The Hopkins Health Watch - Vol 1, Issue 1
& Nutrition News,
Drug Watch and More...
THE BEST OF JOHN R. LEE, M.D.
by John R. Lee, M.D.
More often than one might think, good money is spent on bad science. The causes usually are (a) not understanding the hypothesis being tested or (b) misinterpreting results to prejudice the conclusion. Perhaps an example or two will illustrate my argument.
Christiansen C, Christiansen MS, Transbol I. Bone mass in postmenopausal women after withdrawal of estrogen/gestagen replacement therapy. Lancet 1981; 28: 459-461.
In this study, Christiansen et al showed that postmenopausal women on estrogen/gestagen replacement therapy had a gradual increase in BMD, whereas, after withdrawal of these two hormones, the BMD fell a bit. Dr. Christiansen concluded that estrogen was the factor that accounted for the changes, and totally dismissed any possible bone effect of the gestagen (a synthetic progesterone-like drug). When I challenged him to explain why he chose the estrogen as the functional factor rather than both, or perhaps just gestagen, he was at a loss for words. He first answered by saying the gestagen was used to prevent endometrial cancer that might be activated by the estrogen. On pressing him, he admitted that the idea never entered his mind that the gestagen had a hand in the test outcome.
Prestwood KM, Kenny AM, Kleppinger A, Kuldorff M. Ultralow-dose micronized 17?-estradiol and bone density and bone metabolism in older women. JAMA 2003; 290: 1042-1048.
In this study, the authors gave 0.25 mg of estradiol (83) or placebo (84) to healthy women over age 65. In addition, women without hysterectomy (the majority of the women, one would expect) were given 100 mg of oral micronized progesterone two weeks every 6 months. Here again, the researchers observed modest increase (2-3%) of BMD after 3 years, and little or no BMD gain in those receiving placebo. And here, again, the authors credited the BMD gain to the estradiol and not to the combination of estradiol plus progesterone. The thought simply never entered their heads. And, unfortunately, most readers will see only the title, which never mentioned the progesterone. The study also measured blood serum levels of estradiol, estrone, and SHBG, but never the progesterone levels. How sad that saliva tests were not done, and saliva progesterone levels never measured. A wonderful opportunity lost. These folks make the same mistake made by Christiansen et al in 1981.
I should also point out that a 2-3% BMD increase in a woman who has lost 20-30% of her bone mass is not much of a gain and certainly of very little clinical importance. If the researchers had given the progesterone monthly, they would likely be able to show a clinically relevant increase of bone mass.
The TV news recently announced that a new drug trade name Femara has been found to reduce breast cancer in menopausal women by 50%. The new drug, it turns out, is a well- known aromatase inhibitor (letrozolel) made by Novartis. Inhibiting aromatase inhibits estrogen production that normally occurs in body fat. In menopausal women, this is their only source of endogenous estrogen. Without estrogen, progesterone receptors disappear, making it impossible for progesterone to perform any of its multitude of beneficial roles. The only sex hormone left functioning is testosterone. The point of this treatment, if there is any, is that it illustrates rather well that estrogen causes breast cancer. But the woman is living without any estrogen or progesterone. Consider the osteoporosis, the rampant vaginal atrophy, the rapid aging, and the many other symptoms of hormone deficiency. Estrogen and progesterone are important to women at all ages. The estrogen cancer risk is due to unopposed estrogen; restore proper hormone balance and the breast cancer risk fades away. Conventional medicine in the past 40 years veered into estrogen dominance and the disaster that caused, and now this new treatment veers into extreme sex hormone deficiency. Doesn’t anyone consider the desirability of proper hormone balance?
Time magazine (20 October issue) featured this drug and its breast cancer sparing effect, without explaining clearly what it does or what problems it caused. The drug’s inhibition of estrogen production in breast and body fat is not news. My 2000 PDR makes the same claim. The source was a study reported online by the New England Journal of Medicine, but not printed in the journal. I don’t know about you, but the whole thing strikes me as an advertisement dressed up as a legitimate medical article.
John R. Lee, M.D.
WHAT CAUSES BONE LOSS IN YOUNG WOMEN
The bone building that goes on in a girl’s teens and twenties lays the foundation for bone health later in life. We know that moderate exercise builds bone. It also helps keep insulin, estrogen and other hormones balanced. But did you know that young women who eat a restricted diet and go to extremes of exercise (e.g. ballet dancers, runners) often stop ovulating, and may even stop having periods altogether? If you’re not ovulating you’re not making progesterone, and you’re not having periods you’re not making much in the way of estrogen either. Since progesterone plays a role in building bone, and estrogen plays a role in keeping bone loss under control, suppressing hormone production in early adulthood can have an effect on whether bones are healthy around the time of menopause.
Canadian research done by a team that included Jerilyn Prior, M.D. also shows that increased cortisol levels caused by extreme exercise may also contribute to bone loss in young women. The researchers measured cortisol levels as well as bone content and density, and had the women fill out questionnaires regarding their eating and exercise habits. The women were similar in age, weight and body mass (amount of fat on the body), but those who went to extremes of dieting and exercise had much poorer bone quality.
Extreme exercise raises cortisol levels, and a chronically high cortisol level depletes bone. Dr. Lee felt that this was because progesterone and cortisol compete for receptor sites in bone, and while progesterone builds bone, cortisol depletes it.
Another cause of bone loss in young women is taking birth control pills. The progestins in the birth control pills block ovulation, and thus hormone production, and most progestins don’t build bone the way that progesterone does. In other words, the non-bone-building progestins replace the bone-building progesterone and interfere with bone building.
Since we also know that using oral contraceptives during adolescence increases the risk of breast cancer, it seems evident that they should be used with caution.
McLean JA, Barr SI, Prior JC, “Dietary restraint, exercise, and bone density in young women: are they related?” Med Sci Sports Exerc. 2001 Aug;33(8):1292-6
Prior JC, Kirkland SA et al, “Oral contraceptive use and bone mineral density in premenopausal women: cross-sectional, population-based data from the Canadian Multicentre Osteoporosis Study,” CMAJ. 2001 Oct 16;165(8):1023-9.
For information by Dr. Lee about oral contraceptives, please read What Your Doctor May Not Tell You About PREmenopause.
EATING FOR A HEALTHY PROSTATE
We know that men who eat tomato sauce and who have higher levels of folic acid and zinc have less prostate cancer. A recently published study added a few more pieces to the prostate cancer/diet puzzle. This was a large study, comparing 858 men with prostate cancer with 905 men without it. The men who didn’t have prostate cancer ate more olive oil, more vegetables in general, and specifically more tomatoes and allium vegetables, which includes onions and garlic. The men who did have prostate cancer ate more margarine—yet another reason to avoid this fake food. There was no association between alcohol consumption and prostate cancer.
Dr. John Lee wrote in detail about prostate enlargement and prostate cancer in his booklet, HORMONE BALANCE FOR MEN: What Your Doctor May Not Tell You About Prostate Health and Natural Hormone Supplementation.
Hodge AM, English DR et al, “Foods, Nutrients and Prostate Cancer,” Cancer Causes & Control:15 (1): 11-20, February 2004.