The solutions are straightforward when you understand the problem. If you know a man over the age of 50 who’s not sleeping well, chances are good it’s because he’s got prostate problems that require visits to the bathroom a couple of times a night. It’s estimated that benign prostate
disease affects over 40 percent of American men by age 50 and over 70 percent by age 60. The most common symptom is trouble with urination. Such men may have urinary frequency (hence getting up at night), their urine flow may be decreased in force or rate, they may have urinary urgency, and they may feel that they haven’t emptied the bladder (a sign of urinary
retention), especially after drinking coffee. Urinary retention also makes them more susceptible to urinary tract infections. When such men consult with their doctor, he will usually examine the
prostate gland through the rectum (a digital exam) and diagnose the problem as BPH, an acronym meaning benign prostate hypertrophy (enlarged cells in the prostate gland) or hyperplasia (enlarged by an increase in the number of cells in the gland). The two meanings of BPH are used interchangeably. BPH, like most conditions, varies in how it manifests itself. In some men, the obstruction of urine flow is due to prostate tissue overgrowth and the gland
will be definitely enlarged. In others, however, the obstruction is due to smooth muscle contraction of the urinary sphincters in the prostate gland,
causing the same urinary problems without much prostate enlargement. In some
men, the problem is mixed.
Conventional Medicines for the Prostate
The doctor may prescribe the drug terazosin (Hytrin) to relax urinary
sphincter muscles, or the drug finasteride (Proscar) which inhibits the
enzyme 5-alpha reductase, which converts testosterone into
dihydrotestosterone (DHT, a compound believed to stimulate prostate cell
growth, or hyperplasia). Or, he may recommend transurethral resection of the
prostate (TURP), the surgical coring-out of the urine passageway through the
prostate, quite often resulting in undesirable dribbling problems.
The success rate of the two drugs listed above is not uniform or consistent.
Both drugs were tested in an interesting study in the New England Journal of
Medicine (NEJM) in 1996. It was found that finasteride (the hyperplasia
inhibitor) helped men with considerable prostate gland enlargement, but not
those with more normal-sized prostate glands. Interestingly, saw palmetto
berry and nettle root similarly inhibit 5-alpha reductase, and are just as
effective as finasteride. Though often beneficial in BPH, neither saw
palmetto berry nor finasteride prevent prostate cancer.
Terazosin (the smooth-muscle relaxer) helped men with less gland
enlargement, but not men with larger prostate glands. None of these
treatments recognise the true importance of sex hormones that underlie the
cause of BPH.
The Role of Sex Hormones
Conventional medicine is beginning to recognise the true role of sex
hormones in prostate disease. For example, like a woman, a man’s body fat
will convert male hormones into oestrogen. Some physicians advocate using
aromatase-inhibiting drugs (such as Arimidex) that inhibit the conversion of
adrenal generated androstenedione (a male hormone) into oestrone (an
oestrogen) in body fat. Oestrone is then available to be converted to
oestradiol. The rationale for this treatment is the understanding that
oestrogen is a growth-stimulating hormone in prostate tissue. This leads us
to the hypothesis that the balance of oestradiol to progesterone and/or to
testosterone is an important factor in prostate disease.
As men age, prostate levels of oestradiol gradually rise, and levels of
progesterone and testosterone decline. The decline in testosterone and
progesterone levels is greater than the rise of oestradiol. The ratio of
testosterone to oestradiol (T/B2), for instance, is dramatically lower in
men over 60 than it is at age 40. Studies in the U.S., Germany and Japan
have reached similar conclusions: not only is the T/E2 ratio lower in men
after age 40, but also those men with the lowest T/E2 ratio are the ones
most likely to develop BPH. Conventional medicine, stuck in the outdated and
unfounded paradigm that claims testosterone is dangerous, opts to attack and
destroy oestrogen production rather than supplement testosterone in their
effort to raise the T/E2 ratio and protect men against prostate disease. Why
not raise the low testosterone levels by supplementing physiological doses
of testosterone to restore the ratio of T/B2 to that of younger men? There
is no evidence that the high levels of testosterone in young men puts them
at any risk of BPH. Or of prostate cancer, for that matter.
Progesterone plays several roles in the protection against prostate disease.
Progesterone, like finasteride and saw palmetto berry, inhibits 5-alpha
reductase, thus inhibiting the conversion of testosterone to DHT. In this
manner, progesterone helps raise testosterone levels, and helps lower the
level of the more growth stimulating DHT. Progesterone, like testosterone,
is an anabolic hormone, meaning that it helps burn fat for energy. Thus, it
helps keep men from becoming obese. With less body fat, there is less
endogenous (within the body) oestrone production. Further, both progesterone
and testosterone stimulate gene p55, the product of which protects us from
the oncogene (cancer-causing) Bc1-2, and stimulates healthy apoptosis
(normal cell death). Oestradiol, on the other hand, stimulates Bc1-2
production, which increases the risk of cancer. These are all good reasons
to restore the same progesterone and testosterone levels that younger men
Restoring Hormone Balance
Restoring proper hormone levels is not difficult. The best place to begin is
with a saliva hormone test, so that you have clinical evidence of a hormone
imbalance. Saliva hormone testing reflects the total blood levels of
non-protein-bound (“free”) sex hormones. The free hormone is bioavailable
and filters into saliva, whereas the protein-bound (non-bioavailable)
hormones do not. Conventional blood serum tests of oestradiol, for example,
are essentially irrelevant since they do not distinguish between free and
protein-bound oestradiol. I usually recommend ZRT Lab in Oregon; you can
order a kit through their Web site www.salivatest. com, or you can call them
at (503) 466-2445. You do not need a doctor’s prescription to get a saliva
hormone test, although I do recommend that you work with a qualified health
professional to help interpret the results.
The ratio of saliva progesterone to oestradiol in healthy young men is
usually greater than 200:1. Similarly, the ratio of saliva testosterone to
oestradiol is also about 200 to 300:1. These ratios can be used as a
guideline for the transdermal supplementation of progesterone and
testosterone in older men with E2 dominance and low P/E2 and T/E2 ratios.
>From experience, we have found that just 6 to 8 mg per day of progesterone
(in a cream) will raise low saliva progesterone levels to normal healthy
levels. In a two-ounce jar or tube of cream containing 960 mg of
progesterone, this would be a bit less than 1/8 tsp of cream daily, and it
would last for about 140 days, or about four and a half months.
Testosterone, being a stronger hormone, usually requires just l to 2 mg per
day by transdermal cream to raise low levels to healthy normal levels.
Creams with the proper testosterone content are not readily available, so a
patient with BPH should ask his doctor to write a prescription for the
cream, then take it to a compounding pharmacist. It is essential that the
pharmacist use real testosterone, and not one of the synthetic versions such
as methyl testosterone.
I have seen remarkable benefits and no side effects in men who use hormones
this way. The low doses used attest to the excellent absorption of these
hormones when applied transdermally. As an interesting aside, in a recent
study of women with low free testosterone levels (in women after removal of
their ovaries), the researchers found that the optimal dose of transdermal
testosterone for them was just 0.25 mg per day.
Defence Against Prostate Cancer
Research has shown that BPH is not a risk factor for prostate cancer.
Nevertheless, defence against prostate cancer follows the same precepts. Men
with aggressive prostate cancer have higher numbers of progesterone
receptors (PRs), relative to men with less aggressive cancer. This does not
mean that progesterone increases the aggressiveness of prostate cancer.
Progesterone receptors are made only by oestrogen. An increase of PRs in
prostate tissue is a sign of oestradiol dominance (relative progesterone
deficiency). In other studies it is found that prostate cancer incidence is
greater in men with lower T/E2 ratios (lower testosterone and higher E2
levels) than in men with higher T/E2 ratios.
Conventional medicine’s fear of testosterone is unfounded. In clinics that
routinely treat men with even higher doses of testosterone, the incidence of
prostate cancer is usually less than in men without supplemental
testosterone. While it is true that, in 1941, Dr. Huggins claimed to have
demonstrated that castration (removal of testes) in men with prostate cancer
delayed death (a bit) from their cancer, it does not mean that testosterone
reduction was the cause of this observed benefit. Dr. Huggins forgot that
the testes also supply oestrogen. It is far more likely that the oestrogen
reduction was the source of the benefit. Since that time, it is now clear
that total androgen blockade does not enhance longevity compared to men
without total androgen blockade. It is time to recognise that progesterone
and testosterone are important hormones in men, ant that normal
physiological levels of these hormones do not increase the risk of prostate
cancer but, on the other hand, may help prevent prostate cancer.
Some research indicates that BPH and prostate cancer correlate with higher
levels of sex hormone binding globulin (SHBG). As a result, some have
hypothesised that SHBG may play a role in the cause of BPH and of prostate
cancer. SHBG is the binding hormone for oestradiol. Excessive levels of
oestradiol activate the liver to make more SHBG. Thus, it is likely that the
elevated SHBG is merely a marker for excessive oestradiol. Observations are
one thing, but the conclusions that one draws from them are quite something
else. Conclusions often follow underlying assumptions that may be erroneous,
and are subject to observer bias.
Xenoestrogen (petrochemical toxins often used as pesticides, etc.) exposure
during embryo life may damage gonadal and prostate tissue, making these
tissues more susceptible to carcinogens later in life. Although one can’t
change these circumstances, one can take preventive steps to reduce
oestrogen levels and maintain hormone balance. Our new book, What Your
Doctor May Not Tell You About Breast Cancer, goes into some detail about how
to avoid xenoestrogens.
Some Non-Drug Treatments for BPH
Certain botanicals have been found to be of benefit in treating prostate
disease though their mechanisms of action are still unclear. These
botanicals, and a few others like them, deserve further research. Many
products for the prostate found at health food stores contain various
combinations of these ingredients.
€ Saw Palmetto berry extract, according to Jonathan Wright, M.D., not only
inhibits 5 alpha-reductase but also blocks DHT binding to prostatic androgen
receptors, reduces prostatic oedema (swelling), inhibits oestradiol and
antagonises alpha-adrenergic receptors.
€ Nettle root (may inhibit aromatase, reducing conversion of androgens to
€ Antioxidants, such as vitamin E, lycopene (found in cooked tomatoes), and
€ Polyphenole (e.g., catechins, found in green tea.)
€ Ellagic acid (found in nuts and raspberries) may trigger beneficial
€ Zinc (low zinc levels correlate with increased prostate disease). Be sure
to get extra copper if you’re taking zinc for longer than a few weeks.
€ NATURAL Progesterone Therapy to bring about correct hormonal balance is essential.