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        <h1></h1>

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        <blockquote>
            <strong><span style="color: #222222"><span style="font-family: georgia, times, serif"><span
                            style="font-size: large"
                        >Hot flashes, energy, and aging</span></span></span></strong>
        </blockquote>
        <blockquote></blockquote>
        <blockquote>
            <span style="color: #222222"><span style="font-family: georgia, times, serif"><span
                        style="font-size: medium"
                    >Around the time that menstruation and fertility are ending, certain biological problems are more
                        likely to occur. Between the ages of 50 and 55, about 60% of women experience repeated episodes
                        of flushing and sweating. Asthma, migraine, epilepsy, arthritis, varicose veins, aneurysms,
                        urticaria, reduced lung function, hypertension, strokes, and interstitial colitis are some of
                        the other problems that often begin or get worse at the menopause, but that normally aren't
                        considered to be causally related to it.</span></span></span>
        </blockquote>
        <blockquote></blockquote>
        <blockquote>
            <span style="color: #222222"><span style="font-family: georgia, times, serif"><span
                        style="font-size: medium"
                    >Recently, hot flashes are being taken more seriously, because of their association with increased
                        inflammation, heart disease, and risk of dementia. Around the same age, late 40s to mid-50s, men
                        begin to have a sudden increase of some of the same health problems, including night sweats,
                        anxiety, and insomnia. In both sexes, the high incidence of depression in this age group has
                        usually been explained "psychologically," rather than biologically.</span></span></span>
        </blockquote>
        <blockquote></blockquote>
        <blockquote>
            <span style="color: #222222"><span style="font-family: georgia, times, serif"><span
                        style="font-size: medium"
                    >When the estrogen industry began concentrating on women of menopausal age (after the disastrous
                        years of selling it as a fertility drug), "estrogen replacement" therapy was promoted as a cure
                        for the problems associated with menopause, including hot flashes, which were explained as the
                        result of a deficiency of estrogen. However, in recent years, the phrase "estrogen deficiency"
                        has begun to be replaced by the phrase "estrogen withdrawal," because it has been found that
                        women with hot flashes don't necessarily have less estrogen in their blood stream than women who
                        don't have hot flashes.</span></span></span>
        </blockquote>
        <blockquote></blockquote>
        <blockquote>
            <span style="color: #222222"><span style="font-family: georgia, times, serif"><span
                        style="font-size: medium"
                    >Associated with this change of terminology, there has been a recognition that changes in the
                        temperature regulating system in the brain, rather than changes in the amount of estrogen, are
                        responsible for the hot flashes, but mainstream medicine has carefully avoided the investigation
                        of this subject. The effects of estrogen on the thermoregulatory system are very clear, but the
                        standard medical view is that the physiology of hot flashes simply isn't understood.</span
                    ></span></span>
        </blockquote>
        <blockquote></blockquote>
        <blockquote>
            <span style="color: #222222"><span style="font-family: georgia, times, serif"><span
                        style="font-size: medium"
                    >Since the medical literature boldly describes the mechanisms of the circulatory system and the
                        causes of major problems such as heart attacks, high blood pressure, and strokes, it's odd that
                        it doesn't have an explanation for "hot flashes."</span></span></span>
        </blockquote>
        <blockquote>
            <span style="color: #222222"><span style="font-family: georgia, times, serif"><span
                        style="font-size: medium"
                    >But looking at this historically, I think this selective ignorance is necessary, for the protection
                        of some doctrines that have become very important for conventional medicine.</span></span></span
            >
        </blockquote>
        <blockquote></blockquote>
        <blockquote>
            <span style="color: #222222"><span style="font-family: georgia, times, serif"><span
                        style="font-size: medium"
                    >When doctors are talking about diseases of the heart and circulatory system, it's common for them
                        to say that estrogen is protective, because it causes blood vessels to relax and dilate,
                        improving circulation and preventing hypertension. The fact that estrogen increases the
                        formation of nitric oxide, a vasodilator, is often mentioned as one of its beneficial effects.
                        But in the case of hot flashes, dilation of the blood vessels is exactly the problem, and
                        estrogen is commonly prescribed to prevent the episodic dilation of blood vessels that
                        constitutes the hot flash. Nitric oxide increases in women in association with the menopause
                        (Watanabe, et al., 2000), and it is increased by inflammation, and hot flushes are associated
                        with various mediators of inflammation, but, as far as I can tell, no one has measured the
                        production of nitric oxide during a hot flash. Inhibitors of nitric oxide formation reduce
                        vasodilation during hot flushes (Hubing, et al., 2010).</span></span></span>
        </blockquote>
        <blockquote></blockquote>
        <blockquote>
            <span style="color: #222222"><span style="font-family: georgia, times, serif"><span
                        style="font-size: medium"
                    >Starting in the 1940s, the doctrine that menopause is the result of changes in the ovaries,
                        involving a depletion of eggs and an associated loss of estrogen production, was widely taught
                        to medical students. By the 1970s, the taboo against discussing menopause publicly was fading,
                        and the mass media began teaching the public that hot flashes are the result of an estrogen
                        deficiency, and that "estrogen replacement" is the most appropriate and effective treatment, and
                        in the next 20 years almost half the women in the US began taking it around the time of
                        menopause. This practice became routine at a time when "evidence based medicine" was being
                        promoted as a new standard, but there was no evidence that women experiencing hot flashes were
                        deficient in estrogen (in fact, there was evidence that they weren't), and there was evidence
                        that hot flashes began when the first menstrual period was missed, which coincided with, and
                        resulted from, a failure to produce a functional corpus luteum, preventing the production of a
                        normal amount of progesterone. But the silly old doctrine of deficiency is often restated by
                        professors, as if there was no doubt about it (for example, Rance, 2009; Bhattacharya and
                        Keating, 2012).</span></span></span>
        </blockquote>
        <blockquote></blockquote>
        <blockquote>
            <span style="color: #222222"><span style="font-family: georgia, times, serif"><span
                        style="font-size: medium"
                    >This extremely persistent disregard for important evidence about the nature of menopause and its
                        symptoms was guided by the estrogen industry, which began in the 1930s to call estrogen "the
                        female hormone," disregarding the facts about the biological roles of estrogen and progesterone,
                        because chemicals with estrogenic effects were numerous and cheap, while progesterone was
                        expensive, and had no synthetic equivalents. At the time the pharmaceutical industry began
                        promoting estrogen as the female hormone to prevent miscarriage, it was already well known that
                        it could produce abortion, as well as causing inflammation and cancer, and some of the most
                        famous estrogen researchers were warning of its multiple dangers in the 1930s.</span></span
                ></span>
        </blockquote>
        <blockquote></blockquote>
        <blockquote>
            <span style="color: #222222"><span style="font-family: georgia, times, serif"><span
                        style="font-size: medium"
                    >Menopause is a major landmark of aging, and if its meaning is radically misunderstood, a coherent
                        understanding of aging is unlikely, and without an understanding of the loss of functions with
                        age, we won't really understand life. More specifically, the real causes of the many serious
                        problems occurring in association with the menopause will be ignored. Finding the causes of the
                        seemingly trivial hot flash will affect the way we understand aging and its diseases.</span
                    ></span></span>
        </blockquote>
        <blockquote></blockquote>
        <blockquote>
            <span style="color: #222222"><span style="font-family: georgia, times, serif"><span
                        style="font-size: medium"
                    >If a common occurrence is thought to have some importance in itself, or to relate closely to
                        something of importance, it will be described carefully, and its general features will become
                        part of the common understanding. It's clear that our medical culture hasn't considered the hot
                        flash to be important, because there are still physicians who believe that the hot flash
                        represents a rise of body temperature caused by a sudden increase of heat production, which they
                        sometimes explain as an upward fluctuation of thyroid gland activity. Measurement of body
                        temperature before and during hot flashes has shown clearly that the internal temperature is
                        lowered slightly by the hot flash, as heat is lost from the skin, as a result of vasodilation.
                        Physiologists have been studying the differences in temperature regulation between men and
                        women, and the effects of hormones on temperature regulation, for more than 70 years, but the
                        medical profession in the United States showed almost no interest in the subject for about 50
                        years.</span></span></span>
        </blockquote>
        <blockquote></blockquote>
        <blockquote>
            <span style="color: #222222"><span style="font-family: georgia, times, serif"><span
                        style="font-size: medium"
                    >August Weismann's doctrine of "mortal soma, immortal germ line," led people to postulate that
                        "primordial germ" cells migrated into the ovary (consisting of "somatic" cells) during embryonic
                        development, and that the baby was born with a supply of germ cells that was used up during the
                        reproductive lifetime, accounting for the decline of fertility with aging. The fact that
                        menstrual cycles ended around the time that fertility ended was explained by the idea that
                        ovulation caused the release of estrogen, and that the absence of eggs caused a failure to
                        produce estrogen, and that the absence of estrogen led to the failure of the cyclical uterine
                        changes. It was all deduced from a mistaken ideology about the nature of life.&nbsp;</span
                    ></span></span>
        </blockquote>
        <blockquote></blockquote>
        <blockquote>
            <span style="color: #222222"><span style="font-family: georgia, times, serif"><span
                        style="font-size: medium"
                    >Cancer of the endometrium (lining) of the uterus and breast cancer were known to be the first and
                        second cancers, respectively, produced by uninterrupted exposure to estrogen (for example,
                        Lipshutz, 1950). Investigation of the causes of endometrial cancer showed that women with
                        anovulatory cycles, that failed to produce progesterone, or who had a reduced production of
                        progesterone, developed overgrowth of the endometrium, and that these were the women who were
                        later most likely to develop cancer of the endometrium. The peak incidence of endometrial cancer
                        is in the postmenopausal years, resulting from prolonged exposure to estrogen, unopposed by
                        progesterone. The medical belief* that "ovulation produces estrogen," and that the absence of
                        menstruation means an absence of estrogen, has been very harmful to women's health.</span></span
                ></span>
        </blockquote>
        <blockquote></blockquote>
        <blockquote>
            <span style="color: #222222"><span style="font-family: georgia, times, serif"><span
                        style="font-size: medium"
                    >Several laboratories, from the 1950s through the 1980s, investigated the causes of age-related
                        infertility. A.L. Soderwall, among others, demonstrated that an excess of estrogen makes it
                        impossible for the uterus to maintain a pregnancy.&nbsp;</span></span></span>
        </blockquote>
        <blockquote>
            <span style="color: #222222"><span style="font-family: georgia, times, serif"><span
                        style="font-size: medium"
                    >Subsequently, his lab showed that neither changes in the eggs nor changes in the uterus could
                        explain age related infertility. Altered pituitary hormone cycles, resulting from changes in the
                        brain, could account for the major changes in the ovaries and uterus.</span></span></span>
        </blockquote>
        <blockquote></blockquote>
        <blockquote>
            <span style="color: #222222"><span style="font-family: georgia, times, serif"><span
                        style="font-size: medium"
                    >Other experimenters, including P.M. Wise, V.M. Sopelak and R.L. Butcher (1982), P. Ascheim (1983),
                        and D.C. Desjardins (1995) have clarified the interactions between the ovaries and the brain.
                        For example, when the ovaries of an old animal are transplanted into a young animal, they are
                        able to function in response to the new environment, but when the ovaries of a young animal are
                        transplanted into an old animal, they fail to cycle. However, if the ovaries are removed from an
                        animal when it's young, so that it lives to the normal age of infertility without being
                        regularly exposed to surges of estrogen, it will then be able to support normal cycles when
                        young ovaries are transplanted into it. But if it received estrogen supplements throughout its
                        life, transplanted young ovaries will fail to cycle.</span></span></span>
        </blockquote>
        <blockquote></blockquote>
        <blockquote>
            <span style="color: #222222"><span style="font-family: georgia, times, serif"><span
                        style="font-size: medium"
                    >The work of Desjardins and others has demonstrated that free radicals generated by interactions of
                        estrogen and iron with unsaturated fatty acids are responsible for damage to brain cells
                        (Desjardins, et al., 1992). The damaged inhibitory nerve cells allow the pituitary to remain in
                        a chronically active state; in old rats, this can produce a state of constant estrus. Several
                        groups (Powers, et al., 2006; Everitt, et al., 1980; Telford, et al., 1986) have shown that
                        removal of the pituitary gland can greatly extend lifespan, if thyroid hormone is
                        supplemented.</span></span></span>
        </blockquote>
        <blockquote></blockquote>
        <blockquote>
            <span style="color: #222222"><span style="font-family: georgia, times, serif"><span
                        style="font-size: medium"
                    >One of the animal "models" used to study hot flashes is morphine withdrawal.&nbsp; The model seems
                        relevant to human hot flashes, because estrogen can stop the morphine withdrawal flushing, and
                        estrogen's acute and chronic effects on the brain-pituitary-ovary system involve the endorphins
                        and the opioidergic nerves (Merchenthaler, et al., 1998; Holinka, et al., 2008).</span></span
                ></span>
        </blockquote>
        <blockquote>
            <span style="color: #222222"><span style="font-family: georgia, times, serif"><span
                        style="font-size: medium"
                    >In young rats, sudden morphine withdrawal caused by injecting the anti-opiate naloxone, causes the
                        tail skin to flush, with a temperature increase of a few degrees, and causes the core body
                        temperature to fall slightly. However, old animals respond to the withdrawal in two different
                        ways. One group responded to the naloxone with an exaggerated flushing and decrease of core
                        temperature. The other group of old rats, which already had a lower body temperature, didn't
                        flush at all (Simpkins, 1994). I think this provides an insight into the reason that menopausal
                        treatment with estrogen can relieve some hot flashes--estrogen treatment might create a flush
                        resistant state similar to that of the cooler old animals in Simpkins' experiment.</span></span
                ></span>
        </blockquote>
        <blockquote>
            <span style="color: #222222"><span style="font-family: georgia, times, serif"><span
                        style="font-size: medium"
                    >It has been known for a long time, from studies in animals and people, that estrogen lowers body
                        temperature, and that this involves a tendency to increase blood flow to the skin in response to
                        a given environmental temperature, that is, the temperature "set-point" is lowered by estrogen.
                        Besides increasing heat loss, estrogen decreases heat production. These physiological effects of
                        estrogen can be seen in the normal menstrual cycle, with progesterone having the opposite effect
                        of estrogen on metabolic rate, skin circulation, body temperature, and heat loss. This causes
                        the familiar rise in temperature when ovulation occurs. Occasionally, young women will
                        experience hot flashes during the luteal phase of their menstrual cycle because of insufficient
                        progesterone production, or at menstruation, when the corpus luteus stops producing
                        progesterone.</span></span></span>
        </blockquote>
        <blockquote></blockquote>
        <blockquote>
            <span style="color: #222222"><span style="font-family: georgia, times, serif"><span
                        style="font-size: medium"
                    >Estrogen increases the free fatty acids circulating in the blood, and this shifts metabolism away
                        from oxidation of glucose to oxidation of fat, and it also reduces oxidative metabolism, for
                        example by lowering thyroid function (Vandorpe and Kühn, 1989). These changes are analogous to
                        those of fasting, in which metabolism shifts to the oxidation of fatty acids for energy, causes
                        decreased body temperature, and in some animals leads to a state of torpor or hibernation.</span
                    ></span></span>
        </blockquote>
        <blockquote></blockquote>
        <blockquote>
            <span style="color: #222222"><span style="font-family: georgia, times, serif"><span
                        style="font-size: medium"
                    >Despite decreasing oxidative metabolism, estrogen stimulates the adrenal cortex, both directly and
                        indirectly through the brain and pituitary, increasing the production of cortisol. Cortisol, by
                        increasing protein turnover, can increase heat production, but this effect isn't necessarily
                        sufficient to maintain a normal body temperature. It increases blood glucose, mainly by blocking
                        its use for energy production, but the glucose is derived from the breakdown of muscle protein.
                        It allows some glucose to be stored as fat. Sudden increases in the amount of glucose can lower
                        adrenaline, and chronically excessive cortisol tends to suppress adrenaline. Cushing's syndrome
                        (produced by excessive cortisol) commonly involves flushing and depression, both of which are
                        likely to be related to the decreased action of adrenaline.</span></span></span>
        </blockquote>
        <blockquote></blockquote>
        <blockquote>
            <span style="color: #222222"><span style="font-family: georgia, times, serif"><span
                        style="font-size: medium"
                    >While the biological changes occurring at menopause and during hot flashes are very similar to some
                        of the direct actions of estrogen, and although the menopause itself is the result of prolonged
                        exposure to estrogen, very large doses of estrogen can, in many women (as well as in morphine
                        addicted rats), stop the flushing. In some of the published animal experiments, effective doses
                        of estrogen were about 2000 times normal, and in some human studies, the dose was 30 times
                        normal. By blocking the production of heat, the estrogen treatments might be creating conditions
                        similar to those in Simpkin's cooler old rats, which failed to flush during morphine withdrawal.
                        Menopausal estrogen treatment is known to lower temperature (Brooks, et al., 1994).</span></span
                ></span>
        </blockquote>
        <blockquote></blockquote>
        <blockquote>
            <span style="color: #222222"><span style="font-family: georgia, times, serif"><span
                        style="font-size: medium"
                    >Since the Women's Health Initiative publicized the dangers of estrogen, there has been some
                        interest in alternative treatments for hot flashes. Since a reduced production of progesterone
                        has been associated with hot flushes for several decades, it isn't surprising that it is now
                        being tested as an alternative to estrogen. Recently, 300 mg of oral progesterone was found to
                        be effective for decreasing hot flashes, and a month after discontinuing it, the hot flushes
                        were still less frequent than before using it (Prior and Hitchcock, 2012). Previously,
                        transdermal progesterone was found to be effective (Leonetti, et al., 1999).</span></span></span
            >
        </blockquote>
        <blockquote></blockquote>
        <blockquote>
            <span style="color: #222222"><span style="font-family: georgia, times, serif"><span
                        style="font-size: medium"
                    >One of the things progesterone does is to stabilize blood sugar. In one experiment, hot flashes
                        were found to be increased by lowering blood sugar, and decreased by moderately increasing blood
                        sugar (Dormire and Reame, 2003).</span></span></span>
        </blockquote>
        <blockquote>
            <span style="color: #222222"><span style="font-family: georgia, times, serif"><span
                        style="font-size: medium"
                    >Hypoglycemia increases the brain hormone, corticotropin release hormone, CRH (Widmaier, et al.,
                        1988), which increases ACTH and cortisol. CRH causes vasodilation (Clifton, et al., 2005), and
                        is more active in the presence of estrogen. Menopausal women are more responsive to its effects,
                        and those with the most severe hot flushes are the most responsive (Yakubo, et al., 1990).</span
                    ></span></span>
        </blockquote>
        <blockquote></blockquote>
        <blockquote>
            <span style="color: #222222"><span style="font-family: georgia, times, serif"><span
                        style="font-size: medium"
                    >The first reaction to a decrease of blood glucose, at least in healthy individuals, is to increase
                        the activity of the sympathetic nervous system, with an increase of adrenaline, which causes the
                        liver to release glucose from its glycogen stores. The effect of adrenaline on the liver is very
                        quick, but adrenaline also acts on the brain, stimulating CRH, which causes the pituitary to
                        secrete ACTH, which stimulates the adrenal cortex to release cortisol, which by various means
                        causes blood sugar to increase, consequently causing the sympathetic nervous activity to
                        decrease. Even when the liver's glycogen stores are adequate, the system cycles rhythmically,
                        usually repeating about every 90 minutes throughout the day.</span></span></span>
        </blockquote>
        <blockquote></blockquote>
        <blockquote>
            <span style="color: #222222"><span style="font-family: georgia, times, serif"><span
                        style="font-size: medium"
                    >Sympathetic nervous activity typically causes vasoconstriction in the skin and extremities,
                        reducing heat loss, but the small cycles in the system normally aren't noticed, except as small
                        changes in alertness or appetite. With advancing age, most tissues become less sensitive to
                        adrenaline and the sympathetic nervous stimulation, and the body relies increasingly on the
                        production of cortisol to maintain blood glucose. Many of the changes occurring around the
                        menopause, such as the rise of free fatty acids and decrease of glucose availability, increase
                        the sensitivity of the CRH nerves, causing the fluctuations of the adrenergic system to cause
                        larger increases of ACTH and cortisol. Estrogen is another factor that increases the sensitivity
                        of the CRH nerves, and unsaturated fatty acids (Widmaier, et al. 1995) and serotonin
                        (Buckingham, et al., 1982) are other factors stimulating it. Serotonin, like noradrenalin, rises
                        with hypoglycemia (Vahabzadeh, et al., 1995), and estrogen contributes to hypoglycemia, by
                        impairing the counterregulatory system (Cheng and Mobbs, 2009).</span></span></span>
        </blockquote>
        <blockquote></blockquote>
        <blockquote>
            <span style="color: #222222"><span style="font-family: georgia, times, serif"><span
                        style="font-size: medium"
                    >With the reduced vasoconstrictive effects of the sympathetic nerves, and the increased activity of
                        CRH, cyclic vasodilation under the influence of cortisol will become more noticeable. With the
                        onset of menopause, and in proportion to the number and intensity of symptoms (on the Greene
                        Climacteric Scale), the daily secretion of cortisol was increased (Cagnacci, et al.,
                        2011).</span></span></span>
        </blockquote>
        <blockquote></blockquote>
        <blockquote>
            <span style="color: #222222"><span style="font-family: georgia, times, serif"><span
                        style="font-size: medium"
                    >Once the ideologically based doctrine of menopause as estrogen deficiency is discarded, it's
                        possible to see its features as clues to the ways in which "stress" contributes to the
                        age-related degeneration of the various systems of the body--not just the reproductive system,
                        but also the immune system, the nutritive, growth, and repair processes, and the motivational,
                        emotional, and cognitive processes of the nervous systems. The changes around menopause aren't
                        the same for all women, but the ways in which they vary can be understood in terms of the basic
                        biological principles of energy and adaptation that are universal.</span></span></span>
        </blockquote>
        <blockquote></blockquote>
        <blockquote>
            <span style="color: #222222">&nbsp;<span style="font-family: georgia, times, serif"><span
                        style="font-size: medium"
                    ><span style="font-style: normal"><span style="font-weight: normal"
                            >Each type of cell and organ is subject to injury, and in some cases these injuries are
                                cumulative. In the healthy liver, which stores glycogen, toxins can be inactivated, for
                                example by combining with glucuronic acid, derived from the stored glucose. With injury,
                                such as alcoholism combined with a diet containing polyunsaturated fats, the liver's
                                detoxifying ability is reduced. Even at an early stage, before there is a significant
                                amount of fibrosis, the reduced activity of the liver causes estrogen to accumulate in
                                the body. Estrogen's valuable actions are, in health, exerted briefly, and then the
                                synthesis of estrogen is stopped, and its excretion reduces its activity, but when the
                                liver's function is impaired, estrogen's activity continues, causing further
                                deterioration of liver function, as well as injury of nerves such as Desjardins
                                described, and the systemic energy shifts and stress activations mentioned above.</span
                            ></span></span></span></span>
        </blockquote>
        <blockquote></blockquote>
        <blockquote>
            <span style="color: #222222"><span style="font-family: georgia, times, serif"><span
                        style="font-size: medium"
                    >Besides lowering the liver's detoxifying ability, stress, hypoglycemia, malnutrition,
                        hypothyroidism, and aging can cause estrogen to be synthesized inappropriately and continuously.
                        With aging, estrogen begins to be produced throughout the body--in fat, muscles, skin, bones,
                        brain, liver, breast, uterus, etc. Polyunsaturated fats are a major factor in the induction and
                        activation of the aromatase enzyme, which synthesizes estrogen.</span></span></span>
        </blockquote>
        <blockquote></blockquote>
        <blockquote>
            <span style="color: #222222"><span style="font-family: georgia, times, serif"><span
                        style="font-size: medium"
                    >Increased synthesis of estrogen, with aromatase, and decreased excretion of it, by the liver and
                        kidneys, are only two of the processes that affect the influence of estrogen during aging.
                        Cellular stress (chemical, mechanical, hypoxemic, hypoglycemic [Clere, et al., 2012; Aguirre, et
                        al., 2007, Zaman, et al., 2006, Saxon, et al., 2007; Tamir, et al., 2002; Briski, et al., 2010])
                        increases estrogen receptors (which activate CRH and the stress response). The presence of
                        estrogen receptors means that estrogen will be bound inside cells, where it acts to modify those
                        cells. Before estrogen can reach the liver to be inactivated, it must be released from cells.
                        Ordinarily, the cyclic production of progesterone has that function, by destroying the
                        estrogen-binding proteins. Progesterone also inhibits the aromatase which synthesizes estrogen,
                        and shifts the activities of other enzymes, including sulfatases and dehydrogenates, in a
                        comprehensive process of eliminating the presence and activity of estrogen. At menopause, when
                        the ovary fails to produce the cyclic progesterone, all of these processes of estrogen
                        inactivation fail. In the absence of progesterone, cortisol becomes more active, increasing
                        aromatase activity, which now becomes chronic and progressive. The decrease of progesterone
                        causes many other changes, including the increased conversion of polyunsaturated fatty acids to
                        prostaglandins, and the formation of nitric oxide, all of which contribute to the tendency to
                        flush.</span></span></span>
        </blockquote>
        <blockquote>
            <span style="color: #222222">&nbsp; <span style="font-family: georgia, times, serif"><span
                        style="font-size: medium"
                    ><span style="font-style: normal"><span style="font-weight: normal"><hr /></span></span></span
                    ></span></span>
        </blockquote>
        <blockquote>
            <span style="color: #222222"><span style="font-family: georgia, times, serif"><span
                        style="font-size: medium"
                    >*The limits of the belief system or consciousness of US medicine are nicely defined by the topics
                        included in the Index Medicus, which was published from 1879 to 2004, by the Surgeon General's
                        Office of the U.S. Army, the American Medical Association, and the National Library of Medicine,
                        at different times. If you look up any important topic in physiology or biochemistry in an index
                        of scientific publications such as Biological Abstracts or Chemical Abstracts, and then look for
                        the same subject in the Index Medicus, you will find some startling differences--long delays and
                        antagonistic attitudes. At first the discrepancies seem ludicrous and hard to account for, but I
                        think they can be explained by recognizing that the editors of medical journals consider science
                        to be their enemy.</span></span></span>
        </blockquote>
        <blockquote></blockquote>
        <blockquote>
            <span style="color: #222222">&nbsp;&nbsp;&nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; &nbsp; <span
                    style="font-family: georgia, times, serif"
                ><span style="font-size: medium"><span style="font-style: normal"><span style="font-weight: normal"><h3>
                                    REFERENCES
                                </h3></span></span></span></span></span>
        </blockquote>
        <blockquote>
            <span style="color: #222222"><span style="font-family: georgia, times, serif"><span
                        style="font-size: medium"
                    >J Biol Chem. 2007 Aug 31;282(35):25501-8. A novel ligand-independent function of the estrogen
                        receptor is essential for osteocyte and osteoblast mechanotransduction. Aguirre JI, Plotkin LI,
                        Gortazar AR, Millan MM, O'Brien CA, Manolagas SC, Bellido T.</span></span></span>
        </blockquote>
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