-IBIS-1.7.6-
tx
reproductive system
menopause
Nutrition
dietary guidelines
eating principles:
low fat, low animal protein diet
therapeutic foods:
black beans, sesame seeds, soybeans, walnuts, lycium fruit, mulberries, yams, licorice, black jujube, lotus seeds, chrysanthemum flowers (Ni, 147.)
estrogenic foods: animal products, apples, cherries, olives, plums, carrots, yams, nightshade family, peanuts, soy products, coconut, brown rice, barley, oats, wheat
See: Foods that contain estrogen-like sterols in Materia Medica
fresh juices:
carrot, celery, spinach, and parsley (Walker, 146.)
carrot and spinach (Walker, 146.)
carrot, beet, lettuce, and turnip (Walker, 146.)
specific remedies:
cook black beans with rice into porridge and eat twice daily (Ni, 147.)
steam chicken with lycium fruit and yam (Ni, 147.)
porridge from rice, walnuts, lotus seeds and sunflower seeds (Ni, 147.)
hot flashes: simmer 60 g celery and 30 g Leonurus cardiaca (Motherwort) then serve (Chao-liang, Qing-rong, Bao-zhen, 47.)
avoid:
meat, alcohol, fried foods, fatty foods, rich foods, salty foods, coffee, caffeine, sweet foods and sugar, alcohol, cow's milk and other dairy products, white bread, refined foods, processed foods, smoking
if hot flashes: hot sauces, spicy foods, hot drinks, especially coffee
supplements
Vitamin B6: 150 mg per day
Vitamin E 400-2500 IU per day, with a typical dose of 800 IU per day; many clinicians have reported that water-soluble forms of vitamin E have been more effective with some patients. Researchers in nearly all studies have demonstrated benefits in reducing many menopausal symptoms. A clinical trial of 3-4 weeks will usually establish efficacy for an individual. (Rubenstein BB. Fed Proc 1948;7:106; Perloff WH. Am J Obstet Gynecol 1949;58:684-694; Finkler RS. J Clin Endocrinol Metab 1949;9:89-94; Kavinoky, 1950; Gozan HA. NY State J Med 1952;52:1289; Christy CJ. Am J Obstet Gynecol 1945:50:84; Blatt MHG et al. Arch Intern Med 1953;91:792-799; Barton DL, et al. J Clin Oncol 1998;16:495-500.)
Progesterone:
Women who are perimenopausal (still menstruating, but with menopausal symptoms and/or PMS -- not ovulating):
Day 1 (first day of bleeding) - 6: do not use transdermal progesterone cream (450 mg P/oz)
Day 7-20: use 1/4 teaspoon transdermal progesterone cream (450 mg P/oz) twice a day
Day 21-27: use up to 1/2 teaspoon if necessary for PMS symptoms. If no PMS symptoms occur, continue using 1/4 teaspoon twice a day.
If the period begins early, stop using the transdermal progesterone cream (450 mg P/oz) while bleeding, count the first day of bleeding as day one, and begin the cycle again.
If the period is late, use the cream for up to 3 weeks (day 28 of your cycle), then take a week off. If the period has not started by the end of the week, resume the cream until the period starts. STOP the cream when the period begins, count the first day of bleeding as day one of the cycle, and begin the cycle over again.
Women who are post-menopausal for bone health:
Choose a calendar day (e.g. first day of the month) as day one
Days 1-25: use 1/4 teaspoon of transdermal progesterone cream (450 mg P/oz) twice a day.
Days 25-30 (or 31): do not use transdermal progesterone cream (450 mg P/oz).
For severe menopausal symptoms: use up to 1/2 teaspoon a day according to the same schedule.
The best areas to apply the transdermal progesterone cream (450 mg P/oz) are the palms, inner arms, inner thighs, abdomen, and chest, rotating the areas applied. Transdermal progesterone cream (450 mg P/oz) is best applied twice daily due to the short half-life of progesterone in the blood.
Due to anovulatory cycles, progesterone levels typically decline first peri-menopausally, followed by a decline in estrogen. Progesterone levels fall to near zero levels due to anovulatory cycles, while estrogen levels only decline to about 40-60 % of pre-menopausal levels. This precipitous drop in progesterone levels can lead to an imbalance between estrogen and progesterone, causing a relative estrogen dominance within the body. Many women find that supplementing progesterone alleviates many of the menopausal symptoms they are experiencing. Progesterone has a number of important roles relative to menopause. Progesterone is the natural balancer to estrogen, as well as being necessary for optimum estrogen utilization. The presence of progesterone in the body sensitizes estrogen receptor sites, enabling circulating estrogen to work better. Biochemically, progesterone is a precursor to other hormones, including estrogens, testosterone, aldosterone, and corticosteriods.
Women have been found to gain an average of 10-15 pounds at menopause. These added fat cells are a site of estrogen production once the ovaries retire at menopause. Estrogen can affect weight in several ways. Estrogen not only affects water metabolism and contributes to bloating, but it can also affect the bodys ability to utilize thyroid hormone. Low thyroid function can slow down metabolism and increase weight gain. There is some research linking estrogen to an increase in insulin production, which can cause an increase in fat storage. Since the fat cells are a source of estrogen production, increased body fat coupled with elevated estrogen levels can cause a pattern of escalating weight gain. Progesterone supplementation may balance these effects found with estrogen excess.
DHEA:
Low doses of DHEA (usually 5-10 mg/day) may be especially appropriate for postmenopausal women whose serum DHEA-S levels are near or below the lower limit of normal. In some cases, DHEA relieves symptoms such as hot flashes that are usually attributed to estrogen deficiency. A combination of DHEA and identical-to-natural progesterone (usually given as a topical cream may be more effective against hot flashes than either treatment alone. (Gaby AR. Alt Med Rev. 1996:1(2);66)
It has been shown that menopause is associated with a reduction in DHEA levels. DHEA is manufactured by the adrenal glands. In the adrenals, DHEA is a source of estrogen and testosterone and may be capable of raising the levels of progesterone. DHEA is also one of the four major hormones produced by the ovaries; the others being estrogen. progesterone. and testosterone. At the time of menopause, the amount of DHEA manufactured by the ovaries declines. And, even though the ovaries are not the major source of DHEA, serum DHEA levels decline by more than 60% after menopause. After menopause, when ovarian production of DHEA slows down. the adrenal glands may not be not capable of taking over, and a marked deficiency of DHEA results. It is quite possible that giving DHEA to postmenopausal women with adrenal insufficiency would prevent the accelerated bone loss that these women experience. In one study. the average plasma level of DHEA (ng/100 ml) was 542 in premenopausal women, 197 in post-menopausal women, and only 126 in women whose ovaries had been surgically removed. (Monroe SE, Menon KMJ. Clin Obstet Gynecol 1977:20:113-122)
Recent research has also found that hormone replacement therapy using 2mg/day of oral micronized estradiol reduced the mean blood levels of DHEA-S by 23% and of testosterone by 42%. (Casson PR, et al. Obstet Gynecol 1997.90:995-998.)
The decline in DHEA levels appears to be a factor in age-related bone loss. In one important study, bone mineral density was measured at the lumbar spine, hip, and radius in 105 women, aged 45-69. Fifty women had normal measurements, whereas 55 had low bone density. The average serum DHEA-S level was 60% lower in the women with low bone density than in those with normal bones. Women with low DHEA values were 40 times more likely to have osteoporosis than were women with normal DHEA levels. In contrast, there was no relationship between estrogen levels and bone densitv. (Szathmari M, et al. Osteoporsis Int 1994:4:84-88) In a group of 29 post-menopausal women. there was a significant positive correlation between bone mineral content of the distal radius and ulna and age-adjusted serum DHEA levels. (Brody S, et al. Maturitas 1987:9:25-32) A study of Belgian women found significant correlations were found between bone mineral content and DHEA levels (measured as DHEA-S ), even after correcting for the effects of age. These studies support the proposed role of DHEA in maintaining bone mass.
There are several mechanisms by which DHEA might prevent osteoporosis.
The partial conversion of DHEA to estrogen and testosterone would be expected to provide additional protection against bone loss. DHEA is converted into both estrogen and testosterone, both of which play a role in prevention of bone loss. In a study of postmenopausal women, administering DHEA increased serum levels of both testosterone and estrogens (estradiol and estrone).
Although DHEA is not converted directly into progesterone, it may, through a feedback mechanism, indirectly increase the production of progesterone. Both DHEA and progesterone are produced from the same precursor hormone, pregnenolone. If DHEA levels are adequate, then pregnenolone will be converted primarily to progesterone, rather than to DHEA.
One of the breakdown products of DHEA, a compound called 5-androstene-3B, 178-diol, is known to bind strongly to estrogen receptors. Therefore, DHEA. like estrogen, might inhibit bone resorption.
Androgens, a class of hormones which includes DHEA and testosterone, stimulate bone formation and calcium absorption. DHEA might.therefore. augment the bone-building effect of progesterone.
DHEA appears to be the only hormone which appears capable of both inhibiting bone resorption and stimulating bone formation.
(Casson, PR, et al. Fertil Steril 1995;63:1027-1031; Labrie, F, et al. Ann NY Acad Sci 1995;774:16-28; Buster JE, et al. Am J Obstet Gynecol 1992;166:1163-1168; Mortola, JF, and Yen, SS. J Clin Endocrinol Metab 1990;71:696-704; Weinstein, RE, et al. J Allerg Clin Immunol 1996;97:1-8; Yen, SS, et al. Ann NY Acad Sci 1995;774:128-142)
bioflavonoids, such as hesperidin 1-3 g per day
(Smith CJ. Chicago Med 1964;67:193-195.)
L-tryptophan (for depression)
essential fatty acids 1-2 Tbsp per day
soy isoflavones: Soy contains weak phytoestrogens which can affect the menstrual cycles of premenopausal women and often alleviate menopausal symptoms. In one human study conducted by Albertazzi et al, 104 postmenopausal women were given daily servings of either 60 grams isolated soy protein, or a placebo for twelve weeks. Those receiving the soy reported a 26% reduction in the mean number of hot flashes by the third week, a 33% reduction by the fourth week, and an overall reduction of 45% in their daily hot flashes at the conclusion of the study. In a subsequent double-blind clinical trial involving breast cancer survivors with histories of substantial hot flashes, Quella et al found no suggestion that a soy product was more effective than placebo in reducing hot flashes.
(Baird DD, et al. J Clin Endocrinol Metab 1995;80:1685-1690; Cassidy A, et al. Am J Clin Nutr 1994;60:333-340; Albertazzi P, et al. Obstet Gynecol 1998;91:6-11; Knight DC, Eden JA. Obstet Gynecol 1996;87:897-904; Murkies AL, et al. Maturitas 1995;21:189-195; Brezinski A, et al. Menopause 1997;4:89-94.; Quella SK, et al. J Clin Oncol. 2000 Mar;18(5):1068.)
» drug interactions:
Calcium and thyroid medication [dessicated thyroid, Synthroid (T4), Cytomel (T3)]: causes increased urinary excretion of Calcium.
(Paul, et al., 1988; 259: 3137-3141; Kung, Pun, 1991; 265: 2688-2691; Adlin, et al., 1992; 128: 210-213.)
Recent research has also found that hormone replacement therapy using 2mg per day of oral micronized estradiol reduced the mean blood levels of DHEA-S by 23% (and of testosterone by 42%).
(Casson PR, et al. Obstet Gynecol 1997.90:995-998.)
footnotes
Albanese. Effects of Calcium and micronutrients on bone loss of pre-and postmenopausal women. Paper presented at Am. Med. Assoc. Meeting, Jan.1981.
Abstract: 12 healthy women, ages 39-65, whose usual daily diets contained 200-425mg of Calcium took a supplement containing 600mg of Calcium and all known micronutrients at RDA levels. 11 healthy women with comparable diets took 700-800mg of Calcium per day without the additional nutrients. Periodic x-ray measurements showed that, within 9-11 months, the rate of bone density increase was 2-3 times greater in the women receiving the Calcium plus micronutrients than in those taking the Calcium alone.
Albertazzi P, Pansini F, Bonaccorsi G, et al. The effect of dietary soy supplementation on hot flushes. Obstet Gynecol 1998;91:6-11.
Anderson JJ, Ambrose WW, Garner SC. Biphasic effects of genistein on bone tissue in the ovariectomized, lactating rat model. Proc Soc Exp Biol Med. 1998 Mar;217(3):345-350.
Baird DD, Umbach DM, Landsedell L, et al. Dietary intervention study to assess estrogenicity of dietary soy among postmenopausal women. J Clin Endocrinol Metab 1995;80:1685-1690.
Barton DL, Loprinzi CL, Quella SK, et al. Prospective evaluation of vitamin E for hot flashes in breast cancer survivors. J Clin Oncol 1998;16:495-500.
Blatt MHG et al. Vitamin E and climacteric syndrome: failure of effective control as measured by menopausal index. Arch Intern Med 1953;91:792-799.
Brattstriom. Folic acid responsive postmenopausal homocysteinemia. Metabolism 1985;34(11):1073-1077.
Abstract: 5mg folate daily for 4 weeks substantially reduced homocysteine concentrations (p less than 0.01) both before a methionine load and afterwards (despite the fact that subjects had normal levels of serum and RBC folate) in normal men and pre- and postmenopausal women, suggesting that folic acid may have a prophylactic action against postmenopausal osteoporosis if moderate homocysteinemia promotes its development (homocysteine which is increased in postmenopausal women, interferes with collagen cross-linking leading to defective bone matrix and osteoporosis.
Brezinski A, Adlercreutz H, Shaoul R, et al. Short-term effects of phytoestrogen-rich diet on postmenopausal women. Menopause 1997;4:89-94.
Brody S, et al. Adrenal steroids in post-menopausal women: relation to obesity and to bone mineral content. Maturitas 1987:9:25-32.
Bullock JL, Massey FM, Gambrell RD Jr. Use of medroxyprogesterone acetate to prevent menopausal symptoms. Obstet Gynecol 1975;46:16568.
Buster JE, Casson PR, Straughn AB, et al. Postmenopausal steroid replacement with micronized dehydroepiandrosterone: preliminary oral bioavailability and dose proportionality studies. Am J Obstet Gynecol 1992;166:1163-1168.
Abstract: Eight postmenopausal women randomly received either a placebo or 150 or 300 mg of oral micronized dehydroepiandrosterone in a lipid matrix. Serum dehydroepiandrosterone, dehydroepiandrosterone sulfate, testosterone, and estradiol were measured periodically over the 12 hours after each dose. Mean peak steroid concentrations after 150 mg (300 mg) doses were dehydroepiandrosterone 1617 (2639) ng/dl, 7 (11.5)-fold above placebo; dehydroepiandrosterone S 1185 (1688) micrograms/dl, 14 (20)-fold above placebo; and testosterone 183 (311) ng/dl, 4 (7)-fold above placebo. Estradiol concentrations remained less than 20 pg/ml, but androgen concentrations rose by 1 hour and remained elevated through the twelfth hour. Peak androgen concentrations and areas under the curves exhibited proportionality with both doses. A testosterone radioimmunoassay revealed a 300% overestimation for testosterone. Thus after appropriate readjustment maximum testosterone concentrations were observed consistently within physiologic premenopausal ranges after the 150 mg dose. The study concluded that micronized dehydroepiandrosterone may provide a steroidal postmenopausal replacement that is adjunctive to estrogens and worthy of further investigation.
Cassidy A, Bingham S, Setchell KDR. Biological effects of a diet of soy protein rich in isoflavones on the menstrual cycle of premenopausal women. Am J Clin Nutr 1994;60:333-340.
Casson PR, Elkind-Hirsch KE, Buster JE, Hornsby PJ, Carson SA, Snabes MC. Effect of postmenopausal estrogen replacement on circulating androgens. Obstet Gynecol 1997 Dec;90(6):995-998.
Abstract: OBJECTIVE: To determine the effect of estrogen replacement therapy (ERT) on serum androgen levels in postmenopausal women. METHODS: We measured serum dehydroepiandrosterone (DHEA), DHEA-sulfate, testosterone, estradiol (E2), LH, FSH, and sex hormone binding globulin in 8:00 AM fasting serum samples from a previous randomized, blinded, placebo-controlled crossover study in which 28 postmenopausal women (27 naturally menopausal) were given 2 mg/day of oral micronized estradiol. The treatment arms were 12 weeks with a 6-week washout. RESULTS: Estrogen replacement therapy raised mean (+/- standard error of the mean [SEM]) serum E2 from 8.7 +/- 1.0 to 117 +/- 18.7 pg/mL (P < .001 from baseline). Concurrently, mean (+/- SEM) DHEA-sulfate fell from 67.3 +/- 9.6 to 52.1 +/- 6.4 micrograms/dL (P < .001), and mean (+/- SEM) testosterone fell from 16.1 +/- 2.4 to 9.4 +/- 1.4 ng/dL (P = .006). Both FSH and LH declined significantly. Sex hormone binding globulin increased by 160% with ERT (P < .001). CONCLUSION: Menopausal ERT decreases serum androgen levels, decreasing DHEA-sulfate and testosterone by 23% and 42%, respectively. Whereas the decline in testosterone is likely due to decreased LH-driven ovarian stromal steroidogenesis, the declining levels of DHEA-sulfate also may imply a direct adrenal effect of estrogen. Bioavailable testosterone likely is reduced even more profoundly because sex hormone binding globulin is increased 160% by estrogen. Thus, menopausal ERT may induce relative ovarian and adrenal androgen deficiency, creating a rationale for concurrent physiologic androgen replacement.
Casson, PR, Faquin, LC, Stentz, FB, et al. Replacement of dehydroepiandrosterone enhances T-lymphocyte insulin binding in postmenopausal women. Fertil Steril 1995;63:1027-1031.
Abstract: Oral micronized DHEA (50 mg/d) was administered in 3-week treatments to 11 postmenopausal women in a prospective, placebo-controlled, randomized, blinded, crossover trial with an interarm washout. After dose (23 hour) serum DHEA, DHEAS, T, and cortisol levels were measured, as were fasting lipoproteins, oral glucose tolerance tests (OGTT), T-lymphocyte insulin binding and degradation, and urine collagen cross-links. Morphometric changes were determined by hydrostatic weighing. Dehydroepiandrosterone sulfate, DHEA, T, and free T increased up to two times premenopausal levels with treatment. Fasting triglycerides declined; no change in collagen cross-links or morphometric indexes was noted. Oral glucose tolerance test parameters did not change, but both T-lymphocyte insulin binding and degradation increased with DHEA. Fifty milligrams per day of oral DHEA gives suprahysiologic androgen levels; 25 mg/d may be more appropriate. Dehydroepiandrosterone enhanced tissue insulin sensitivity and lowered serum triglycerides. Rationale is provided for postmenopausal replacement therapy with this androgen.
Christy CJ. Vitamin E in menopause: Preliminary report of experimental and clinical study. Am J Obstet Gynecol 1945:50:84.
Cohen, Kitzes. Infrared spectroscopy and magnesium content of bone mineral in osteoporotic women. Israel J Med Sci. 1981;17:1123-1125.
Abstract: 16 of 19 Osteoporotic patients had lower than normal trabecular bone magnesium content (by infrared spectrophotometry) and clinical magnesium deficiency.
Finkler RS. The effect of vitamin E in the menopause. J Clin Endocrinol Metab 1949;9:89-94.
Gaby AR. Commentary. Nutr Healing 1996;June:1,1011.
Gaby AR. Dehydroepiandrosterone: Biological Effects and Clinical Significance. Alternative Medicine Review. 1996:1(2);60-69.
Gaby AR. Preventing and Reversing Osteoporosis. Prima Publishing: Rocklin, CA, 1993.
Gaby AR. Research Review. Nutr Healing Jun 1997: 8.
Gozan HA. The use of vitamin E in treatment of the menopause. NY State J Med 1952;52:1289.
Greendale GA, Reboussin BA, Hogan P, et al. Symptom relief and side effects of postmenopausal hormones: results from the Postmenopausal Estrogen/Progestin Interventions Trial. Obstet Gynecol 1998;92:982-988.
Hart JP, Hearer MJ, Klenerrman L, Shearer MJ, Caterall A, et al. Electrochemical detection of depressed circulating levels of vitamin K in osteoporosis. J Clin Endocrinol Metab 1985;60:1268-1269.
Abstract: 16 patients with osteoporosis were found to have mean serum vitamin K concentrations only 35% of aged matched controls.
Harvey JA, Zobitz MM, Pak CYC. Dose dependency of calcium absorption: a comparison of calcium carbonate and calcium citrate. J Bone Min Res 1988;3(3): 253-258.
Abstract: It was found that a 500mg dose of calcium citrate resulted in a greater amount of absorption than a 2000mg load of calcium carbonate. The authors suggest that just prescribing higher amounts of the carbonate form doesn't necessarily increase the total amount of calcium absorbed.
Knapen MHJ, Hamulyak K, Vermeer C. The effect of vitamin K suppl on circulating osteocalcin and urinary calcium excretion Ann Intern Med 1989;111:1001-1005.
Abstract: In postmenopausal women, osteocalcin levels were 50% that of premenopausal women. Vitamin K induced increased serum immunoreactive osteocalcin concentration; normalization of HAB capacity of serum immunoreactive osteocalcin.
Knight DC, Eden JA. A review of the clinical effects of phytoestrogens. Obstet Gynecol 1996;87:897904. (Review)
Labrie F, Belanger A, Simard J, et al. DHEA and peripheral androgen and estrogen formation: Intracrinology. Ann NY Acad Sci 1995;774:16-28.
Lee JR. Natural Progesterone. The multiple roles of a remarkable hormone. Sebastipol, CA: BLL Publishing, 1993, 31-37.
Lee JR, Hopkins V. What Your Doctor May Not Tell You About Menopause. Warner Books, NY: 1996.
Massey LK, Berg TA. The effect of dietary caffeine on urinary excretion of Calcium, Magnesium, Phosphorus, Sodium, Potassium, Chloride, and Zinc in healthy males. Nutr Res 1985;5:1281-1284.
Abstract: 15 males drank decaffeinated coffee to which 0, 150, or 300mg caffeine had been added. Total urinary 3 hour excretion of calcium, magnesium, sodium, and chloride, increased significantly after caffeine intake, while zinc, phosphorus, creatinine, and volume were unchanged.
Morrison JC, Martin DC, Blair RA, et al. The use of medroxyprogesterone acetate for relief of climateric symptoms. Am J Obstet Gynecol 1980 138:99-104.
Murkies AL, Lombard C, Strauss BJ, et al. Dietary flour supplementation decreases post-menopausal hot flushes: effect of soy and wheat. Maturitas 1995;21:189-195.
Nielsen FH, Hunt CD, Mullen LM, Hunt JR. Effect of dietary boron mineral, estrogen, and testosterone metabolism in postmenopausal women. FASEBJ 1987;1:394-397.
Abstract: Postmenopausal women were fed a standard diet for 119 days consisting of 0.25mg boron. Supplementing this diet with 3mg boron reduced urinary calcium excretion by 44% and markedly increased serum concentrations of the estrogenic hormone, 17ß-estradiol. The increased levels of 17ß-estradiol were the same as in women receiving estrogen therapy.
Perloff WH. Treatment of the menopause. Am J Obstet Gynecol 1949;58:684-694.
Quella SK, Loprinzi CL, Barton DL, Knost JA, Sloan JA, LaVasseur BI, Swan D, Krupp KR, Miller KD, Novotny PJ. Evaluation of Soy Phytoestrogens for the Treatment of Hot Flashes in Breast Cancer Survivors: A North Central Cancer Treatment Group Trial. J Clin Oncol. 2000 Mar;18(5):1068.
Abstract: PURPOSE: Hot flashes represent a significant clinical problem for some breast cancer survivors. Safe, effective treatment is needed for this prominent clinical problem. Although it has been shown that estrogen or progesterone replacement therapy can alleviate this problem, there are continued safety concerns regarding the use of hormonal therapies in these women. Based on anecdotal information, we hypothesized that soy-derived phytoestrogens, weak estrogen-like substances in the soybean that demonstrate estrogen agonist and/or antagonist effects when they bind to estrogen receptors, could alleviate hot flashes. This current trial was designed to investigate this hypothesis. PATIENTS AND METHODS: This double-blind clinical trial involved breast cancer survivors with substantial hot flashes. After randomization, patients underwent a 1-week baseline period with no therapy. This was followed by 4 weeks of either soy tablets or placebo. The patients then crossed over to the opposite arm in a double-blind manner for the last 4 weeks. Patients completed a daily questionnaire documenting hot flash frequency, intensity, and perceived side effects. RESULTS: Of the 177 women who were randomized and started the study substance, 155 (88%) provided useable data over the first 5 weeks; 149 provided usable data over the entire 9 weeks. There was no suggestion that the soy product was more effective in reducing hot flashes than the placebo. At study completion, patients preferred the soy product 33% of the time, the placebo 37% of the time, and neither substance 31% of the time. No toxicity was observed. CONCLUSION: The soy product did not alleviate hot flashes in breast cancer survivors.
Rubenstein BB. Vitamin E diminishes the vasomotor symptoms of menopause. Fed Proc 1948;7:106. (Abstract)
Schiff I, Tulchinsky D, Cramer D, Ryan KJ. Oral medroxyprogesterone in the treatment of postmenopausal symptoms. JAMA 1980;244:1443-1445.
Smith CJ. Non-hormonal control of vaso-motor flushing in menopausal patients. Chicago Med 1964;67:193-195.
Wright JV. Hormones for menopause. Nutr Healing 1996;June:1-2,9.
Yen, SS, Morales, AJ, and Khorram, O. Replacement of DHEA in aging men and women. Potential remedial effects. Ann NY Acad Sci 1995;774:128-142.
Abstract: DHEA in appropriate replacement doses appears to have remedial effects with respect to its ability to induce an anabolic growth factor, increase muscle strength and lean body mass, activate immune function, and enhance quality of life in aging men and women, with no significant adverse effects. Further studies are needed to confirm and extend our current results, particularly the gender differences.