADPH declines, GSSG cannot be recycled back into GSH to protect the hair follicle from oxidative stress. In 2015, a group found that balding dermal papilla cells have “significantly higher concentrations of GSSG” compared to occipital dermal papilla cells, and that the balding hair follicles “appear to be less able to handle oxidative stress”. The group concluded the abstract with, “there may be a role for oxidative stress in the pathogenesis of [male-pattern baldness]”.[14]

The energy metabolism done by G6PDH in hair follicles of male-pattern alopecia may be related to the hair growth, and activation of the energy metabolism may be a new strategy to prevent and cure male-pattern alopecia.
— Activity of glucose-6-phosphate 1-dehydrogenase in hair follicles with male-pattern alopecia (1999)

If supporting energy metabolism can be thought of as ‘a strategy for preventing and curing so-called male-pattern baldness,’ as Adachi et al. suggested, I think it’s important to look at factors in the environment that contribute to decreasing the activity of G6PDH and production of NADPH. 

III: G6PDH Regulation

Unsaturated fatty acids have increased 1000 fold from 1909 to 1999,[15] and have a dominant position in the world's food supply. In addition to being the precursor for the prostaglandin Garza et al. discovered accumulated in the scalp's of balding men and inhibited hair growth,[16] they appear to be inhibitors of G6PDH. In one experiment, rats were switched from a non-fat diet to one containing 15% unsaturated fatty acids and there was an 8-fold decrease in the level of G6PDH. When the rats fasted for two days and were fed a high-carbohydrate, non-fat diet, the activity of G6PDH increased to an amount larger than that of the "normal" fed state.[17]

In contrast to the unsaturated fats, adding saturated fats (palmitate or stearate), or a monounsaturated fat (oleate), does not inhibit, or inhibits G6PDH activity to a lesser degree,[18] suggesting that the inhibition of G6PDH is not solely a consequence of reduced carbohydrate intake. In an experiment with rodents, 20% of calories from safflower oil inhibited the activity of G6PDH to a greater degree than 20% of calories from beef tallow.[19] Similar to safflower oil, the so-called "essential fatty acids" were found to inhibit G6PDH activity, too.[20]

In comparison to the inhibitory effect of the unsaturated fats, carbohydrates appear to stimulate G6PDH activity. The greatest change in G6PDH activity is observed when rats are fed diets containing glucose or fructose, compared with starch, and stimulation by fructose is greater than by glucose.[21] In diabetic rats, fructose increased the activity of G6PDH more than glucose, suggesting that it might be the most useful carbohydrate for increasing G6PDH activity.[22]

IV: Recharging The Mosaic Cycle

The microinflammatory process of baldness suggests that the hair follicle is undergoing stress,[23] and the energy requirements for highly proliferative tissues are amplified in stress. For example, in 3-day old wounds, the activities of glycolytic enzymes increase 4 times over normal levels, there's a 5-fold increase in oxygen uptake, and the rate of lactate production is tripled. G6PDH activity triples in psoriasis increases 5-fold in tumors and hyperplasia and 7-fold in the epidermis during wound healing. There is a 50% increase in glucose flow along the pentose phosphate pathway during wound healing.[24] 

Sugars stimulate the hormone insulin, an “inducer“ of G6PDH. In rats, when insulin levels drop, there is a concomitant decrease in G6PDH activity, and when animals are refed, G6PDH activity is restored. Moreover, administration of insulin alone increased G6PDH enzyme in a dose-dependent manner. It was proposed in Montagna's epic, The Biology of Hair Growth that insulin—and not glucose—might be the critical factor in the growth of hair follicles.[25] 

In addition to inducing G6PDH, insulin activates another regulator of G6PDH, thyroid hormone.[26] Thyroid hormone is essential for the initiation as well as the maintenance of hair growth, and the main effect of this hormone is to preserve the anagen state. Low thyroid function is associated with an increase in the percentage of telogen to anagen hairs, as well as higher levels of total cholesterol.[27] In 2010, it was found that men and women with androgenic alopecia had higher levels of cholesterol, and that the anomalous lipid values "...may contribute, alongside other mechanisms, to the development of cardiovascular disease in patient with androgenic alopecia."[28] 

Both thyroid hormones, T2 and T3, increased the activity of G6PDH in hypothyroid rats, and G6PDH activity was elevated in patients with thyrotoxicosis.[29] As I’ve mentioned previously, Vidali, et al. called for a repositioning of thyroid hormone as “mitochondrial hair medicine” in 2013.[30] 

Disturbances of hair cycles involve modification of the relative duration of the phases of the cycle and are most characteristically determined by excess or deficiency of glucocorticosteroids or thyroid hormones. They are usually completely reversible.
— Rook, A. Endocrine Influences on Hair Growth. 1965.

Insulin and thyroid hormone tend to shift the metabolism away from the oxidation of free fatty acids and the production of the adaptive "stress" hormones and toward the constructive use of sugar. A lowered rate of metabolism (or the "stress" metabolism)—and not “bad genes” or an excess of masculinity—I think, is the most coherent explanation for the development of pattern baldness in both men and women. 

References

  1. Lesko, S.M., et al. A case-control study of baldness in relation to myocardial infarction in men. JAMA. 1993 Feb 24;269(8) “The relationship between vertex baldness and myocardial infarction was consistent within strata defined by age and other risk factors for coronary artery disease.””These data support the hypothesis that male pattern baldness involving the vertex scalp is associated with coronary artery disease in men under the age of 55 years.”
  2. Morteza, et al. Prevalence of Dermatologic Features in Patients With Ischemic Heart Disease. Shiraz E-Medical Journal. 2015 January. “Male pattern baldness, hair graying, xanthoma, and earlobe crease are associated with increased risk of ischemic heart disease. These dermatologic signs can be considered as CVD risk factors for screening.”
  3. Lotufo, P.A., et al. Male pattern baldness and coronary heart disease: the Physicians’ Health Study. Arch Intern Med. 2000 Jan 24;160(2):165-71. “Vertex pattern baldness appears to be a marker for increased risk of CHD events, especially among men with hypertension or high cholesterol levels.”
  4. Agac, M.T., et al. Androgenetic alopecia is associated with increased arterial stiffness in asymptomatic young adults. J Eur Acad Dermatol Venereol. 2014 Mar 14. “We concluded that, AGA might be an indicator of arterial stiffness in asymptomatic young adults.”
  5. Su, L.H., et al. Association of Androgenetic Alopecia with Metabolic Syndrome in Men: A Community-based Survey. Br J Dermatol. 2010 Aug;163(2):371-7. “Conclusions: Our population-based study found a significant association between AGA and MetS; among MetS components, HDL was found to be of particular importance. This finding may have significant implications for the identification of MetS in moderate or severe AGA patients. Early intervention for MetS is critical to reduce the risk and complications of cardiovascular disease and type 2 diabetes mellitus later in life.”
  6. Arias-Santiago, S., et al. A comparative study of dyslipidaemia in men and woman with androgenic alopecia. Acta Derm Venereol. 2010 Sep;90(5):485-7. doi: 10.2340/00015555-0926. “A higher prevalence of dyslipidemia in women and men with androgenic alopecia has been found. The elevated lipid values in these patients may contribute, alongside other mechanisms, to the development of cardiovascular disease in patient with androgenic alopecia.”
  7. Morton, D.J., et al. Premature graying, balding, and low bone mineral density in older women and men: the Rancho Bernardo study. J Aging Health. 2007 Apr;19(2):275-85. “Balding men averaged 5% lower total body BMD (p </= 0.05), and balding women had ~24% higher mean hip BMD (p </= 0.05). Graying and balding women reported a higher proportion of current estrogen use; balding women reported more use of glucocorticosteroids. Balding women using estrogen may explain the higher BMD.”
  8. Zhou, C., et al. Relationship Between Male Pattern Baldness and the Risk of Aggressive Prostate Cancer: An Analysis of the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. 2014. “Our analysis indicates that frontal plus moderate vertex baldness at age 45 years is associated with an increased risk of aggressive prostate cancer and supports the possibility of common pathophysiologic mechanisms.”
  9. Kleenmann, D., et al. [The effect of hormonal agents on the development of chronic laryngitis and tumor disease. Report of two cases]. HNO. 2010 Mar;58(3):305-12. “In the first case of a patient suffering from chronic hyperplastic laryngitis for 17 years, a close correlation was found between the treatment with the 5alpha-reductase inhibitor Finasteride, the drop in serum levels of dihydrotestosterone (DHT), and the appearance of an invasive squamous cell carcinoma of the vocal cord. During the postoperative 7-year follow-up without recurrence the androgen serum levels were within normal range.” “ In the second patient, who had undergone previous surgery for mesopharyngeal cancer at another site before the present tumor operation, rapid recurrence was seen within 2 years. Despite radical revision surgery and subsequent irradiation the patient insisted on carrying on with his work. He complained about a general lack of stamina and libido. His androgen serum levels were at the low-end of the normal range and even below that. The daily administration of 25 mg dehydroepiandrosterone (DHEA) resulted in normal androgen serum levels and improved his wellbeing. He has been free of recurrence for 10 years.” “”…cofactor in the genesis and development of malignant tumors of the upper aerodigestive tract.”
  10. Badawi, A.F. The role of prostaglandin synthesis in prostate cancer. BJU Int. 2000 Mar;85(4):451-62. “It was suggested recently that PGE2 plays a major role in the growth of prostate cancer cells through the activation of COX-2 expression. Increased levels of PGs have been widely reported in malignant human prostate tumours and in carcinogen-induced rat and mouse prostate cancers. In vitro studies with tissue explants or primary cultures of prostate tumour cells have also shown higher PG production in malignant tissue than in benign or normal tissue. Increased synthesis of PGs was associated with advancing prostate cancer and the concentrations increased as the degree of tumour differentiation progressed, i.e. a worse prognosis.”
  11. Greenhough, A., et al. The COX-2/PGE2 pathway: key roles in the hallmarks of cancer and adaptation to the tumour microenvironment. Carcinogenesis. 2009 Mar;30(3):377-86. “It is widely accepted that alterations to cyclooxygenase-2 (COX-2) expression and the abundance of its enzymatic product prostaglandin E(2) (PGE(2)) have key roles in influencing the development of colorectal cancer.” “Future studies into the emerging players within the COX-2/PGE2 pathway may reveal novel approaches for more safely targeting this pathway for both cancer chemoprevention and therapy.”
  12. Motagna, W. The Structure and Function of Skin. 1974. The general metabolic pattern is extremely “glycolytic,” i.e., more than 85% of the glucose consumed is reduced to lactate. When the various glucose pathways are studied in growing and resting follicles, the metabolic activities are found to be much higher during the growing phase. For example, in growing follicles glucose utilization increases 200%, glycolysis 200%, the activity of pentose cycle 800%, metabolism by other pathways 150%, and ATP production via the respiratory chains 270%.” “Clearly, by activating the pentose cycle, glucose assimilation in growing hair follicles produces not only sufficient energy for itself but also essential substances (TPNH, ribose, etc.) for the follicle to metabolize fatty acid, nucleic acids, and steroid hormones. When the enzymes of carbohydrate metabolism were assayed with the microtechnique of Lowry (1953), the results agreed with those obtained above. For example, in the bulb portion of growing follicles, the activity of glucose-6-phosphate dehydrogenase, a key enzyme of the pentose cycle, increased 350% over that in resting follicles.”
  13. Rushton, H., et al. The unit area trichogram in the assessment of androgen-dependent alopecia. Br J Dermatol. 1983 Oct;109(4):429-37.
  14. Upton, J.H., et al. Oxidative stress-associated senescence in dermal papilla cells of men with androgenetic alopecia. J Invest Dermatol. 2015 May;135(5):1244-52. “Balding DPCs had higher levels of catalase and total glutathione but appear to be less able to handle oxidative stress compared with occipital DPCs. These in vitro findings suggest that there may be a role for oxidative stress in the pathogenesis of AGA both in relation to cell senescence and migration but also secretion of known hair follicle inhibitory factors.”
  15. Blasbalg, T.L., et al. Changes in consumption of omega-3 and omega-6 fatty acids in the United States during the 20th century. Am J Clin Nutr. 2011 May;93(5):950-62. “The estimated per capita consumption of soybean oil increased >1000-fold from 1909 to 1999.”
  16. Garza, L.A., et al. Prostaglandin d2 inhibits hair growth and is elevated in bald scalp of men with androgenetic alopecia. Sci Transl Med. 2012 Mar 21;4(126):126ra34. “Given the androgens are aromatized into estrogens, these results may be relevant to hair growth and alopecia in both men and women. Thus, these or similar pathways might be conserved in the skin and suggest that sex hormone regulation of Ptgds may contribute to the pathogenesis of AGA.” “…demonstrates elevated levels of PGD2 in the skin and develops alopecia, follicular miniaturization, and sebaceous gland hyperplasia, which are all hallmarks of human AGA. These results define PGD2 as an inhibitor of hair growth in AGA and suggest the PGD2-GPR44 pathway as a potential target for treatment.”
  17. Gozukara, E.M., et al. The effect of unsaturated fatty acids on the rate of synthesis of rat liver glucose-6-phosphate dehydrogenase. Biochim Biophys Acta. 1972 Nov 24;286(1):155-63.
  18. Salati, L.M., et al. Dietary regulation of expression of glucose-6-phosphate dehydrogenase. Annu Rev Nutr. 2001;21:121-40. “G6PD activity is enhanced by dietary carbohydrates and is inhibited by dietary polyunsaturated fats.” “Addition to the diet of saturated fatty acids, such as palmitate (16:0) and stearate (18:0), and of monounsaturated fatty acids, such as oleate (18:1), do not inhibit G6PD activity.”
  19. Clarke, S.D., et al. Inhibition of triiodothyronine’s induction of rat liver lipogenic enzymes by dietary fat. J Nutr. 1990 Jun;120(6):625-30. “The objective of these studies was to demonstrate that the reduction in lipogenic enzymes caused by ingestion of dietary polyunsaturated fat can in part be attributed to an inhibition of triiodothyronine’s induction of hepatic lipogenic enzymes.” “Triiodothyronine (T3) administration induced (p less than 0.05) the activity of malic enzyme, fatty acid synthase and glucose-6-phosphate dehydrogenase in a dose-dependent manner.” “Beef tallow and safflower oil supplementation of the high glucose, fat-free diet significantly reduced the T3 induction of all the enzymes. Safflower oil was more effective than tallow as a repressor of T3 action. The effect of dietary fat, particularly safflower oil, was to increase the amount of T3 required to induce the activity of lipogenic enzymes.” “These data support the hypothesis that polyunsaturated fats uniquely suppress the gene expression of lipogenic enzymes by functioning as competitive inhibitors of T3 action, possibly at the nuclear receptor level.”
  20. Clarke, S.D., et al. Specific inhibition of hepatic fatty acid synthesis exerted by dietary linoleate and linolenate in essential fatty acid adequate rats. Lipids. 1976 Jun;11(6):485-90. “However, 18:2 addition to the basal diet did result in a significant (P less than 0.05) decline of liver fatty acid synthetase (FAS) and glucose-6-phosphate dehydrogenase (G6PD) activities. When the safflower oil content of the basal diet was reduced to 1%, the addition of 3% 18:2 or linolenate 18:3 significantly (P less than 0.05) depressed hepatic FAS, G6PD, and in vivo fatty acid synthesis by 50%.”
  21. Kastrouni, E., et al. Activity changes of glucose-6-phosphate dehydrogenase in response to diet and insulin. Int J Biochem. 1984;16(12):1353-8.
  22. Fukuda, H., et al. Effects of high-fructose diet on lipogenic enzymes and their substrate and effector levels in diabetic rats. J Nutr Sci Vitaminol (Tokyo). 1983 Dec;29(6):691-9. “When rats adapted to a stock diet were fed on various high-carbohydrate diets, the hepatic activities of glucose-6-phosphate dehydrogenase, malic enzyme and acetyl-CoA carboxylase were more greatly increased by fructose than by any other carbohydrate. Even in the diabetic state, the enzyme activities were somewhat increased by fructose feeding.”
  23. Mahe, Y.F., et al. Androgenetic alopecia and microinflammation. Int J Dermatol. 2000 Aug;39(8):576-84. "Despite such a reduction of circulating 5-DHT levels, however, a number of individuals (60–70%) still remained unresponsive to this treatment, indicating again that simple dysregulation of 5-DHT synthesis levels or a genetic polymorphism of 5α-R genes cannot account for all cases of AGA, and a polygenic etiology should be considered.” "The fact that the success rate of treatment with either antihypertensive agents, or modulators of androgen metabolism, barely exceeds 30% means that other pathways may be envisioned.” "Once aa is released from the cell membrane phospholipids by phospholipase A2,18,19 it is metabolized through a complex equilibrium between two families of enzymes, generating either prostaglandins (PGs) (through the activity of PGH synthases, PGHSs) or leukotrienes…” "This upregulation of androgen metabolism by proinflammatory cytokines remains, however, to be established at the pilosebaceous unit level.” "We know now that, at least in about one-third of cases, the tool which causes the lethal damage is a microinflammatory process."
  24. Motagna, W. The Structure and Function of Skin. 1974. “A specific feature of the epidermis—intense glycolytic activity in the presence of oxygen—is amplified by trauma. For example, during wound healing, glycolytic activity increases in the regenerating epidermis and a minor alteration in glucose catabolism occurs through the tricarboxylic acid cycle. Wounded skin also exhibits increased glucose utilization and lactate production. The activities of glycolytic enzymes increase 4 times over normal levels, and the rate of lactate production from uniformly labeled glucose-14C is tripled in 3-day-old wounds. The activities of key glycolytic enzymes increase in some skin disorders and in experimental lesions.” “Healing wounds show a fivefold increase in oxygen uptake.” “However, a small part of glucose metabolism through the tricarboxylic acid cycle decreases to half that of normal skin. Presumably, then, the fuel for increased respiratory oxidation in healing skin comes from other sources of nutrient. Glucose metabolism through the pentose phosphate shunt supplies the pentose needed for nucleic acid formation and for reduced nicotinamide denucleotide phosphate (NADPH), a reducing equivalent needed for lipogenesis and indirectly for keratinization. Increased activity in this shunt in psoriasis, hyperplasia, tumors, and wound healing reflects the increased demands of the epidermis for synthetic activities. Glucose-6-phosphate dehydrogenase activity of the pentose phosphate shunt triples in psoriasis, increases 5-fold in tumors and hyperplasia, and 7-fold in the migrating epidermis during wound healing. There is a 50% increase in glucose flow along the pentose phosphate shunt during wound healing.” 
  25. Montagna, W. The Biology of Hair Growth. 1958. “Insulin and not glucose seems to be the critical factor in the growth of hair follicles. Unlike the epidermis, hair follicles are able to grow normally despite changes in the concentration of blood glucose. Although both oxygen and a carbohydrate source are essential for maintaining the mitotic activity of a hair follicle in vitro, drastic conditions such as starvation or shock are required to influence such activity in vivo. The abundant supply of glycogen in growing hair follicles may partially account for the relative independence of the hair follicle from the level of circulating glucose.”
  26. Jennings, A.S., et al. Regulation of hepatic triiodothyronine production in the streptozotocin-induced diabetic rat. Am J Physiol. 1984 Oct;247(4 Pt 1):E526-33. “Induction of diabetes with streptozotocin resulted in decreased serum thyroxine (T4) and T3 levels and a progressive decline in hepatic T3 production over 5 days. The decline in T3 production resulted from decreased conversion of T4 to T3, whereas T4 uptake was unchanged. Insulin administration restored serum T4 and T3, hepatic conversion of T4 to T3, and T3 production to normal levels. When serum T4 levels in diabetic rats were maintained by T4 administration, the conversion of T4 to T3 and T3 production returned to control levels. However, restoration of serum T4 levels in fasted rats failed to correct the decrease in hepatic T4 uptake or T3 production.” “These data suggest that the fall in serum T4 levels observed in diabetic rats is important in mediating the decreased hepatic conversion of T4 to T3 and T3 production.”
  27. Saito, R. and Nishiyama, S. Alopecia in Hypothyroidism. Hair Research 355-357 (1981). "Freinkel and Freinkel studied the relative proportions of telogen to anagen hairs in the scalps of hypothyroid subjects with hair loss and found that deficiency of thyroid hormone was associated with an increase in the percentage of telogen hairs in all instances.” "Not only the duration and grade of hypothyroidal condition, but also anemia, hypercholesteremia, disturbances of Vitamin A metabolism, and local deposition of mucin induced by hypothyroidism must be considered as factors inducing hair loss in hypothyroidism.” "Vitamin A is essential for preserving the function of the epidermis, and deficiency of Vitamin A may induce dyskeratosis of follicular openings and hair loss. Inasmuch as deposition of mucin in whole tissues (including perifollicular tissue) is observed, mucin may have some effect of keratin synthesis."
  28. Arias-Santiago, S., et al. A comparative study of dyslipidaemia in men and woman with androgenic alopecia. Acta Derm Venereol. 2010 Sep;90(5):485-7. doi: 10.2340/00015555-0926. "A higher prevalence of dyslipidemia in women and men with androgenic alopecia has been found. The elevated lipid values in these patients may contribute, alongside other mechanisms, to the development of cardiovascular disease in patient with androgenic alopecia."
  29. Yilmaz, S., et al. Oxidative damage and antioxidant enzyme activities in experimental hypothyroidism. Cell Biochem Funct. 2003 Dec;21(4):325-30. “Several studies have demonstrated that thyroid hormones regulate G6PD activity. Lombardi et al. generated experimental hypothyroidism in rats by i.p. injection of PTU and iopanic acid in combination. This type of combined application of drugs for induction of hypothyroidism causes serious hypothyroidism and the three known types of diodinase were also inhibited. Rats with serious hypothyroidism were injected with different doses of T2 and T3 for 2 weeks and effects on their livers were evaluated. G6PD activity levels in the liver of rats with hypothyroidism were determined to be 28% lower than that in the control animals, whereas a reduction in the thymus was not significant. T2 and T3 administration caused an increase in the G6PD activity levels. G6PD activity was reported to be mainly regulated by T2. In rats with thyroidectomy, G6PD activity levels were found to be lower compared to controls, but T3 application reversed the effect of thyroidectomy. G6PD activity levels were reported to be increased in patients with thyrotoxicosis compared to controls. In the present study, we found that in the rats with hypothyroidism, G6PD activity levels were not changed in the thymus but were reduced in liver tissues compared to controls. These findings are in agreement with those of Lombardi et al.”
  30. Vidali, S., et al. Hypothalamic-Pituitary-Thyroid Axis Hormones Stimulate Mitochondrial Function and Biogenesis in Human Hair Follicles. J Invest Dermatol. 2013 Jun 27. “HPT-axis hormones did not increase reactive oxygen species (ROS) production. Rather, T3 and T4 reduced ROS formation, and all tested HPT-axis hormones increased the transcription of ROS scavengers (catalase, superoxide dismutase 2) in HF keratinocytes. Thus, mitochondrial biology, energy metabolism, and redox state of human HFs are subject to profound (neuro-)endocrine regulation by HPT-axis hormones. The neuroendocrine control of mitochondrial biology in a complex human mini-organ revealed here may be therapeutically exploitable.“ “The current data also provide clinically relevant pointers to how HF aging and disease correlated with declining mitochondrial function might be effectively counteracted in the future by endogenous neurohormones produced in the human epithelium, e.g., TRH and TSH. This also applies to THs [thyroid hormones], which have long been known to modulate hair shaft quality and/or pigmentation. Both TRH and T4 are administered routinely in thyroid medicine and are FDA-approved agents with a well-known toxicity profile. Therefore, regulatory hurdles to reposition these hormones for novel ‘mitochondrial hair medicine’ approaches are relatively low.” 

Generative Energy #18: Q and A with Danny and Georgi

 
 

“The true method of knowledge is experiment.” —William Blake

“Experience is, for me, the highest authority. The touchstone of validity is my own experience. No other person’s ideas, and none of my own ideas, are as authoritative as my experience. It is to experience that I must return again and again, to discover a closer approximation to truth as it is in the process of becoming in me. Neither the Bible nor the prophets — neither Freud nor research — neither the revelations of God nor man — can take precedence over my own direct experience. My experience is not authoritative because it is infallible. It is the basis of authority because it can always be checked in new primary ways. In this way its frequent error or fallibility is always open to correction.” —Carl Rogers

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01:17 - How an episode is made
02:44 - Georgi’s general thoughts on taking thyroid hormone
11:36 - Weird symptoms when taking T4 or T3?
13:49 - A bioenergetic view of acne and skin health
15:12 - A bioenergetic view of exercise
19:10 - Georgi’s favorite books
20:20 - Georgi’s approach to learning
24:38 - A bioenergetic view of sleep
28:08 - Mitigating anger and aggression
32:50 - Clarifying “so-called receptors”
38:16 - Thoughts on tinnitus (ear ringing)
39:59 - MTHFR mutation—a plausible mechanism for disease?
42:12 - A reasonable supplement regimen for a healthy person
46:35 - Problems with cancer as a genetic disease
48:39 - Antiphospholipid syndrome and breast cancer
51:00 - Georgi, where can we find more of your work?
51:50 - Next week’s episode

Generative Energy #17: PMS, PCOS, and Breast Cancer

 
 

01:17 - “Female hormones” and stress, aging, and inflammation
01:50 - Estrogen—not the “female hormone”
03:10 - Levels of estrogen rise with metabolic stress
03:42 - Estrogen is a carcinogen and mutagen
04:30 - How could estrogen cause so many problems?
07:48 - PUFA are estrogenic
09:17 - PCOS and breast cancer are tightly related
10:38 - Bleeding, poor mood, mental disorders—estrogen problems
11:53 - Estrogen increases cortisol—influences mood
12:46 - Mianserin (antiserotonin drug) for symptoms of PMS
13:51 - Estrogen suppresses pituitary menopausal hormones
16:12 - Are progestins the same as progesterone?
18:26 - PMS, PCOS, and breast cancer—excess estrogen?
20:15 - A hyperestrogenic environment
25:35 - Actionable things to lower estrogen, cortisol, etc.
32:55 - Low blood sugar and metabolic stress
34:08 - Calcium, parathyroid hormone (PTH), and prolactin
35:12 - Is the estrogen in milk a problem?
38:00 - A bioenergetic view of breast cancer
40:30 - Aspirin for breast cancer?
42:00 - Tetraclycine antibiotics, natural progesterone, methylene blue, and the anti-estrogenic fat-soluble vitamins
44:29 - Toxinless.com—a great resources for supplements
45:09 - The centrality of the liver for regulating estrogen
47:38 - Georgi, where can we find more of your work on the Internet this week?
48:14 - Outro and next week’s episode

Generative Energy #16: Hair Loss and Prostate Cancer

 
 

Listen to Georgi and me discuss a bioenergetic view of hair loss and prostate cancer on episode #16 of The Generative Energy Podcast! 

“The true method of knowledge is experiment.”
—William Blake

“Experience is, for me, the highest authority. The touchstone of validity is my own experience. No other person’s ideas, and none of my own ideas, are as authoritative as my experience. It is to experience that I must return again and again, to discover a closer approximation to truth as it is in the process of becoming in me. Neither the Bible nor the prophets — neither Freud nor research — neither the revelations of God nor man — can take precedence over my own direct experience. My experience is not authoritative because it is infallible. It is the basis of authority because it can always be checked in new primary ways. In this way its frequent error or fallibility is always open to correction.”
—Carl Rogers

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• Download Danny’s Book ► http://bit.ly/maindrod
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01:16 - ‘Keeping the Pipeline Filled at Merck’ (http://nyti.ms/1QtJN23)
02:26 - The mainstream view of baldness and prostate cancer (Julianne Imperato-McGinley and the Guevedoces)
03:59 - Does DHT cause baldness and prostate cancer?
04:39 - The difference between finasteride and dutasteride
05:18 - The overcomplicated genetic-androgen theory
06:22 - Prostate cancer and baldness are associated
07:25 - “Castration-resistant prostate cancer” 
08:14 - “The five year survival rate in the United States is 99%.” (http://1.usa.gov/1m8W5QB)
09:10 - The Dark Side of 5α-Reductase Inhibitors’ Therapy: Sexual Dysfunction, High Gleason Grade Prostate Cancer and Depression (http://1.usa.gov/1IzqsHs)
10:34 - Georgi goes over the risks for 5α-reductase inhibitors
11:46 - Finasteride and chemical castration
12:02 - Is “post-finasteride syndrome” permanent?
13:09 - 5α-reductase inhibitors and depression (pregnenolone and DHT)
14:14 - What’s the ‘bioenergetic view’ of baldness and prostate cancer?
15:11 - Prostate cancer and baldness are associated with aging
16:04 - Premature baldness and skin aging
16:46 - The hair follicle has high-energy requirements (http://1.usa.gov/1m90m6y)
17:36 - Danny’s thoughts on measuring the temperature and pulse (http://1.usa.gov/1m90pzo)
17:56 - Georgi discusses biomarkers for prostate cancer and baldness (http://bit.ly/1m90zqq)
20:17 - Dietary and supplemental suggestion for reducing estrogen, cortisol, serotonin, and prolactin (or metabolic stress)
23:50 - Ray’s article on prostate cancer (http://bit.ly/1m91l6F)
24:20 - Prolactin’s role in prostate cancer
26:00 - Vitamin A—an important factor in steroid synthesis
26:33 - Learning from female’s with “male-pattern baldness”
27:13 - Are finasteride and dutasteride similar to progesterone?
29:20 - Cyproterone acetate as a progesterone-like substance
31:27 - Baldness is associated with many other health problems
33:32 - Young males with “mpb” have high levels of DHEA (http://1.usa.gov/1m94ymF)
35:16 - A higher ration of “free” to “bound” testosterone in “mpb”
36:55 - The relationship between prolactin and calcium (and vitamin D)
38:40 - Are topicals useful for hair loss?
40:33 - Georgi, where can we find more of your work on the internet this week?