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September 2003 - Part II: Is Conventional Medicine (CM) Evidence-Based
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Last month we featured excerpted highlights of a paper titled, “Is Conventional Medicine (CM) Evidence-Based?” by recognized hormone replacement researcher, John Lee MD. This month we continue with Dr. Lee’s observations on the qualitative differences between Conventional Medicine (CM) and Alternative Medicine (AM), based on his collection of high quality references that refute the notion that conventional medicine is truly evidence-based. These references focus on hormones and their application to health, which has been the focus of study by Dr. Lee for over 23 years.
- Conventional Medicine promotes the notion that there is no proof that estrogen causes breast or other cancers, despite evidence showing that estrogen is involved in these cancers, and that estrogen-progestin replacements are even worse.16-23
- Conventional Medicine doesn’t recognize that progesterone protects against breast cancer, or that this benefit can be provided by transdermal application. Conversely, the evidence shows that a deficiency of progesterone leads to a greater than five-fold increase in the incidence of breast cancer. Furthermore, there is good evidence that transdermal progesterone greatly reduces human breast epithelial cell proliferation, the hallmark of impending breast cancer. At least eight different metabolic mechanisms of progesterone are known to be protective against breast cancer. Overall survival of node-positive patients 20 years after breast surgery is 50 percent less in women with low progesterone levels on the day of surgery than in women with normal progesterone levels on the day of surgery.24-29
- Conventional Medicine believes that “normal” hormone levels are, in fact, healthy. The truth is that laboratory ranges of hormone levels merely represent statistically common levels found in a certain population. When US ranges of estrogen are compared to world-wide ranges, estrogen levels in the US and industrialized nations are abnormally high prior to menopause. Experts, such as Dr. Peter Ellison, believe that this is a major factor in the higher breast cancer incidence found in industrialized countries.30
- Conventional Medicine has long argued that birth control pills are not a significant cause of breast cancer. The evidence is that oral contraceptives prior to 1976 significantly increased the risk of breast cancer among women with a strong family history (sisters and mothers) of breast cancer.31
- Conventional Medicine believes that oral contraceptives do not cause cervical dysplasia. The evidence is that they do.33
- Conventional Medicine accepts the fact that estrogen is the only known cause of endometrial cancer but doubts that progesterone will prevent endometrial cancer. The evidence is that oral progesterone (200 mg/day) prevents endometrial cell proliferation and atypical hyperplasia in postmenopausal women receiving estrogen therapy. There is good evidence that topically applied progesterone does the same thing.34-36
- Conventional Medicine believes that estrogen falls essentially to zero after menopause. The evidence is that at least two-thirds of postmenopausal women continue to produce sufficient estradiol years after menopause. The problem is that, in the absence of sufficient progesterone, sex hormone binding globulin (SHBG) rises and inhibits estrogen function.37
- Conventional Medicine believes that serum levels of hormone are accurate measurements of bioavailable hormone. The evidence is that serum levels are irrelevant unless one also knows the concurrent concentration of sex hormone binding protein (SHBG) and can somehow calculate its inhibiting
effect.37-39
- Conventional Medicine believes that low endogenous estrogen after menopause is the cause of osteoporosis. The fact is that bone mass begins to fall at age 36 in US women, a time when estrogen levels remain high. Even after menopause, the evidence is that two-thirds of US women produce sufficient endogenous estrogen for optimal estrogen bone benefit. The problem is that, when progesterone is deficient, SHBG levels rise and inhibit estrogen bioavailability. Among 107 postmenopausal women who are truly estrogen-deficient and given estradiol in doses of 1 mg, 0.5 mg, or 0.25 mg, the 0.25 mg/day dose is optimal for inhibiting bone resorption. Conventional Medicine customarily prescribes 0.5–2 mg doses, which are 2-8 times higher than needed.37,40
- Conventional Medicine prescribes estrogen supplements to postmenopausal women in the belief they need it to prevent memory loss and decline in cognitive function. The evidence is that estradiol does help brain function but the optimal concentration, measured as the “free” non-protein-bound fraction, is often within the range of that found in postmenopausal women, and not at the higher levels found in premenopausal women. Serum levels that do not distinguish between protein-bound and “free” estradiol are irrelevant. Estrogen supplements are needed only in those women who are truly estrogen deficient!
Thank you Dr. Lee! More to come next month.
Robert Watson
President/CEO
References:
16. National Cancer Institute symposium, March 1998, Estrogens as Endogenous Carcinogens
in the Breast and Prostate, available as Monograph #27, from the Oxford University Press
(800-852-7323).
17. Formby B, & Wiley TS. Progesterone inhibits growth and induces apoptosis in breast cancer cells: inverse effects on Bcl-2 and p53. Annals of Clin and Lab Science 1998; 28: 360-369.
18. Cavalieri EI, Stack DE, Devanesan PD, Todorovic R, et al. Molecular origin of cancer: catechol estrogen-3,4-quinones as endogenous tumor initiators. Proc. Natl. Acad. Sci. 1997; 94:10937-42.
19. Bergkvist L, Adami H-O, Persson I, Hoover R, Schairer C. The risk of breast cancer after estrogen and estrogen-progestin replacement. NEJM 1989; 321: 293-297.
20. Colditz GA, Stampfer MJ, Willett WS, et al. Cancer Causes Control. 1992; 3: 433-439.
21. Schairer C, Lubin J, Troisis R, Sturgeon S, et al. Menopausal estrogen and estrogen-progestin replacement therapy and breast cancer risk. JAMA 2000; 283: 485-497.
22. Clemons M & Goss P. Estrogen and the risk of breast cancer. NEJM 2001; 344: 276-285.
23. Raafat AM, Li S, Bennett JM, Hofseth LJ, Haslam SZ. Estrogen and estrogen plus progestin act directly on the mammary gland to increase proliferation in a postmenopausal mouse model. J Cell Physiol 2001; 187: 81-9.
24. Cowan LD, Gordis L, Tomascia JA, Jones GS. Breast cancer incidence in women with a history of progesterone deficiency. Am J Epidemiology 1981; 114: 209-217.
25. Chang K-J, Lee TTY, Linares-Cruz G, Fournier S, and de Lignieres, B. Influences of percutaneous administration of estradiol and progesterone on human breast epithelial cell cycle in vivo. Fertility and Sterility 1995; 63: 785-791.
26. Foidart J-M, Colin C, Denoo X, Desroux J, et al. Estradiol and progesterone regulate the proliferation of human breast epithelial cells. Fertility and Sterility 1998; 69: 963-969.
27. Hrushesky. Breast cancer, timing of surgery, and menstrual cycle: Call for prospective trial. Journal of Women’s Health 1996; 5: 555-566.
28. Mohr PE, Wang DY, Gregory WM, Richards MA, & Fentiman IS. Serum progesterone and prognosis in operable breast cancer. British J of Cancer 1996; 73: 1552-1555.
29. Gompel A, Somai S, Chaouat M, Kazem A, et al. Hormonal regulation of apoptosis in breast cells and tissues. Steroids 2000; 65: 593-8.
30. Ellison PT, Lipson SF, O’Rourke MT, Bentley GR, et al. Population variation in ovarian function (letter). Lancet 1993; 342: 433-434.
31. Grabrick DM, Hartmann LC, Cerhad JR, Vierkant RA, et al. Risk of Breast cancer with oral contraceptive use in women with a family history of breast cancer. JAMA 2000; 284: 1791-98.
32. Isaksson E, von Schoultz E, Odlind V, Soderqvist G, et al. Effect of oral
contraception on breast epithelium proliferation. Breast Cancer Res Treat 2001;
65: 163-9.
33. Salazar EL, Sojo-Aranda I, Lopez R, Salcedo M. the evidence for an etiological relationship between oral contraceptive use and dysplastic change in cervical tissues. Gynecol Endocrinol 2001; 15: 23-8.
34. PEPI study, Effects of estrogen/progestin regimens on heart disease risk factors in post-menopausal women. JAMA 1995; 273: 199-208.
35. Levine H, Watson N. Fertility & Sterility 2000; 73: 516-521.
36. Anasti JN, Leonetti HB, Wilson KJ. Topical progesterone cream has antiproliferative effect on estrogen-stimulated endometrium. Obstet Gynecol 2001 Apr; 97(4 Suppl 1):S10.
37. Cummings SR, Browner WS, Bauer D, Stone K, et al. Endogenous hormones and the risk of hip and vertebral fracture among older women. NEJM, 10 September 1998; 339: 733-738.
38. Letter to Lancet on saliva RIA hormone assay. Lancet 12 Sept 1998; vol. 352.
39. Verkasalo PK, Thomas HV, Appleby PN, Davey GR, Key TJ. Cancer Causes Control 2001; 12: 47-59.
40. J Clin Endocrinol Metab 2000; 85: 4462-69. (Reported also in Lancet, 2000; 356, 1988.)
41. Yaffe K, Lui L-Y, Grady D, Cauley J, et al. Cognitive decline in women in relation to non-protein-bound oestradiol concentrations. Lancet August 2000; 356: 708-712