- Mitochondria - The structure inside the cell in which energy is produced by respiration is called the mitochondria. The vitality of the mitochondria, their capacity for oxidative energy production, is influenced by nutrition and hormones.
- Thyroid - Thyroid hormone is necessary for respiration on the cellular level, and makes possible all higher biological functions. Without the metabolic efficiency, which is promoted by thyroid hormone, life couldn’t get much beyond the single-cell stage. Without adequate thyroid, we become sluggish, clumsy, cold, anemic, and subject to infections, heart disease, headaches, cancer, and many other diseases, and seem to be prematurely aged, because none of our tissues can function normally.
- Fermentation (Non-Oxidative Metabolism or Sometimes Just "Glycolysis") - The conversion of glucose to lactic acid, providing some usable energy, but many times less than oxidation provides. Lactic acid, produced by splitting glucose to pyruvic acid followed by its reduction, is associated with calcium uptake and nitric oxide production, depletes energy, contributing to cell death. The presence of oxygen normally restrains fermentation so that glucose is converted to carbon dioxide instead of lactic acid.
- Oxidation - Oxidation refers to the combination of a substance with oxygen. This can be beneficial, as in normal respiration that produces energy, or harmful, as in rancidity, irradiation, or stress reactions.
- Oxidative Metabolism (Mitochondrial Respiration or Respiratory Energy) - The ability of cells to consume oxygen and produce useful biological energy.
- Carbon Dioxide - Carbon dioxide, produced in the cells, releases oxygen into the tissues, relaxes blood vessels, prevents edema, eliminates ammonia, and increases the efficiency of oxidative metabolism.
- Estrogen - Estrogen is a hormone that stimulates cell division (mainly in the breast, uterus, and prostate gland, and in the pituitary gland) and is normally produced in a monthly surge at the time of ovulation and during pregnancy. Women normally have higher levels in their blood than men do.
- Prolactin - Prolactin is a hormone secreted by the pituitary gland during pregnancy, and during stress. It promotes milk production, removes calcium from the bones, and inhibits progesterone formation.
- Progesterone - Progesterone is the main female hormone, and is a protective hormone during pregnancy, but it is also important in men since it is a general brain regulating and protective hormone. It has direct effects on mitochondria, promoting energy production, and it facilitates thyroid hormone functions in various ways. It promotes the elimination of estrogen from tissues, and is a "diuretic" in several benign ways, that are compatible with maintenance of blood volume. Progesterone is an anti-androgen and blocks testosterone's effects.
Because some of the ideas progressed in HAIR LIKE A FOX are consistently misrepresented (or misinterpreted), I thought it might be useful to attempt to mimic a Q and A format in order to provide clarity on topics I might have failed to address clearly in the book.
Q: CAN YOU BRIEFLY GO OVER THE HISTORY OF THE IDEA THAT MASCULINITY, AND MORE SPECIFICALLY "MALE" ANDROGENS, CAUSE BALDNESS WITHOUT GETTING OVERLY TECHNICAL?
In the 1940s, it was believed that testosterone caused pattern baldness due the fact that men without functioning testicles did not lose their hair (no matter how strong the disposition towards familial baldness).
"No matter how strong the inherited predisposition to baldness, alopecia will not result if inciting agents, such as androgens, are missing. This is illustrated by the luxuriant scalp hair in old eunuchs who were castrated prior to sexual maturation." —Dr. James B. Hamilton (1942)
While pattern baldness is often said to be a feature of masculinity—and very often contextualized in the male vs. female—early research was careful to point out that a “normal” amount of androgenic hormones were associated with the advent of pattern baldness:
“As shown by bioassay studies in eunuchoid and eunuchs, titers of urinary androgens one-third, or less, of those in normal men are not accompanied by baldness even in the man later shown to be susceptible to alopecia. There is as yet, however, no proof that common baldness or unusually rapid loss of hair is caused by excessive quantities or unusual types of androgens." —Dr. James B. Hamilton (1942)
A decade later, the originator of this idea, Dr. James B Hamilton, cast doubt on his own findings acknowledging that baldness was probably more complicated:
"Instead, there is the paradox that the androgen-dependent condition of common baldness increases in frequency and extent with age, whereas the quantity of these stimulating agents [androgens] decreases with age. The explanation of this paradox is of some importance, since baldness is a condition which may be paralleled to some extent by many of several hundred pathological conditions that select males preferentially and occur with increasing frequency with advance in age.” “This paradox is discussed at length elsewhere and the conclusion is drawn that, although the quality of maleness is the basis of this sex difference in viability and in susceptibility to a host of pathological conditions, the role of testicular secretions is but a ‘setting of the stage’, the action on which is controlled by genetic, aging, environmental, and other factors."—Dr. James B. Hamilton (1951)
He mentioned estrogen as an interesting area of research in a few of his papers:
"Decrease in androgenic secretion can be attained also upon administration of estrogens, either as a result of inhibiting gonadotropic secretions or possible by direct antagonism between androgens and estrogens, but estrogens in themselves have been demonstrated to prevent the proper growth of hair." —Dr. James B. Hamilton (1942)
In 1974, Dr. Imperato-McGinely found a group of pseudohermaphrodites in the Dominican Republic that mimicked Hamilton’s baldness-resistant castrates. Her team found that the pseudohermaphrodites testosterone levels were normal, but they lacked the enzyme that converted testosterone into the more potent androgen, DHT.
"Free" Testosterone > 5-Alpha Reductase > Dihydrotestosterone (DHT)
Taken together, presumably, castrates and pseudohermaphrodites were protected from baldness because of the lack of the androgen, dihydrotestosterone.
In 1975, Merck got wind of Imperato-McGinley’s research and began working on a pharmaceutical to block the enzyme that synthesized DHT from testosterone (5-alpha reductase or 5-AR) to treat prostate disorders that affect a large number of men in old age. During this time, Merck discovered that the drug was somewhat effective at growing hair, and in 1997 Merck received FDA-approval for their "blockbuster" drug, Finasteride (marketed under the name Propecia).
Q: WHAT CAN WE CONCLUDE FROM THE FOUNDATIONS OF PATTERN BALDNESS RESEARCH?
Almost immediately, we can dismiss the "genetic determinism" mindset. For example, "no matter how strong the familial inherited disposition to baldness” castrates and pseudohermaphrodites did not go bald. To me, this suggests that baldness is an environmental problem rather than the result of inherited “bad genes” (more about "genetic determinism" here). I think it also means that the “protective” physiological state is possible to replicate without becoming a castrate or a pseudohermaphrodite, but we’ll get to that.
A problem with drawing finite conclusions from Hamilton's research is that castrates produce scant amounts of estrogen and prolactin, in addition to virtually no testosterone.
Testosterone > Aromatase Enzyme > Estrogen > Prolactin
Additionally, both castrates and pseudohermaphrodites are unified by the production of larger amounts of the strongly “hair-protective” hormone, progesterone. For example, one of the clearest examples of how the hormones estrogen and progesterone affect hair growth is during pregnancy, when there is an increase in hair growth rate, hair diameter, and ratio of growing hairs to resting hairs – all of which result in a “lush head of hair.” In fact, in some cases pregnancy reverses “male-pattern” baldness in women.
“Little attention has been paid in medical literature to changes of the scalp hair during pregnancy. Behrman observed that women 'with the seborrheic diatheses and even male pattern alopecia' improved at the end of the second month of gestation: 'Their scalps are less oily, and the sebum diminished to a normal amount, and the amount of hair fall is temporarily arrested.’” —Lynnfield, Y.L. Effect of pregnancy on the human hair cycle. J Invest Dermatol. 1960 Dec;35:323-7.
In contrast to the beneficial effects of pregnancy on hair growth, postpartum women routinely experience dramatic hair loss. But after giving birth, when progesterone levels fall sharply and estrogen and prolactin (the "lactation" or "molting hormone") levels increase, the lush head of hair that had developed during pregnancy – when progesterone levels were soaring – disappears.
Q: INTERESTING, BUT DON’T ALL MEN AND WOMEN WITH PATTERN BALDNESS HAVE INCREASED LEVELS OF ANDROGENS?
"The widespread assumption that androgen levels are in general elevated in bald-trait men must therefore be rejected" —Knussman et, al. (1992)
"It is well-known that the androgenic alopecia (AGA) patients’ blood concentration levels of male hormones are not different from those people without alopecia." —(2014) Androgenic alopecia: an evaluation of the thyroid hormones and male hormones as prognostic factors.
This should have been the first clue that something was very wrong with the genetic-androgen hypothesis, and was noted very early on by Dr. James B. Hamilton.
Sadly, today, it’s not uncommon to read a paper that starts with, ‘…baldness is caused by increased levels of androgens’ or something similar. The idea is practically ingrained in the cultural zeitgeist (e.g., ‘fish oil is good for you,’ ‘serotonin makes you feel good,’ ‘sugars cause diabetes,’ etc.).
Q: WELL YEAH, BUT EVERYONE KNOWS THAT IT’S NOT THE AMOUNT OF ANDROGENS IN THE BLOOD, IT’S THE "AMOUNT" OR "SENSITIVITY" OF THE ANDROGEN RECEPTORS IN THE SCALP.
A posthoc addition to the genetic-androgen hypothesis is the ever-changing role of the androgen receptor. Androgen receptors are believed to be sensitive parts of cells that have an affinity for androgens, mostly dihydrotestosterone.
It’s very important to note that the “genetically inherited” aspect of baldness (i.e., you are born with these receptors and they cannot be changed) is supposed to play out through the androgen receptors in the scalp.
One idea is that balding people have “hypersensitive” androgen receptors (i.e., a very high affinity for DHT), which somehow terminates the hair follicle. However, in 2008, Valerie Randall suggest that wasn't the case:
"However, the similar steroid-binding capacity of androgen receptors from balding and non-balding follicle dermal papilla cells does not support increased sensitivity." —Randal, V. 2008
Another idea is that the balding have more androgen receptors. The evidence is conflicting, sometimes finding that there are more androgen receptors in balding areas, while other pieces of evidence massively confuse the issue:
"Dermal papilla cells derived from balding scalp hair follicles contained significantly more androgen receptors than those derived from the non-balding ones" —Randall, et. al. (1998)
"Senescent thinning was indistinguishable from androgenetic alopecia in older males." "Biochemical analysis for androgen receptors, 5.-reductase type 1 and 2, and aromatase, in scalp biopsies from older males showed nearly a two fold decrease in levels compared to levels in young males with AGA." —Price et, al. (2010)
"...For example, treatment of animals with 5-alpha reductase inhibitors resulted in marked increase in the expression of the androgen receptor." —Traish, et. al., 2014
"However, the androgen receptor may not be the sole determinant of androgen action on scalp hair follicles, as a high level of receptor was found in a dermal papilla culture from the vertex of a non bald man of 73 years." —The Molecular and Structural Biology of Hair, 1991
Q: FOR THE SAKE OF CONVERSATION, LET'S SAY AN INCREASED AMOUNT OF ANDROGEN RECEPTORS IN BALDING AREAS OF THE SCALP IS A FEATURE OF BALDNESS. IF THAT WERE TRUE, WOULD IT BE A SMOKING GUN?
I don’t think so.
The androgen receptor count in any given tissue seems to be easily modifiable through its interactions with the environment. For example, vitamin A decreased the androgen receptor activity of prostate tissue by 30-40%.
"Using a radioligand binding assay, we found that androgen-binding activity was reduced 30-40% in cells treated with 10(-5) M RA [vitamin A] plus 6 nM dihydrotestosterone (DHT), as compared to cells with the androgen alone." "These data suggest that the suppression of proliferation and function of prostatic cells by RA [vitamin A] may be via modulatory effects on the androgen receptor" — Young, et. al. (1994)
Moreover, the androgen receptor is located on heat shock proteins (HSPs) in the cytoplasm of the cell.
"The androgen receptor is located in the cellular cytoplasm bound to heat shock proteins (HSP) which give the androgen receptor molecule stability and an optimal conformation for binding to the androgen lignand." —The endocrinology of baldness (2014)
Nobel laureate Barbara McClintock found that heat shock proteins can be activated in response to immediate environmental danger, influencing the genome:
"Examples are the “heat shock” responses in eukaryotic organisms, and the “SOS” responses in bacteria. Each of these initiates a highly programmed sequence of events within the cell that serves to cushion the effects of the shock. Some sensing mechanism must be present in these instances to alert the cell to imminent danger, and to set in motion the orderly sequence of events that will mitigate this danger. The responses of genomes to unanticipated challenges are not so precisely programmed. Nevertheless, these are sensed, and the genome responds in a discernible but initially unforeseen manner." —The Significance of responses of the genome to challenge by Nobel Laureate Barbara McClintock (1983)
Here's Raymond Peat's take on the androgen receptor; he likens it to the effects of concentric exercise on mitochondrial function:
"I think the androgen receptor is a kind of leverage point in the cell, tipping the balance in an anabolic direction, favoring glucose oxidation, and opposing catabolic influences of all sorts, in a sort of "loading" function, the way "concentric" exercise has many protective effects. As the organism ages, the meaning of that kind of loading will change, especially with the accumulation of PUFA." —Ray Peat, PhD (2014 email correspondence)
Taken together, I think these suggest that the organism's interaction with the environment may influence androgen receptors, however, if a change in the androgen receptor was a feature of baldness, it would support a "Lamarckian" or environmental view of pattern baldness, not a genetic-androgen explanation.
Q: IF BALDNESS DOESN'T RESULT FROM HIGHER LEVELS OF ANDROGENS OR THROUGH SOME MYSTERY MECHANISM THROUGH THE ANDROGEN RECEPTOR, WHY IS FINASTERIDE (PROPECIA) SO EFFECTIVE?
According to different sources, finasteride is less than 50% effective.
"Till date, only two FDA-approved synthetic drugs, minoxidil and finasteride, are used to cure AGA with only 35 and 48% success, respectively; therefore, a search for new drug based on the mechanism of androgens action is still needed." "It is unlikely that single targeted agents will be sufficient for treating AGA, and therefore, it would be a challenge to obtain compounds with multiple activities." —Jain, R. et al. Potential targets in the discovery of new hair growth promoters for androgenic alopecia. July 2014, Vol. 18, No. 7 , Pages 787-806
I’m constantly in doubt on whether or not finasteride is that efficacious, however. I only have to venture to a major street in San Francisco to find that if there were an "effective" treatment for baldness, a majority of men are either not aware of it, or are choosing to be bald.
Jonathan J. Jarrow has written a great piece of Merck’s manipulative marketing of Finasteride’s so-called effectiveness.
Q: IF FINASTERIDE DOESN’T EXERT IT’S EFFECTS BY DECREASING ANDROGENS, HOW DOES IT WORK?
I think finasteride is essentially a derivative of progesterone, but it probably lacks most of the "protective" effects of natural progesterone.
A few pieces of evidence support this view:
1) Finasteride and progesterone are chemically similar.
2) Finasteride and progesterone are both feminizing.
3) It was found that finasteride is more effective in younger men that older men. I think this might be because older men are more "estrogenized" than younger men (progesterone and estrogen work in the opposite direction).
As for the safety of finasteride, a 2014 paper concluded:
"However, a substantial body of evidence exists which points to serious and potentially ill-health effects of 5α-RIs’ therapy. These include loss or reduced libido, erectile dysfunction, orgasmic and ejaculatory dysfunction, development of high grade PCa tumors, potential negative cardiovascular events, and depression. The side effects are potentially harmful in some individuals and in young men may be persistent or irreversible. The argument that the benefits of these drugs outweighs the risks is slowly eroding in the face of new emerging scientific evidence from preclinical and clinical studies." —Traish, A.M., et al. The Dark Side of 5α-Reductase Inhibitors’ Therapy: Sexual Dysfunction, High Gleason Grade Prostate Cancer and Depression. Korean J Urol. 2014 Jun;55(6):367-79. doi: 10.4111/kju.2014.55.6.367. Epub 2014 Jun 16.
Q: IN THE 2013 (FREE) #1 SELLING AMAZON BOOK, HAIR LIKE A FOX: A BIOENERGETIC VIEW OF PATTERN HAIR LOSS, YOU MADE THE CASE THAT BALDNESS IS THE RESULT OF METABOLIC STRESS. CAN YOU BRIEFLY EXPLAIN THAT WITHOUT GETTING TOO TECHNICAL?
The thesis of the book was that pattern hair loss is the result of a chronic interference with respiratory energy ("efficient" energy generation through the mitochondria, or oxidative metabolism) and an increased reliance on the adaptive "stress" substances that cause unfavorable changes to the scalp overtime leading to the decreased efficiency of hair growth.
The hormone responsible for "efficient" energy generation through the mitochondria is active thyroid hormone (i.e., triiodothyronine, or T3). Thyroid hormone is sometimes referred to as "the hormone of respiration" and supports the oxidation of glucose to carbon dioxide, which in return allows cells to use glucose and oxygen.
Q: INTERESTING, BUT IS THERE ANY EVIDENCE TO SUPPORT THIS "ENVIRONMENTAL" HYPOTHESIS?
I tried to include as much context and evidence in the book, but here are a few pieces of evidence:
1) The discovery by Vitali, et al. that degenerative hair conditions were related to a decline in mitochondrial function and that thyroid hormones act as "mitochondrial hair medicine".
"The current data also provide clinically relevant pointers to how hair follicle 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 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." —Vidali, S., et al. Hypothalamic-Pituitary-Thyroid Axis Hormones Stimulate Mitochondrial Function and Biogenesis in Human Hair Follicles. J Invest Dermatol. 2013 Jun 27.
2) Baldness is clearly associated with a "higher functioning" of the adaptive "stress" substances that interfere with "efficient" energy metabolism (i.e., glucose to carbon dioxide), and decrease the rate of metabolism.
"Our findings showed a significant elevation of cortisol in both male and female androgenic alopecia patients compared to controls, pointing to the suprarenes as a contributing factor in androgenic alopecia. This is confirmed by the observation of exacerbated androgenic alopecia in periods of increased stress." "...elevated E2 levels in males..." "Another significant finding was elevated PRL after TRH stimulation." —Schmidt, J.B. Hormonal basis of male and female androgenic alopecia: clinical relevance. Skin Pharmacol. 1994;7(1-2):61-6.
DHEA tends to increase during stress:
"Eighteen men aged 18 to 32 with rapidly progressive male pattern baldness had serum dehydroepiandrosterone sulfate and testosterone measured.Dehydroepiandrosterone sulfate levels were elevated in all patients, ranging from 340 to 730 micrograms/dl. The patients were otherwise healthy and serum testosterone levels were within normal limits. A control group of men of similar age without hair loss had lower dehydroepiandrosterone sulfate levels ranging from 124 to 300 micrograms/dl (p less than 0.005). The biochemistry of androgens, particularly dehydroepiandrosterone sulfate, suggests that adrenal hyperactivity may initiate alopecia in young men who are genetically susceptible." — Pitts, R.L. Serum elevation of dehydroepiandrosterone sulfate associated with male pattern baldness in young men. J Am Acad Dermatol. 1987 Mar;16(3 Pt 1):571-3.
Polycystic ovarian syndrome can be characterized as an increase in the adaptive "stress" hormones (e.g., estrogen, cortisol, etc.), along with a decrease in the protective "youth-associated substances" (e.g., pregnenolone, progesterone, thyroid):
"The hormonal pattern of a substantial number of men with premature balding resembles in some respects the hormonal pattern of women with polycystic ovary syndrome." —Starka, L., et al. Hormonal profile of men with premature balding. Exp Clin Endocrinol Diabetes. 2004 Jan;112(1):24-8.
In my personal research, higher levels of TSH and prolactin are common in both men and women with pattern baldness:
"31 female patients suffering from androgentic alopecia were examined by means of the TRH test with regard to hypothyroidism and hyperprolactinemia." "In 48% of the patients, we found either hypothyroidism or hyperprolactinemia." "This suggests that both conditions may contribute to the clinical picture of female androgenetic alopecia, as they interfere with the androgen metabolism." —Schmidt, et al. [Hypothyroidism and hyperprolactinemia as a possible cause of androgenetic alopecia in the female]. Z Hautkr. 1989 Jan 15;64(1):9-12.
3) Finally, the current rationale for pattern hair loss is fragmented, that is, different explanations are used for the occurrence of pattern baldness in men, men and women during old age, women after pregnancy, women taking contraceptives, newborn babies of both sexes, and even in animals during plumage or molting. The proposed explanation of pattern baldness as the result in a disturbance of energy metabolism over time (i.e., a 'bioenergetic' view of pattern baldness) readily explains all of these situations with one explanation rather than several. Reductionism in the place of a holistic context can probably account for the lack of progress in baldness research for the last several decades.
"Recent years have witnessed a considerable progress in the research focused on treatment of hair disorders, but with limited success. Therefore, one of the prime challenges of modern hair research is a more profound understanding of the molecular controls of hair follicle cycling. Common diseases such as alopecia areata, telogen effluvium and AGA, until than will remain the unsolved medical problems." —Brajac, I. et al. Human Hair Follicle: An Update on Biology and Perspectives in Hair Growth Disorders Treatment. Hair Transplant 4:115.
There will never be "a cure" for pattern baldness, just like there won't be "a cure" for osteoporosis. Both of these problems are the result of life-long developmental processes.
"It is unlikely that single targeted agents will be sufficient for treating AGA, and therefore, it would be a challenge to obtain compounds with multiple activities." —Jain, R. et al. Potential targets in the discovery of new hair growth promoters for androgenic alopecia. July 2014, Vol. 18, No. 7, Pages 787-806
Q: LOW SEX-HORMONE BINDING GLOBULIN (SHBG) IS A HALLMARK OF PATTERN BALDNESS. HOW DO YOU EXPLAIN THAT?
SBHG is produced in a healthy liver, but not in adequate amounts in the balding male.
Thyroid hormone is integral to liver’s functioning, and without it, the liver cannot store it’s sugar, glycogen—which is needed to energize the liver locally. In fact, without adequate thyroid hormone, the strongly lipogenic (i.e., fat liberating) pituitary hormones can induce non-alcoholic fatty liver disease quickly.
In his 1983 book, Hope for Hypoglycemia, Dr. Broda Barnes found that his patients with impaired livers (hypoglycemia) tended to benefit from thyroid supplementation.
Q: IF YOU'RE NON-GENETIC ENVIRONMENTAL ("LAMARCKIAN") THEORY OF BALDNESS IS CORRECT, WHY THEN DO MEN AND WOMEN “INHERIT” BALDNESS?
I think a physiological state is passed on, similar to what James Vaupel stated:
"...what children inherit from their parents is not their longevity per se but rather their frailty, that is, a set of susceptibilities and risk factors that alter their chances of death at different ages." - James Vaupel. Inherited Frailty and Longevity (1988)
The physiological state inherited in pattern baldness is probably the tendency towards metabolic stress.
Q: YOU SAY THAT ESTROGEN IS INTEGRAL FOR THE GENESIS OF PATTERN BALDNESS, HOWEVER, VARIOUS PIECES OF RESEARCH SHOW THAT ESTROGEN GROWS HAIR. HOW DO YOU EXPLAIN THIS?
Estrogen is among the "very best" of the growth hormones. By inhibiting a cell’s oxidative metabolism, estrogen causes a cell to take up water and divide. In the studies that show that topical estrogen caused hair growth, I think estrogen is stimulating mitosis or the formation of new cells under stressful conditions.
This is interesting in a laboratory setting, however; I’m unaware of anyone in the last ten years or so that made any kind of progress supplementing estrogen. Transgenders who have completely regrown their hair are all—to my knowledge—using a form of progesterone alone, or alongside estrogen. One transgender who had incredible results decided to ditch estrogen because of various reasons.
Q: YOU THINK THAT THE TISSUE LEVEL OF POLYUNSATURATED FATS IS ONE OF THE MOST IMPORTANT CONTRIBUTORS TOWARDS THE GENESIS OF PATTERN BALDNESS. YOU CAN EXPLAIN THAT IN A NON-TECHNICAL WAY?
In 2012, Garza, et al. found an increased level of the "essential fat" breakdown product, prostaglandin d2 (PGD2) in the scalps of balding men. They stated that the accumulation of PGD2 was inhibitory towards hair growth, and its accumulation was largely related to an increase in estrogen, which promotes the formation of prostaglandins.
Prostaglandins are produced from the so-called "essential fat" arachidonic acid, which is largely formed in the liver from linoleic acid (LA). The discussion of the essentiality of any fat is discussed in HAIR LIKE A FOX, however, suffice it to say, so-called essential fats appear to be essential for pattern baldness to occur.
Q: YOU THINK THAT NUTRITION AND SUPPLEMENTATION SHOULD BE GEARED TOWARDS SUPPORTING THYROID FUNCTION. CAN YOU EXPLAIN THIS IN A NON-TECHNICAL WAY?
Given the totality of the evidence, I think nutrition and supplementation should be utilized to support resistance to stress, or the ability of cells to produce "efficient" (useful) energy, which limits the need for the adaptive "stress" substances. While it may sound far-fetched to influence how our cells produce energy, there are many environmental factors that affect the creation, transport, and activation of the thyroid hormones.
A general overview—which is heavily extended and supported in the book—may look something like this:
- Regularly measuring the resting pulse rate and body temperature in an attempt to gather information about the metabolic rate. Obtain lab tests for thyroid stimulating hormone, carbon dioxide (or bicarbonate), serum calcium, serum phosphate, prolactin, parathyroid hormone, vitamin D, iron saturation, etc. [Measuring and collecting data, in my estimation, is extremely important.]
- Consuming a favorable calcium to phosphate ratio. Milk and cheese are high-calcium foods (if allergic, sometimes powdered eggshell calcium can help). The calcium co-factors vitamin D, vitamin K, vitamin E, vitamin A, and copper are worth monitoring as well. Cronometer.com is helpful for this.
- An emphasis on saturated over unsaturated fats in the daily diet (e.g., butter, animal fats, coconut oil, etc.).
- Consuming an adequate amount of protein with an emphasis on milk, cheese, eggs, and gelatinous cuts of meat (i.e., gelatin). Beef liver and shellfish (i.e., oysters, shrimp, squid, etc.) weekly or bi-weekly for the micronutrients they provide.
- Consuming more carbohydrate than protein (to avoid the insulinogenic actions of protein) with an emphasis on fruits over starches.
- Consciously limiting iron intake, or inhibiting its absorption by consuming coffee and/or calcium foods with iron-rich foods.
- Consuming salt to taste (or a slight excess).
- While not explicitly recommended in the book, some might benefit from a thyroid supplement.