Microsoft word - leereport.doc

SLOWING THE AGING PROCESS WITH NATURAL PROGESTERONE Aging is as inevitable as death and taxes, but prevention of premature aging is a goal towhich we all should (and can) aspire. In this regard, the role of natural progesterone shouldbe re-examined. In women, progesterone and estrogen are produced primarily by the ovaryduring normal menstrual cycles. Progesterone maintains the secretory endometrium and, inthe case of a fertilized ovum, is necessary for the survival of the embryo and the developmentof the growing fetus throughout gestation. Also, progesterone is an important precursor inthe biosynthesis of adrenal corticosteroids and of all the sex hormones, and provides manyimportant intrinsic physiological functions, the lack of which can lead to symptoms oftenassociated with aging as well.
Thus, natural progesterone is one of the body’s most important hormones and has benefitsfar beyond its role in menstrual cycles and pregnancy. As menopause approaches and thenumber of ovarian follicles decrease, progesterone levels also decrease. With menopause,progesterone levels fall close to zero, whereas some estrogen continues to be synthesizedwithin fat and muscle cells. The pre and postmenopausal loss of progesterone can becorrelated not only with osteoporosis, but with many bodily changes commonly interpretedas aging. Proper supplementation with natural progesterone prevents and commonly reversesthese supposed aging effects. Good health during the latter half of one’s life is not a forlornhope; it can become a reality if we learn to support rather than impair or neglect our naturalhealth giving capabilities. In this regard, natural progesterone has a key role.
[Natural progesterone should not be confused with the synthetic progesterone promoted bythe pharmaceutical industry and so often prescribed by physicians as progesteronesubstitutes. The truth is that these synthetic versions do not duplicate natural progesterone’sfull spectrum of benefits, and all carry multiple potential undesirable side effects. This willbe more fully discussed later in the paper.] Diagram 1. The multiple roles of natural progesterone helps normalize blood sugar levelsnormalizes zinc and copper levelsmaintains proper cell oxygen levelsprotects against breast cystsprotects against breast cancerprotects against endometrial cancerwhen used topically, moisturizes skincounteracts estrogen side effects Our present preoccupation with supplemental estrogen and our neglect of naturalprogesterone is a medical oddity peculiar to the past 3-4 decades. The reasons for this arecomplex, but include incomplete knowledge among most physicians and the pressures onresearch funds driven by pharmaceutical profits. At this time, it is important to understandthe known physiological effects of these two important hormones.
Comparison of Estrogen’s and Progesterone’s Physiologic Effects stimulates osteoblast bone buildingnecessary for survival of embryoprecursor of cortisone and sex hormones Further, estrogen is an end-product hormone and does not participate in the biosynthesis ofother hormones or active compounds; whereas progesterone, while active in its own right,also is a precursor to other vital hormones in the body.
When one observes the many benefits of progesterone, one must wonder why this valuablehormone has been so long neglected. Let us more closely review the various roles of naturalprogesterone.
The female role in the propagation of the human species includes, of course, the menstrualcycle. Both sets of ovarian hormones, estrogens and progesterone, are pare of a complex,interconnected and closely coordinated system of hypothalamic brain centers and pituitaryhormones involving feedback controls designed to produce a wide array of physiologicaleffects, the purpose of which is to prepare the uterus (and the body as well) for pregnancyand to produce an ovum ready for fertilization by sperm. Simply put, hypothalamic nucleiwithin the limbic brain monitor serum levels of estrogen and progesterone; when levels fall(bringing on menstruation), the hypothalamic nuclei produces gonadotropin releasinghormone (GnRH) which causes the pituitary secretion of follicle stimulating hormone (FSH) which stimulates the ovary to synthesize estrogen which (a) initiates proliferation of the endometrium, and (b) initiates ovarian follicles to prepare an ovum for ovulation. Asthe follicle matures in this activity, pituitary luteinizing hormone (LH) rises to a peak coinciding with ovulation. With ovulation, the successful ovarian follicle becomes thecorpus luteum which then synthesizes progesterone, often as much as 20-25 mg per day.
Progesterone transforms the proliferative endometrium into the secretory form necessary forsuccessful implantation of a fertilized ovum, should one occur. If fertilization does not occurin a week or so, the levels of both ovarian hormones decline, leading to menstruation, and thecycle begins anew.
In this system, estrogen is the dominant hormone during the first two weeks of the cycle(prior to ovulation) and, after ovulation, progesterone soon becomes the dominant hormone.
If fertilization does not occur, progesterone declines after day 26 or 27 of the typicalmenstrual cycle, bringing on menstruation.
In the event of a successful fertilization of an ovum and its implantation in the uterus,progesterone secretion by the corpus lelteum is enhanced by a hormone (chorionicgondotropin) produced by the developing zygote (fertilized ovum). As the placentadevelops, it takes over production of progesterone, increasing the production greatly. Duringthe third trimester of pregnancy, for example, placental progesterone production reaches 300-400 mg per day.
Interestingly, all the ovarian follicles from which future ova will spring are present in theovaries at birth. In fact, there may be 300,000 follicles initially present. With the onset ofpuberty (menarche) and the monthly surges of follicle stimulating hormone (FSH) andluteinizing hormone (LH), the monthly development of ova begins. One would think that theplentiful initial supply of follicles would yield ova sufficient to last until the cessation ofmenstrual cycles (menopause) at age 50-55. This, however, is not the case in North America.
It has become quite common that unusual follicle “burn-out” occurs as early as age 35 andthus many women have anovulatory (and thus, lacking progesterone) cycles for 15 years ormore before actual menopause. This results in sustained monthly estrogen dominance,leading to a wide variety of medical problems stemming from unopposed estrogen sideeffects. Such women present with water retention, increased fat deposition about the hipsand lower abdomen, hypertension, lack of libido, irritability and depression, fibrocysticbreasts, endometrial cancer and breast cancer.
Since these complaints are far less common in “undeveloped” countries, it is natural tospeculate that the cause of follicle burn-out is environmental, probably a toxic contaminant towhich we are exposed, or possibly some dietary deficiency. The leading candidates for thisendemic malady at this time are our pervasive petrochemical derivatives, principally thepetrochemically derived insecticides and herbicides which, being fat-soluble, becomeconcentrated in animal fat food chain products. Many of these compounds act as estrogenmimics and, in this regard are amazingly potent, being active at nanogram (one-billionth[109] of a gram) levels. They include pesticides such as DDT, DDE, Kepone, dieldrin,dicofol, and methoxychlor; and polychlorinated biphenyls (PCB’s), anthracene, alkyl phenolsand bisphenol A (the monomer that is condensed to make polycarbonate plastic). These estrogen mimics are highly lipophilic (fat soluble), very persistent (not biodegradable or wellexcreted), and accumulate in fat tissue of animals and humans over a lifetime. 1,2 The toxicity of DDT was recognized sometime ago and its use has been severely restrictedin the US and European countries. However, it is still being used in third world countries,especially for mosquito control, and new DDT production plants are still being funded by theWorld Bank. The DDT does not remain in the country where it is used. It, or its metabolite,DDE, can be carried by the wind to incorporation in the food chain of all sea life, includingthe fish we eat; and its use on food crops becomes international when the foods are soldworldwide. The other pesticides, PCB’s, and plastics are particularly prevalent in our societytoday and the full panoply of their toxic results is yet to be revealed.
Thus, it should be clear that anovulatory cycles, whether created by environmental toxinsor other causes, lead to progesterone deficiency and estrogen dominance, with all its potentialfor undesirable side effects. When this hormone imbalance is present, supplementation withnatural progesterone is paramount.
Menopause, were it only the cessation of menses and the loss of fecundity, would beviewed with relief by most women. In the US and most “advanced” nations, however,menopause is viewed as a portent of disagreeable symptoms and progressive physicaldeterioration. The prospect of unpredictable hot flushes, night sweats and mood swings, andthe seemingly inevitable progress of osteoporosis with its ultimate consequence of fracture istroublesome, if not downright fearsome. Estrogen supplementation may reduce hot flushesand can, for a while, slow osteoporotic bone loss. However, estrogen also increases one’srisk of fibrocystic breast, edema, uterine fibroids, endometrial cancer, and most probably,breast cancer. Menopause is a continental divide in a woman’s life beyond which the view isone of trouble and eventual disaster. In large pare, this bleak outlook is due, in reality, to ourpresent neglect of using natural progesterone.
Menopause results from lowered estrogen levels such that monthly blood-richendometrial development and its shedding does not occur. It does not mean that estrogenlevels have fallen to zero. Estrogen continues to be produced, in somewhat lesser amounts,by conversion of a sterol, androstenedione, which is found in fat, including the fat in ourmuscle cells. Menopause merely means that ovarian production of estrogen declines tolevels which do not induce endometrial response. It is a natural phenomenon indicating onlythat one’s period of fertility is over.
Of greater importance is the fact that, in the US, it is common that women’s production ofprogesterone falls to near zero at least 6-8 years before actual menopause, due to theanovulatory periods described above. This is rarely recognized by typical physicians whomore or less automatically prescribe estrogen for many “menopausal” symptoms which, in actuality, result from progesterone deficiency, not estrogen deficiency. Not only are womensubject to estrogen dominance and its attendant symptoms, but they arrive at menopause withosteoporosis well underway, a clear indication that osteoporosis is not due to estrogendeficiency, but more likely due to progesterone deficiency (see below). All this could beprevented by timely supplementation during the menstrual cycle of natural progesteroneduring the pre and peri-menopausal period.
The doctor is told that estrogen helps delay osteoporosis, is good for hot flashes, and mayhelp prevent cardiovascular disease; and that these benefits outweigh the various estrogenrisks suck as fibroids, breast fibrocysts and/or cancer, and endometrial cancer. He is furthertold that synthetic progesterone will decrease estrogen’s risk of endometrial cancer and that itis up to the patient to decide if she is willing to accept the risks of progestin’s side effects.
The fact is, there is a degree of falsity in each of these claims. For now, let us focus on theosteoporosis problem.
Bones are living tissue, constantly being made, unmade (resorbed), and made anew. Theycan be broken and then healed; they can grow as we grow; and they can restore their mineralswhen such are taken from them. Within bones are cells (osteoblasts) that make new bone;and there are cells (osteoclasts) that resorb bone previously made. Bone mass and bonemineral density represent the relative contribution of osteoclast-mediated bone resorption andosteoclast-mediated new bone formation. Others factors remaining equal, bones remainstable when osteoblast and osteoclast actions are in equilibrium. Osteoporosis is a conditioninvolving relative osteoblast deficiency.
The only proven bone function of estrogen is to deter osteoclast-mediated boneresorption.3 Progesterone, on the other hand, stimulates osteoblast-mediated new boneformation.4 At menopause, the decline of estrogen levels allow a temporary increase in boneresorption; estrogen supplementation will retard this accelerated bone loss but it will notstimulate new bone formation and thus can not correct the loss that has occurred. Five yearsafter menopause, this benefit of estrogen disappears; with or without estrogen supplements,bone loss progresses at the same rate (of approximately 1.5% per year). 5 Bone formation in the adult woman is the function of progesterone, not estrogen. In myclinical experience since 1982, I have found that osteoporosis can be reversed in manywomen by restoring adequate natural progesterone, along with a program of diet, a fewvitamin and mineral supplements and exercise. Several of the synthetic progestins have amodest effect6,7 (at most a 5% increase bone mass in two years), but none are as effective asnatural progesterone is (typically a 15% increase in 2-3 years), depending on degree ofprevious bone loss) with or without supplemental estrogen8,9. Further, the progestins areknown to cause many side effects, whereas natural progesterone has no known side effects.
Hot flushes (or flashes) are vasomotor disturbances emanating from homeostatic controlcenters within the hypothalamus leading to inappropriate dilation of skin capillaries and/orsweating. During menopause, they correlate with high levels of pituitary follicle stimulatinghormone (FSH), resulting from low estrogen and progesterone levels. When estrogen issupplemented, FSH levels fall and so does the incidence of hot flushes. The most likelyscenario for this phenomenon is that low hormone levels stimulate the hypothalamic centersresulting not only the FSH elevation, but also the activation of nearby hypothalamic neuralnuclei controlling vasomotor responses. Although estrogen supplementation is effective inreducing hot flushes, later attempts to reduce estrogen supplementation often results inrecurrence of the symptoms.
There are other ways to deal with hot flushes. Experience shows that a diet rich in freshvegetables and low in sugar and refined carbohydrates, along with vitamin E and aerobicexercise, will often decrease the intensity and frequency of these symptoms. Also,replacement of natural progesterone alone and in sufficient doses will frequently result inelimination or decreased severity of hot flushes. Since the hypothalamic centers monitorboth estrogen and progesterone, it should not be surprising that sufficient naturalprogesterone will be effective in treating hot flushes. Because of the inherent toxicity ofunopposed estrogen, these methods should be thoroughly tried before resorting to estrogensupplements.
Recent pharmaceutical advertisements claim that estrogen supplementation reduces therisk of cardiac death. Despite the evidence of numerous studies showing otherwise,10-13 thisclaim is based on a nurses questionnaire report which found a slightly lower incidence ofcardiac deaths in estrogen using nurses, compared to non-estrogen using nurses. In thisreport,14 the total number of cardiac deaths among the nurse population constitutes less than0.5% of the total number in the study. Further, it is revealed that among the nurses for whomestrogen had not been prescribed, there was a higher proportion of nurses with diabetes,obesity, cigarette smoking and little or no exercise. These are all risk factors for heartdisease, and therefore the doctors for these nurses had wisely refrained from prescribingestrogen for them. The claim of lower relative risk for estrogen users is based solely on thestatistical “adjustment” of the risk factors listed above. With a slightly different“adjustment”, the putative estrogen benefit disappears.
Furthermore, the pharmaceutical advertisements do not mention the fact the ischemic(thrombo-embolic) stroke death incidence was higher among the estrogen users. This isentirely understandable since estrogen increases the tendency of blood to form clots. If oneis offered estrogen supplements, shouldn’t he/she be told that such treatment increased thechance of dying from a stroke? Natural progesterone, on the other hand, normalizes blood clotting. The message to be learned is that, if estrogen is to be prescribed, it should alwaysbe accompanied by natural progesterone.
Fibroids are non-malignant nodules or masses of connective tissue within or extendingfrom the walls of the uterus. They tend to develop during the pre or peri-menopausal phasewhen estrogen is dominant; they atrophy after menopause when estrogen levels fall. Propersupplementation with natural progesterone during these critical times of estrogen dominancewill prevent or reduce the size of uterine fibroids. If a woman can prevent or reverseosteoporosis by using natural progesterone instead of estrogen replacement therapy (ERT),she need not risk the development of fibroids.
Progesterone Prevention of Fibrocystic Breasts and Mastodynia Estrone and estradiol, the two estrogens most often prescribed in ERT, both stimulatebreast tissue, especially if unopposed by natural progesterone. Thus, during thepremenopausal estrogen-dominant phase, breast fibrocysts and painful breast swelling(mastodynia) are common. These problems are perpetuated after menopause by ERT. Thepresence of fibrocystic breasts in the premenopausal phase is sufficient evidence ofunopposed estrogen and should be treated with adequate natural progesteronesupplementation. When this is done, the fibrocystic problem usually disappears in 2-3months, as does mastodynia. Very few medical conditions are this easy to treat. It isstaggering to consider the many women who suffer needlessly from these problems.
The cause of causes of breast cancer are not known. Some argue that dietary fats (such asthe trans-fatty acids) are involved, but the available references are mixed. More recently, acorrelation between certain environmental pesticides (especially the fat-soluble ones) andother petrochemical derivatives with breast cancer incidence has begun to attract attention.
Many of these chemicals act as extremely potent estrogen mimics, are lipophilic, andaccumulate in fat tissue in animals and humans. The importance of these chemicals inexplaining the rising incidence of breast cancer may be appreciated by understanding theworrisome connection between estrogen and breast cancer. Consider the following evidence: 1. Early pregnancy conveys protection against breast cancer; women bearing their first child after age 30 have a higher risk than nulliparous women.
2. Only the first, full term, early pregnancy conveys protection; aborted or interrupted pregnancies do not afford protection.
3. Married women without children are at a higher risk than those with one or more children; unmarried women and nuns are a higher risk than women who have experiencedpregnancy.
4. The risk of breast cancer is significantly less in women subjected to oophorectomy prior 5. Protective effect of early oophorectomy are negated by supplemental estrogen (ERT).
6. Treatment of males with estrogen (for prostate cancer or after trans-sexual surgery) is associated with an increased risk of breast cancer.
7. Survival time after mastectomy for cancer is improved by Tamoxifen, a weak estrogen that acts as an anti-estrogen to inhibit estrogen receptors.
It should be recalled that during pregnancy, the dominant estrogen is estriol, rather thanestrone and estradiol, which are the major estrogens produced during the menstrual cycle andas given in ERT. Similarly, during pregnancy, placental synthesis of progesterone isextraordinarily increased to levels 10-20 times the amount normally synthesized by the ovaryduring the menstrual cycle. It is likely that both estriol and progesterone provideprotection against breast cancer. This benefit of natural progesterone is further confirmedby the recent finding that pre-menopausal women having mastectomy for cancer suffer fewermetastases and late recurrences if their surgery were performed during the latter two weeksof their menstrual cycle (when progesterone is dominant), rather than during theearlier two weeks (when progesterone is absent).15 Synthetic progestins do not convey thisprotection and may, in fact, increase the risk of breast cancer, especially when used inconjunction with supplemental estrone or estradiol.16 The only known cause of endometrial cancer is unopposed estrogen. Since the mid-1970’s, it has been known that estrogen should never be given without being opposed bysupplemental progesterone or one of the progestins. The work of Gambrell,17 for example, isespecially important in illustrating this cancer risk of unopposed estrogen and the protectionby progestin supplementation. Further, Hargrove18 showed the superiority of naturalprogesterone over progestins by comparing the endometrial effects of (a) progestin[medroxyprogesterone acetate] given with estrone, to that of (b) natural progesterone whengiven with estradiol. He found that estradiol and natural progesterone supplementation inmenopausal women resulted in symptomatic improvement, minimal side effects, an improvedlipid profile, and amenorrhea without endometrial proliferation or hyperplasia (emphasisadded). Endometrial proliferation and/or hyperplasia are considered to be early steps in theendometrial cellular changes that can lead to cancer.
From what is already known, one could reasonably hope that if clinicians were alert to theestrogen dominance that can occur in premenopausal women and would supplement themwith natural progesterone, the risk of endometrial cancer would be dramatically reduced,perhaps to zero.
Progestin (also called progestagen or gestagen) refers to the class of synthetically createdpatentable compounds which share the ability to sustain human secretory endometrium and,if given early enough in the menstrual cycle, to prevent ovulation. In this they are similar tonatural progesterone, the specific hormone produced by the corpus luteum after ovulation andalso by the placenta. Progestins are widely used in oral contraceptives and in hormonereplacement therapy (HRT). In medical and lay writing, many authors confuse the twowords, progestin and progesterone. This is a great error, since they are not the same anddiffer in many important aspects. Progestins are foreign to all living things and have atomsintroduced at unusual positions in their molecules such that their metabolism and excretionare inhibited and they induce actions not consistent with natural progesterone. Specifically,they lack intrinsic physiologic benefits of progesterone, they can not function in the majorbiosynthetic pathways as progesterone does, and they carry a wide array of potentialundesirable side effects.
One of the most commonly used progestins, medroxyprogesterone acetate (Provera),carries the warning that its use in women during early pregnancy can increase the risk ofearly abortion or cause congenital abnormalities in the fetus. Since natural progesterone isnecessary for the survival of the embryo and the normal development of the fetus throughoutpregnancy, it is clear that Provera is not progesterone. A partial list of progestin side effectsfollows: POTENTIAL SIDE EFFECTS OF SYNTHETIC PROGESTINS
Increased risk of birth defects such as heart and limb defects if taken during the first four months of pregnancy.
Beagle dogs given this drug developed malignant mammary nodules.
Discontinue this drug if there is sudden or partial loss of vision.
This drug passes into breast milk, consequences unknown.
May contribute to thrombophlebitis, pulmonary embolism, and cerebral thrombosis.
Thrombophlebitis, thromboembolic disorders, cerebral apoplexy, liver dysfunction ordisease, known or suspected malignancy of breast or genital organs, undiagnosed vaginal bleeding,missed abortion or known sensitivity.
May cause fluid retention, epilepsy, migraine, asthma, cardiac or renal dysfunction.
May cause breakthrough bleeding or menstrual irregularities.
May cause or contribute to depression.
The effect of prolonged use of this drug on pituitary, ovarian, adrenal, hepatic or uterine function is unknown.
May decrease glucose tolerance, diabetes patients must be carefully monitored.
May increase the thrombotic disorders associated with estrogens.
May cause breast tenderness and galactorrhea.
May cause sensitivity reactions such as urticaria, pruritis, edema or rash.
May cause acne, alopecia and hirsutism.
Edema, weight changes (increase or decrease).
Cervical erosions and changes in cervical secretions.
Cholestatic jaundice.
Mental depression, pyrexia, nausea, insomnia or somnolence.
Anaphylactic reactions and anaphylaxis (severe acute allergic reactions).
Thrombophlebitis and pulmonary embolism.
Breakthrough bleeding, spotting, amenorrhea or changes in the menses.
When taken with estrogen, the following have been observed: Rise in blood pressure, headache, dizziness, nervousness, fatigue.
Changes in libido, hirsutism and loss of scalp hair, decrease in T-3 uptake values.
Premenstrual-like syndrome, changes in appetite.
Cystitis-like syndrome.
Erythema multiforme, erythema nodosum, hemorrhagic eruption, itching.
The reader can note the number of symptoms and medical problems in the list above whichare commonly attributed to aging. Natural progesterone, on the other hand, has no knownside effects. Need more be said? Premenstrual syndrome (PMS) refers to a group of symptoms occurring consistentlyduring the l0-14 days before menses and clearing 2-3 days after the onset of menses. Thesesymptoms include depression, irritability, anger and other mood swings, headache, fatigue,edema and a consequent weight gain, and loss of libido. The timing of these symptomscorresponds precisely to the time when, under normal circumstances, progesterone should bethe dominant hormone. If progesterone is absent, however, then estrogen dominance prevailsthroughout the menstrual month. Side effects of unopposed estrogen include many of thesymptoms listed above. In addition, the lack of progesterone would upset the complexinterplay between the hypothalamus and the pituitary, and lead to the full display of PMS symptoms. Thus, PMS may result in whole or in great part from anovulatory cycles insensitive women whose emotional and physiological balance is upset by stress and/orimproper diet. When sufficient natural progesterone is supplemented during the 10-14 daysbefore menses, along with a diet avoiding stimulants, caffeine and sugar, or highly refinedstarches, PMS symptoms will disappear or be greatly reduced. In some cases, smallsupplements of magnesium and vitamin B6 (pyridoxine) are also helpful.
It should be recalled that the word “syndrome” implies that the etiology and mechanism(s)of action underlying the disorder are not completely understood or validated by presentscientific research. This should not deter a trial of treatment with natural progesterone. If apatient’s typical pre-menstrual weight gain is found not to occur when on naturalprogesterone treatment, it is objective evidence that estrogen dominance, due to deficiency ofnatural progesterone, is playing a strong role, at least in the etiology of the condition.
Further, serum progesterone levels can be obtained during day 20-23 of the cycle; a lowfinding corroborates the progesterone deficiency hypothesis.
Other Anti-Aging Benefits of Natural Progesterone As women approach menopause, they commonly find themselves losing energy, retainingfluids, fighting fat, developing wrinkles and facial hairs, prone to headaches and depressionand less interest in sex. They see their doctors, take their diuretics and, occasionally, thyroidmedication and face the future with fading enthusiasm. They seek out cosmeticians for theirwrinkles, visit their beauticians more often for their thinning hair, and take calciumsupplements for their thinning bones. What they are unaware of is the importance of properhormonal balance, particularly the lack of this singularly important hormone, naturalprogesterone. Consider the following: 1. Progesterone is a primary precursor in the biosynthesis of the adrenal corticosteroids.
Without adequate progesterone, syntheses of the cortisones is impaired and the bodyturns to an alternative pathway, via adrenal production of dihydro-epiandrosterone(DHEA) and androstenedione, produced by fat in the body. These alternative pathwayshave androgenic side effects which cause the long facial hairs of elderly postmenopausalwomen and thinning of their scalp hair. When natural progesterone is supplemented, it isquite common to witness the disappearance of facial hair and the return of healthy scalphair.
Further, impaired corticosteroid production results in a decrease in one’s ability to handlestress, e.g., surgery, trauma or emotional. With restoration of adequate progesterone, one’sability to deal with stress improves.
2. In many peri or post-menopausal women, symptoms of hypothyroidism occur despite normal serum levels of thyroid hormone. Estrogen interferes with intracellular utilizationof thyroid hormone. Thus, many women with clinical signs of hypothyroidism such asfatigue, lack of energy, intolerance to cold, etc., are actually suffering from unrecognizedestrogen dominance and will benefit from supplementation with natural progesterone.
Women who are already placed on thyroid supplements will find that their dose can bereduced or eliminated when natural progesterone is restored to adequate levels. In thisregard, the test for thyroid stimulating hormone (TSH) is a better guide for thyroiddosage than are the T-3 or T-4 tests.
Estrogen and most of the synthetic progestins increase intracellular sodium and wateruptake. The effect of this on the aldosterone system is hypertension. Since the true causeis rarely recognized, this condition is called “essential” hypertension by most cliniciansand is commonly treated with diuretics. Natural progesterone, on the other hand, is anatural diuretic and prevents the cell’s uptake of sodium and water, thus preventinghypertension. In treating a hypertensive woman taking estrogen and/or a progestin, thefirst step should be to discontinue the hormones; the second step is to switch to a diet offresh vegetables, eliminating high sodium processed foods and severely limit red meatfrom the diet; and the third step is to provide supplemental natural progesterone. In thismanner, drug treatment for hypertension is commonly unnecessary.
3. Whereas estrogen impairs homeostatic control of glucose levels, natural progesterone stabilizes them, thus, natural progesterone can be beneficial to both those with diabetesand those with reactive hypoglycemia. Estrogen should be contraindicated in patientswith diabetes.
4. Loss of libido is common with menopause. To the surprise (and delight) of many postmenopausal women, progesterone often restores normal libido. Estrogensupplementation, as is known, usually results in a decrease of libido. It is a falseassumption that the enjoyment of full sexual activity is not in the province of post-menopausal women; it is merely a matter of a correctable hormone balance.
5. Thinning and wrinkled skin is a sign of lack of hydration in the skin. It is common in peri and post-menopausal women and is a sure sign of hormone depletion. Transdermalnatural progesterone is a skin moisturizer. When used as a skin cream, not only isprogesterone well absorbed, but it restores skin hydration . The skin becomes moreyouthful in appearance and most small wrinkles disappear.
6. Recent research has found that recovery from brain injury in male test animals is enhanced by pre-treatment with progesterone. Further, brain cells are well supplied withprogesterone receptors and the brain content of progesterone, as well as pregnenelone andDHEA, is normally 20-30 times higher than serum levels. It is suggested, therefore, that 7. progesterone serves a role in keeping brain cells healthy and that disorders such as premature senility (Alzheimer’s disease) may be, at least in part, another example ofdisease secondary to progesterone deficiency.
Why Natural Progesterone is so Neglected by Contemporary Medicine It should not require a PhD in physiology to realize that unopposed estrogen is largelydisadvantageous and progesterone is remarkably beneficial. Yet, this view is not shared (orunderstood) by many physicians and medical writers. Why should this be? One answer is,of course, that many doctors have simply not kept up with advances in medical science. Themore sanguine answer is that doctors have come to rely on pharmaceutical advertising astheir education sources and do not fully realize that they, themselves, are the targets of clevercampaigns inducing them to prescribe what the industry sells. Natural progesterone, thougheasily and relatively inexpensively derived from plant sterols, (e.g., diosgenin, present inyams and many other plants) is not offered by the major pharmaceutical firms since, being anatural substance it is not patentable, and thus not profitable. Natural progesterone isroutinely used by the pharmaceutical industry for synthesis of progestins. The availabilityand superiority of natural progesterone is a secret carefully kept from physicians.
Premature aging remains a great concern in our present society. It is entirely likely thatmany factors play a role: nutritional deficiencies, alcoholism, cigarette smoking,environmental toxins and others may all be implicated. But present knowledge suggests alarge factor is our misdirected attention to estrogen and our neglect of natural progesterone.
Proper understanding and supplementation with natural progesterone promises to restore ahealthy zestful life, where before the only prospect was one of early aging and progressivedeterioration. It is time for natural progesterone to take its place along with proper nutrition,exercise and a clean environment in the preservation of good health.
Dr. Lee has recently published Natural Progesterone: the Multiple Roles of a RemarkableHormone, BLL Publishing, P.O. Box 2068, Sebastopol, CA 95473, recently reviewed byTownsend Letter for Doctors, April 1994. The reviewer calls it “the most informative andlucid explanation of the female hormone cycle” that the reviewer had ever encountered andthat it “contains priceless information for women wrestling with the effects of menopauseand hormone imbalance and for the doctors who treat them.” 1. Raloff, J. EcoCancers: do environmental factors underlie a breast cancer epidemic? 2. Hileman, B. Environmental estrogens linked to reproductive abnormalities, cancer.
3. Manolagas, SC, Jilka, RL, Hangoc, G., et al. Increased osteoclast development after estrogen loss: mediation by interleukin-6. Science 1992; 257:88-91.
4. Prior, JC. Progesterone as a bone-trophic hormone. Endocrine Reviews 1990; 11:386- 5. 6. Felson, DT, Zhang, Y, Hannan, MT, Kiel, DP, Wilson, PWF, Anderson, JJ. The effect of post-menopausal estrogen therapy on bone density in elderly women. N Engl J Med1993; 329:1141-1146.
7. Prior, JC, Vigna, YM, Burgess, R. Medroxyprogesterone acetate increases trabecular bone density in women with menstrual disorder. Presented at the annual meeting of theEndocrine Society, June 11, 1987, Indianapolis.
8. Munk-Jensen, N, Nielsen, SP, Obel, EB, Erikson, PB. Reversal of postmenopausal vertebral bone loss by oestrogen and progestagen: a double-blind placebo-controlledstudy. Br Med J 1988; 296:1150-1152 9. Lee, JR. Osteoporosis reversal: the role of progesterone. Intern Clin Nutr Rev 1990; 10. Lee, JR. Is natural progesterone the missing link in osteoporosis prevention and treatment? Medical Hypotheses 1991; 35:316-318.
11. von Kaullia, F, et al. Conjugated oestrogens and hypercoagulability. Am J Obstet Gyn 12. Bonnar, J, et al. Coagulation system changes in postmenopausal women receiving oestrogen preparation. Postgrad Med J 1976; 52:30 13. Boston Collaborative Drug Surveillance Program: Surgically confirmed gallbladder disease, venous thromboembolism, and breast tumors in relation to menopausal oestrogentherapy. N Engl J Med 1974; 290:15.
14. Nabulsi, AA, Folsom, AR, White, A, et al. Association of hormone replacement therapy with various cardiovascular risk factors in postmenopausal women. N Engl J Med 1993;328: 1069-75.
15. “Late-cycle mastectomies may reduce recurrences.” Reported in Med Trib May 7, 1992.
16. Bergkvist, L, Adami, HO, Persson, I, Hoover, R, Schairer, C. The risk of breast cancer after estrogen and estrogen-progestin replacement. N Engl J Med 1989; 321:293-297.
17. Gambrel, RD. The menopause: benefits and risks of estrogen-progestogen replacement therapy. Fertil Steril 1982; 37:457-474.
18. Hargrove, JT, Maxson, WS, Wentz, AC, Burnett, LS. Menopausal hormone replacement therapy with continuous daily oral micronized estradiol and progesterone. OB&BYN1989; 73:606-612

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