Stay Young & Sexy with Bio-Identical Hormone Replacement: The Science Explained by Jonathan V. Wright, Lane Leanard
In addition to its large proportion, estriol is a very “gentle” or low-potency estrogen , only about one-quarter as potent as estradiol and only one-eighth as potent as equilin. Research indicates that, due in part to its low potency, estriol may provide invaluable built-in protection against the carcinogenic (cancer-causing) potential of other more potent estrogens.
My estrogen replacement prescriptions should be 80% estriol, 10% estradiol, 10% estrone, just as Nature appeared to intend.
Progesterone helps prevent endometrial cancer in two ways. First, it reduces the number of estrogen receptors (sites on cells where estrogen molecules normally bind, or attach themselves), such as those in the uterine lining or the breasts; estrogen molecules that are prevented from binding by the action of progesterone cannot then stimulate cell growth. Second, progesterone directly regulates cell division/replication of fully mature endometrial cells, thus inhibiting estrogen-stimulated cellular overgrowth (called hyperplasia) and sometimes cancer.9
The primary estrogen circulating before menopause is estradiol ; after menopause it is estrone , which comes from three sources: 1) cells in the adrenal glands (cortex); 2) fat cells, which convert the androgen androstenedione to the estrogen estrone; and 3) the ovaries, which continue producing small quantities of androgens, which are converted to estrogens, primarily estrone.
However, the risk of abnormal blood clotting from the estriol in topically applied BHRT is extremely small (For more on this topic, see Chapter 9). Nevertheless, there are safe, natural measures women can take to reduce their risk even further. Over the years, I’ve (JVW) observed that combinations of cod liver oil (1 – 1½ tablespoons daily) and vitamin E (400 – 800 IU of “mixed tocopherols” daily) help enormously in preventing phlebitis. When taken regularly, these items are nearly 100% effective for preventing abnormal blood clotting, even during pregnancy.
What the hip, spine, and other vulnerable bones have in common is a high proportion of sponge-like cancellous (or trabecular) bone beneath their thin, smooth surfaces (Fig. 6-3). Cancellous bone is found at the ends of long bones of the arms and legs (eg, hip (femoral neck), shoulder, and wrist) and the inner parts of flat bones (eg, ribs). By contrast, the main body of long bones like the femur (thigh bone) are composed primarily of harder, denser cortical bone, which makes them much more resistant (but not invulnerable) to osteoporotic wasting and fracture.8 The major advantage of softer cancellous bone is its ability to be rapidly reshaped or remodeled in response to the body’s physical and metabolic needs. The idea of skeletal remodeling, or turnover , may sound strange, because people sometimes forget that, for all bones’ rigidity and strength, they are living tissue that is constantly renewing and reshaping itself, albeit at a much slower rate than soft tissues, such as muscle and skin. That is, after all, how fractures heal. Although adult bones have long stopped growing in length, they continue to remodel themselves under the influence of such factors as exercise and weight distribution, as well as the actions of various hormones, vitamins, minerals, and other natural biochemicals.
But estrogen is not the only hormone active in bone metabolism. Just as estrogen and progesterone are the Yin and Yang of the menstrual cycle (See Chapter 3.), so the two steroid hormones are also inextricably linked in the life cycle of bone tissue. Progesterone is a key – but widely overlooked – factor needed by osteoblasts to build new bone . While estrogen is linked to the function of osteoclasts, the decline in progesterone in the years before, during, and after menopause deprives your bone-building osteoblasts of a growth factor that is essential to their efficient activity.
But while estrogen helps slow bone loss, it is of virtually no help in rebuilding new bone to replace that which has already been lost.12 Thus, “estrogen” replacement, primarily using Premarin® slows the rate of bone loss by only about one-third overall and decreases the fracture risk by only about 50%.13 For the rebuilding task, you also need progesterone. In addition, parathyroid hormone, the androgens (“male” hormones) − testosterone and DHEA − are important, as are foods and supplements containing calcium , magnesium , strontium , vitamin D , and other nutrients, along with regular and frequent weight-bearing exercise .
Overall, her findings lead us to a startling conclusion: that bone loss actually begins long before menopause – sometimes as early your 30s – while your estrogen levels are still essentially normal. Between the ages of 35 and 50, you might lose as much as 75% of your progesterone. So that when you enter the perimenopausal period, with estrogen loss just beginning in earnest, your progesterone has been declining for 15 years.17, 18, 19, 20
Getting back to calcium supplements, then, to get the most out of a calcium supplement, regardless of how much acid our stomachs may be capable of churning out, it’s usually best to avoid calcium carbonate altogether and instead take supplements that supply calcium citrate or calcium malate . Unlike calcium carbonate, these have no trouble dissolving and dissociating, no matter how much acid your stomach is producing.
Most nutritionally-oriented physicians now recommend taking 3,000 to 4,000 IU supplemental vitamin D daily, depending on the amount of sunlight exposure. For many individuals, blood tests show that even higher amounts are necessary to achieve optimal levels. However, since taking too much vitamin D for too long can be dangerous, it’s always best, when embarking on a serious nutritional supplement program with vitamin D (or any other nutrient) to consult with a physician who is skilled and knowledgeable in natural medicine. (See Chapter 11 to learn how to locate such a doctor.)
Here’s the remarkable thing about strontium: once it gets into bone tissue (in physiologic amounts), it slows osteoclastic resorption while at the same time enhancing osteoblastic bone building. In other words, it mimics the effects of estrogen, progesterone, testosterone, and DHEA, but without any other hormonal effects.51 This means that, all by itself, strontium can help prevent and even reverse osteoporosis.
Bones need both calcium and strontium to stay strong, with a preference for more calcium than strontium.
Let us emphasize an important point about these studies: Postmenopausal women without osteoporosis who took no replacement hormones still had increases in BMD when they used strontium. So not only did strontium repair existing damage, it actually helped prevent the women from suffering with osteoporosis in the first place. But, remember this, it doesn’t matter whether it’s strontium gluconate, strontium lactate, strontium carbonate, or even strontium ranelate; as long as it’s strontium (along with a greater quantity of calcium), it’s good for you! Remember, never take strontium without taking more calcium than strontium.
However, helpful as they may be in this regard in the uterus, progestins have their own carcinogenic potential in the breast, where they might even contribute to “estrogen”-induced cell proliferation. By contrast, bio-identical progesterone has little or no built-in carcinogenic potential, either in the uterus or breast (or anywhere else), and it also helps modulate the cancer-causing effects of potent estrogens.1
Three years later, the International Agency for Research on Cancer, a division of the World Health Organization (WHO), issued a statement declaring that, “… combined “estrogen”-progestogen contraceptives and menopausal therapy are carcinogenic to humans.”5 As described in Chapter 1, the final shoe dropped when researchers from the MD Anderson Cancer Center in Houston, Texas, produced the “smoking gun,” a rock-sold link between the use of conventional HRT and an increased risk of breast cancer.6-8
The MISSION study compared the incidence of breast cancer in women who had been “exposed” to some form of hormone replacement therapy within the prior 5 years with the breast cancer incidence in women who had never used hormone replacement therapy or had stopped using it more than 5 years before the study. The average exposure to hormones in the MISSION study was 8.3 years, 5 years longer than exposure to conventional HRT in the WHI study. Yet, unlike the WHI, the MISSION study found no increased risk of breast cancer in women exposed to hormone replacement therapy. Why the difference? The primary reason, according to the MISSION researchers, was likely that women in France for the most part do not use American-style conventional HRT. Instead, at least three-fourths of the participants used topical estradiol combined with either bio-identical progesterone (44%) or a progestin other than Provera® (56%). Although there were no significant differences in the incidence of breast cancer among the various hormone replacement regimens used in the MISSION study, the safest one included topical estradiol + bio-identical progesterone (an oral micronized formulation) .
Estrogens influence the growth (or not) of breast cell proliferation and possibly cancer by binding to (and stimulating) two different estrogen receptors, identified as α and β receptors − or ER- α and ER- β .1 Estrogens that stimulate ER- α tend to promote breast cell proliferation. By contrast, estrogens that stimulate ER- β inhibit breast cell proliferation, and consequently, protect against breast cancer development. Research has shown that estradiol stimulates ER- α and ER- β receptors about equally, but estrone is about five times more potent in stimulating ER- α vs. ER- β receptors. This helps explain why elevated estrone levels are considered such a high risk for breast cancer. On the other hand, estriol stimulates ER- β receptors about three times more than ER- α receptors, making it less likely to promote breast cancer.
What about horse estrogens? They’re worst of all. Not only do CEEs favorably stimulate ER- α receptors, they also block (or downregulate) ER- β receptors. To make matters worse, one horse estrogen − 4-hydroxequilenin, never found in humans (See Chapter 1.) − induces DNA damage, making it a particularly potent carcinogen.
While cumulative exposure to some estrogens may be a factor in breast cancer development in some women, it is clearly far from the whole story. For example, the long-term exposure hypothesis is not supported by the following highly valid observation: even as ovarian estrogen secretion falls sharply during and after menopause, women’s risk of breast cancer during these years continues to rise. Dr. Richard A. Wiseman of the London School of Hygiene and Tropical Medicine observes that a 75-year-old woman (not on HRT), who has spent her last 25 years without significant ovarian estrogenic stimulation, nevertheless, has a considerably higher risk of breast cancer than a 50-year-old woman, who is just coming to the end of her maximum estrogen-secreting years.
sex steroid hormones. As shown in Figure 7-2, the USPHS investigators found a strong and statistically significant inverse association between estriol levels during pregnancy and the later occurrence of breast cancer. That is, women who had the highest levels of estriol during their pregnancies, had a 77% lower breast cancer risk later in life, while those with the lowest levels of estriol had just a 58% reduction.*
Dr. Lemon found that about two-thirds of Caucasian women diagnosed with breast cancer had subnormal urinary EQs (less than 1.0).25 In his small study, in 34 women with no signs of breast cancer, Dr. Lemon found the median EQ to be 1.3 before menopause and 1.2 postmenopause. The EQ was below 1.0 – a possible danger sign – in only 21% of these healthy women (Fig. 7-3). In 26 other women who had breast cancer, the picture was quite different; their median EQ was low – 0.5 before menopause and 0.8 postmenopause. Nearly two-thirds (62%) of the women with breast cancer had an EQ below 1.0. Thus, relative to the estrone and estradiol, the women without breast cancer seemed to be excreting substantially more estriol than the women with breast cancer.28
Anything that alters the balance of “good” to “bad” estrogens – the 2-hydroxyestrone/16α -hydroxyestrone ratio (also called the 2/16 ratio , for short) – may alter the risk of estrogen-related cancer. The optimal ratio (as measured in samples of urine) appears to be about 2:1 (ie, twice as much “good” estrogen to “bad” estrogen).
For every 10 grams of cruciferous vegetables you eat each day, your 2/16 ratio increases by 8%.68
The phytochemical that seems to be most effective against estrogen-based cancers (eg, breast, uterine, ovary) in lab animals is called indole-3-carbinol (I3C) . When placed in an acidic environment, like a healthy stomach, I3C molecules chemically bond together to form a variety of different biologically active products, the most prominent of which is 3,3’-diindolylmethane (DIM). Each DIM molecule has 10 times the potency of an individual I3C molecule,
Daily oral doses of 300 to 400 mg of I3C per week – equivalent to about 300 to 400 grams of raw vegetables (about one-third of a head of cabbage) – significantly improved the 2/16 ratios in women who were at increased risk for breast cancer.72-75 If eating I3C/DIM raises our 2/16 ratios , and if raising the ratio reduces our risk of cancer, is it possible to cut our risk of cancer simply by consuming more I3C/DIM?
We should also point out that some studies in lab animals have shown that long-term use of I3C supplements (but not DIM) can actually promote or enhance the growth of some cancers. However, this effect has never been seen in humans or with the consumption of cruciferous vegetables. Nevertheless, it has led some researchers to caution against the use of I3C supplements until their risks and benefits are more clearly spelled out.
“The results of the present study indicate a synergistic effect of estrogen and progesterone, but not estrogen and MPA [Provera®] , on exercise time to myocardial ischemia. This is a novel finding in the setting of CAD [coronary artery disease].24
Provera® is worse than no treatment at all.
For both hormones, the upper limit of normal was about 40 micrograms. In other words, 24 hours’ worth of urine in normal, nonpregnant, premenopausal women should contain no more than 40 micrograms each of estradiol and estrone. Because excessive amounts of estradiol and estrone are potentially carcinogenic, women who have 24-hour urinary levels of these hormones above the 40-microgram line may be at increased risk for breast cancer.
A close look at Figure 9-1 reveals that urinary levels of estradiol close to the upper limit of normal occurred when the women took oral estradiol at doses between 0.2 and 0.5 milligrams. At the FDA-recommended daily dose of 1 milligram, urinary estradiol levels rose to about 70 to 100 micrograms – 2- to 3-fold higher than the normal level .
While estradiol doses as high as 0.5 milligrams per day produced safe levels of estradiol, this same dose produced estrone levels that were about 3 times higher. In other words, the 1-milligram FDA-“approved” dose of estradiol resulted in estrone levels 4 to 6 times above safe, normal levels . Thus, a safe dose of oral estradiol turns out to be about 0.25 milligrams (or 250 micrograms) per day – about 4 times lower than the FDA-“approved” level found in commercial “drugstore” varieties, the kind touted as FDA-“approved” BHRT.
Thus, the recommended oral dose of Activella® produced serum levels of estrone that were about 5 times higher than safe, normal levels.
Reminder: The widely recommended, commercially available, FDA-“approved” dose of oral estradiol – considered by some to be an FDA-“approved” version of BHRT – is 1 to 2 milligrams per day – which results in circulating estradiol and estrone levels 4 to 8 times higher than the upper limit of normal (safe natural level).
It is for these reasons that Tri-Est and Bi-Est formulations always contain a relatively high dose of estriol (2.0-2.25 milligrams) and very small doses of the carcinogenic estrogens, estradiol (0.25 milligrams) and sometimes estrone (0.25 milligrams).
during first-pass metabolism. Even though first-pass metabolism of oral estradiol does not produce any overtly toxic metabolites (as it does with Premarin®), the liver rapidly and extensively transforms most of an oral estradiol dose into estrone, which then circulates in the blood stream, serving as an inert reservoir for continuous re-supply of estradiol. Circulating estrone − which has been linked to increased risk of breast cancer − can remain at excessively high levels for more than 12 hours after dosing, and only slowly decline over time. (See Figs. 9-1, 9-2, and 9-3.)1,
In addition, FDA-“approved” oral doses of estradiol (1-2 milligrams) can cause the liver to produce dangerously high levels of substances, such as C-reactive protein and blood clotting factors, which increase the risks of heart attacks, strokes, and deep vein thromboses (blood clots). By contrast, topical estrogens have no such effects.
If you take progesterone by mouth, liver enzymes break it down into more than 30 different metabolites, but very little of the original progesterone, which is what your body really needs, actually ever makes it into the bloodstream.1
cycle. By contrast, oral dosing led to large pulses of estradiol and estrone shortly after administration and average daily plasma concentrations that were 12 times and 9.4 times higher , respectively, than those typically seen following topical application.12
In other words, regardless of dose, following transdermal administration of estradiol, all circulating levels of estradiol and estrone remained very close to the 1:1 ratio of free estradiol and free estrone found during the menstrual cycles of normal premenopausal women.
However, when women took their estrogen orally , the estradiol:estrone ratios were abnormally high. For oral estradiol (2 milligrams per day), the ratio was 1:5 in one study and 1:6.7 in another. That means that estrone levels were 5 to 7 times higher than estradiol levels. In women taking oral Premarin® (0.625 milligrams per day), the ratio was 1:3.2; estrone levels were 3 times higher than estradiol levels. Thus, again we see that taking estradiol or horse estrogens by mouth yields excessively high levels of estrone, the estrogen most closely linked to breast cancer.
Reduced plasma triglyceride levels . Topical, but not oral, administration of estrogen reduces serum concentrations of triglyceride, a fatty substance related to cholesterol. Elevated triglycerides levels are an important risk factor for coronary heart disease.14, 15 Less LDL-cholesterol oxidation. Both topical and oral estrogen administration can reduce the levels of low-density lipoprotein (LDL) cholesterol (the “bad” cholesterol). However, LDL levels are only part of the story. LDL becomes a much greater danger after it has been oxidized.* Ovarian estrogen has natural antioxidant effects, which help protect LDL from oxidation. This may be one of the reasons premenopausal women have such a low risk of heart disease.16-18 However, only topical administration of replacement estrogen preserves, or even improves, this valuable antioxidant effect in women after postmenopause. When you take estrogen orally, even bio-identical estrogens do not prevent LDL oxidation.† Normalized blood coagulation and clotting. Blood clotting, a perfectly normal and healthy reaction when we have a cut or scrape, can also occur inside blood vessels, and contribute to the formation of plaque and eventually a dangerous thrombus (blood clot) at sites of minor irritation or inflammation. If one of these thrombi should break loose, it can travel through the bloodstream until it blocks a small artery, possibly causing a heart attack or stroke.
Lower levels of C-reactive protein. C-reactive protein (CRP) has been identified as a sensitive sign of underlying inflammation and is now recognized as a direct promoter of the growth and progression of atherogenic plaques. This makes high levels of CRP an important independent risk factor for heart attacks, strokes, and related cardiovascular events – just like fatty diets, obesity, and smoking.
The reason seems to lie in the hormone’s first-pass through the liver, since CRP levels rise only after estrogen is metabolized in the liver. Elevated levels of CRP were noted in the WHI study after women took Premarin® by mouth, and where they were also associated with a 200% increase in the risk of coronary heart disease.28
Because estrogen taken orally readily activates abnormal blood coagulation and clotting, it increases the risk of VTE in postmenopausal women. In the WHI study, oral Premarin® doubled the risk of VTE compared with placebo.30
What does estrogen replacement have to do with diabetes in postmenopausal women? Again, it depends largely on how you take the estrogen. Taking estrogen orally, whether it’s estradiol or Premarin®, increases insulin resistance, reducing blood sugar control, and consequently, elevating the risk of cardiovascular disease and other serious diabetes complications. By contrast, topical administration of estrogen (usually estradiol in these studies, but BHRT should work equally well) has the exact opposite – and healthier – effects: decreasing insulin resistance, improving blood sugar control , and decreasing the risk of cardiovascular disease and other adverse consequences of diabetes.15, 25, 33-41
However, we have found that when we switch the route of administration from transdermal to transvaginal – without altering the dose – their urinary levels rise right back up to their target range, and any symptoms of low estrogen they might have been experiencing quickly disappear. We have attributed this loss of effect of transdermal administration to a factor we term “dermal absorption fatigue:” repeated transdermal applications over many months seem to cause the skin to lose some of its ability to transport the hormones into the blood stream. Why this happens remains a mystery, but we know it happens, and we know that switching to intravaginal dosing avoids it or reverses it. Improving Progesterone Absorption Not only does transvaginal application prevent dermal absorption fatigue for estrogens, but it also facilitates progesterone absorption. We have long known that progesterone absorption through the skin is not very efficient. This has led some critics of BHRT to argue that topical progesterone administration is useless, and might even be dangerous, since progesterone might not be available to “oppose” the potentially carcinogenic effects of potent estrogens in the uterus. However, when progesterone cream is applied to the vaginal tissue, its rate of absorption is much higher, quite enough to elevate serum progesterone levels higher and keep them elevated longer, compared with oral administration. Vaginal administration also minimizes drowsiness, the primary side effect of excessive doses of oral progesterone.1 Because of all these factors, we now routinely recommend transvaginal administration as the best method for using BHRT.
Therefore, if any physician insists on prescribing any form of estrogen without also an adequate amount of progesterone – whether you still have a uterus or not – we recommend that you insist that he/she do some basic research (perhaps by reading this book!) or that you find yourself another, better informed doctor.
It is my observation that DHEA replacement is essential for maintaining optimum immune function and for helping to reduce the risk of cancer.* Some women report that DHEA does more for libido than testosterone, usually thought to be the major libido-enhancer in both sexes.
A reasonable, conservative starting dose of DHEA for most women is 15 milligrams per day, although for a few women, follow-up testing may indicate that the daily dose needs to be raised to 30 milligrams.
If testing shows that a woman’s DHEA is not getting metabolized to produce sufficient testosterone, she can also take testosterone (at an average dose of 2.5 to 5 milligrams daily). It’s
Figure 9-5 shows the dosing pattern I usually recommend starting out with for the average woman, who had a “typical” 26 to 30 day cycle during her menstruating years. Remember, this is not my plan; it’s the one designed by Mother Nature.
Although our basic schedule calls for adding progesterone midway through the “cycle,” some women find they feel much better with continuous progesterone. For these women, we have found that we can modify their regimen by adding a small amount of progesterone (eg, 10-20 milligrams per day), depending on whether she is having a “bleeding cycle” or not. The highest daily dose of progesterone – about 25 to 50 milligrams – should be used during the “luteal phase” (Days 12-25 in Fig. 9-5). If she needs to use it the rest of the month, a “step-down” dose of about 10 milligrams per day should be adequate.
A number of minerals are known to affect the function of these enzymes. Among these, cobalt had been shown to be safe and effective for “down-regulating” the overactive enzymes,45 which should put the brakes on estrogen metabolism.
Sure enough, we found that daily microdoses of cobalt chloride are usually quite effective in arresting estrogen hyperexcretion and restoring the efficacy of BHRT. Although many women need only about 500 micrograms of cobalt chloride per day to “reset” their estrogen metabolism and help normalize their menopausal symptoms, some have occasionally needed up to 1,000 micrograms. (These doses of cobalt are quite harmless and are no greater than those found in the daily diets in some areas of the world.) In nearly all cases, cobalt supplementation can be discontinued without need for resumption once 24-hour urine tests show that estrogen metabolism has returned to normal, which usually takes about 10 to 20 weeks.
Noting the importance of using a “relatively low dose” of progesterone with every cycle, they concluded, in part, “Induction of withdrawal bleeding and endometrial secretory transformation, which require larger doses of progesterone, do not provide additional benefit for prevention of hyperplasia.
Not only is it important to measure levels of hormones prescribed as part of BHRT (ie, estradiol, estriol, estrone, progesterone, testosterone, and DHEA), it is equally essential that we measure their “downstream metabolites,” including – but not limited to – the important “procarcinogens” 16 α -hydroxyestrone, 4-hydroxyestrone, and dihydrotestosterone (DHT), as well as the even more important “anticarcinogen” metabolites, 2-methoxyestradiol, 2-hydroxyestrone, and androstanediol. Relatively high levels of procarcinogenic metabolites and/or low levels of anticarcinogenic metabolites do not cause overt symptoms, but their effects can be profound and, best of all, they can almost always be favorably altered with diet and supplementation.
Saliva Testing: Inexpensive, Convenient, and Highly Unreliable
Saliva testing is not useful and not recommended for women on BHRT , because it is very likely to indicate “sky high” hormone levels that bear no relation to their actual physiologic levels and may falsely suggest a hormone overdose. Nor can saliva testing show the wide range of procarcinogenic and anticarcinogenic metabolites of estrogens and testosterone.
Blood Testing: Sometimes Useful but Difficult to Interpret
However, interpretation of hormone levels based on blood tests must be done carefully, because levels may vary depending on the timing of the test. Keep in mind that a blood test provides a kind of “snapshot” of what’s going on in your body at the moment blood is drawn.
Nor are blood tests ideal for monitoring the levels of estriol, one of the most important protective estrogens. In fact, estriol is practically unmeasurable in serum by most labs. The reason for this is not completely understood, but according to one research study,48 estriol gets “cleared” from the blood rapidly due to its very short half-life (rapid metabolism).
Serum levels also differ depending on whether you take a hormone orally or topically. Estradiol taken via a lozenge (partially topical, partially oral) reaches its peak blood level about 1 hour after dosing and then declines rapidly, suggesting rapid metabolism. By contrast, estriol taken orally causes a peak blood level about 3 to 4 hours after dosing (slower metabolism). However, a second peak occurs if you consume a meal about 4 hours after taking an oral dose. If you apply estriol topically, though, food consumption does not affect serum levels.
Another disadvantage of blood/serum testing is that no assays are currently available to practicing physicians for measuring the many steroid metabolites that have recently been shown to influence the risk for cancer, such as 2-methoxyestradiol (a “good” estrogen), 4-methoxyestrone (one of the “worst” estrogens), androstanediol, and others. As noted below, 24-hour urine testing is far superior for detecting, not only these metabolites, but also for measuring estriol levels.
24-Hour Urine Testing: The “Gold Standard”
Not only does this method even out all the peaks and valleys that complicate analysis of blood test results, it also facilitates the measurement of “unbound” (ie, “free”) levels of estradiol, estrone, estriol, progesterone, testosterone, and DHEA. Urine testing does not measure protein-bound hormones, which comprise the largest portion of “total” hormone production but are functionally irrelevant.*
24-hour urine collections are also preferable for two other reasons. First, they give the careful physician so much more information, including whether the hormones taken as BHRT are getting metabolized to mostly “safe” metabolites, or excessively to “unsafe,” possibly procarcinogenic metabolites. Second, the expense for capturing a 24-hour urine “picture” of 25 to 30 metabolites of the hormones administered as BHRT is very much lower than checking for all these metabolites in blood. In fact, as noted above, many of these metabolites can’t even be measured with standard blood tests.
Only a few small studies have prospectively examined the effects of testosterone replacement on cholesterol levels.21-24 In one such study, 22 men with low testosterone levels were given biweekly testosterone injections for a year. As shown in Figure 10-4, their total cholesterol levels fell from a mean of 225 mg/dL (“borderline high”*) at the start of treatment to 198 mg/dL (“optimal”) after 12 months. LDL-cholesterol levels dropped from 139 mg/dL (“borderline high”) to 118 mg/dL (“near or above
fat. Not only did testosterone replacement make the men stronger and leaner, it also helped improve their mood and sexual function – sexual performance, motivation, and desire, as well as an increase in spontaneous erections.37
Testosterone may act as an antidepressant
Testosterone replacement significantly improved cognitive function
Testosterone replacement significantly improved verbal memory
Lowering testosterone levels in normal, healthy young men caused a significant decrement in verbal memory
Chemical castration can impair memory in older men.
Testosterone supplementation improved working memory in older men
A good deal of recent evidence suggests that abnormal prostate growth may actually be related to an imbalance between testosterone and estradiol, ie, too much estradiol relative to testosterone, which commonly occurs as men age. If that turns out to be the case, low testosterone levels may be a greater danger to the prostate than high levels, and testosterone replacement – and/or estrogen suppression – may be a good way to prevent or even treat prostate hypertrophy.
Most recently, a well-controlled Swedish study measured testosterone and other hormones in 392 men with prostate cancer, comparing them with 392 healthy controls.57 The researchers found no significant associations between androgen levels and the risk of prostate cancer. Similarly, a smaller study from the UCLA School of Medicine found that 6 months of testosterone injections in men with declining testosterone levels had little effect on prostate volume or functions.58 There is still much to be learned about the causes of and treatments for prostate diseases. Nevertheless, one thing seems abundantly clear: currently “approved” treatments – drugs that basically inhibit androgenic activity (to try to shrink enlarged prostates) or dilate the ureters (to facilitate urine flow despite prostate enlargement) – act merely as symptom suppressors with limited efficacy, no effect on the course of the disease, and lots of potential side effects. On the other hand, they do earn patent medicine companies billions of dollars.
Maximize Your Vitality & Potency for Men Over 40 (Smart Publications).
Other Good Sources of Information about Bio-Identical Hormones