October 20, 1997

CyberHealth Index

CONTENTS:

1. Body fat, exercise, estrone, and Dr. Susan Love
2. Why rice may be better for you than wheat
3. Great quotations: postmeno years are the best

Body Fat, Exercise, Estrone and Dr. Susan Love

On page 10 of her “Hormone Book,” Dr. Love summarizes the study done by Jane Cauley, which showed that the main determinant of postmenopausal estrone and estradiol production is the amount of body fat. Dr. Cauley also examined the relationship between estrogen levels and the amount of physical activity of her subjects (white Pittsburgh women, average age 58, not on HRT).

Describing Cauley’s study, Love writes: “Women who were physically active also had higher blood levels of estrone. Although some active women had lower levels of estrone (because they were thinner), paradoxically those with more muscle mass had higher estrogen levels.”

Sounds great, doesn’t it? If women who were physically active also had higher levels of estrone, than exercise sounds like a wonderful way to increase one’s own estrone production. Unfortunately Cauley’s study says nothing of the sort.

In fact Cauley repeatedly stresses that physical activity LOWERS estrogen levels.

Let me quote some of Cauley’s statements: “Physical activity was an independent predictor of serum estrone. More active women had lower levels of estrone.” “The relation remained significant after controlling for obesity.”

“Obesity was the primary determinant of estrone and estradiol even after controlling for androstenedione.” “Both estrone and estradiol were positively correlated with the degree of obesity” (the estrone level of obese women [defined as BMI above 30] was 41% higher than that of normal-weight women; their estradiol was twice as high; their testosterone was also significantly higher).

“A negative correlation was present between physical activity and estrone and estradiol. This was true whether an objective or subjective measure of activity was used.

Because more active women tend to be less obese, the authors controlled for obesity. The magnitude of the correlation decreased, but the coefficients remained statistically significant.” “WOMEN WHO WERE THE MOST ACTIVE HAD THE LOWEST ESTROGEN LEVELS.” (My emphasis)

To drive her point home, Cauley stresses that EVEN MODERATE PHYSICAL ACTIVITY LOWERED ESTRONE. As for more intense exercise, Cauley cites a 1988 study by Nelson which showed that postmenopausal women who ran 23 miles a week had lower estrone levels than age-matched sedentary women.

In other words, Cauley is almost unusually insistent and absolutely clear in stating that physical activity and lower estrogen levels go hand in hand, and not just because the women who exercise are thinner (though that certainly is an important factor; certainly none of Nelson’s runners could have a high BMI — even though muscle weighs more than fat).

There is nothing surprising about this finding. We have known for a long time that physical exercise can delay puberty and generally lower steroid levels. If it’s strenuous enough, exercise can lead to serious endocrine deficiencies in female athletes to the point of anovulation and osteoporosis (certain types of male athletes, such as long-distance runners, may also develop testosterone deficiency and fertility problems).

A lean, muscular, small-breasted female athlete (or a ballerina) is not anyone’s image of an estrogenic woman. We think rather of Marilyn Monroe; we think of cleavage.

How does exercise lower estrogen levels? Exercise raises the resting metabolic rate (in other words, a regular exerciser has a higher metabolic rate even when not exercising), and thus the body burns more calories even during sleep, making obesity unlikely.

Furthermore, the higher metabolic rate also means faster hormone metabolism and clearance (nicotine and high levels of the thyroid hormones have a similar effect). Add to this the finding that exercise even affects the nature of estradiol metabolites, favoring the production of 2-hydroxyestrone, which is a potent antioxidant but has practically no estrogenic activity and in breast tissue it could even be called an anti-estrogen (athletes have a significantly lower risk of breast cancer, ovarian cancer, and endometrial cancer).

If exercise ever led to increased estrogen levels, then breast cancer patients and women at high risk would be warned to move as little as possible, and exercise would not be one of the chief battle cries of breast cancer prevention.

Parenthetically, I can’t resist pointing out that looking at estrone in relation to exercise may be really missing the bigger point, which isTHE DRAMATIC IMPACT OF EXERCISE ON INSULIN LEVELS. Insulin is a major tumor growth factor; excess insulin has been strongly implicated in both cancer and heart disease. Exercise may derive its anticarcinogenic and life-extending effects chiefly from its ability to lower insulin.

Still, I think I can guess why Dr. S. Love made the statement that’s the opposite of Cauley’s findings. (Note that I’m not interested in attacking Love; I think it’s more useful simply to probe the subject at greater depth.) Cauley found a very weak (.14) positive correlation between grip strength and estrone and estradiol levels.

But when she analyzed her data differently, separating women into tertiles according to grip strength, she found that “there was little difference in estrone and estradiol when the low and middle tertiles were compared.

However, women who had the highest grip strength had significantly higher estrone and estradiol levels” (looking at Cauley’s figures, their testosterone levels were much higher also). It’s possible that Love concluded that higher grip strength was due to more exercise, and thus indirectly, through building muscle mass, more exercise resulted in higher estrogen levels.

However, another interpretation is also possible. We know that estrone affects muscle formation (myoblasts have estrone receptors just as osteoblasts in the bone have them), and that muscle atrophy, in parallel with bone loss, accelerates after menopause, presumably due to hormone deficiencies.

Thus, one could hypothesize that obese women, with their higher estrogen and testosterone levels, would lose muscle mass more slowly. And there is indeed a 1994 study by Kritz-Silverstein which showed that overweight women had significantly stronger grip strength in both hands, while exercisers had significantly stronger grip in the non-dominant arm.

Cauley checked the grip strength only in the dominant arm. Thus it is likely that again it was the obese women, with their higher estrone and estradiol, who had superior grip strength, not the women who were the most physically active, and who in Cauley’s study were found to have the lowest estrogen levels.

Both growth hormone and sex steroids, including estrogens (though estrogens are apparently not as anabolic in regard to muscle tissue as testosterone), are well known to affect muscle mass and the muscle to fat ratio, which even in athletes decline with age. Regelson is adamant in pointing out that EXERCISE ALONE CANNOT PREVENT AGE-RELATED MUSCLE ATROPHY.

It is also interesting to recall the PEPI findings on hormones and weight gain (see CyberHealth #2): women assigned to placebo gained on the average twice as much weight as those assigned to hormone treatment.

PEPI findings confirmed the epidemiological findings that women on long-term HRT maintained lower BMI, but this time, because of random assignment rather than self-selection, the criticism that women who opt for HRT are thinner to start with did not hold.

Rather, it seems that in the more youthful hormonal state (much higher estradiol levels than in untreated postmenopausal women, even the obese ones), the body resists obesity.

Now, there exists a certain “let-them-eat-cake” school of thought about menopause, which encourages the acquiring of “a few extra pounds” as a means of increasing your estrone production.

True, obese women tend to have a late and relatively easy menopause; gynecologists have long ago realized that there was a considerable difference in the severity of symptoms between “the thin woman’s menopause” and what Gail Sheehy euphemistically calls “the plump woman’s menopause.”

(One theory is that it is the magnitude of the drop in estrogen levels that determines the severity of the withdrawal symptoms, rather than the levels per se. Thus a thin woman who is quite hypoestrogenic to start with, as is true of some vegetarian women, for instance, might also have an easy menopause, according to this theory.)

Likewise, obese women don’t have to worry about osteoporosis. And they do tend to preserve better skin and youthful-looking face. But these benefits are canceled by the much greater risk of heart attack, stroke, diabetes, and many kinds of cancer, to mention just the most serious diseases.

It’s now politically correct to sing the praises of postmenopausal body fat “taking over” when the ovaries shut down; it’s poetic to liken adipose tissue to an alchemist transforming the lead of androstenedione into the gold of estrone.

But a warning must be sounded: after menopause, there is no progesterone to oppose the action of estrone on the endometrial and breast tissue. Nature’s system of hormonal checks and balances is no longer in place. Since endometrial cancer is particularly estrogen-dependent, it is no surprise that obesity is the prime risk factor. Being 25-50 lbs overweight triples the risk; being more than 50 lbs overweight increases the risk nine times.

It would be insane to recommend that a woman become obese and sedentary as a means of increasing endogenous estrogen levels. Building muscle mass through weight lifting would be a fabulous alternative, but the evidence just isn’t in. Weight lifting that results in significant muscle increase is still pretty vigorous exercise, and increased muscle mass definitely means a higher resting metabolic rate, so a possible increase might be canceled by the other effects of exercise.

Unfortunately, all the evidence we have so far indicates that exercise results in LOWER estrogen levels, both in premenopausal and postmenopausal women. Obesity, on the other hand, reliably raises estrogen levels—in both sexes.

Growing fat feminizes men. Obese men may in fact produce so much estrone and estradiol that they start growing breasts. I’ve always found it amusing that the statues of the fat Buddha are far more “bosomy” than those of the willowy goddess of mercy, Quan-Yin.

As for Love’s credibility, the point that I raise is a minor one next to the big storm over her misstatement of the heart disease and breast cancer statistics. Somehow she got it in reverse: in every postmenopausal age category, there are more deaths from heart disease than from breast cancer. For women under 75, there are three times as many deaths from heart disease as from breast cancer; for women over 75, there are twenty times as many deaths from heart disease as from breast cancer.

Interestingly, however, exercise protects against BOTH heart disease and breast cancer (and various other types of cancer). Postmenopausal obesity, on the other hand, magnifies the risk of both disorders, and this vastly outweighs the benefits of extra estrone.

So Love is certainly not wrong in recommending exercise and increased muscle mass. Start with a light set of weights and don’t worry; you’ll reap health benefits no matter what happens to your endogenous estrone levels.

(Sources:

Cauley J et al. Epidemiology of serum sex hormone levels in postmenopausal women. American Journal of Epidemiology 1989; 129: 1120-31;

Kritz-Silverstein D et al. Grip strength and BMD in older women. Journal of Bone and Mineral Research 1994; 9: 45-51;

Kritz-Silverman D and Barrett-Connor E. Long-term postmenopausal hormone use, obesity, and fat distribution in older women. JAMA 1996; 275 (January 3), p. 46-49;

Gladwell M. The estrogen question: How wrong is Dr. Susan Love? The New Yorker, June 9, 1997 [Gladwell also points out Love’s inaccuracy on phytoestrogens; Trien S, The Menopause Handbook;

Ballantine Books, 1986; Regelson W. The Superhormone Promise. Simon and Schuster 1996, p. 208.)

RICE COULD BE BETTER FOR YOU THAN WHEAT

Jim Barron, who’s done a lot of research on nutrition for his planned book on life extension, writes:

Rice is “better” than more traditional western grains in one important respect: Grains such as wheat (which are a relatively recent introduction to our (H. sapiens) diet) provoke damaging immune reactions in many individuals (those with celiac disease). It has been found that the more recent the introduction of wheat and associated grains into the diet in an area, the higher the incidence of celiac disease (CD has been shown to be a GENETIC condition).

This is generally interpreted to mean that the alleles which cause the CD type reaction to wheat are in the process of being selected out of our species. [If anyone wants further information on this, I can supply e-mail addresses of individuals who have accumulated a lot of information on this topic.] In areas where wheat has been used much longer, the incidence of the CD alleles is much lower. There are SOME authorities who feel that wheat is somewhat damaging to most individuals and that CD is just an extreme example of such damage.

Wheat and closely related grains also have other problems: They are prone to contamination with molds that produce very potent toxins (Aspergillus flavus producing aflatoxin, etc.)

As far as I know, rice is not prone to the molds that cause such problems in wheat, etc. FONT FACE=”Arial” COLOR=”#ff0000″>****But rice may have its own problems – I just don’t know.****

The introduction of grains seems to have been a trade-off (“double edged sword”) of accepting the associated problems (or just not being aware of them) in order to get the benefits of long term storage at a time when more modern and reliable methods of long-term food storage were not available. They also, of course, make possible higher population densities (more food per acre as well as increased transportability, length of storage, etc.).

Interestingly, rice (and corn) do not affect MOST celiacs, but a small percentage (myself included, unfortunately) DO react quite strongly to them.

***There are NO essential nutrients in ANY grains which cannot be obtained in adequate amounts from non-grain sources.***

Rice has one more important advantage over other grains: It has traditionally been grown as part of a sophisticated, integratedsystem of agriculture: Fish in the water eat various things that would otherwise damage the rice and fertilize the water and provide dietary protein. There are also a number of other symbiotic relationships involved in the system (algae that provide nitrogen, etc.).

There are countries that have used rice as part of a SUSTAINABLE, stable system of agriculture for many thousands of years (until the introduction of recent “improvements”). Western agriculture (like much of the REST of western culture), IMHO, has yet to grasp the basic concept of sustainability.

*******What foods are BEST for an individual is, to a great extent, determined by his genetic heritage: which area his ancestors came from and what their traditional diet was. Much of the genetic variation in Homo sapiens involves adaptation to a wide variety of local conditions, including local diets. ********

IMHO, fundamental to the significant extension of lifespans will be learning to identify individual variations (NOT the same thing as genetic defects!) and learning to optimize adjustment to them. The current approach of identifying what is “best” (in terms of diet, lifestyle, etc) by CRUDE statistics which apply to the population as a whole have VERY limited effectiveness: They may improve lifespan in some **at the expense of ** shortened lifespan in others. Future application of genetics in making many more types of biological testing MUCH cheaper and more widely available will make optimization of lifestyle **tailored to individuals** possible and practical. IF we chose to apply the technology this way.

Sir Archibald Garrod wrote his prescient essay on “Biochemical Individuality” many decades ago, but we STILL haven’t incorporated this very important concept into our thinking. (Probably because it conflicts with our cultural fixation on the concept of “interchangeable parts” and mass production. Seems like every good new idea gets overused.. And the better it is (when APPROPRIATELY applied) the more it will be OVERused..

Ivy replies:

Thank you, Jim, for excellent information. The lower cancer rates among rice-eating people may have something to do with their immune systems being less suppressed with allergens and fungal toxins. It’s quite interesting that some authorities think that wheat may be harmful to most of us, causing some degree of immunosuppression.

Another nutrition expert I’ve contacted also confirmed that wheat tends to be stored for a long time before use, sometimes for over a decade, while rice is consumed relatively fresh.

I’d also like to add that RICE CONTAINS MELATONIN. Maybe that’s why it feels so especially soothing, and is so appropriate with an evening meal. Rice is also a good source of MAGNESIUM, a natural tranquilizer.

In addition, BROWN RICE contains SILICON (in the bran), important for the building of all connective tissue, including bone and the walls of blood vessels. And rice bran also contains TOCOTRIENOLS, which are apparently very effective antioxidants and anticarcinogens. And brown rice is less glycemic, which is welcome news to those of us on a low-glycemic diet.

It has also been suggested that no whole grain is digested as easily as rice is. It does not burden your digestive system. Gail Peterson, our editorial assistant, reminds us that rice cereal is the first solid food usually given to infants, that’s how safe and digestible it is.

In order to make rice less glycemic (that is, to lower its ability to raise your blood sugar and consequently your insulin levels), be sure to favor brown rice over white rice, and to eat it slightly undercooked (the equivalent of “al dente”), and with lots of high-fiber vegetables—briefly stir-fried in healthy fat, of course (I find that a mixture of olive oil and sesame oil imparts a wonderful flavor). Fat is just as important as fiber, or maybe even more so, in slowing down glucose release.

Another valuable wheat alternative is rye, which is remarkably nutrient rich and high in fiber. Dark pumpernickel bread is not loaded with yeast the way wheat breads are; note how dense it is. But be sure to read the label; these days one practically has to be buy imported German pumpernickel to get real rye and real old-fashioned leavened bread (traditional bread was basically a healthy fermented food; today most of mass-produced bread is white-flour junk food.. Sometimes the flour is colored with caramel to mislead the health-conscious into thinking they are not buying what is still, despite the color, white bread.).

If you have a tendency to abdominal bloating (I do not mean water retention, but a digestive problem: you wake up with a relatively flat stomach, but by evening you get that distended, pregnant look), try an experiment: eliminate all bread, cereal, and bakery products. (No, no bun with your hamburger. Have a salad instead.) It could be some degree of intolerance to wheat, or to a combination of wheat and yeast.

As for “biochemical individuality,” there is no excuse for disregarding it. Laboratory animals, for instance, get hormones and other treatments in dosages based on body weight; with humans, not even body weight is typically taken into account. That’s why the CyberHealth nutrition philosophy is:

Above all, listen to your own body.