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!this thread will be very long, but it should settle many questions which course around in the internet and will also show a bit how kiked this world is!
Reversing pattern baldness requires a radically different context for viewing health problems than most physicians are capable of accepting.
It’s time to take your health into your own hands and become your own expert. Think for yourself and question authority. Do whatever it takes to find the best information available.
THE ANDROGEN HYPOTHESIS
In 1942 Dr. James B. Hamilton changed the course of hair loss research with his groundbreaking study in a group of 104 men who failed to mature sexually (i.e., eunuchs or eunachoids).1 Both young and old, the men were unified by testicular insufficiency, which Dr. Hamilton found to give rise to three anomalies: 1. A lack of balding and retention of all scalp hair. 2. Less sebaceous gland activity, compared to normal men of comparable age, that resulted in a reduced oiliness of the face, hair, and scalp and a complete lack of acne. 3. Dandruff that was either absent or present in such small amounts such that only a few white flakes could be brushed off from the scalp. In stark contrast, mature young men of the same age had copious amounts of dandruff. Faced with the obvious correlation between castration and hair retention, Dr. Hamilton administered "male" hormone injections (i.e., testosterone propionate) to men who were not bald. Upon receiving these injections, those with a family history of baldness experienced a pronounced loss of hair; however, halting the treatment ceased all further hair loss. In castrates who received the same injections without interruption, not only was hair loss induced, but it also continued unabated.
The Androgen Paradox?
Nearly a decade after his original discovery, Hamilton cast doubt on his own findings, invoking the word "paradox" to explain the role of "male" hormones in baldness. Hamilton's paradox came in the form of an observation that baldness increased in severity and frequency with age, whereas the stimulating agents (i.e., "male" androgens) very often decreased with age.9 This paradox is further supported by the fact that the androgens are known to produce long, thick, pigmented scalp hairs in youth, yet produce baldness later in life. How could the androgens be responsible for vigorously growing hair during adolescence and later for terminating hair growth in adulthood when the concentrations of the androgens decrease?
B-But Dr. Shekelberg, balding men aren't necessarily producing more androgens; they're simply more sensitive to them because of an inherited genetic defect.
When examination is applied, this "sensitivity" argument becomes a stretch. Although there are no precise statistics, the incidence of pattern baldness in whites is often quoted as approaching 100 percent; less grandiose estimates suggest that half of all men and women above 40 experience pattern hair loss. Wouldn’t these kinds of statistics require an impossibly high rate of gene mutation? Moreover, balding is increasingly becoming a metabolic marker for future and current health problems, including metabolic syndrome, insulin resistance, hyper tension, polycystic ovarian syndrome, heart disease, and cancer.
How does an ‘enhanced sensitivity to androgens in the scalp’ help to explain the association between hair loss and these health problems?
Finally, while heavily relied upon to explain the genesis of balding in men, this theory is completely abandoned in other cases of “male-pattern baldness”. For instance “male-pattern” hair loss is observed in females (female androgenic alopecia), in newborns during the first year of life, women taking oral contraceptives, postpartum mothers, post-menopausal women, and senescent alopecia (hair loss in those over 50 years of age). These situations are believed to be age-related or androgenindependent or both. A “genetic sensitivity to androgens in the scalp” isn’t usually invoked. Why is the aging male subjected to the androgen hypothesis, while children, women and the elderly are subject to a completely different theory?
Androgens or Aging?
We find that baldness is incontrovertibly associated with aging, with research actually suggesting that premature baldness is a sign of premature aging. An understanding of the mechanisms behind degeneration and regeneration would not only help to form a more coherent picture of pattern hair loss, but would also help to establish a context for devising effective and rational therapies for reversing it. The new context would need to reconcile the following observations: why balding occurs in both men and women, why balding is associated with aging, why castrates and pseudohermaphrodites are immune to baldness, and why drugs like Finasteride are effective for roughly half of those who use them.
A Shift in the "balding" archetype
The process of regeneration and the ability to avoid the ravages of stress correspond to the degree of metabolic intensity, and therefore the ability to sufficiently deliver glucose and oxygen to cells. Youth is associated with an uncanny ability to regenerate and a resiliency to stressors, whereas adulthood is deemed a declining state of imperfect repair and associated with an impaired ability to bounce back from those same stressors
this sounds like @x30001 level gibberish, right ? ahaha ... It gets better
A BIOENERGETIC VIEW OF PATTERN HAIR LOSS
People with sleep apnea also age quickly (incl. hairloss), so MSE and other surgeries for Airways may actually be mandatory if you want to stay young longer
Carbon dioxide allows cells, tissues, and organs to better absorb oxygen, essentially “breathing oxygen into us.” The Danish physician Christian Bohr is credited for elucidating the details of this finding, showing in 1903 that carbon dioxide, produced by properly respiring cells, caused hemoglobin molecules (the proteins on which red blood cells bind and transport molecular oxygen) to release their oxygen atoms, increasing the availability of oxygen to cells (i.e., the Bohr effect). In this respect, carbon dioxide and lactate share an inverse relationship, evidenced by the fact that lactate levels are no higher during bouts of exertion as a person acclimates to a higher altitude, where oxygen levels are lower than they are at sea level. This phenomenon is called the lactate paradox. It indicates that at high altitude some sort of acclimatization occurs in which more carbon dioxide is retained in the tissues than is normal, such that the delivery of oxygen to tissues keeps up with demand, despite the fact that oxygen concentrations in the atmosphere are markedly reduced. If energy is generated without producing sufficient amounts of carbon dioxide, a situation similar to hyperventilation occurs, where large amounts of carbon dioxide are blown off through the lungs, which, in turn, leads to cellular hypoxia, despite the fact that normal amounts of oxygen are being carried by the blood.
This cyclical process hinges on the availability of active thyroid hormone or triiodothyronine (T3), which is predominantly synthesized in the liver from the “prohormone” thyroxine (T4). For the genesis of baldness, we are concerned with the active thyroid hormone’s dual role as “the hormone of respiration”—stimulating oxygen consumption through the efficient breakdown of carbohydrates, fats, and proteins into carbon dioxide—and as a cofactor (along with cholesterol and vitamin A) 31 in the production of the “youth-associated” steroid hormones (e.g., pregnenolone, progesterone and DHEA). Changes in hair growth, color and texture are famously associated with low thyroid function, which coincides with the age-associated decline in the production, transport, and activation of the thyroid hormones. Without the active thyroid hormone, and the corresponding respiratory efficiency that it provides, tissues would not function properly, leading to a laundry list of symptoms including weakness, dry skin, lethargy, slow speech, edema, sensation of cold, decreased sweating, thick tongue, pallor of skin, impaired memory, constipation, and mitochondrial dysfunction.
Oxygen, carbon dioxide, active thyroid hormone, and the vitality of the mitochondria form the foundation of our ‘bioenergetic’ view of pattern baldness. Since cells form tissues, tissues form organs, and organs form whole organisms, it follows as a matter of course that energy generated by cells, either "inefficiently" or "efficiently", has a "ripple effect" throughout the entire organism. The hair follicle itself is a complicated mini-organ that stands to be negatively affected by even subtle shifts in the efficiency with which energy is generated. In fact, because of the already inherent inefficiency of metabolism present therein, the hair follicle is one of the most sensitive among all the organs to these shifts.
Hormones and proper breathing might be more important than a proper diet
Mechanisms of Pattern Hair Loss
Various adaptive “stress” substances that suppress thyroid function may explain the pathological changes seen in pattern baldness. For example, a characteristic of low thyroid is the accumulation of mucopolysaccharides – combinations of proteins and sugars that deposit in the area between cells called the extracellular space. Evidence suggests that mucopolysaccharides, a hallmark of low thyroid, accumulate in the scalps of those men with pattern baldness and can act as a matrix for calcification. ( @Deliciadecu )
At the cell level, “inefficient” respiration (i.e., glucose to lactate) provides a viable mechanism for the higher functioning of adaptive "stress" hormones, poor bone mineral density, reduced follicular blood supply, scalp hypoxia, increased oxidative stress, and other unfavorable changes seen in pattern baldness. While these problems are traditionally viewed in a compartmentalized fashion, our bioenergetic view of the organism redirects our main focus to the mitochondria. The mitochondria need glucose and oxygen to produce energy, with oxygen being the ultimate “bottleneck” in “efficient” mitochondrial energy production. Regulating the availability of oxygen is the so-called “waste product” carbon dioxide, a product of oxidative metabolism, whose formation is empowered by the active thyroid hormone T3.
Estrogen ...
The last chapter solidified our bioenergetic concept of pattern baldness, noting that aging typically coincides with reduced energy expenditure and increases the reliance on the adaptive "stress" hormones that interfere with thyroid hormone production to promote "inefficient" cellular respiration. Over time, this leads to unfavorable changes in energy metabolism within hair follicles, degrading its structure. It also leads to pathological changes in the scalp tissue that can temporarily, or permanently, inhibit hair growth (e.g., inflammation, calcification, reduced follicular blood flow, hypoxia, oxidative stress).
B-But Dr. Shekelberg, all this gibberish does not directly address the evidence that Eunuchs for example had no hairloss, and that Propecia (Finasterid) might stop hairloss
The idea of "gender" hormones (i.e., testosterone is the "male" hormone and estrogen is the "female" hormone) extends to other diseases including polycystic ovarian syndrome, prostate cancer, menopause and, most recently, the so-called andropause. However, when adopting a “whole organism view of physiology,” hormone gender specificity becomes untenable. For example, testosterone can be converted to estrogen by an enzyme whose activity increases during stress, aging and malnutrition. Estrogen can also act on the adrenal glands, causing them to secrete an androgen responsible for causing whisker growth and chest hair.1 While the concept of “male hormone” and “female hormone” makes it easier to sell drugs like Propecia, it makes little sense physiologically.
Perhaps the largest casualty of this medical reductionism is the physiological role of estrogen. Commonly believed only to support everything feminine, estrogen's negative influence on energy metabolism speaks to an alternative view of estrogen as an agent of stress, aging, and pattern baldness.
Estrogen, Progesterone and Hair Growth
This may not seem important because it is for/about women, but it makes you understand the hormones
In women, estrogen is normally produced in monthly surges during ovulation or pregnancy, inducing a temporary loss of coherence within the organism. The monthly estrogen surge inhibits "efficient" oxidative mitochondrial metabolism and stimulates cell division.3 In good health, this intense but brief stimulation is useful in situations that require rapid growth (i.e., for growing the uterus, breasts, and pituitary or for tissue repair following injury), but in other situations, can become degenerative if unopposed by large amounts of progesterone.
Progesterone acts as an anti-estrogen, supporting oxidative mitochondrial respiration and resolving the temporary growth-state induced by estrogen. However, if the factors needed to produce progesterone – such as thyroid hormone and vitamin A – are deficient, as they typically are in advanced age, estrogen can accumulate in the tissues to lower the metabolic rate and the efficiency by which energy is generated. The anti-respiratory, pro-inflammatory nature of estrogen, a systemic problem, has many anti-hair qualities.
One of the clearest examples of how 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. 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.
In stark contrast to the hair-supportive conditions of pregnancy, menopausal conditions favor the development of “male-pattern baldness”. While professionals often proclaim menopause as an “estrogen deficiency”—as if there were no doubt about it— it is very clear, instead, that an elevated ratio of estrogen to progesterone is involved. Estrogen concentrations in tissues correlate positively with aging and with body fat levels. Because there is much misunderstanding, it is worth stating here that blood levels of estrogen do not necessarily reflect tissue concentrations of estrogen. Increased by estrogen, prolactin often becomes excessive around menopause, slows the metabolic rate, and inhibits the production of progesterone.
Estrogen and prolactin tend to cause hair loss in animals too. In one study, administering estrogen to rodents caused hair loss, while an antiestrogen drug renewed hair growth. In another experiment, dogs treated with large doses of estrogens lost their coats, which persisted even after the experiment ended. Similarly, prolactin treated rodents experience hair loss, and both estrogen and prolactin work together to initiate molting in birds.
Estrogen and prolactin both suppress thyroid function and interfere with the "efficient" production of energy, while progesterone opposes both hormones and supports respiration. Not surprisingly, estrogen and prolactin were increased in those with pattern baldness.
Estrogen, Prolactin & Osteoporosis
Estrogen's "anti-hair" "anti-respiratory" qualities are further supported by what is considered its greatest strength: its effect on bone health. Estrogen is said to help prevent osteoporosis by decreasing the production of cells that destroy bone called osteoclasts. While estrogen does slow osteoclast production, it also decreases the rate of bone renewal and promotes the deposition of calcium in soft tissue.
Fail jfl
Perhaps the most striking anti-bone quality of estrogen is that it stimulates the secretion of the pituitary hormone prolactin. A well-known function of prolactin is to break down bone to provide calcium for milk production during lactation. Unsurprisingly, lactating mothers are at very high risk for osteoporosis, as well as other ailments that include depression and hair loss. A hormone that tends to increase with prolactin (and vice versa) and also removes calcium from the bones is parathyroid hormone (PTH). While the increased secretion of parathyroid hormone is adaptive in the short-term (normalizing blood calcium levels when they fall below normal), low levels of parathyroid hormone are essential for maintaining bone health. Consistent with its role in causing errant calcification processes, parathyroid hormone has also been shown to influence hair growth in animal experiments.
Estrogen, prolactin, and parathyroid hormone tend to suppress thyroid function, reducing the concentration of carbon dioxide, promoting "inefficient" respiratory energy, the production of lactic acid, all of which lead to an increased reliance on the classical stress hormone cortisol. Cortisol, secreted from the adrenal glands during stress, degrades the body’s proteins before turning them into glucose so as to quickly provide large amounts of glucose to cells to deal with the stressors. When energy metabolism is inhibited, as it is in diabetes, cortisol rises despite high blood glucose levels. Because the exposure to cortisol is increased in age-related bone loss and in patternbaldness, cortisol is thought to at least contribute to those conditions.
Progesterone's opposition towards estrogen, prolactin, cortisol, and parathyroid hormone helps clarify the complex relationships among the endocrine factors involved in bone loss.
Finasteride may have progesterone-like qualities. Chemically similar to progesterone, Finasteride is helpful for the types of hair loss that are arbitrarily deemed to be “androgen independent”. For instance, in a study of eight females with normal levels of androgens, Finasteride arrested the progression of hair loss for half of the women who used it. Another piece of evidence showing that Finasteride has progesterone-like qualities came in the form of an observation that younger men respond better to Finasteride than older men do. Because estrogen tends to accumulate with aging at the same time testosterone, an anti-estrogen, declines, the “estrogenized” aging male may have more difficulty experiencing the full force of Finasteride’s feminizing effects, provided Finasteride did, in fact, have progesterone-like qualities. According to its most recent package insert, Finasteride is so potently feminizing in some males that it has been shown to induce breast development, reduce beard growth, and eliminate libido – all confirming Finasteride’s progestogenic qualities.
Anything but the “female hormone”, estrogen is involved in the genesis of stress, aging, and pattern baldness. Its effects on hair growth are most clearly seen in pregnancy and menopause. During pregnancy progesterone, which opposes estrogen, increases roughly 100 times more than normal, often resulting in a “lush head of hair” and reversing so-called female androgenic alopecia. During lactation, when progesterone levels fall, and prolactin, estrogen, and cortisol increase, postpartum mothers notoriously experience hair loss that is often considered excessive. Similarly, during menopause—also an estrogen dominant state—women often experience “male-pattern baldness”. Changes in hair growth during pregnancy and menopause are further elucidated by these hormones’ influence on energy metabolism. For example, estrogen and prolactin promote the energetically inefficient non-oxidative metabolism, while progesterone supports the creation of thyroid hormones and, therefore, the energetically efficient oxidative metabolism. So, it’s all but fair to suppose that because an interference in energy metabolism induces temporary hair loss, when estrogen and prolactin are activated chronically, pathological changes in the scalp develop, ultimately leading to permanent pattern baldness by way of hypoxia, soft tissue calcification, poor blood flow, nutrient loss, oxidative stress, and so forth.
SEROTONIN - Depression, Stress & Energy
Although it is stated with great confidence that depression involves low levels of serotonin, it’s never been definitively proven in humans that a deficiency of serotonin causes depression. Serotonin reuptake inhibitors (SSRIs), which prolong the effects of serotonin in the brain, among other places, are about as effective as a placebo.2 Accumulating cases of children, teens, and young adults (ages 18 to 24) committing suicide and developing suicidal thinking patterns have even led the FDA to force drug manufacturers to add a black box warning – the most serious of all warnings – to all the drugs in the SSRI class, warning prescribers, pharmacists, and patients of this very serious risk.3 However, some people find great relief with these antidepressants, but that may have nothing to do with serotonin per se, as serotonin increases the adaptive “stress” hormone, cortisol4,5,6 that can result in a sense of “extraordinary wellbeing and buoyancy” followed by “mood swings” and “suicidal tendencies”
I propose that a “higher functioning” of serotonin is probably involved in the pathology of depression. Depression is the result of energy problems, the ones I’ve been describing, exacerbated by all the things that interfere with energy generation, including an excessive exposure to serotonin. Thyroid hormone and aspirin (salicylic acid) stimulate uncoupling of the mitochondria, thereby increasing oxygen consumption, carbon dioxide production, and heat generation. In short, all the things associated with efficient oxidative metabolism. Is it then any wonder that the supplementation of thyroid hormone and aspirin has been shown to help alleviate depression?
Studies have confirmed the anti-metabolic effects of serotonin.
In animals, serotonin appears to be crucially involved in the transition to the hibernation state(winter sleep). Serotonin slows the respiratory rate by increasing the activity of the enzyme (carbonic anhydrase) that degrades carbon dioxide. On the other hand, administering thyroid hormone to hibernating animals wakes them up.
Serotonin & Hair Growth
Serotonin’s inhibition of “efficient” energy metabolism has adverse effects on the mini-organ known as the hair follicle. Like all tissues, the hair follicle is composed of collection of cells and depends on the “flow” of energy to function. Thyroid hormones regulate this process, controlling hair follicle energy metabolism as well as mitochondrial function. As we saw in the hibernating animals, serotonin shares an inverse relationship with the thyroid hormones. For example, individuals with low thyroid tend to have higher levels of serotonin.
Carbon dioxide, produced under the direction of the thyroid hormones, stabilizes circulating mast cells, preventing them from releasing their serotonin into the blood
In addition to its inverse relationship with the thyroid hormones, serotonin increases and synergizes with a variety of hormones associated with baldness. It, for instance, increases estrogen (and estrogen, in turn, increases serotonin jfl).
Increased prolactin is a typical side effect of SSRIs and serotonin precursor supplements (such as 5-HTP and tryptophan), sometimes inducing gynecomastia (i.e., male breast growth) in men. Like estrogen and prolactin, serotonin causes bone loss and inhibits bone formation; on this basis, anti-serotonin drugs have been used to inhibit bone loss. Bone health is of particular interest given that the factors in bone health usually intersect with the factors in hair health (e.g., carbon dioxide, thyroid, estrogen, prolactin, parathyroid hormone, etc.).
Serotonin & Bacterial Endotoxin
A factor in stress, aging, and pattern hair loss that has yet to be mentioned is endotoxin, or lipopolysaccharide (LPS), which is a toxic, outer-cell wall component of certain bacteria that, like estrogen, produces shock and interferes with cells’ use of oxygen. This hair loss factor is normally produced by common colonic bacteria and released into the surrounding area upon their destruction or death. In stress, deenergized intestinal cells (enterocytes) become more promiscuous in the substances that they allow to enter the body, including endotoxin, which, upon slipping past this intestinal firewall, gets into the general circulation, through which it does almost all of its damage to the host.
Endotoxin synergizes with and increases many of the bioenergetic factors contributing to pattern baldness, especially serotonin. While often referred to as a brain neurotransmitter, the intestines produce about 95 percent of the body’s serotonin, whose basic function is to produce intestinal contractions.
Endotoxin causes the release of serotonin. Serotonin, in turn, causes inflammation in the intestines and appears in excess in inflammatory bowel diseases, such as irritable bowel syndrome (IBS), celiac disease, and Crohn’s disease.
Endotoxin also interacts with two other factors in baldness, cortisol and estrogen. Cortisol increases blood levels of endotoxin in a dose-dependent fashion, and endotoxin activates the enzyme that synthesizes new estrogen. In a vicious cycle, estrogen increases cortisol and causes intestinal cells to become permeable. Constipation increases estrogen, too.
In context, serotonin—in its role as an inhibitor of the metabolic rate—seems to be a contributor to the pathology of pattern baldness. Serotonin’s synergy with estrogen, prolactin, cortisol and endotoxin further elucidates its mechanism in the advent of hair loss. The evidence provided suggests a rethinking of a substance that is subject to as much bias and misinformation as the topic of our previous chapter, estrogen.
Diet - The Rock in the Surf?
Our bioenergetic view of estrogen and serotonin establishes a foundation for reviewing what is perhaps the largest factor in our bioenergetic view of pattern baldness: the types of fat we consume. While dietary fat has been a focal point in nutrition research for the last several decades, the so-called deleterious fat, saturated fat, as part of the 'diet-heart-hypothesis', has been vindicated by the forward thinking pioneers like Dr. Chris Masterjohn, Uffe Ravnskov and others. Solving the riddle of pattern baldness may require a similar pioneering attitude towards the role of fatty acids in stress, aging and pattern hair loss. More specifically, the case will be made that the current darling of the nutrition industry, the polyunsaturated fats (including omega-3s) are uniquely harmful for hair growth, and may even be a prerequisite for pattern baldness.
THE “ESSENTIAL” FATTY ACIDS
While the hair-loss-o-sphere was confused and excited at the same time, elevated levels of PGD2 in the scalps of balding men is to be expected given our bioenergetic context of hair loss. However, the current doctrine of the “essentiality” of certain fats has muddied the waters of baldness research, effectively handicapping progressive thought on the subject. Therefore, the role of the various types of dietary fats in human health, and by extension balding, demands a reimagining; a reimagining that turns the current ideas on the topic, including the current darling of the nutritional world – the polyunsaturated fats – on its head.
Dietary Fats
Although all fats and oils, whether of vegetable or plant origin, contain a mixture of saturated, monounsaturated, and polyunsaturated fats, they differ in the proportions of each of these fats; that is to say, the main difference is a matter of degree, not kind. Highly unsaturated fats (polyunsaturated fats, or PUFA) have more carbon double bonds and are more susceptible to spontaneous oxidation, while saturated fats have fewer double bonds and more hydrogen atoms, making them less susceptible to errant oxidation processes.
While oxidation in the context of mitochondrial oxidative metabolism is beneficial and desired, unsaturated fats that react with oxygen-derived free radicals lead to oxidative stress to produce the conditions that favor the generation of the previously mentioned PUFA breakdown products, the prostaglandins, that, in one way or another, irreversibly damage the mitochondria.
In nature, we find that PUFA is appropriate for animals preparing for hibernation or living in cold climates, such as sardines in the ice-cold waters of the arctic. If we were to exchange the high concentration of PUFA in the tissue of sardines for an equally high concentration of saturated fatty acids, as is found in warm-blooded animals, those sardines would become stiff and unable to maneuver in the cold water.
Likewise, a higher concentration of PUFA in warm-blooded animals would increase the fat’s likelihood of oxidizing because of the higher temperatures, as well as the higher oxygen concentrations, present therein. Plants, nuts and seeds are the most concentrated sources of PUFA, whose degree of saturation depends on the climate in which the plants are grown. For instance, soybeans grown in tropical climates have the same degree of saturation that coconuts do.
Humans have a high rate of metabolism and a body that operates optimally at a temperature around 98.6 degrees Fahrenheit/ 37 degrees Celsius, suggesting that saturated fats – which are stable against relatively high concentrations of oxygen and used exclusively to generate heat – are more appropriate for humans than unsaturated fats are.
However, the 1970s birthed the poorly substantiated "lipid hypothesis" and a medical doctrine which put forth the idea that saturated fats were responsible for heart disease, polluting lipid research for the next several decades. The cultural response to the lipid hypothesis was to minimize the consumption of saturated fats in favor of the cheap "heart healthy" refined oils (e.g., soybean oil, corn oil, cottonseed oil, vegetable oil, rapeseed oil, peanut oil, sesame oil, canola oil, etc.). In particular, it was estimated that the consumption of soybean oil has gone up 1000% in the last decade.
Rather than preventing heart disease, the increased consumption of unsaturated fats has coincided with the rapid decline of U.S. health, some even hypothesizing that the promotion of unsaturated fats have been partially responsible for the obesity epidemic.
While the topic continues to baffle the mainstream, Uffe Ravnskov, Dr. Chris Masterjohn and others have thoroughly picked apart the flaws in the "the lipid hypothesis," vindicating saturated fats in the process (for many of the same reasons that are discussed in this chapter).
Even more controversial than the role of unsaturated and saturated fats in human physiology is the role of the so-called "essential fatty acids," or EFAs, which include
Insulin Resistance & Baldness
In September 2000, researchers raised the question of whether insulin resistance was a mechanism or promoting factor in early pattern baldness. Early on, insulin resistance is characterized by high blood levels of insulin, a ‘compensation’ for the resistance to insulin that develops in the body. Later on, when insulin secretion begins to fall off, high blood glucose levels (hyperglycemia) develops, and a diagnosis of type II diabetes is made.
Excess carbohydrate consumption is often thought to cause or greatly exacerbate these issues, and some have suggested that limiting our overall intake of carbohydrates, especially of sugar, would greatly ameliorate these problems.
Rather than excess carbohydrate, however, the preponderance of evidence suggests that excess fat, by elevating free fatty acids (non-esterified fatty acids or NEFA), causes insulin resistance. The accumulation of free fatty acids in the blood can be thought of as a condition brought about by stress (any kind), executed by way of the adaptive “stress” hormones. These stress hormones are all “lipolytic”—meaning that they liberate fatty acids into the blood. Adrenaline, cortisol, estrogen, growth hormone, and aldosterone (among others), inhibit the use of glucose in various tissues in order to spare that glucose for certain areas of the brain and the muscles as means to supply energy to power short bursts of explosive activity. While “burning fat” has become synonymous with meaningless diet jargon, Wolfe and his colleagues noted that “the enhanced mobilization and oxidation of fat is a fundamental response to stress,” and that there was “little doubt that there are signals for the increased mobilization of fat [present] in shock, trauma, and sepsis.”
Free fatty acids interfere with energy metabolism in both the short-term and the long-term. In the short-term fatty acid metabolism inhibits the uptake and oxidation of glucose, as the British biochemist Sir Phillip Randle’s hypothesis states. In the long-term, free fatty acids have been referred to as a “toxic candidate” for the insulinsecreting pancreatic beta cells. In fact, it was found that chronic exposure to even moderate amounts of fatty acids dysregulates and impairs the functioning of the beta cells, even destroying them in severe cases. In contrast to the beta cell destroying effect of fatty acids, glucose has been shown to initiate the regeneration of beta cells, thereby restoring the physiological proportion of insulin secretion to glucagon secretion by the pancreas. For example, experiments with animals showed that infusions of glucose increased the mass of beta cells by 250 percent over the course of 4 days. By reducing the cell’s exposure to free fatty acids, glucose, by way of insulin, actually protects the mitochondria from harm.
Unsaturated fatty acids are specifically detrimental to energy production by interfering with oxygen use. Raymond Peat (god sent), PhD has brought attention to cardiolipin, a unique (double) phospholipid found exclusively in the mitochondria. In physical proximity, cardiolipin supports the activity of cytochrome c oxidase, an enzyme that occupies the last crucial step in the process of energy generation by way of oxidative phosphorylation. The fatty acid composition of cardiolipin changes with aging, “specifically [by] an increase in highly unsaturated fatty acids,” and these changes decrease the activity of cytochrome c oxidase.
Perhaps the largest contribution of free fatty acids to the genesis of pattern baldness is their degradation into hormone-like inflammatory substances called prostaglandins. While the common belief is that there are both "good" and "bad" prostaglandins, in the context of baldness they seem to be exclusively bad. In stress, the cyclooxygenase (COX) enzymes are activated, metabolizing the “essential” fat arachidonic acid into prostaglandins. One of these prostaglandins, prostaglandin E2, activates aromatase, increasing estrogen, which is associated with pattern baldness. In a vicious cycle, estrogen activates the fat-liberating enzyme (phospholipase A2) that releases arachidonic from cells allowing prostaglandins to form. Although correlational data cannot be magically turned into proof of cause and effect, balding men were found to have accumulated higher levels of prostaglandin D2 in their scalps, an observation that supports the body of evidence and mechanisms implicating COX, arachidonic acid, and prostaglandins in pattern baldness. Estrogen, arachidonic acid, and prostaglandins all stimulate the synthesis of prolactin, which is also associated with pattern baldness.
In addition to inhibiting glucose metabolism, the efficiency of which is central to hair growth, elevated levels of free fatty acids have two well-defined negative effects on hormonal metabolism. The first is that free fatty acids, especially when unsaturated, facilitate the entry of estrogen into cells, possibly by lowering levels of sex hormone binding globulin (SHBG), whose function is to bind and keep estrogen out of cells and in the blood. Lower levels of SHBG are associated with pattern baldness. The second is that free fatty acids increase the activity of the ratelimiting enzyme (tryptophan hydroxylase) of the pathway that converts tryptophan to serotonin. While this is considered to be beneficial by the rest of the world, as described in the last chapter, serotonin is a factor in pattern baldness that should be tightly regulated.
Before closing this chapter, it is important to bear in mind that overeating that leads to weight gain represents a stressor that can lead to chronically elevated levels of the free fatty acids. When energy intake exceeds energy requirements, over time, adipose tissue becomes overstuffed with fat and as a result, fatty acids leak out from the adipose tissue and into the blood, thereby raising the levels of free fatty acids. At the same time, the overstuffed adipose tissues increase the body's overall inflammatory burden, which, in a positive feedback loop, liberate even more fatty acids from the adipose tissue.
Although all free fatty acids, saturated or unsaturated, are harmful in excess, when they are saturated, the positive feedback loop just described would short circuit itself, as saturated fatty acids suppress the body's adaptive responses to stressors and are quickly burnt to counteract the hypercaloric imbalance. But when the liberated fatty acids are unsaturated, as is undoubtedly now the case in those who eat the standard American, PUFA-laden diet, there is no such off switch as there is for saturated fatty acids, as unsaturated fatty acids interfere with the creation, release, transport, and activation of the thyroid hormone. Unsaturated fatty acids also irreversibly damage the mitochondria, increase estrogen and prolactin, and perpetuate the body's inflammatory state.
STEPS TOWARDS A LOGICAL “PRO-HAIR” LIFESTYLE
Our ability to defend against these adaptive "stress" substances depends on our ability to sufficiently deliver oxygen and glucose to our cells. Because carbohydrate, protein, and fat can provide glucose, oxygen is the ultimate bottleneck in the “efficient” production of energy through the mitochondria. Oxygen is regulated in large by thyroid hormones, and more specifically, active thyroid hormone, triiodothyronine (T3), which is produced predominantly in the liver from the “pro-hormone” thyroxine (T4).
Thyroid hormones regulate the rate of oxygen consumption in two ways; by stimulating the production of carbon dioxide and acting as a cofactor in the synthesis of various "youth-associated" hormones (e.g., pregnenolone, progesterone, DHEA). Thus, a lifestyle that supports hair growth can also be thought of as an "anti-stress" or "pro-thyroid" lifestyle. 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.
The Importance of Self-Diagnostics
Before we get into the dietary and lifestyle suggestions, it’s imperative that you, Cels, be aware of self-diagnostics that should be employed during any dietary and lifestyle endeavor. Adopting an arbitrary list of dietary recommendations without collecting objective data is a waste of time. In my estimation, the two most revealing objective data that could be obtained are body temperature and pulse rate.
The body temperature, for all intents, reflects the intensity of the metabolic rate, which, in turn, governs the amount of heat that is generated. Anything but merely a sign of excess food intake, the production of heat is needed to maintain the temperatures for the continued optimal functioning of all the enzymes in the body, and thus, processes such as tissue renewal and repair. After all, nearly all the food we eat is ultimately converted to heat, in one way or another. An intense metabolic rate also ensures a continuous supply of energy (while limiting the storage of the food we eat as fat), which is essential for the organization and functioning of all living cells.
The intolerance to cold is often disregarded, yet seems to be highly common among people, especially among women. From my own research and observations, cold intolerance – in the hands, feet, genitals, and nose – is among the most intolerable symptoms I’ve ever encountered. Keeping track of your body temperature (I recommend the axillary [armpit] temperature) every morning, afternoon (after lunch), and evening (before bed) for about a month will help to reveal your temperature rhythms, and therefore your state of health and metabolism. The famous “thyroidologist” Dr. Barnes found that those temperature readings should hover around 97.8 to 98.6 degrees Fahrenheit / 36, 5 to 37 degree Celsius, rising to a peak in the afternoon.
It is important to bear in mind that although the body temperature is a relatively accurate means of assessing your metabolism and state of health, it can be misleading because the stress hormones can also elevate the body temperature to apparently optimal levels – especially during times of intense stress. However, you can easily determine whether the stress hormones are keeping your body temperature up: If after eating breakfast your body temperature rapidly declines, then the stress hormones are at play, and you have some work to do.
The pulse rate, another self-diagnostic tool that complements the body temperature, reflects the rate at which the heart is pumping blood, oxygen, and nutrients to cells throughout the body. While many physicians subscribe to idea that “lower is better,” they tend to justify this theory using athletes as shining examples. Besides the fact that it is not uncommon for athletes to spontaneously drop dead, a lower pulse rate is suggestive of reduced blood flow, which, in effect, limits the rate at which cells can generate energy. Similar to the body temperature, there are some caveats to a higher pulse rate. In stress, the pulse rate can be maintained by adrenaline, sometimes elevating the pulse rate to over 100 beats per minute (BPM). Instead of feeling pleasant, elevated adrenaline causes anxiety and poor sleep. In all, a pulse rate of about 85 BPM and body temperature of about 98.6 degrees Fahrenheit / 37 degrees Celsius are suggestive of high rates of efficient energy production, rather than a metabolism maintained by the stress hormones.
Dietary Samples
Reversing pattern baldness requires a radically different context for viewing health problems than most physicians are capable of accepting.
“Without self knowledge, without understanding the working and functions of his machine, man cannot be free, he cannot govern himself and he will always remain a slave.”
—G. I. Gurdjieff
—G. I. Gurdjieff
It’s time to take your health into your own hands and become your own expert. Think for yourself and question authority. Do whatever it takes to find the best information available.
THE ANDROGEN HYPOTHESIS
In 1942 Dr. James B. Hamilton changed the course of hair loss research with his groundbreaking study in a group of 104 men who failed to mature sexually (i.e., eunuchs or eunachoids).1 Both young and old, the men were unified by testicular insufficiency, which Dr. Hamilton found to give rise to three anomalies: 1. A lack of balding and retention of all scalp hair. 2. Less sebaceous gland activity, compared to normal men of comparable age, that resulted in a reduced oiliness of the face, hair, and scalp and a complete lack of acne. 3. Dandruff that was either absent or present in such small amounts such that only a few white flakes could be brushed off from the scalp. In stark contrast, mature young men of the same age had copious amounts of dandruff. Faced with the obvious correlation between castration and hair retention, Dr. Hamilton administered "male" hormone injections (i.e., testosterone propionate) to men who were not bald. Upon receiving these injections, those with a family history of baldness experienced a pronounced loss of hair; however, halting the treatment ceased all further hair loss. In castrates who received the same injections without interruption, not only was hair loss induced, but it also continued unabated.
The Androgen Paradox?
Nearly a decade after his original discovery, Hamilton cast doubt on his own findings, invoking the word "paradox" to explain the role of "male" hormones in baldness. Hamilton's paradox came in the form of an observation that baldness increased in severity and frequency with age, whereas the stimulating agents (i.e., "male" androgens) very often decreased with age.9 This paradox is further supported by the fact that the androgens are known to produce long, thick, pigmented scalp hairs in youth, yet produce baldness later in life. How could the androgens be responsible for vigorously growing hair during adolescence and later for terminating hair growth in adulthood when the concentrations of the androgens decrease?
B-But Dr. Shekelberg, balding men aren't necessarily producing more androgens; they're simply more sensitive to them because of an inherited genetic defect.
When examination is applied, this "sensitivity" argument becomes a stretch. Although there are no precise statistics, the incidence of pattern baldness in whites is often quoted as approaching 100 percent; less grandiose estimates suggest that half of all men and women above 40 experience pattern hair loss. Wouldn’t these kinds of statistics require an impossibly high rate of gene mutation? Moreover, balding is increasingly becoming a metabolic marker for future and current health problems, including metabolic syndrome, insulin resistance, hyper tension, polycystic ovarian syndrome, heart disease, and cancer.
How does an ‘enhanced sensitivity to androgens in the scalp’ help to explain the association between hair loss and these health problems?
Finally, while heavily relied upon to explain the genesis of balding in men, this theory is completely abandoned in other cases of “male-pattern baldness”. For instance “male-pattern” hair loss is observed in females (female androgenic alopecia), in newborns during the first year of life, women taking oral contraceptives, postpartum mothers, post-menopausal women, and senescent alopecia (hair loss in those over 50 years of age). These situations are believed to be age-related or androgenindependent or both. A “genetic sensitivity to androgens in the scalp” isn’t usually invoked. Why is the aging male subjected to the androgen hypothesis, while children, women and the elderly are subject to a completely different theory?
Androgens or Aging?
"The suspicion arises that androgens are not the 'directly causative' agent in baldness, but only one member—albeit a frequently effective one—of a family of remote causes that affect local areas capable of reacting in a special manner."
-Dr. Watson (what a fitting name)
Seven decades later, it’s safe to say that androgens are not the “directly causative” agents in baldness. Rather, like other multicellular tissues, the function and longevity of the hair follicle is dependent on the energetic state of the cells that make up its structure. Pattern baldness in both sexes is characterized by a shift from “efficient” to “inefficient” cellular energy metabolism, evidenced by an increase in the adaptive “stress” substances. Over time, these adaptive “stress” substances cause pathological changes in the scalp, including the accumulation of mucopolysaccharides, deranged calcification processes, reduced follicular blood flow, hypoxia, oxidative stress, and mitochondrial dysfunction, all of which predispose to temporary or permanent baldness. These changes just so happen to be the same changes seen in the tissues of aging organisms; we now have a rational starting point for a new paradigm.-Dr. Watson (what a fitting name)
We find that baldness is incontrovertibly associated with aging, with research actually suggesting that premature baldness is a sign of premature aging. An understanding of the mechanisms behind degeneration and regeneration would not only help to form a more coherent picture of pattern hair loss, but would also help to establish a context for devising effective and rational therapies for reversing it. The new context would need to reconcile the following observations: why balding occurs in both men and women, why balding is associated with aging, why castrates and pseudohermaphrodites are immune to baldness, and why drugs like Finasteride are effective for roughly half of those who use them.
A Shift in the "balding" archetype
“The cells in hair follicles produce hair when they are furnished with everything they need. But in the scalp of a balding man, they do not get everything they need and as a result, the hair-producing cells gradually die off. Here we have an example of a mild ‘disease’ which is caused by cellular malnutrition.”
-Dr. Williams
In the last chapters I covered why hairloss is not necessarily a by-product of "bad genes" or Androgens.-Dr. Williams
"Mainly because the pathogenesis mechanisms of androgenic alopecia are not fully understood, the treatments available are limited and vary in effectiveness. Over the centuries a wide range of remedies have been suggested for androgenic alopecia and currently treatments include wigs and hairpieces, surgery, hormone action modifiers, and non-hormonal therapy. Several of these are based on our understanding of the mechanisms of androgen action within the follicle. "
Hairloss = Aging?
The process of regeneration and the ability to avoid the ravages of stress correspond to the degree of metabolic intensity, and therefore the ability to sufficiently deliver glucose and oxygen to cells. Youth is associated with an uncanny ability to regenerate and a resiliency to stressors, whereas adulthood is deemed a declining state of imperfect repair and associated with an impaired ability to bounce back from those same stressors
this sounds like @x30001 level gibberish, right ? ahaha ... It gets better
A BIOENERGETIC VIEW OF PATTERN HAIR LOSS
"He was started on thyroid therapy with the suggestion that after a time this should make him feel better, but there was little hope of recovering his hair. Two months later, when I saw him again, his depression had lifted, his blood pressure was down to normal, he was energetic, interested in life, and, to my own as well as his astonishment, hair was growing all over his head.”
-Dr. Barnes
In the last chapters I showed that stress and deficient cellular energy are directly linked to both aging and baldness. We also learned that energy production becomes less efficient with age and that the adaptive “stress” hormones and signaling substances make up for this lost energy, with some people even suggesting that aging is caused by a maladaptation to stress. The provision of glucose and oxygen to cells determines our ability to generate energy and therefore our ability to tolerate the ravages of the stressors we encounter all day long. Because protein, and fat can be converted to glucose, oxygen is the ultimate bottleneck in the ability to meet energy requirements by way of glucose oxidation.-Dr. Barnes
People with sleep apnea also age quickly (incl. hairloss), so MSE and other surgeries for Airways may actually be mandatory if you want to stay young longer
Carbon dioxide allows cells, tissues, and organs to better absorb oxygen, essentially “breathing oxygen into us.” The Danish physician Christian Bohr is credited for elucidating the details of this finding, showing in 1903 that carbon dioxide, produced by properly respiring cells, caused hemoglobin molecules (the proteins on which red blood cells bind and transport molecular oxygen) to release their oxygen atoms, increasing the availability of oxygen to cells (i.e., the Bohr effect). In this respect, carbon dioxide and lactate share an inverse relationship, evidenced by the fact that lactate levels are no higher during bouts of exertion as a person acclimates to a higher altitude, where oxygen levels are lower than they are at sea level. This phenomenon is called the lactate paradox. It indicates that at high altitude some sort of acclimatization occurs in which more carbon dioxide is retained in the tissues than is normal, such that the delivery of oxygen to tissues keeps up with demand, despite the fact that oxygen concentrations in the atmosphere are markedly reduced. If energy is generated without producing sufficient amounts of carbon dioxide, a situation similar to hyperventilation occurs, where large amounts of carbon dioxide are blown off through the lungs, which, in turn, leads to cellular hypoxia, despite the fact that normal amounts of oxygen are being carried by the blood.
This cyclical process hinges on the availability of active thyroid hormone or triiodothyronine (T3), which is predominantly synthesized in the liver from the “prohormone” thyroxine (T4). For the genesis of baldness, we are concerned with the active thyroid hormone’s dual role as “the hormone of respiration”—stimulating oxygen consumption through the efficient breakdown of carbohydrates, fats, and proteins into carbon dioxide—and as a cofactor (along with cholesterol and vitamin A) 31 in the production of the “youth-associated” steroid hormones (e.g., pregnenolone, progesterone and DHEA). Changes in hair growth, color and texture are famously associated with low thyroid function, which coincides with the age-associated decline in the production, transport, and activation of the thyroid hormones. Without the active thyroid hormone, and the corresponding respiratory efficiency that it provides, tissues would not function properly, leading to a laundry list of symptoms including weakness, dry skin, lethargy, slow speech, edema, sensation of cold, decreased sweating, thick tongue, pallor of skin, impaired memory, constipation, and mitochondrial dysfunction.
Oxygen, carbon dioxide, active thyroid hormone, and the vitality of the mitochondria form the foundation of our ‘bioenergetic’ view of pattern baldness. Since cells form tissues, tissues form organs, and organs form whole organisms, it follows as a matter of course that energy generated by cells, either "inefficiently" or "efficiently", has a "ripple effect" throughout the entire organism. The hair follicle itself is a complicated mini-organ that stands to be negatively affected by even subtle shifts in the efficiency with which energy is generated. In fact, because of the already inherent inefficiency of metabolism present therein, the hair follicle is one of the most sensitive among all the organs to these shifts.
Hormones and proper breathing might be more important than a proper diet
Mechanisms of Pattern Hair Loss
Various adaptive “stress” substances that suppress thyroid function may explain the pathological changes seen in pattern baldness. For example, a characteristic of low thyroid is the accumulation of mucopolysaccharides – combinations of proteins and sugars that deposit in the area between cells called the extracellular space. Evidence suggests that mucopolysaccharides, a hallmark of low thyroid, accumulate in the scalps of those men with pattern baldness and can act as a matrix for calcification. ( @Deliciadecu )
At the cell level, “inefficient” respiration (i.e., glucose to lactate) provides a viable mechanism for the higher functioning of adaptive "stress" hormones, poor bone mineral density, reduced follicular blood supply, scalp hypoxia, increased oxidative stress, and other unfavorable changes seen in pattern baldness. While these problems are traditionally viewed in a compartmentalized fashion, our bioenergetic view of the organism redirects our main focus to the mitochondria. The mitochondria need glucose and oxygen to produce energy, with oxygen being the ultimate “bottleneck” in “efficient” mitochondrial energy production. Regulating the availability of oxygen is the so-called “waste product” carbon dioxide, a product of oxidative metabolism, whose formation is empowered by the active thyroid hormone T3.
Estrogen ...
The last chapter solidified our bioenergetic concept of pattern baldness, noting that aging typically coincides with reduced energy expenditure and increases the reliance on the adaptive "stress" hormones that interfere with thyroid hormone production to promote "inefficient" cellular respiration. Over time, this leads to unfavorable changes in energy metabolism within hair follicles, degrading its structure. It also leads to pathological changes in the scalp tissue that can temporarily, or permanently, inhibit hair growth (e.g., inflammation, calcification, reduced follicular blood flow, hypoxia, oxidative stress).
B-But Dr. Shekelberg, all this gibberish does not directly address the evidence that Eunuchs for example had no hairloss, and that Propecia (Finasterid) might stop hairloss
The idea of "gender" hormones (i.e., testosterone is the "male" hormone and estrogen is the "female" hormone) extends to other diseases including polycystic ovarian syndrome, prostate cancer, menopause and, most recently, the so-called andropause. However, when adopting a “whole organism view of physiology,” hormone gender specificity becomes untenable. For example, testosterone can be converted to estrogen by an enzyme whose activity increases during stress, aging and malnutrition. Estrogen can also act on the adrenal glands, causing them to secrete an androgen responsible for causing whisker growth and chest hair.1 While the concept of “male hormone” and “female hormone” makes it easier to sell drugs like Propecia, it makes little sense physiologically.
Perhaps the largest casualty of this medical reductionism is the physiological role of estrogen. Commonly believed only to support everything feminine, estrogen's negative influence on energy metabolism speaks to an alternative view of estrogen as an agent of stress, aging, and pattern baldness.
In 1947, pioneering endocrinologist Hans Selye discovered that estrogen mimicked the most severe state stress, shock. Rather than “producing estrus,” (i.e., the female readiness to mate), administering estrogens to animals interrupted estrus and were actually “anti-estrogenic.” Rejecting the name, Selye preferred to call estrogen “adipin”, because of its production in the fat tissue (adipocytes), or “folliculin”, because of the ovarian follicle's significant role in its production.2 Today, however, estrogen has shed its identity as the "shock hormone", and has been ingrained into the cultural zeitgeist as the "female hormone" through a bizarre course of events.
In her 2005 essay, “The Rise and Fall of Estrogen Therapy: The History of HRT,” Carla Rothenberg explains that over several decades, estrogen acquired a reputation as an antidote for many of the illnesses associated with aging, and even as a preventative drug for such diseases as osteoporosis, benign prostate hyperplasia (BPH), heart disease, and Alzheimer’s disease. As part of a billion dollar business, estrogen "replacement" of 15 times the amount a young woman would produce normally has been embraced by doctors, drug manufacturers, and advertising agencies in a supposed effort to support femininity into old age. What could go wrong? After all, estrogen is “the female hormone” and scores of observational and case studies have supported an overwhelmingly positive view of replacing “lost” estrogen.
In 1991, the National Institutes of Health announced The Women's Health Initiative, a large clinical trial designed to test the effectiveness of various hormones and supplements compared to placebos. The largest study ever conducted of its kind, the trial involved a total of 161,808 healthy postmenopausal women. The morning of July 9, 2002, however, things went really wrong. A safety-monitoring board suddenly halted a part of the study involving 16,608 women because those women who were taking estrogen had more breast cancer, heart attacks, strokes, pulmonary embolisms, and blood clots than the women who were taking placebos. This was surprising to many physicians who were prescribing estrogen for the very illnesses estrogen was apparently causing; but if they had been aware of the effect of estrogen on cellular respiration, and if they had implemented a bioenergetic framework in the provision of care in their medical practice, it wouldn't have been.
In her 2005 essay, “The Rise and Fall of Estrogen Therapy: The History of HRT,” Carla Rothenberg explains that over several decades, estrogen acquired a reputation as an antidote for many of the illnesses associated with aging, and even as a preventative drug for such diseases as osteoporosis, benign prostate hyperplasia (BPH), heart disease, and Alzheimer’s disease. As part of a billion dollar business, estrogen "replacement" of 15 times the amount a young woman would produce normally has been embraced by doctors, drug manufacturers, and advertising agencies in a supposed effort to support femininity into old age. What could go wrong? After all, estrogen is “the female hormone” and scores of observational and case studies have supported an overwhelmingly positive view of replacing “lost” estrogen.
In 1991, the National Institutes of Health announced The Women's Health Initiative, a large clinical trial designed to test the effectiveness of various hormones and supplements compared to placebos. The largest study ever conducted of its kind, the trial involved a total of 161,808 healthy postmenopausal women. The morning of July 9, 2002, however, things went really wrong. A safety-monitoring board suddenly halted a part of the study involving 16,608 women because those women who were taking estrogen had more breast cancer, heart attacks, strokes, pulmonary embolisms, and blood clots than the women who were taking placebos. This was surprising to many physicians who were prescribing estrogen for the very illnesses estrogen was apparently causing; but if they had been aware of the effect of estrogen on cellular respiration, and if they had implemented a bioenergetic framework in the provision of care in their medical practice, it wouldn't have been.
Estrogen, Progesterone and Hair Growth
This may not seem important because it is for/about women, but it makes you understand the hormones
In women, estrogen is normally produced in monthly surges during ovulation or pregnancy, inducing a temporary loss of coherence within the organism. The monthly estrogen surge inhibits "efficient" oxidative mitochondrial metabolism and stimulates cell division.3 In good health, this intense but brief stimulation is useful in situations that require rapid growth (i.e., for growing the uterus, breasts, and pituitary or for tissue repair following injury), but in other situations, can become degenerative if unopposed by large amounts of progesterone.
Progesterone acts as an anti-estrogen, supporting oxidative mitochondrial respiration and resolving the temporary growth-state induced by estrogen. However, if the factors needed to produce progesterone – such as thyroid hormone and vitamin A – are deficient, as they typically are in advanced age, estrogen can accumulate in the tissues to lower the metabolic rate and the efficiency by which energy is generated. The anti-respiratory, pro-inflammatory nature of estrogen, a systemic problem, has many anti-hair qualities.
One of the clearest examples of how 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. 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.
In stark contrast to the hair-supportive conditions of pregnancy, menopausal conditions favor the development of “male-pattern baldness”. While professionals often proclaim menopause as an “estrogen deficiency”—as if there were no doubt about it— it is very clear, instead, that an elevated ratio of estrogen to progesterone is involved. Estrogen concentrations in tissues correlate positively with aging and with body fat levels. Because there is much misunderstanding, it is worth stating here that blood levels of estrogen do not necessarily reflect tissue concentrations of estrogen. Increased by estrogen, prolactin often becomes excessive around menopause, slows the metabolic rate, and inhibits the production of progesterone.
Estrogen and prolactin tend to cause hair loss in animals too. In one study, administering estrogen to rodents caused hair loss, while an antiestrogen drug renewed hair growth. In another experiment, dogs treated with large doses of estrogens lost their coats, which persisted even after the experiment ended. Similarly, prolactin treated rodents experience hair loss, and both estrogen and prolactin work together to initiate molting in birds.
Estrogen and prolactin both suppress thyroid function and interfere with the "efficient" production of energy, while progesterone opposes both hormones and supports respiration. Not surprisingly, estrogen and prolactin were increased in those with pattern baldness.
Estrogen, Prolactin & Osteoporosis
Estrogen's "anti-hair" "anti-respiratory" qualities are further supported by what is considered its greatest strength: its effect on bone health. Estrogen is said to help prevent osteoporosis by decreasing the production of cells that destroy bone called osteoclasts. While estrogen does slow osteoclast production, it also decreases the rate of bone renewal and promotes the deposition of calcium in soft tissue.
Fail jfl
Perhaps the most striking anti-bone quality of estrogen is that it stimulates the secretion of the pituitary hormone prolactin. A well-known function of prolactin is to break down bone to provide calcium for milk production during lactation. Unsurprisingly, lactating mothers are at very high risk for osteoporosis, as well as other ailments that include depression and hair loss. A hormone that tends to increase with prolactin (and vice versa) and also removes calcium from the bones is parathyroid hormone (PTH). While the increased secretion of parathyroid hormone is adaptive in the short-term (normalizing blood calcium levels when they fall below normal), low levels of parathyroid hormone are essential for maintaining bone health. Consistent with its role in causing errant calcification processes, parathyroid hormone has also been shown to influence hair growth in animal experiments.
Estrogen, prolactin, and parathyroid hormone tend to suppress thyroid function, reducing the concentration of carbon dioxide, promoting "inefficient" respiratory energy, the production of lactic acid, all of which lead to an increased reliance on the classical stress hormone cortisol. Cortisol, secreted from the adrenal glands during stress, degrades the body’s proteins before turning them into glucose so as to quickly provide large amounts of glucose to cells to deal with the stressors. When energy metabolism is inhibited, as it is in diabetes, cortisol rises despite high blood glucose levels. Because the exposure to cortisol is increased in age-related bone loss and in patternbaldness, cortisol is thought to at least contribute to those conditions.
Progesterone's opposition towards estrogen, prolactin, cortisol, and parathyroid hormone helps clarify the complex relationships among the endocrine factors involved in bone loss.
Finasterid
Finasteride may have progesterone-like qualities. Chemically similar to progesterone, Finasteride is helpful for the types of hair loss that are arbitrarily deemed to be “androgen independent”. For instance, in a study of eight females with normal levels of androgens, Finasteride arrested the progression of hair loss for half of the women who used it. Another piece of evidence showing that Finasteride has progesterone-like qualities came in the form of an observation that younger men respond better to Finasteride than older men do. Because estrogen tends to accumulate with aging at the same time testosterone, an anti-estrogen, declines, the “estrogenized” aging male may have more difficulty experiencing the full force of Finasteride’s feminizing effects, provided Finasteride did, in fact, have progesterone-like qualities. According to its most recent package insert, Finasteride is so potently feminizing in some males that it has been shown to induce breast development, reduce beard growth, and eliminate libido – all confirming Finasteride’s progestogenic qualities.
Anything but the “female hormone”, estrogen is involved in the genesis of stress, aging, and pattern baldness. Its effects on hair growth are most clearly seen in pregnancy and menopause. During pregnancy progesterone, which opposes estrogen, increases roughly 100 times more than normal, often resulting in a “lush head of hair” and reversing so-called female androgenic alopecia. During lactation, when progesterone levels fall, and prolactin, estrogen, and cortisol increase, postpartum mothers notoriously experience hair loss that is often considered excessive. Similarly, during menopause—also an estrogen dominant state—women often experience “male-pattern baldness”. Changes in hair growth during pregnancy and menopause are further elucidated by these hormones’ influence on energy metabolism. For example, estrogen and prolactin promote the energetically inefficient non-oxidative metabolism, while progesterone supports the creation of thyroid hormones and, therefore, the energetically efficient oxidative metabolism. So, it’s all but fair to suppose that because an interference in energy metabolism induces temporary hair loss, when estrogen and prolactin are activated chronically, pathological changes in the scalp develop, ultimately leading to permanent pattern baldness by way of hypoxia, soft tissue calcification, poor blood flow, nutrient loss, oxidative stress, and so forth.
SEROTONIN - Depression, Stress & Energy
Although it is stated with great confidence that depression involves low levels of serotonin, it’s never been definitively proven in humans that a deficiency of serotonin causes depression. Serotonin reuptake inhibitors (SSRIs), which prolong the effects of serotonin in the brain, among other places, are about as effective as a placebo.2 Accumulating cases of children, teens, and young adults (ages 18 to 24) committing suicide and developing suicidal thinking patterns have even led the FDA to force drug manufacturers to add a black box warning – the most serious of all warnings – to all the drugs in the SSRI class, warning prescribers, pharmacists, and patients of this very serious risk.3 However, some people find great relief with these antidepressants, but that may have nothing to do with serotonin per se, as serotonin increases the adaptive “stress” hormone, cortisol4,5,6 that can result in a sense of “extraordinary wellbeing and buoyancy” followed by “mood swings” and “suicidal tendencies”
I propose that a “higher functioning” of serotonin is probably involved in the pathology of depression. Depression is the result of energy problems, the ones I’ve been describing, exacerbated by all the things that interfere with energy generation, including an excessive exposure to serotonin. Thyroid hormone and aspirin (salicylic acid) stimulate uncoupling of the mitochondria, thereby increasing oxygen consumption, carbon dioxide production, and heat generation. In short, all the things associated with efficient oxidative metabolism. Is it then any wonder that the supplementation of thyroid hormone and aspirin has been shown to help alleviate depression?
Studies have confirmed the anti-metabolic effects of serotonin.
In animals, serotonin appears to be crucially involved in the transition to the hibernation state(winter sleep). Serotonin slows the respiratory rate by increasing the activity of the enzyme (carbonic anhydrase) that degrades carbon dioxide. On the other hand, administering thyroid hormone to hibernating animals wakes them up.
Serotonin & Hair Growth
Serotonin’s inhibition of “efficient” energy metabolism has adverse effects on the mini-organ known as the hair follicle. Like all tissues, the hair follicle is composed of collection of cells and depends on the “flow” of energy to function. Thyroid hormones regulate this process, controlling hair follicle energy metabolism as well as mitochondrial function. As we saw in the hibernating animals, serotonin shares an inverse relationship with the thyroid hormones. For example, individuals with low thyroid tend to have higher levels of serotonin.
Carbon dioxide, produced under the direction of the thyroid hormones, stabilizes circulating mast cells, preventing them from releasing their serotonin into the blood
In addition to its inverse relationship with the thyroid hormones, serotonin increases and synergizes with a variety of hormones associated with baldness. It, for instance, increases estrogen (and estrogen, in turn, increases serotonin jfl).
Increased prolactin is a typical side effect of SSRIs and serotonin precursor supplements (such as 5-HTP and tryptophan), sometimes inducing gynecomastia (i.e., male breast growth) in men. Like estrogen and prolactin, serotonin causes bone loss and inhibits bone formation; on this basis, anti-serotonin drugs have been used to inhibit bone loss. Bone health is of particular interest given that the factors in bone health usually intersect with the factors in hair health (e.g., carbon dioxide, thyroid, estrogen, prolactin, parathyroid hormone, etc.).
Serotonin & Bacterial Endotoxin
A factor in stress, aging, and pattern hair loss that has yet to be mentioned is endotoxin, or lipopolysaccharide (LPS), which is a toxic, outer-cell wall component of certain bacteria that, like estrogen, produces shock and interferes with cells’ use of oxygen. This hair loss factor is normally produced by common colonic bacteria and released into the surrounding area upon their destruction or death. In stress, deenergized intestinal cells (enterocytes) become more promiscuous in the substances that they allow to enter the body, including endotoxin, which, upon slipping past this intestinal firewall, gets into the general circulation, through which it does almost all of its damage to the host.
Endotoxin synergizes with and increases many of the bioenergetic factors contributing to pattern baldness, especially serotonin. While often referred to as a brain neurotransmitter, the intestines produce about 95 percent of the body’s serotonin, whose basic function is to produce intestinal contractions.
Endotoxin causes the release of serotonin. Serotonin, in turn, causes inflammation in the intestines and appears in excess in inflammatory bowel diseases, such as irritable bowel syndrome (IBS), celiac disease, and Crohn’s disease.
Endotoxin also interacts with two other factors in baldness, cortisol and estrogen. Cortisol increases blood levels of endotoxin in a dose-dependent fashion, and endotoxin activates the enzyme that synthesizes new estrogen. In a vicious cycle, estrogen increases cortisol and causes intestinal cells to become permeable. Constipation increases estrogen, too.
In context, serotonin—in its role as an inhibitor of the metabolic rate—seems to be a contributor to the pathology of pattern baldness. Serotonin’s synergy with estrogen, prolactin, cortisol and endotoxin further elucidates its mechanism in the advent of hair loss. The evidence provided suggests a rethinking of a substance that is subject to as much bias and misinformation as the topic of our previous chapter, estrogen.
Diet - The Rock in the Surf?
Our bioenergetic view of estrogen and serotonin establishes a foundation for reviewing what is perhaps the largest factor in our bioenergetic view of pattern baldness: the types of fat we consume. While dietary fat has been a focal point in nutrition research for the last several decades, the so-called deleterious fat, saturated fat, as part of the 'diet-heart-hypothesis', has been vindicated by the forward thinking pioneers like Dr. Chris Masterjohn, Uffe Ravnskov and others. Solving the riddle of pattern baldness may require a similar pioneering attitude towards the role of fatty acids in stress, aging and pattern hair loss. More specifically, the case will be made that the current darling of the nutrition industry, the polyunsaturated fats (including omega-3s) are uniquely harmful for hair growth, and may even be a prerequisite for pattern baldness.
THE “ESSENTIAL” FATTY ACIDS
"Everyone should have the privilege of playing Russian Roulette if it is desired, but it is only fair to have the warning that with the use of polyunsaturated fats the gun probably contains live ammunition."
-Dr. Barnes
Recently, it was found that men with "androgenic alopecia" had higher levels of the polyunsaturated fatty acid breakdown product, prostaglandin D2 (PGD2) in their scalps. Naturally, this created a tidal wave in the hair loss community, lighting various forums ablaze with thread titles such as, "Hope for us all - Source of baldness discovered: Prostaglandin D2", "How can I reduce prostaglandin D2 to save my hair?" and "Prostaglandin inhibitor to cure baldness in two years!”-Dr. Barnes
While the hair-loss-o-sphere was confused and excited at the same time, elevated levels of PGD2 in the scalps of balding men is to be expected given our bioenergetic context of hair loss. However, the current doctrine of the “essentiality” of certain fats has muddied the waters of baldness research, effectively handicapping progressive thought on the subject. Therefore, the role of the various types of dietary fats in human health, and by extension balding, demands a reimagining; a reimagining that turns the current ideas on the topic, including the current darling of the nutritional world – the polyunsaturated fats – on its head.
Dietary Fats
Although all fats and oils, whether of vegetable or plant origin, contain a mixture of saturated, monounsaturated, and polyunsaturated fats, they differ in the proportions of each of these fats; that is to say, the main difference is a matter of degree, not kind. Highly unsaturated fats (polyunsaturated fats, or PUFA) have more carbon double bonds and are more susceptible to spontaneous oxidation, while saturated fats have fewer double bonds and more hydrogen atoms, making them less susceptible to errant oxidation processes.
While oxidation in the context of mitochondrial oxidative metabolism is beneficial and desired, unsaturated fats that react with oxygen-derived free radicals lead to oxidative stress to produce the conditions that favor the generation of the previously mentioned PUFA breakdown products, the prostaglandins, that, in one way or another, irreversibly damage the mitochondria.
In nature, we find that PUFA is appropriate for animals preparing for hibernation or living in cold climates, such as sardines in the ice-cold waters of the arctic. If we were to exchange the high concentration of PUFA in the tissue of sardines for an equally high concentration of saturated fatty acids, as is found in warm-blooded animals, those sardines would become stiff and unable to maneuver in the cold water.
Likewise, a higher concentration of PUFA in warm-blooded animals would increase the fat’s likelihood of oxidizing because of the higher temperatures, as well as the higher oxygen concentrations, present therein. Plants, nuts and seeds are the most concentrated sources of PUFA, whose degree of saturation depends on the climate in which the plants are grown. For instance, soybeans grown in tropical climates have the same degree of saturation that coconuts do.
Humans have a high rate of metabolism and a body that operates optimally at a temperature around 98.6 degrees Fahrenheit/ 37 degrees Celsius, suggesting that saturated fats – which are stable against relatively high concentrations of oxygen and used exclusively to generate heat – are more appropriate for humans than unsaturated fats are.
However, the 1970s birthed the poorly substantiated "lipid hypothesis" and a medical doctrine which put forth the idea that saturated fats were responsible for heart disease, polluting lipid research for the next several decades. The cultural response to the lipid hypothesis was to minimize the consumption of saturated fats in favor of the cheap "heart healthy" refined oils (e.g., soybean oil, corn oil, cottonseed oil, vegetable oil, rapeseed oil, peanut oil, sesame oil, canola oil, etc.). In particular, it was estimated that the consumption of soybean oil has gone up 1000% in the last decade.
Rather than preventing heart disease, the increased consumption of unsaturated fats has coincided with the rapid decline of U.S. health, some even hypothesizing that the promotion of unsaturated fats have been partially responsible for the obesity epidemic.
While the topic continues to baffle the mainstream, Uffe Ravnskov, Dr. Chris Masterjohn and others have thoroughly picked apart the flaws in the "the lipid hypothesis," vindicating saturated fats in the process (for many of the same reasons that are discussed in this chapter).
Even more controversial than the role of unsaturated and saturated fats in human physiology is the role of the so-called "essential fatty acids," or EFAs, which include
• Omega-6 linoleic acid (LA)
• Omega-6 arachidonic acid (AA)
• Omega-3 alpha-linolenic acid (ALA)
• Omega-3 docosahexaenoic acid (DHA)
• Omega-3 eicosapentaenoic acid (EPA)
Found predominantly in oily fish such as salmon, halibut, and sardines, and in dietary supplements derived therefrom (e.g., fish oil, cod liver oil, salmon oil, krill oil), these fats, now universally believed to be beneficial, have been elevated to the status of vitamins. Especially when viewed in our bioenergetic context, however, the early research that deemed certain polyunsaturated fatty acids as “essential” seems, in my estimation, to have been presumptuous.• Omega-6 arachidonic acid (AA)
• Omega-3 alpha-linolenic acid (ALA)
• Omega-3 docosahexaenoic acid (DHA)
• Omega-3 eicosapentaenoic acid (EPA)
Insulin Resistance & Baldness
In September 2000, researchers raised the question of whether insulin resistance was a mechanism or promoting factor in early pattern baldness. Early on, insulin resistance is characterized by high blood levels of insulin, a ‘compensation’ for the resistance to insulin that develops in the body. Later on, when insulin secretion begins to fall off, high blood glucose levels (hyperglycemia) develops, and a diagnosis of type II diabetes is made.
Excess carbohydrate consumption is often thought to cause or greatly exacerbate these issues, and some have suggested that limiting our overall intake of carbohydrates, especially of sugar, would greatly ameliorate these problems.
Rather than excess carbohydrate, however, the preponderance of evidence suggests that excess fat, by elevating free fatty acids (non-esterified fatty acids or NEFA), causes insulin resistance. The accumulation of free fatty acids in the blood can be thought of as a condition brought about by stress (any kind), executed by way of the adaptive “stress” hormones. These stress hormones are all “lipolytic”—meaning that they liberate fatty acids into the blood. Adrenaline, cortisol, estrogen, growth hormone, and aldosterone (among others), inhibit the use of glucose in various tissues in order to spare that glucose for certain areas of the brain and the muscles as means to supply energy to power short bursts of explosive activity. While “burning fat” has become synonymous with meaningless diet jargon, Wolfe and his colleagues noted that “the enhanced mobilization and oxidation of fat is a fundamental response to stress,” and that there was “little doubt that there are signals for the increased mobilization of fat [present] in shock, trauma, and sepsis.”
Free fatty acids interfere with energy metabolism in both the short-term and the long-term. In the short-term fatty acid metabolism inhibits the uptake and oxidation of glucose, as the British biochemist Sir Phillip Randle’s hypothesis states. In the long-term, free fatty acids have been referred to as a “toxic candidate” for the insulinsecreting pancreatic beta cells. In fact, it was found that chronic exposure to even moderate amounts of fatty acids dysregulates and impairs the functioning of the beta cells, even destroying them in severe cases. In contrast to the beta cell destroying effect of fatty acids, glucose has been shown to initiate the regeneration of beta cells, thereby restoring the physiological proportion of insulin secretion to glucagon secretion by the pancreas. For example, experiments with animals showed that infusions of glucose increased the mass of beta cells by 250 percent over the course of 4 days. By reducing the cell’s exposure to free fatty acids, glucose, by way of insulin, actually protects the mitochondria from harm.
Unsaturated fatty acids are specifically detrimental to energy production by interfering with oxygen use. Raymond Peat (god sent), PhD has brought attention to cardiolipin, a unique (double) phospholipid found exclusively in the mitochondria. In physical proximity, cardiolipin supports the activity of cytochrome c oxidase, an enzyme that occupies the last crucial step in the process of energy generation by way of oxidative phosphorylation. The fatty acid composition of cardiolipin changes with aging, “specifically [by] an increase in highly unsaturated fatty acids,” and these changes decrease the activity of cytochrome c oxidase.
Perhaps the largest contribution of free fatty acids to the genesis of pattern baldness is their degradation into hormone-like inflammatory substances called prostaglandins. While the common belief is that there are both "good" and "bad" prostaglandins, in the context of baldness they seem to be exclusively bad. In stress, the cyclooxygenase (COX) enzymes are activated, metabolizing the “essential” fat arachidonic acid into prostaglandins. One of these prostaglandins, prostaglandin E2, activates aromatase, increasing estrogen, which is associated with pattern baldness. In a vicious cycle, estrogen activates the fat-liberating enzyme (phospholipase A2) that releases arachidonic from cells allowing prostaglandins to form. Although correlational data cannot be magically turned into proof of cause and effect, balding men were found to have accumulated higher levels of prostaglandin D2 in their scalps, an observation that supports the body of evidence and mechanisms implicating COX, arachidonic acid, and prostaglandins in pattern baldness. Estrogen, arachidonic acid, and prostaglandins all stimulate the synthesis of prolactin, which is also associated with pattern baldness.
In addition to inhibiting glucose metabolism, the efficiency of which is central to hair growth, elevated levels of free fatty acids have two well-defined negative effects on hormonal metabolism. The first is that free fatty acids, especially when unsaturated, facilitate the entry of estrogen into cells, possibly by lowering levels of sex hormone binding globulin (SHBG), whose function is to bind and keep estrogen out of cells and in the blood. Lower levels of SHBG are associated with pattern baldness. The second is that free fatty acids increase the activity of the ratelimiting enzyme (tryptophan hydroxylase) of the pathway that converts tryptophan to serotonin. While this is considered to be beneficial by the rest of the world, as described in the last chapter, serotonin is a factor in pattern baldness that should be tightly regulated.
Before closing this chapter, it is important to bear in mind that overeating that leads to weight gain represents a stressor that can lead to chronically elevated levels of the free fatty acids. When energy intake exceeds energy requirements, over time, adipose tissue becomes overstuffed with fat and as a result, fatty acids leak out from the adipose tissue and into the blood, thereby raising the levels of free fatty acids. At the same time, the overstuffed adipose tissues increase the body's overall inflammatory burden, which, in a positive feedback loop, liberate even more fatty acids from the adipose tissue.
Although all free fatty acids, saturated or unsaturated, are harmful in excess, when they are saturated, the positive feedback loop just described would short circuit itself, as saturated fatty acids suppress the body's adaptive responses to stressors and are quickly burnt to counteract the hypercaloric imbalance. But when the liberated fatty acids are unsaturated, as is undoubtedly now the case in those who eat the standard American, PUFA-laden diet, there is no such off switch as there is for saturated fatty acids, as unsaturated fatty acids interfere with the creation, release, transport, and activation of the thyroid hormone. Unsaturated fatty acids also irreversibly damage the mitochondria, increase estrogen and prolactin, and perpetuate the body's inflammatory state.
STEPS TOWARDS A LOGICAL “PRO-HAIR” LIFESTYLE
“It’s refreshing to see people beginning to think clearly and rationally and move away from gimmicky diets that have little basis in fact, reality, or objectivity, and to ones that are firmly seated in all aspects of human physiology and science. After all, this is why most of us choose to eat a certain way, that is to be as healthy as we can be, both physically and mentally . . . not to, say, replicate how our caveman ancestors supposedly ate and lived. It’s due to this line of reasoning that carbohydrates, and especially sugar and fructose, have fallen by the wayside of late, driven by an irrational fear, bordering on obsessiveness, that’s evolved to where sugar is now conceived of as a toxic poison and blamed for causing diabetes, cancer, obesity, gout, etc."
-Andrew Kim
Pattern baldness is an energy problem that begins in the cell. Solving that energy problem involves limiting our exposure to adaptive "stress" substances such as cortisol, estrogen, prolactin, serotonin, endotoxin, parathyroid hormone and aldosterone.-Andrew Kim
Our ability to defend against these adaptive "stress" substances depends on our ability to sufficiently deliver oxygen and glucose to our cells. Because carbohydrate, protein, and fat can provide glucose, oxygen is the ultimate bottleneck in the “efficient” production of energy through the mitochondria. Oxygen is regulated in large by thyroid hormones, and more specifically, active thyroid hormone, triiodothyronine (T3), which is produced predominantly in the liver from the “pro-hormone” thyroxine (T4).
Thyroid hormones regulate the rate of oxygen consumption in two ways; by stimulating the production of carbon dioxide and acting as a cofactor in the synthesis of various "youth-associated" hormones (e.g., pregnenolone, progesterone, DHEA). Thus, a lifestyle that supports hair growth can also be thought of as an "anti-stress" or "pro-thyroid" lifestyle. 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.
The Importance of Self-Diagnostics
Before we get into the dietary and lifestyle suggestions, it’s imperative that you, Cels, be aware of self-diagnostics that should be employed during any dietary and lifestyle endeavor. Adopting an arbitrary list of dietary recommendations without collecting objective data is a waste of time. In my estimation, the two most revealing objective data that could be obtained are body temperature and pulse rate.
The body temperature, for all intents, reflects the intensity of the metabolic rate, which, in turn, governs the amount of heat that is generated. Anything but merely a sign of excess food intake, the production of heat is needed to maintain the temperatures for the continued optimal functioning of all the enzymes in the body, and thus, processes such as tissue renewal and repair. After all, nearly all the food we eat is ultimately converted to heat, in one way or another. An intense metabolic rate also ensures a continuous supply of energy (while limiting the storage of the food we eat as fat), which is essential for the organization and functioning of all living cells.
The intolerance to cold is often disregarded, yet seems to be highly common among people, especially among women. From my own research and observations, cold intolerance – in the hands, feet, genitals, and nose – is among the most intolerable symptoms I’ve ever encountered. Keeping track of your body temperature (I recommend the axillary [armpit] temperature) every morning, afternoon (after lunch), and evening (before bed) for about a month will help to reveal your temperature rhythms, and therefore your state of health and metabolism. The famous “thyroidologist” Dr. Barnes found that those temperature readings should hover around 97.8 to 98.6 degrees Fahrenheit / 36, 5 to 37 degree Celsius, rising to a peak in the afternoon.
It is important to bear in mind that although the body temperature is a relatively accurate means of assessing your metabolism and state of health, it can be misleading because the stress hormones can also elevate the body temperature to apparently optimal levels – especially during times of intense stress. However, you can easily determine whether the stress hormones are keeping your body temperature up: If after eating breakfast your body temperature rapidly declines, then the stress hormones are at play, and you have some work to do.
The pulse rate, another self-diagnostic tool that complements the body temperature, reflects the rate at which the heart is pumping blood, oxygen, and nutrients to cells throughout the body. While many physicians subscribe to idea that “lower is better,” they tend to justify this theory using athletes as shining examples. Besides the fact that it is not uncommon for athletes to spontaneously drop dead, a lower pulse rate is suggestive of reduced blood flow, which, in effect, limits the rate at which cells can generate energy. Similar to the body temperature, there are some caveats to a higher pulse rate. In stress, the pulse rate can be maintained by adrenaline, sometimes elevating the pulse rate to over 100 beats per minute (BPM). Instead of feeling pleasant, elevated adrenaline causes anxiety and poor sleep. In all, a pulse rate of about 85 BPM and body temperature of about 98.6 degrees Fahrenheit / 37 degrees Celsius are suggestive of high rates of efficient energy production, rather than a metabolism maintained by the stress hormones.
Dietary Samples
Adequate Protein – A modifier of 1.5 grams of protein per kilogram of body weight can be used to experiment with protein intake. Depending on activity and stress level, some may need more. Given that protein is insulinogenic, consuming more protein during the day and less at night seems reasonable. Sources of protein include, milk, cheese and gelatinous cuts of meat. Supplemental proteins include ruminant liver, shellfish (especially oysters), and eggs (specifically the yolks).
Adequate Carbohydrate – Due to the insulinogenic nature of protein, carbohydrate intake should exceed protein intake. Meat and carbohydrate can be balanced in a 1:1 ratio, while dairy warrants a ratio of 2-3:1 due to its greater stimulation of insulin. Ripe fruits such as oranges, tangerines, watermelon, grapes, lemons, limes, cherries, sapotas, guavas, lychees, papayas, and other citrus and tropical fruits provide enough glucose and fructose for general stress resistance. In addition, these fruits tend to contain low levels of serotonin, which can be problematic in sensitive individuals. Fruit supports respiration, contains low levels of iron and polyunsaturated fats, and contains a favorable calcium to phosphate ratio. Starches such as grains, breads, and beans contain enough iron and phosphate to greatly limit their consumption or eliminate them all together. Additionally, fruit is digested in the upper part of the intestine avoiding complications with bacterial endotoxin, while starches tend to promote the absorption of endotoxin into the blood.
Become Deficient in The “Essential Fatty Acids” – A diet based on nutrientdense proteins and fruits tends to automatically limit the amount of polyunsaturated fats in the diet. Coconut oil, butter, animal fats and cocoa are all highly saturated and safe to consume. Olive oil contains enough unsaturated fat to warrant limiting its consumption. Vegetable and seed oils should be avoided completely. Similarly, the highly unsaturated fats found in fish and flax oils (i.e., the so-called “essential” fatty acids) are not recommended.
Supplements – A majority of dietary supplements are not recommended due to their allergenicity and poor manufacturing quality. Food supplements such as salt (to taste), ruminant liver, oysters, and eggs are highly recommended. Vitamin D is an important regulator of hair health and exposing as much of the body to sunlight without burning as possible is desirable. Cycles of light and darkness seem to have a dramatic effect on hair growth. For example, 90% of hair follicles shift from the resting to growing phase during springtime only to fall out in winter months. This phenomenon may be explained by light exposure, which as many have suspected, is biologically active. Low-level laser therapy makes use of red light initiating regrowth of hair in some individuals. A physiological mechanism for light's effect on hair growth may have to do with its inhibition of the "molting" hormone, prolactin, which is sensitive to light and increased in darkness. For those that cannot spend a significant amount of time in the sun supplementing with vitamin D (if less than ~40 ng/dL) and utilizing red light (600-850nm) around one’s workspace may be warranted.
Haidut approach - You could also additionally "supplement" the hormones like Progesterone, DHEA, Pregnenolone and Thyroid hormones
Cronometer.com is a useful tool for figuring out some of the more nuanced suggestions (i.e., calcium to phosphate ratio)
End
I cant follow a proper diet right now, but when I get home again around summer, then I will definitely follow this.
This is a long term "looksmax" and "healthmax", so, push through and actually live the diet
Thanks to
Danny Roddy (of whom I copy pasta'd nearly everything here)
Haidut
Ray Peat
ReayPeatForum
@x30001 for showing me this path
I will send the studies per enquiry (it is pretty long, I myself did mostly copy pasta lol)
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