Lights Out! Get your melatonin.

From T.S. Wiley’s website:
“People spent summers, before electric lights, sleeping less & eating heavily in preparation for winter because the light triggered the hunger for carbohydrates. Now, light is available 24 hours a day. Heating and air-conditioning climate control our hormonal responses to consume carbohydrates now available year round. This is the scenario for obesity, Type II diabetes, and depression… In Wiley’s opinion, sleep is the best medicine.”

And Wikipedia:
“Wiley’s main thesis in Lights Out is that light is a physiological trigger that controls dopamine and hormones like cortisol. Wiley posits that with the extension of the natural day through artificial lighting, rest at the hormonal level is rarely adequate for optimum biological needs of the body. In her view, this results in both fatigue and unnatural appetite, which leads to weight gain, exhaustion, and disease. Wiley theorizes that the body’s responses are cyclical, reflecting the seasons of the year, and that the body’s needs vary seasonally. According to Wiley, during the winter months the body needs more sleep, and carbohydrates should be restricted as they would have been naturally during hunter-gatherer times.”

melatonin

Most of the first third of Wiley’s book “Lights Out: Sleep, Sugar, and Survival” centers around light exposure, melatonin, and the many, many effects of a screwed up circadian cycle.  Jane Plain and Jack Kruse have written volumes on the subject, please see their websites for more in-depth analyses and practical applications…

Much of this blog post is my take on that first third (I couldn’t wait to finish it before writing about it), plus a little input from Google, Pubmed, et al; some commentary & pseudo-fact-checking as well.  I’m going to finish the book, and hopefully it will inspire a few more blog posts as opposed to a tin foil hat.  Most of the stuff in Lights Out makes incredibly good sense, but: 1) that doesn’t mean it’s true; and 2) the strings of logic are far too long to do a proper fact-check.  But really it’s how well it makes sense (mostly) that has me intrigued.

divide and conquer

Melatonin is a sleep-inducing hormone controlled by the light-dark cycle.  It is known.  On the day-to-day, melatonin increases at night and decreases during the daytime.  From Wiley: on a seasonal level, longer days during the summer meant less melatonin overall during these months.  Since melatonin suppresses sex hormones (inconsistent? Eg, Smith et al., 2013), summer is supposed to be breeding time, so the baby is born in spring when food is plenty (I’m OK with this now, but will certainly disagree come December).  Melatonin also suppresses metabolic rate, so the decreased daylight and thus increased melatonin during the winter months helped to survive on less food (supported by Marrin et al., 2013).

Disruptions in circadian rhythms royally screws us up.  According to Wikipedia, fireplaces/candles and incandescent bulbs produce less of the melatonin-suppressive blue lights… use these at night in winter?


Antidepressant and circadian phase-shifting effects of light. (Lewy et al., 1987)
Abstract: Bright light can suppress nighttime melatonin production in humans, but ordinary indoor light does not have this effect. This finding suggested that bright light may have other chronobiologic effects in humans as well. Eight patients who regularly became depressed in the winter (as day length shortens) significantly improved after 1 week of exposure to bright light in the morning (but not after 1 week of bright light in the evening). The antidepressant response to morning light was accompanied by an advance (shift to an earlier time) in the onset of nighttime melatonin production. These results suggest that timing may be critical for the antidepressant effects of bright light.

Next:  Prolactin inhibits sex hormones, and melatonin stimulates prolactin (supported by Gill-Sharma 2009Campino et al., 2008).  Thus, less melatonin in summer means less prolactin = more sex & fertility.  She also says day sex is more likely to result in conception compared to night sex for this reason (couldn’t find a reference for or against this).

Dopamine inhibits prolactin, whereas TRH & melatonin stimulate it.  Melatonin also blunts ACTH-induced cortisol secretion (supported by Torres-Farfan 2003Campino 2008).  Winter = high melatonin, prolactin, and low cortisol & dopamine.  Summer = high dopamine & cortisol, and low melatonin & prolactin.  Prolactin is supposed to be high in winter, during pregnancy; low dopamine would support this.

Circadian rhythm

Dopamine is a summer hormone?  Lu et al. (2006) showed high dopaminergic activity was associated with light and wakefulness (ie, summertime).  However, Venero (2002) showed melatonin stimulated dopamine synthesis in specific brain regions, and Eisenberg (2010) showed increased dopamine synthesis in fall & winter relative to spring and summer.  Two  possible confounding factors come to mind: 1) Location, location, location!  Some of these discrepancies may be due to brain region-specific dopamine metabolism… actually, Lu is the only odd-man out, so perhaps dopamine is a winter hormone?  And 2) Wiley’s main premise is that we pwned the light… epigenetics and the like mean that we, including the people in those studies, have deeply screwed up light/dark summer/winter metabolic programs on an epigenetic level, so it’s possible those studies are riddles with artefacts.  However, Wiley also says that people get sick because they live in perpetual summer (lights on all the time = high dopamine), and Markianos (2013) showed elevated dopamine metabolites in overweight patients; in my experience these studies usually continuously enroll patients, year-round.


I’m really just blazing through abstracts here – this is why I call it “pseudo-fact-checking;” not to be confused with any degree of academic rigor.

To be continued… (no tin foil hats, I promise) (not yet at least)

calories proper

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  • TJ

    Wait, did you really just link to Jack Kruse?

  • http://itsthewooo.blogspot.com/ Jane Plain (Woo)

    Yay a post on sleep season melatonin and neurotransmitters and circadian rhythms and biology! My favorite!

    There is indeed a seasonal trend for testosterone of men to peak in fall. I believe more people are born in early fall, statistically speaking, which is consistent with male reproductive motivation being higher in fall leading to late fall/early winter conceptions.

    Modern women are too overfed/high body weight to exhibit much fertility inhibition from seasonal melatonin shifts, as in humans, seasonal variation of melatonin is only weakly suppressive of gonadotropins. However, women predisposed to anorexia nervosa are more likely to be born in spring, which is consistent with lower weight mothers who have subclinical syndromes / neurotic food avoidance and low body weight and can only ever conceive in summer.

    Interestingly, astrology myth reflects these natural biology effects… winter and early spring births correlate with astrological signs known to be eccentric, detached from others, strange or mentally ill (aquarius and pisces) , whereas late summer early fall births are characterized by the signs known to be socially aware, logical, and well socialized/ adjusted / in tune to environment and others (virgo and libra). This would reflect physical/brain health of biological rhythms and healthy parents.

    Actually, not only are anoretics more likely to be born in spring, but schizophrenics and other severely mentally handicapped people are more likely to be born in later winter/early spring… thus the stereotype (and astrology myth reflection) of “eccentricity” of a late winter/early spring birth.

    Interesting non-sequitur of myth/tradition and biological correlates 😀 .

    I believe the seasonal testosterone elevation of men in fall may reflect the traditional biological rhythm for females to be peak fertility after the summer, when weeks of light has inhibited melatonin, promoted follicular development throughout summer, and plentiful food has also enhanced ability to ovulate and conceive.

    In women who are unhealthy or starving however fertility may only be possible acutely in summer, as melatonin is a starvation signal, promoting energy conservation, starvation increases melatonin levels to conserve energy/inhibit fertility, and a starving woman who is underweight and unhealthy will not be able to conceive in late fall, whereas better nourished healthier women will.

    • http://www.caloriesproper.com/ William Lagakos

      my instinct for most health outcomes, with the rare but obviously genetic exceptions, has always been: nurture > nature. Thus, any correlations between birth month & adult phenotype seem very horoscopey to me at first… but then again some of the theories I find the most interesting end up at a tin foil hat, but that hasn’t stalled my fascination with them.

      On another note, this is an interesting angle on reproductive fitness. Ie, a healthier woman is more fertile “year-round,” whereas a less healthy woman may need to more conditions in her favor to reach a similar level of fertility, like summertime, good recent sleep history, etc. (probably analogous correlations for men, too).

  • http://itsthewooo.blogspot.com/ Jane Plain (Woo)

    Regarding fertility and diurnal rhythms, it is indeed true fertility is superior in the morning and the reason for this is that gonadotropins LH and FSH are made during sleep, peak in the moring, leading to highest estrogen at this time in women, as well as frank ovulation more likely to occur early in morning. Estrogen is responsible for cervical mucous changes that promote successful conception, so ideally if one is attempting to conceive, early morning is best when estrogen levels are highest, especially if trying to have a boy (because estrogen in women is biologically redundant with stored energy/maternal physical health, sperm with a Y chromosome do very poorly in a low estrogen cervical mucous and women who are thin/unhealthy/low estrogenic will statistically give birth to daughters, as female fetus is less energy intensive and more likely to survive )

    It’s often said “men determine sex of child”, but this is not true at all and ultimately the endocrine state of the female biases things considerably, which is actually perfectly logical considering energy inequities between male/female children and the hugely energy intensive prospect of female reproduction… in other words, another feminist myth bites the dust, and ultimately women / females are responsible for the sex of children, and a woman who gives birth to many daughters and no sons is likely under a lot of stress/low body weight/ low estrogen… whereas heavier body weight / better nourished women with high estrogen have more sons.

    • http://itsthewooo.blogspot.com/ Jane Plain (Woo)

      I tried to edit my replies to make them less ridiculously long but failed, sorry :(

    • http://www.caloriesproper.com/ William Lagakos

      +1 for morning sex

    • http://www.dannyroddy.com/ Danny Roddy

      “Estrogen is responsible for cervical mucous changes that promote successful conception…”

      Why do you say that?

      Failure of implantation in human in vitro fertilization and embryo transfer patients: the effects of altered progesterone/estrogen ratios in humans and mice.

      “Daily blood samples were taken for progesterone (P) and estradiol (E2) measurements from women who showed a platelet response consistent with the presence of viable embryos after in vitro fertilization and embryo transfer procedures. A comparison of steroid levels between those women who became pregnant and those who did not revealed the following: at and after the time of transfer, women who failed to become pregnant had significantly higher E2 levels and a lower ratio of P/E2 than women who became pregnant. The P/E2 ratio was a better predictor of implantation failure than was the absolute level of either hormone. Experiments were done in mice to test the hypothesis that P could protect implantation of the embryo against the inhibitory effects of high E2. In mice, implantation was inhibited by relatively high levels of E2. This effect was overcome by concomitant administration of P. There was a significant dose-response-related interaction of P with the E2.”

      Early luteal serum progesterone concentrations are higher in pregnancy cycles.

      “In a consecutive series of 167 patients reaching the stage of embryo transfer after in vitro fertilization and embryo transfer, 19 clinical pregnancies ensued. The serum progesterone (P) levels were significantly greater on the first and second (P less than 0.01) and third (P less than 0.05) postaspiration days for those who conceived. Higher circulating levels of P were achieved on days 1, 2, and 3 (P less than 0.05) by the daily injection of P, 50 mg in oil, given for 5 consecutive days, beginning immediately after follicle aspiration. Both pregnancy and nonpregnancy cycles demonstrated high circulating P levels, but the study implies that relatively higher levels are required for conception, and such levels can be achieved by the use of intramuscular P.”

      • http://itsthewooo.blogspot.com/ Jane Plain (Woo)

        This is what happens when people who don’t understand basic medicine/endocrinology try to give medical advice.

        You are aware that progesterone is made in response to endocrinological correlates of pregnancy, right? This study is directed toward reproductive endocrinologists, to help them develop better medical protocols for women with impaired fertility. Summarized, it says this:

        “Diagnostically, the ratio of progesterone to estrogen is best predictive of embryo implantation failure”

        Only a moron would interpret this as supporting quack progesterone therapy, which would *suppress* follicular development (although may or may not support successful embryo implantation/survival in infertile women receiving IVF, which is of zero relevance to the discussion, BTW).

        Also, just so you know, a high quality oocyte/mature follicle results in a higher progesterone spike at ovulation, and usually always occurs with baseline high estrogen (which is also the result of female reproductive health/successful follicular development). This would explain any correlation of higher early leutal progesterone and successful pregnancy. Again, this does not support quack therapies of using progesterone replacement , as the progesterone is only a sign of healthy follicular development (and also supports embryo survival once conception has occurred, which is a *far cry* from using progesterone replacement to mimic these effects and far more likely to accomplish the opposite of impaired fertility/suppressed ovarian follicular health and development as progesterone is a primary negative feedback regulator of gonadotropins).

        With regard to female fertility, progesterone is never found without complementary high estrogen, both are produced from the follicle at different times in the cycle. Each serve important roles for fertility. Estrogen rules basic conception whereas progesterone only begins to matter after that. High estrogen , and high progesterone, are the result of healthy ovaries and good follicle development. Low progesterone is a sign of failure to ovulate, and the answer/solution is not “more progesterone” any more than the answer to lethargy / fatigue / activity intolerance is to make yourself sweat in a sauna. Sweating is the result of normal metabolism, and progesterone is the result of normal ovulation.

        Why can’t the progesterone quacks comprehend this? IHKNFI.

        • http://www.dannyroddy.com/ Danny Roddy

          Sup, Woo.

          “This is what happens when people who don’t understand basic medicine/endocrinology try to give medical advice.”

          I hate those people.

          “Only a moron would interpret this as supporting quack progesterone therapy, which would *suppress* follicular development (although may or may not support successful embryo implantation/survival in infertile women receiving IVF, which is of zero relevance to the discussion, BTW).”

          Yeah, the rise in estrogen in a healthy woman is intense and brief. I think a lack of progesterone is more likely than an “estrogen deficiency,” though. Estrogen probably increases with age [1,2], and serum values don’t always reflect tissue concentrations [3,4].

          “Again, this does not support quack therapies of using progesterone replacement , as the progesterone is only a sign of healthy follicular development (and also supports embryo survival once conception has occurred, which is a *far cry* from using progesterone replacement to mimic these effects and far more likely to accomplish the opposite of impaired fertility/suppressed ovarian follicular health and development as progesterone is a primary negative feedback regulator of gonadotropins).

          P.M. Wise found that estrogen interferes with the regulation of LH and FSH by desensitizing nerves in the hypothalamus [5].

          We probably just disagree, I think progesterone’s utility goes far beyond pregnancy.

          1. Musey VC, Collins DC, Musey PI, Martino-Saltzman D, Preedy JR. Age-related changes in the female hormonal environment during reproductive life. Am J Obstet Gynecol. 1987 Aug;157(2):312-7. “We found that increased age during reproductive life is accompanied by a significant rise in both basal and stimulated serum follicle-stimulating hormone levels. This was accompanied by an increase in the serum level of estradiol-17 beta and the urine levels of estradiol-17 beta and 17 beta-estradiol-17-glucosiduronate.”

          2. Wilshire GB, Loughlin JS, Brown JR, Adel TE, Santoro N. Diminished function of the somatotropic axis in older reproductive-aged women. J Clin Endocrinol Metab. 1995 Feb;80(2):608-13. “Older reproductive-aged women had lower 12-h integrated daytime GH concentrations (mean +/- SE, 171 +/- 35 vs. 427 +/- 130 micrograms min/L; P = 0.036) than younger controls and a strong trend for lower IGF-I levels (22.7 +/- 2.1 vs. 31.3 +/- 3.5 nmol/L; P = 0.055) than younger controls despite having higher circulating E2 on the day of sampling (368 +/- 51 vs. 167 +/- 20 pmol/L; P = 0.002). We conclude that older reproductive-aged women have lower daytime GH concentrations than younger controls despite having higher E2 levels on the day of sampling and overall normal gonadal hormone parameters.”

          3. Batra S, Bengtsson LP, Sjöberg NO. Interrelations between plasma and tissue concentrations of 17 beta-oestradiol and progesterone during human pregnancy. Clin Endocrinol (Oxf). 1979 Dec;11(6):603-10. “The general conclusion to be drawn from the present study is the lack of correspondence between the plasma concentrations and the tissue concentrations of female sex steroids during pregnancy.”

          4. Vermeulen-Meiners C, Jaszmann LJ, Haspels AA, Poortman J, Thijssen JH. The endogenous concentration of estradiol and estrone in normal human postmenopausal endometrium. J Steroid Biochem. 1984 Nov;21(5):607-12. “The results from the tissue levels of both steroids showed large variations and there was no significant correlation with their plasma levels. The mean E2 concentration in tissue was 420 pg/g, 50 times higher than in plasma and the E1 concentration of 270 pg/g was 9 times higher. The E2/E1 ratio in tissue of 1.6, was higher than the corresponding E2/E1 ratio in plasma, being 0.3.”

          5. Wise, P.M., et al., “Neuroendocrine influences on aging of the female reproductive system,” Frontiers in Neuroendocrinology 12, 323-356, 1991.

          • http://itsthewooo.blogspot.com/ Jane Plain (Woo)

            1)” Yeah, the rise in estrogen in a healthy woman is intense and brief. “

            Quackwatch correction: the estrogen/LH surge at ovulation is intense and brief.
            Higher echelon baseline estrogen, on the other hand, occurs 24/7 in healthy young women.

            The scientific literature is rather uncontroversial regarding the numerous benefits of estrogen for women with regard to mood, energy, appearance, body weight, metabolic and neurological health.

            Female aging is basically summarized as estrogen deficiency. The difference between a young woman, and an old woman, is not merely years, but estrogen level and sensitivity. Low estrogen, low sensitivity = lethargic, diabetic , heart diseased, withered skinned, barrel waisted miserable old crone.

            This is exactly as in men, 40+ andropause and physiological changes are largely related to natural decline of testosterone in older men (loss of muscle mass, motivation, increased body fat, metabolic problems and so on).

            2) “I think a lack of progesterone is more likely than an “estrogen deficiency,” though.”

            Again, this is because you simply don’t understand endocrinology and physiology. Progesterone is a stress hormone, made from adrenal glands and ovaries. It is only ever elevated during actual or potential stressors. Progesterone is not a dominant hormone in women, although it plays important role in female fertility and reproduction and sexual development, it is largely subordinate to estrogen.

            3) ” Estrogen probably increases with age “

            No, it doesn’t. This is quackery. Why do people such as yourself persist in quackery when it’s easily refuted by anyone with the motivation to fact check your arguments?

            Do you have any idea how estrogen is made in women, from the time of puberty onward? If you do understand this very basic endocrinology 101, your statement is quickly revealed to be total nonsense.

            4) “P.M. Wise found that estrogen interfered with the regulation of LH and FSH by desensitizing nerves in the hypothalamus [5].”

            You are describing an endocrinopathy, such as women who fail to ovulate for whatever reason, sometimes perhaps due to exposure to very high levels of synthetic chemical disruptive xenoestrogens prenatally, and various other irrelevant things. The normal estrogen made from a woman’s ovaries cannot ever result in this endocrine dysregulation you reference, once more, *totally* out of context. Yes, xenoestrogens and perhaps birth control have been known to cause dysregulation of the HPO axis and failure to ovulate due to insensitivity to the estrogen production of ovaries; this is of no relevance to normal female reproductive endocrinology and the normal healthy estrogen women make in their bodies.

            If it sounds like i have little tolerance for your nonsense, P.S., it’s because I do have little tolerance for it. I’m tired of refuting basic physiology amongst layquacks who are misleading large groups of people all over the world for profit and attention.

          • http://www.dannyroddy.com/ Danny Roddy

            Hey Homie,

            “Quackwatch correction: the estrogen/LH surge at ovulation is intense and brief. Higher echelon baseline estrogen, on the other hand, occurs 24/7 in healthy young women.”

            Higher baseline estrogen also appears in sepsis [1], breast cancer [2, 3], and general stress.

            Note the progesterone deficiency and prolactin excess in the women with breast cancer.

            In ‘The Textbook of Endocrinology’ Hans Selye preferred to call estrogen “the shock hormone” or “adipin” (because it was produced predominantly in the fat tissue) and found that in animals estrogens interrupted estrus, and were “anti-estrogenic” [4].

            In ‘Endocrine Physiology’ Constance R. Martin found that estrogens were “defeminizing” and that they “mimic testosterone” [5].

            Ditkoff et. al., found that in PCOS estrogen sometimes stimulated the adrenal glands to produce androgens responsible for whisker growth and chest hair [6]. Progesterone opposes estrogen [7], and is an anti-androgen [8].

            And I think all of this makes sense given that estrogen is essentially a growth hormone, reducing the cell and stimulating cell division [9], supporting the growth of the uterus, the breasts, and the pituitary gland.

            “The scientific literature is rather uncontroversial regarding the numerous benefits of estrogen for women with regard to mood, energy, appearance, body weight, metabolic and neurological health.

            I don’t think it’s uncommon in medical culture for people to feel that they have benefitted and understood a therapy, only to find later that it had seriously harmed them, radiation for example.

            “Female aging is basically summarized as estrogen deficiency. The difference between a young woman, and an old woman, is not merely years, but estrogen level and sensitivity. Low estrogen, low sensitivity = lethargic, diabetic , heart diseased, withered skinned, barrel waisted miserable old crone.”

            Estrogen probably increases with age [10,11], and serum values don’t always reflect tissue concentrations [12,13].

            Sustained high estrogen levels increase both insulin requirements and insulin secretion [14]. Lactic acid produced under the influence estrogen, which tends to accumulate in diabetics [15, 16, 17], interferes with respiration. Lactic acid stimulates the release of proinflammatory prostaglandin E2, which increases aromatase. Estrogen also increases PGE2. PGE2 interferes with respiration, too [18].

            “This is exactly as in men, 40+ andropause and physiological changes are largely related to natural decline of testosterone in older men (loss of muscle mass, motivation, increased body fat, metabolic problems and so on).”

            “Andropause” is also associated with an increase in prolactin, which is increased by estrogen [19,20].

            “Again, this is because you simply don’t understand endocrinology and physiology. Progesterone is a stress hormone, made from adrenal glands and ovaries. It is only ever elevated during actual or potential stressors. Progesterone is not a dominant hormone in women, although it plays important role in female fertility and reproduction and sexual development, it is largely subordinate to estrogen.”

            In the context of energy metabolism, estrogen seems disruptive: increasing reliance on “inefficient” glycolytic energy, increasing lactic acid, increasing calcium influx into cells [21], and probably decreases mitochondrial biogenesis [22].

            Progesterone protects mitochondrial function and structure [23], inhibits growth and induces apoptosis in cancer cells [24], and induces differentiation in breast cancer cells [25], and probably increases mitochondrial biogenesis [26].

          • Jannis Dittmer

            “Progesterone is a stress hormone, made from adrenal glands and ovaries.
            It is only ever elevated during actual or potential stressors. Progesterone is not a dominant hormone in women”

            LOL. You shouldn’t be allowed to write anything about health and hormone related topics. Poorly educated people might believe your nonsense. Regarding your position on estrogen you might want to read “The Rise and Fall of Estrogen Therapy” by Carla J. Rothenberg

          • http://www.dannyroddy.com/ Danny Roddy

            Hey Homie,

            “Quackwatch correction: the estrogen/LH surge at ovulation is intense and brief.

            Higher echelon baseline estrogen, on the other hand, occurs 24/7 in healthy young women.”

            Higher baseline estrogen also appears in sepsis [1], breast cancer [2, 3], and general stress.

            Note the progesterone deficiency and prolactin excess in the women with breast cancer.

            In ‘The Textbook of Endocrinology’ Hans Selye preferred to call estrogen “the shock hormone” or “adipin” (because it was produced predominantly in the fat tissue) and found that in animals estrogens interrupted estrus, and were “anti-estrogenic” [4].

            In ‘Endocrine Physiology’ Constance R. Martin found that estrogens were “defeminizing” and that they “mimic testosterone” [5].

            Ditkoff et. al., found that in PCOS estrogen sometimes stimulated the adrenal glands to produce androgens responsible for whisker growth and chest hair [6]. Progesterone opposes estrogen [7], and is an anti-androgen [8].

            And I think all of this makes sense given that estrogen is essentially a growth hormone, reducing the cell and stimulating cell division [9], supporting the growth of the uterus, the breasts, and the pituitary gland.

            “The scientific literature is rather uncontroversial regarding the numerous benefits of estrogen for women with regard to mood, energy, appearance, body weight, metabolic and neurological health.

            I don’t think it’s uncommon in medical culture for people to feel that they have benefitted and understood a therapy, only to find later that it had seriously harmed them, radiation for example.

            “Female aging is basically summarized as estrogen deficiency. The difference between a young woman, and an old woman, is not merely years, but estrogen level and sensitivity. Low estrogen, low sensitivity = lethargic, diabetic , heart diseased, withered skinned, barrel waisted miserable old crone.”

            Estrogen probably increases with age [10,11], and serum values don’t always reflect tissue concentrations [12,13].

            Sustained high estrogen levels increase both insulin requirements and insulin secretion [14]. Lactic acid produced under the influence estrogen, which tends to accumulate in diabetics [15, 16, 17], interferes with respiration. Lactic acid stimulates the release of proinflammatory prostaglandin E2, which increases aromatase. Estrogen also increases PGE2. PGE2 interferes with respiration, too [18].

            “This is exactly as in men, 40+ andropause and physiological changes are largely related to natural decline of testosterone in older men (loss of muscle mass, motivation, increased body fat, metabolic problems and so on).”

            “Andropause” is also associated with an increase in prolactin, which is increased by estrogen [19,20].

            “Again, this is because you simply don’t understand endocrinology and physiology. Progesterone is a stress hormone, made from adrenal glands and ovaries. It is only ever elevated during actual or potential stressors. Progesterone is not a dominant hormone in women, although it plays important role in female fertility and reproduction and sexual development, it is largely subordinate to estrogen.”

            In the context of energy metabolism, estrogen seems disruptive: increasing reliance on “inefficient” glycolytic energy, increasing lactic acid, increasing calcium influx into cells [21], and probably decreases mitochondrial biogenesis [22].

            Progesterone protects mitochondrial function and structure [23], inhibits growth and induces apoptosis in cancer cells [24], and induces differentiation in breast cancer cells [25], and probably increases mitochondrial biogenesis [26].

            References:

            1. Fourrier F, Jallot A, Leclerc L, Jourdain M, Racadot A, Chagnon JL, Rime A, Chopin C. Sex steroid hormones in circulatory shock, sepsis syndrome, and septic shock. Circ Shock. 1994 Aug;43(4):171-8. “High estrogen levels were specifically observed in patients with sepsis and septic shock, either males or females. Decreased LH and FSH levels were consistent with the negative feed-back effect of high estrogen levels on pituitary secretion. Circulating T levels were decreased in all male patients.”

            2. Meyer F, Brown JB, Morrison AS, MacMahon B. Endogenous sex hormones, prolactin, and breast cancer in premenopausal women. J Natl Cancer Inst. 1986 Sep;77(3):613-6. “Breast cancer was associated with high-plasma estradiol and prolactin and with low progesterone.”

            3. Zumoff B. Hormonal profiles in women with breast cancer. Obstet Gynecol Clin North Am. 1994 Dec;21(4):751-72. “It is concluded that four sets of findings are valid: (1) diminished adrenal androgen production, probably genetic, in women with premenopausal breast cancer; (2) ovarian dysfunction (luteal inadequacy plus increased testosterone production) in breast cancer at all ages; (3) increased 16 alpha-hydroxylation of estradiol in breast cancer at all ages; and (4) evidence that prolactin is a permissive risk factor for breast cancer, and that the pregnancy-induced decrease in prolactin levels may account for the protective effect of early pregnancy against breast cancer.”

            4. Selye H. The Textbook of Endocrinology. 1976 pp.59 “…Similarly, in many animal species, the so-called “estrogens” do not in themselves cause estrus or heat without simultaneous progesterone treatment, hence the later hormone could be called “estrogenic” with almost equal justification. Furthermore, folliculoids interrupt the estrous cycle in the intact rodent so that they are actually “anti-estrogenic” under ordinary circumstances of bioassay.”

            5. Martin C. Endocrine Physiology. 1985 pp. 556 “When the effects of perinatal gonadectomy and hormone injection were first observed, it seemed reasonable to conclude that testosterone interacts with androgen receptors in the brain to bring about defeminization. However, the concept had to be revised when it was found that estrogens mimic testosterone, whereas DHT does not.

            6. Ditkoff EC, Fruzzetti F, Chang L, Stancyzk FZ, Lobo RA. The impact of estrogen on adrenal androgen sensitivity and secretion in polycystic ovary syndrome. J Clin Endocrinol Metab. 1995 Feb;80(2):603-7. “Adrenal hyperandrogenism is a common feature of patients with polycystic ovary syndrome (PCO). This may be due to enhanced adrenal sensitivity to ACTH. Because enhanced ovarian androgen secretion does not appear to explain this phenomenon, we explored the role of estrogen in inducing enhanced adrenal sensitivity, in that a state of relative hyperestrogenism exists in PCO” “In conclusion, these data provide evidence that estrogen is at least one factor that influences adrenal androgen sensitivity in PCO and may help explain the frequent finding of adrenal hyperandrogenism in this syndrome.”

            7. Liu JW, Dawson DD, Peters CE, Baker MA, Walker AM. Estrogen replacement in ovariectomized rats results in physiologically significant levels of circulating progesterone, and co-administration of progesterone markedly reduces the circulating estrogen. Endocrine. 1997 Apr;6(2):125-31. “It is reported that estrogen treatment (237.2 +/- 49.2 pg/mL) results in physiologically significant levels of circulating progesterone (11.1 +/- 1.3 ng/mL). Also, co-administration of progesterone (23.7 +/- 2.0 ng/mL) with estrogen decreases the level of estrogen over that seen with estrogen alone (96.7 +/- 19.2 pg/mL with progesterone vs 237.2 +/- 49.2 pg/mL without progesterone). Thus, contrary to expectations, estrogen replacement therapy is not specific to estrogen and some of the antagonistic effects of progesterone are the result of a decrease in circulating estrogen, and not a specific effect on a target tissue.”

            8. Cassidenti DL, Paulson RJ, Serafini P, Stanczyk FZ, Lobo RA. Effects of sex steroids on skin 5 alpha-reductase activity in vitro. Obstet Gynecol. 1991 Jul;78(1):103-7.

            9. Gross. Reproductive cycle biochemistry. 1961 Fertility & Sterility 12(3), 245-260, 1961. “The maintenance of an environment conducive to anaerobic metabolism–which may involve the maintenance of an adequate supply of the substances that permit anaerobiosis…seems to depend primarily upon the action of estrogen.” “Glycolytic metabolism gradually increases throughout the proliferative phases of the cycle, reaching a maximum coincident with the ovulation phase, when estrogen is at a peak. Following this, glycolysis decreases, the respiratory mechanisms being more active during the secretory phase. Eschbach and Negelein showed the metabolism of the infantile mouse uterus to be less anaerobic than that of the adult. If estrogen is administered, however, there is a 98 per cent increase in glycolytic mechanisms.””The effect of the progestational steroids may be such as to interfere with the biochemical pattern required for support of this anaerobic environment.”

            10. Musey VC, Collins DC, Musey PI, Martino-Saltzman D, Preedy JR. Age-related changes in the female hormonal environment during reproductive life. Am J Obstet Gynecol. 1987 Aug;157(2):312-7. “We found that increased age during reproductive life is accompanied by a significant rise in both basal and stimulated serum follicle-stimulating hormone levels. This was accompanied by an increase in the serum level of estradiol-17 beta and the urine levels of estradiol-17 beta and 17 beta-estradiol-17-glucosiduronate.”

            11. Wilshire GB, Loughlin JS, Brown JR, Adel TE, Santoro N. Diminished function of the somatotropic axis in older reproductive-aged women. J Clin Endocrinol Metab. 1995 Feb;80(2):608-13. “Older reproductive-aged women had lower 12-h integrated daytime GH concentrations (mean +/- SE, 171 +/- 35 vs. 427 +/- 130 micrograms min/L; P = 0.036) than younger controls and a strong trend for lower IGF-I levels (22.7 +/- 2.1 vs. 31.3 +/- 3.5 nmol/L; P = 0.055) than younger controls despite having higher circulating E2 on the day of sampling (368 +/- 51 vs. 167 +/- 20 pmol/L; P = 0.002). We conclude that older reproductive-aged women have lower daytime GH concentrations than younger controls despite having higher E2 levels on the day of sampling and overall normal gonadal hormone parameters.”

            12. Batra S, Bengtsson LP, Sjöberg NO. Interrelations between plasma and tissue concentrations of 17 beta-oestradiol and progesterone during human pregnancy. Clin Endocrinol (Oxf). 1979 Dec;11(6):603-10. “The general conclusion to be drawn from the present study is the lack of correspondence between the plasma concentrations and the tissue concentrations of female sex steroids during pregnancy.”

            13. Vermeulen-Meiners C, Jaszmann LJ, Haspels AA, Poortman J, Thijssen JH. The endogenous concentration of estradiol and estrone in normal human postmenopausal endometrium. J Steroid Biochem. 1984 Nov;21(5):607-12. “The results from the tissue levels of both steroids showed large variations and there was no significant correlation with their plasma levels. The mean E2 concentration in tissue was 420 pg/g, 50 times higher than in plasma and the E1 concentration of 270 pg/g was 9 times higher. The E2/E1 ratio in tissue of 1.6, was higher than the corresponding E2/E1 ratio in plasma, being 0.3.”

            14. Briggs M. Oral Contraceptives. Eden Press, Montreal 1977.

            15. Scale T, Harvey JN. Diabetes, metformin and lactic acidosis. Clin Endocrinol (Oxf). 2011 Feb;74(2):191-6 “Diabetes rather than metformin therapy is the major risk factor for the development of LA. Lactic acidosis occurs in association with acute illness particularly in diabetes. Current guidance for the prevention of lactic acidosis may overemphasize the role of metformin.”

            16. Crawford SO, Hoogeveen RC, Brancati FL, Astor BC, Ballantyne CM, Schmidt MI, Young JH. Association of blood lactate with type 2 diabetes: the Atherosclerosis Risk in Communities Carotid MRI Study. Int J Epidemiol. 2010 Dec;39(6):1647-55. Epub 2010 Aug 25. “Plasma lactate was strongly associated with type 2 diabetes in older adults. Plasma lactate deserves greater attention in studies of oxidative capacity and diabetes risk.”

            17. Reaven GM, Hollenbeck C, Jeng CY, Wu MS, Chen YD. Measurement of plasma glucose, free fatty acid, lactate, and insulin for 24 h in patients with NIDDM. Diabetes. 1988 Aug;37(8):1020-4. “Variations in plasma FFA and lactate levels of the three groups were qualitatively similar, with lowest concentrations seen in normal individuals, intermediate levels in the group with mild NIDDM, and the highest concentration in those with severe NIDDM (two-way ANOVA, P < .001). Of particular interest was the observation that plasma FFA concentrations were dramatically elevated from midnight to 0800 in patients with severe NIDDM."

            18. Cherkasskaia MD, Matulis AA, Iasa?tis AA. [Effect of prostaglandin E2 on energy metabolism in isolated rat liver mitochondria]. Vopr Med Khim. 1982 May-Jun;28(3):110-4. "…and in presence of Ca2+–it caused uncoupling and inhibition of mitochondrial respiration, decrease in the rate of phosphorylation and in the ATPase reaction was well as in the efficiency of mitochondrial proton pump, connected with Ca2+ transport."

            19. D'Agata R, Aliffi A, Maugeri G, Mongioi A, Vicari E, Gulizia S, Polosa P, (1982), Hydrotestolactone lowers serum oestradiol and PRL levels in normal men: evidence of a role of oestradiol in prl secretion. Clin Endocrinol (Oxf). 1982 Nov;17(5):495-9.

            20. Nicoletti I, Filipponi P, Fedeli L, Ambrosi F, Gregorini G, Santeusanio F. Testosterone-induced hyperprolactinaemia in a patient with a disturbance of hypothalamo-pituitary regulation. Acta Endocrinol (Copenh). 1984 Feb;105(2):167-72.

            21. Zaitsu M, Narita S, Lambert KC, Grady JJ, Estes DM, Curran EM, Brooks EG, Watson CS, Goldblum RM, Midoro-Horiuti T. Estradiol activates mast cells via a non-genomic estrogen receptor-alpha and calcium influx. Mol Immunol. 2007 Mar;44(8):1977-85. Epub 2006 Nov 3.

            22. Rodríguez-Cuenca S, Monjo M, Gianotti M, Proenza AM, Roca P. Expression of mitochondrial biogenesis-signaling factors in brown adipocytes is influenced specifically by 17beta-estradiol, testosterone, and progesterone. Am J Physiol Endocrinol Metab. 2007 Jan;292(1):E340-6. Epub 2006 Sep 5.

            23. Maria Claudia Gonzalez Denisellea, Juan José Lopez Costab, Susana L. Gonzaleza, Florencia Labombardaa, Laura Garaya, Rachida Guennounc, Michael Schumacherc, Alejandro F. De Nicolaa. Basis of progesterone protection in spinal cord neurodegeneration. The Journal of Steroid Biochemistry and Molecular Biology

            Volume 83, Issues 1–5, December 2002, Pages 199–209

            24. Formby B, Wiley TS. Progesterone inhibits growth and induces apoptosis in breast cancer cells: inverse effects on Bcl-2 and p53. Ann Clin Lab Sci. 1998 Nov-Dec;28(6):360-9.

            25. Lin VC, Jin R, Tan PH, Aw SE, Woon CT, Bay BH. Progesterone induces cellular differentiation in MDA-MB-231 breast cancer cells transfected with progesterone receptor complementary DNA. Am J Pathol. 2003 Jun;162(6):1781-7.

            26. Rodríguez-Cuenca S, Monjo M, Gianotti M, Proenza AM, Roca P. Expression of mitochondrial biogenesis-signaling factors in brown adipocytes is influenced specifically by 17beta-estradiol, testosterone, and progesterone. Am J Physiol Endocrinol Metab. 2007 Jan;292(1):E340-6. Epub 2006 Sep 5.

          • http://itsthewooo.blogspot.com/ Jane Plain (Woo)

            Bill,
            Apologies for responding to Roddy’s progesterone rant.

            It seems the church of progesterone has showed up to defend their religion, making further discourse highly distracting + unproductive.

          • Scott Peterson

            My man boobs hurt

  • http://itsthewooo.blogspot.com/ Jane Plain (Woo)

    I’ve read Wiley’s book and while she has some good ideas her basic premise that people are in an eternal summer is not entirely correct, it is more accurate to say our circadian rhythms are simply dysregulated. Summer is a time of ideal metabolic health actually , whereas the chronic metabolic syndrome/insulin resistance of modern people is more in line with adaptive physiology for fall in winter.

    Modern people are in a limbo zone of triggering the stress/energy conservation systems adaptive for fall and winter prep , without the normal down time , sleep, darkness, and food avoidance that is normally implicit of winter.

    Animals preparing for hibernation induct a physiological syndrome exactly like that of human obesity, and it relates to higher melatonin and lower dopamine sensitivity at the end of summer. They become slothful, gluttonous, store fat, and become infertile, and this is true even if you take away all those fattening nuts.

    Obese humans have higher dopamine which may relate to high insulin and sympathetic nervous system excesses in insulin resistance, but their actual sensitivity to dopamine is very, very poor (just like a hibernating animal) and so the phenotype of obese human is that of dopamine deficiency, just like a hibernating animal. This is why dopamine agonists dont work very well in obese people, but when they are used there is a trend to motivation, weight loss, less food interest, better blood sugar and in PCOS women fertility too.

    • http://www.caloriesproper.com/ William Lagakos

      I’m attracted to Wiley’s “we pwned the light” theory because it is a simple way to explain the circannual dysrhythmia that’s our supposed demise; or somewhat of a grand unifying theory… that said, there are probably other theories leading up to dysregulated circadian rhythms that also *make sense.*
      Currently, however, I’m obsessed with light/dark, DA/5HT, summer/winter, melatonin, etc.

      • http://itsthewooo.blogspot.com/ Jane Plain (Woo)

        I have been obsessed with this for years ;D

        The core of her theory is sold:

        1) Our biology is shaped by genes which assume we still live in a world where nutrition and opportunity for expansion is controlled by sunlight patterns.

        2) Much modern disease relates to abolishing dark/light/seasonal patterns which are in synch with sunlight.

        Details are a bit spotty, but the book is otherwise revolutionary and she wrote it before anyone else was saying these things really.

    • Scott Peterson

      Pathetic low carb cock munching. How does thus really help you live?

      I eat the carbz, so what should I do¿¿¿¿¿

  • http://nigeepoo.blogspot.com/ Nigel Kinbrum

    “According to Wiley, during the winter months the body needs more sleep, and carbohydrates should be restricted as they would have been naturally during hunter-gatherer times.”
    I thought that H-Gs ate roots during the winter months, when there wasn’t much edible plant life above ground level.

    • FrankG

      Try to imagine yourself in Ice-age Europe (or the N American Plains for that matter) in the Winter months… snow on the ground for 3, 4, 5, 6 months?
      Exactly what roots are you planning to eat?

      • http://www.caloriesproper.com/ William Lagakos

        This is all speculation –>
        If you surf around the academic side of the paleo-sphere for long enough, you’ll find a tribe that ate some taters in the winter, and one that didn’t; same is probably true for a lot of foods. While there may be some common themes among them, there were still a lot of different tribes back then.

        • FrankG

          Of course there would have been variability and even today there are Hunter-Gatherer groups in Africa, New Guinea, Australia and elsewhere that include wild tubers (and even starch-rich tree pulp) in their diet. But I don’t think their concept of “Winter” is quite the same as mine… living in NE Canada and coming from ice-age European ancestry (according to my genes) :-)

          Surely potatoes would have been out of the question everywhere except South and Central America? And unless we are are talking about semi-sedentary Hunter-Gatherers I doubt we could assume that any tubers they found would be cultivated, or anything like the starch-rich varieties on offer today.

          I guess to me “Winter” means a covering of snow and ice on the ground. Maybe that is too much of an assumption on my part.

          • http://www.caloriesproper.com/ William Lagakos

            That makes a lot of sense. And of late (ie, Game of Thrones: “winter is coming”), I think of paleo-winter as an acute pseudo-ice age wherein there would indeed be no taters to pull from the ground… but again, there are probably some tribes who would’ve had ’em (it’s hard to make broad statements that apply equally to many different peoples, especially about diet).

      • http://nigeepoo.blogspot.com/ Nigel Kinbrum

        H-Gs would have eaten the stomach contents of animals who could extract edible roots/bulbs/w.h.y. from frozen soil. Eskimos get carbs from chitin in the stomachs of marine animals.
        In warmer parts of the world, the ground isn’t frozen in the Winter months.

        • FrankG

          Sure.. so Hunter-Gatherers eating the plant matter in the intestinal contents of animals during the Winter is the same as “H-Gs ate roots during the winter months”?

          I believe I just commented above that my definition of “Winter” perhaps is too narrow but even where the ground is not frozen you’re not going to be pulling up King Edwards by the spadeful.

          • http://www.caloriesproper.com/ William Lagakos

            https://en.wikipedia.org/wiki/King_Edward_potato
            I inferred as much, but had to google it to be sure.

          • http://nigeepoo.blogspot.com/ Nigel Kinbrum

            When I wrote “H-Gs ate roots”, the source of said roots is irrelevant. H-Gs could have dug up some roots using tools, but it’s easier to let herbivores dig them up & chew them for you (provided you can catch the herbivores). If you can’t dig up your own food or catch herbivores during Winter months, you die. If you catch a herbivore, are you going to throw away food that’s in its gut? I think not.

            King Edwards are stem tubers. Edible roots are root tubers, which can be eaten raw. See http://en.wikipedia.org/wiki/Tuber#Root_tubers

          • George

            I’ve seen a doco on taiga/tundra dwellers whose main source of carbohydrate was the stashes they pilfered from burrowing rodents – handfuls of oca-sized corms or tubers. This supplemented a carnivorous diet, and this form of carb piracy/scavenging in cold conditions is undoubtedly an ancient product of human smartness.
            Any herbivore that stores food can be robbed as well as eaten.

      • http://www.wild-aurochs.com/ Ballomar Cingetorigis

        Interestngly, across the great ice age steppe that stretched from Europe, through Asia and into north America there was very little snow, because so much water was locked up in the ice sheets.

        It’s likely that at least some of our ancestors followed the herds as they migrated.

        • http://www.caloriesproper.com/ William Lagakos

          Following the herd was an option?! That’s probably where you would’ve found me.

          • http://www.wild-aurochs.com/ Ballomar Cingetorigis

            It almost certainly was an option. It would have been cold but, if you had this moving larder in front of you, why wouldn’t you follow it?

  • http://www.caloriesproper.com/ William Lagakos

    TSH restores a summer phenotype in photoinhibited mammals via the RF-amides RFRP3 and kisspeptin.
    http://www.ncbi.nlm.nih.gov/pubmed/23538709

  • Jack Kruse

    Jeff Rothschild gave an excellent AHS 2013 talk. Here is his slides. Slide 7 and 8 big……but slide 13 holds the magic. http://www.slideshare.net/ancestralhealth/jeffrey-rothschild-timerestricted-feeding-an-overview-of-the-current-research-and-practical-applications-ahs13

    • http://www.caloriesproper.com/ William Lagakos

      Hi Jack, thanks for the link – that’s a very compelling presentation. I’m rather convinced that light exposure and meal timing are two very important inputs into circadian rhythms… but still trying to wrap my head around how the circadian impact on physiological insulin resistance was maintained in these mice seemingly independent of both: http://caloriesproper.com/?p=3494.

      Slides 7 & 8: Circadian integration of metabolism and energetics (Bass and Takahashi 2010). http://www.ncbi.nlm.nih.gov/pubmed/21127246

      Slide 13: Peripheral circadian oscillators in mammals: time and food Schibler et al., 2003). http://www.ncbi.nlm.nih.gov/pubmed/12828282

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  • Micah

    Jane Plain Woo, I am going to tell you right now you are absolutely wrong on many of these points, and I only study physiology as a hobby. Calm down and ready Danny’s comments again!

    On a side note, isn’t it common knowledge that estrogen feeds cancer, causes weight gain,etc..?? Hence why when men take aromatase inhibitors, they lose weight, have more sex drive?

    • http://itsthewooo.blogspot.com/ Jane Plain (Woo)

      Sorry you think I am wrong Micah.This seems to be the popular consensus among peatarians and magic progesterone disciples.

      “Men” do not take aromatase inhibitors, competitive athletes and body builders who are abusing steroids, whether they are male or female, take aromatase inhibitors.

      The function of this pharmacological intervention is to drive testosterone levels high and prevent estrogen metabolites antagonism of testosterone activity. Testosterone naturally breaks down into estrogen which exerts negative feedback control over testosterone activity and production in males.

      Please note, the behavior of steroid abusing athletes to use aromatase inhibitors to rig testosterone levels extremely high, is diametrically opposed to Roddy’s earlier comments that estrogen is post natally , post pubertally masculinizing.

      • http://www.dannyroddy.com/ Danny Roddy

        Hey Woo,

        Those steroid abusing athletes tend to have high levels of prolactin, too.

        Estrogen increases prolactin [1,2] and prolactin is associated with gynecomastia.

        Also, those suffering from PCOS tend to suffer from masculinity. Elevated estrogen is a feature of PCOS [3] and estrogen can antagonize the adrenal glands to secrete hormones responsible for whisker growth and chest hair [4].

        References:

        1. D’Agata R, Aliffi A, Maugeri G, Mongioi A, Vicari E, Gulizia S, Polosa P, (1982), Hydrotestolactone lowers serum oestradiol and PRL levels in normal men: evidence of a role of oestradiol in prl secretion. Clin Endocrinol (Oxf). 1982 Nov;17(5):495-9.

        2. Nicoletti I, Filipponi P, Fedeli L, Ambrosi F, Gregorini G, Santeusanio F. Testosterone-induced hyperprolactinaemia in a patient with a disturbance of hypothalamo-pituitary regulation. Acta Endocrinol (Copenh). 1984 Feb;105(2):167-72.

        3. Am J Obstet Gynecol. 1993 Nov;169(5):1223-6. Excessive estradiol secretion in polycystic ovarian disease. Benjamin F, Toles AW, Seltzer VL, Deutsch S. Polycystic ovarian disease is both a hyperestrogenic and a hyperandrogenic syndrome, and all studies have shown that hyperestrogenemia is the result of an elevation of estrone with plasma estradiol levels in the normal follicular range. Because a literature search failed to reveal any report of polycystic ovarian disease with significantly elevated estradiol levels, we report a case in which the plasma estradiol was so massively elevated as to mimic an estrogen-producing neoplasm. This case also suggests that although polycystic ovarian disease is a very rare cause of such excessive estradiol production, it should be included in the differential diagnosis of estrogen-producing neoplasms.

        4. Ditkoff EC, Fruzzetti F, Chang L, Stancyzk FZ, Lobo RA. The impact of estrogen on adrenal androgen sensitivity and secretion in polycystic ovary syndrome. J Clin Endocrinol Metab. 1995 Feb;80(2):603-7. “Adrenal hyperandrogenism is a common feature of patients with polycystic ovary syndrome (PCO). This may be due to enhanced adrenal sensitivity to ACTH. Because enhanced ovarian androgen secretion does not appear to explain this phenomenon, we explored the role of estrogen in inducing enhanced adrenal sensitivity, in that a state of relative hyperestrogenism exists in PCO” “In conclusion, these data provide evidence that estrogen is at least one factor that influences adrenal androgen sensitivity in PCO and may help explain the frequent finding of adrenal hyperandrogenism in this syndrome.”

        • http://itsthewooo.blogspot.com/ Jane Plain (Woo)

          The androgenic symptoms of PCOS are mediated by testosterone, not estrogen. PCOS women have normal to high estrogen (although, often *lower* estrogen than age/weight matched control female) and abnormally elevated testosterone, free testosterone, and DHEA-S (which is androgenic, and BTW, a metabolite of adrenal gland hormones / closely related to progesterone. Think about it for a second.)

          Sigh. This is blatant medical misinformation you are writing.

          The primary regulator of prolactin is dopamine, and any time testosterone is reduced / estrogen is augmented, prolactin will elevate, largely secondary to dopamine vs serotonin balance of nervous system. The association of prolactin with gynecomastia in men would relate to gonadotropin suppression and low testosterone with a relative dominance of estrogen. Prolactin suppresses gonadotropins.

          • Cow

            Cowrinthians 1, Chapter 3, Verse 13:
            “And Wooo was a keeper of sheep, but Peat was a tiller of the ground.
            “And in process of time it came to pass, that Peat brought of the citrus fruit and sugar cane of the ground an offering unto the Lord.
            “And Wooo, she also brought of the firstlings of her flock and of the fat thereof. And the Lord had respect unto Wooo and to her offering.
            “But unto Peat and to his offering he had not respect.”
            Amen.

          • http://itsthewooo.blogspot.com/ Jane Plain (Woo)

            Roddy , you may have peatarians, but I have cow minions.

            I clearly win.

        • http://itsthewooo.blogspot.com/ Jane Plain (Woo)

          Oh and BTW I have totally resolved my PCOS, much as you’ve resolved your balding. Congrats on that, I see you are very proud of not being bald :)

          I do not and never did have chest hair, and most PCOS women don’t have “chest hair” either.

          If only we could all be perfect human paleo specimens like Danny Roddy, carefully studying the good word of Peatarianism and raking in the $$$s at the same time. Some of us, like wooo, are just so imperfect and will surely be destroyed when the paleo revolution happens. I can never live up to the standards of human perfection set by Ray Peat and his son on earth Danny Roddy.

          • http://www.dannyroddy.com/ Danny Roddy

            “Oh and BTW I have totally resolved my PCOS”

            Rad.

            “much as you’ve resolved your balding. Congrats on that, I see you are very proud of not being bald :)”

            It’s, like, a dream come true.

            “If only we could all be perfect human paleo specimens like Danny Roddy, carefully studying the good word of Peatarianism and raking in the $$$s at the same time. Some of us, like wooo, are just so imperfect and will surely be destroyed when the paleo revolution happens. I can never live up to the standards of human perfection set by Ray Peat and his son on earth Danny Roddy.”

            I wish Ray was my Dad. That would be so cool!

          • http://itsthewooo.blogspot.com/ Jane Plain (Woo)

            I find it funny you’ve called PCOS women hairy man beasts with chesthair, meanwhile 18% bodyfat the one true grokette is supporting you on facebook… when she, as well, has PCOS.

            Someone should ask Gokaleo if “grokette” has chest hair? We know grokette isn’t a fat low carber, but the possibility remains grokette might have been a hairy man beast with chesthair. It’s definitely true grokette had 18% bodyfat ,however.

          • Mary Lewis

            The Estrogen Errors – Baxter, PhD, Prior, MD (endocrinologist.)

            http://www.cemcor.ubc.ca/help_yourself/articles/progesterone_therapy_menopause

            Suggest exploring the entire site thoroughly.

  • http://www.caloriesproper.com/ William Lagakos

    Danny, does your assessment also apply to seasonal breeding? This is far from my area of expertise, but it seems as though there are other factors besides progesterone/estrogen in favor of it, eg, melatonin & light cycles, prolactin/dopamine, and if I were a hunter-gatherer I would definitely want my progeny born in spring (admittedly that last one isn’t really a biological mechanism, but it *makes sense*).

    • http://www.dannyroddy.com/ Danny Roddy

      I try to look at health problems through the lens of energy metabolism. More specifically, cell excitation/relaxation, lactic acid/carbon dioxide, water retention/water loss, salt regulation, pH and energy levels, and the biochemical and physiological processes that reinforce or modify them (e.g., hormones, signaling substances, nutritional adequacy, light and the type of fuel used).

    • George

      Would you want young born in spring if it meant pregnancy was carried over winter? I wonder what sun sign is nutritionally optimal in Northern hemisphere?

      • http://www.caloriesproper.com/ William Lagakos

        clearly a two-edged sword, and seasonal breeding probably wasn’t a universal phenomenon. (but I sure like speculating about it.)

        • George

          Lambs are born in early spring but mating is controlled and winter feed supplied. Birds mate in early spring, raise young in summer. But with a 9 month gestation?
          Here’s a paper on human seasonality:
          http://jbr.sagepub.com/content/5/3/217.short

          Our results show for the first time on a global scale that photoperiod, as shown for many animals, may also influence the physiology of human reproduction. At higher latitudes, where changes in daylength are pronounced, a steep increase in human conceptions coincides with the vernal equinox. Temperature also appears to be a major influencing factor. Conception rates are above the annual mean at temperatures between 5° and 20°C, and temperature extremes decrease the probability of conceptions. In regions with cold winters and moderate summers, the number of conceptions correlates positively with temperature; close to the equator, where winters are more moderate than the hot summers, this correlation is negative. Regions with both hot summers and cold winters tend to have a bimodal conception rhythm. The influence of photoperiod is dominant before 1930, whereas the impact of temperature dominates in later years.

          • http://www.caloriesproper.com/ William Lagakos

            Interesting! December births… but I can also see how this too might be confounded by cultural influences (in humans). I used to work with horses – pregnant mares and their foals – and I remember a lot of cold nights in the barn waiting for them to give birth. (come to think of it, though, I’m not sure if the timing of their pregnancies was natural or manipulated by outside influences.)

          • George

            Pregnancy requires energy, especially in later months – but so does breast feeding. With 9mth gestation and even longer lactation (6-24mth) at 500Kcal daily, perhaps little human advantage from seasonal delivery. Fertility is not-to-be-missed opportunity, because certain, infancy just a gamble.

  • Scott Peterson

    carbs = BAD

    • Scott Peterson

      con mucho terrible.

      Por favor no los comen

  • http://www.caloriesproper.com/ William Lagakos

    +1 for morning sex –> “How much sex is considered exercise?”
    http://www.cnn.com/2013/09/17/health/sex-calorie-burn-upwave/

    From the article: “Having sex in the morning is a great idea for several reasons. A man’s testosterone levels are the highest between 7 and 8 a.m., for one. Also, if you make time for a half-hour morning session, you can roll out of bed and right into your morning workout and you’re already warmed up! Now that’s something worth setting your alarm for.”