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Hair Loss Guide, References & Glossary
Finasteride,
Dutasteride & Gynecomastia
This is
not a medical report. Its information is presented by non medical
personnel. Any drug program should be discussed with your physician or
endocronologist!
Gyno is short for
gynecomastia (male breast tissue formation!)
5 alpha reductase (5AR)
such as Finasteride (Proscar/Propecia) and dutasteride (Avodart) have
been shown to increase both testosterone and estrogen while lowering
serum levels of DHT. Some suggested that this increase in estrogen may
compromise its effectiveness in treating hair loss. More importantly,
the increase in estrogen creates side effect called Gynecomastia or
breast enlargement in some men, along with increased body fat and loss
of libido.
Based on discussions
from forum members, the best way to counter gynecomastia is with:
a) Arimidex (Anastrazole) - Estrogen blocker
b) Super Miraforte (natural Estrogen Blocker)
"This combination
reduces excess estrogen, raises free testosterone, and potentiates the
hair growth effects of 5-alpha-reductase inhibitors. It also increases
libido and reduces body fat, both potential problematic areas of concern
for those using Propecia alone."
As for Arimidex dosage,
some forum members recommend half a tablet twice per week. It is as
"safe" a drug as you can get as ".
"If all of the
above fail to increase free testosterone and lower excess estradiol,
then ask your doctor to prescribe the potent aromatase inhibiting drug
Arimidex (anastrozole) in the very low dose of one-half (0.5 mg) mg,
twice a week. Arimidex is prescribed to breast cancer patients at the
dose of 1 to 10 mg a day. Even at the high dose prescribed to cancer
patients, side effects are rare. In the minute dose of 0.5 mg twice a
week, a man will see an immediate drop in estradiol levels and should
experience a rise in free testosterone to the optimal range."
(source: http://www.lef.org/protocols/prtcl-130cold.shtml)
Final note: Normal
Estradiol range for a male is 15-30 pg/ml. High Estrogen levels in males
(above 30 pg/ml) blocks the production and effect of testosterone
throughout the body, dampens sexuality, and increases the risk of
prostate and cardiovascular disease.
Also note that these
reference ranges indicate that it can be normal for a man to have no
estrogen. The fact that most aging men have too much estrogen does not
mean it is acceptable for a man to have NO (or virtually no) estrogen.
Estrogen is used by men to maintain bone density and abnormally low
estrogen levels may increase the risk for prostate cancer and
osteoporosis."
 Gynecomastia discussion from the
archives
Study which shows
that "Gynecomastia produced by Propecia is transient and disappears
if the treatment is discontinued."
Click here.
UNILATERAL
GYNECOMASTIA INDUCED BY 1 mg ORAL FINASTERIDE. REPORT OF 3 CASES
1Ferrando J, 1Grimalt R, 1Alsina M, 1Bulla F, 2Manasievska E. Depts. of
Dermatology. 1Hospital Clínic. University of Barcelona. Spain. 2Centro
Medicinal Kumanovo. University of Skopje. Macedonia.
Since 1998 1 mg oral finasteride (PropeciaTM) has been widely used for
treament of male androgenic alopecia (MAGA). Side effects have been
described in less than 2% of cases (transitory impotence, libido
decrease or ejaculation disorder) and they did not imply treatment
discontinuation. Five clinical trials submitted by Merck to the FDA
refer those data, but only quoted a “breast enlargement and
sensitivity, occasionally reported”. We had the opportunity to observe
painful unilateral gynecomastia in three males under 1 mg oral
finasteride regimen.
Three males aged 18 to 29 with grades II to IV of the Hamilton/Norwood
classification developed unilateral gynecomastia after 2 to 6 months on
treatment with 1 mg oral finasteride (one case with ProscarTM, 1/5 of
tablet per day, two cases with PropeciaTM). In two cases the diagnosis
was confirmed by mamography and in the third case by aspiration-biopsy.
In all cases gynecomastia disappeared between 2 to 6 months after the
treatment was discontinued.
Five mg oral finasteride (ProscarTM) used for treatment of benign
prostatic hypertrophy can produce gynecomastia, so it would not be rare
to find that effect with PropeciaTM. Gynecomastia is mainly caused by
alterations of estrogen/androgen ratio. Finasteride decreases
circulating dihydrotestosterone levels, increasing serum estradiol, so
it could produce gynecomastia.Gynecomastia produced by PropeciaTM is
transient and disapears if the treatment is discontinued.
Pathogenesis and diagnosis of gynecomastia -
by Dr. Braunstein
DEFINITION — Gynecomastia is defined histologically as a benign
proliferation of the glandular tissue of the male breast and clinically by
the presence of a rubbery or firm mass extending concentrically from the
nipple(s). Fat deposition without glandular proliferation is termed
pseudogynecomastia (often seen in obese men). These two entities may be
distinguished by having the patient lie on his back with his hands behind
his head. The examiner then places his or her thumb and forefinger on each
side of the breast, and slowly brings them together.
In true gynecomastia, a ridge of glandular tissue will be felt that is
reasonably symmetrical to the nipple-areolar complex.
In pseudogynecomastia, the fingers will not meet any resistance until they
reach the nipple.
Gynecomastia can usually be detected when the size of the glandular tissue
exceeds 0.5 cm in diameter.
The most important differentiation is between gynecomastia and breast
carcinoma. Carcinoma is much less common, is generally unilateral, is
eccentric in location rather than symmetrical to the nipple, is hard or
firm, and may be associated with skin dimpling, nipple retraction or
discharge, and axillary lymphadenopathy [3]. Less common conditions
leading to breast enlargement include neurofibromas, lymphangiomas,
hematomas, lipomas, and dermoid cysts.
Physical examination method to distinguish gynecomastia, due to
enlargement of the glandular tissue, from pseudogynecomastia, due to
excessive adipose tissue. The thumb and forefinger are placed on opposite
sides of the breast and slowly brought together towards the areolar-nipple
complex. Gynecomastia is appreciated as a concentric, rubbery-to-firm disk
of tissue, often mobile, located directly beneath the areolar area.
Pseudogynecomastia presents no discrete mass, and other masses due to
disorders such as cancer tend to be eccentrically positioned. Adapted from
Braunstein, GD, Hosp Pract 1993; 28:37. See graphic illustration at
HairSite forum.
Drugs commonly associated with Gynecomastia
Gynecomasty: histological aspects in a surgical material
TI - Gynecomasty: histological aspects in a surgical material.
AU - Andersen JA; Gram JB
SO - Acta Pathol Microbiol Immunol Scand [A] 1982 May;90(3):185-90.
In a consecutive and unselected series of 83 patients operated upon for
gynecomasty, the histological and related clinical aspects were studied.
It was convincingly demonstrated that gynecomasty begins in an active
proliferating phase and ends in a fibrous inactive phase. Contrary to
previous authors we found it justified that the formation of lobules,
indistinguishable from what is seen in the reproduceable age in the female
breast, is not necessarily related to the administration of exogenic
hormones. In five (6.5%) cases, typical multicentric foci of intraductal
epithelial hyperplasia were demonstrated--of the atypical hyperplastic or
early intraductal carcinoma type. It was concluded that the clinical
significance of such morphological changes must not be overestimated.
PMID- 6285666
Detailed Arimidex and Gynecomastia
information,
click here.
Arimidex and Gyno info
Here's the Arimidex summary from the archives:
Arimidex general info
http://www.hairsite7.com/m563finas17/_disc563/0000019f.htm
http://www.hairsite7.com/m563finas17/_disc563/0000018d.htm
http://www.hairsite7.com/m563finas17/_disc563/000001ae.htm
1)Arimidex is not an estroten blocker but an aromatase inhibitor
http://www.hairsite7.com/m574dutas24/_disc574/0000004a.htm
2) Quick reference on a good Arimidex dosage, +
arimidex is BETTER than nolvadex:
http://www.hairsite7.com/m563finas17/_disc563/00000001.htm
http://www.hairsite8.com/m572ru16/_disc572/0000029b.htm
http://www.hairsite7.com/m563finas17/_disc563/00000225.htm
3) Reference with good overview and commentary
http://www.hairsite7.com/m563finas17/_disc563/00000003.htm
http://www.hairsite7.com/m563finas17/_disc563/00000005.htm
4) Posts against using Arimidex
http://www.hairsite7.com/m563finas17/_disc563/00000008.htm
4a) Bryan's analysis: caution against using
arimidex because of beneficial role of estrogen in mpb:
http://www.hairsite8.com/m572ru16/_disc572/000002e4.htm
5) Why Arimidex works
http://www.hairsite7.com/m563finas17/_disc563/0000001f.htm
http://www.hairsite7.com/m563finas17/_disc563/00000132.htm
6) Posters who said Arimidex doesn't work:
http://www.hairsite7.com/m563finas17/_disc563/00000007.htm
http://www.hairsite7.com/m563finas17/_disc563/00000250.htm
http://www.hairsite7.com/m581finas18/_disc581/0000001f.htm
http://www.hairsite7.com/m581finas18/_disc581/00000058.htm
7) Posters who said Arimidex / Liquidex works
http://www.hairsite7.com/m567dutas23/_disc567/000001ae.htm
http://www.hairsite7.com/m563finas17/_disc563/0000000f.htm
http://www.hairsite7.com/m563finas17/_disc563/0000001c.htm
http://www.hairsite7.com/m563finas17/_disc563/00000167.htm
http://www.hairsite7.com/m563finas17/_disc563/000001bf.htm
http://www.hairsite7.com/m563finas17/_disc563/000001ce.htm
http://www.hairsite7.com/m563finas17/_disc563/00000188.htm
http://www.hairsite7.com/m563finas17/_disc563/000001ca.htm
http://www.hairsite7.com/m563finas17/_disc563/00000072.htm
http://www.hairsite8.com/m572ru16/_disc572/00000295.htm
http://www.hairsite7.com/m563finas17/_disc563/0000025e.htm
(not hair related results)
7a) Arimidex shedding
http://www.hairsite7.com/m581finas18/_disc581/00000044.htm
8) Availability
WWW.HAIRLOSSDRUGS.8M.COM
http://www.hairsite7.com/m563finas17/_disc563/00000091.htm
http://www.hairsite7.com/m563finas17/_disc563/0000013c.htm
http://www.rxworld.com
http://www.syntholdirect.com
(liquidex)
http://www.pumpnpose.com/
www.valuepharmaceuticals.com
http://www.hairsite7.com/m581finas18/_disc581/0000001d.htm
9) Arimidex / liquidex Side effects
http://www.hairsite7.com/m563finas17/_disc563/00000194.htm
(side effects for women only)
http://shop.valuepharmaceuticals.com/public/med_info/arimidex.htm
http://www.hairsite7.com/m563finas17/_disc563/000001ae.htm
http://www.hairsite7.com/m563finas17/_disc563/0000012e.htm
http://www.hairsite7.com/m563finas17/_disc563/00000131.htm
http://www.hairsite7.com/m563finas17/_disc563/00000132.htm
http://www.hairsite7.com/m563finas17/_disc563/00000133.htm
http://www.hairsite7.com/m563finas17/_disc563/000001bf.htm
http://www.hairsite7.com/m563finas17/_disc563/000001af.htm
http://www.hairsite7.com/m563finas17/_disc563/00000072.htm
10) Liquidex vs Arimidex
http://www.hairsite7.com/m563finas17/_disc563/00000140.htm
11) Dosage reference: 1/2 tablet (0.25mg) twice a
week
http://www.hairsite8.com/m572ru16/_disc572/0000029b.htm
http://www.hairsite7.com/m581finas18/_disc581/00000004.htm
http://www.hairsite7.com/m581finas18/_disc581/00000005.htm
http://www.hairsite7.com/m574dutas24/_disc574/00000046.htm
12)Alternative to Arimidex - Clomid: Follow this
thread
http://www.hairsite4.com/dcforum/DCForumID5/1212.html
OTHER INFO:
Excerpts from Mesomorphosis.com
http://www.mesomorphosis.com/articles/pharmacology/
anti-aromatases-versus-estrogen-antagonists.htm
What does "anti-estrogen" mean? How are anti-estrogens like
Cytadren, Clomid, and Nolvadex different from each other? Is Proviron an
anabolic steroid, or not?
Anti-estrogens are drugs which act to reduce estrogenic activity in the
body. This can be done either by reducing the amount of estrogen, or by
reducing the activity of whatever estrogen is present.
Competitive aromatase inhibitors, such as Cytadren, Arimidex, and
probably Proviron, bind to the same binding site on the aromatase enzyme
that testosterone does. By doing this, they allow less testosterone to
bind to aromatase. So, less testosterone is converted to estradiol
(estrogen).
Here’s an important thing: the effectiveness of competitive inhibitors
decreases as the amount of the normal substrate increases. Suppose that
you had equal amounts of inhibitor and normal substrate in the blood,
and they bound to the enzyme equally well. Then the inhibitor would at
any moment be taking up half the sites that the normal substrate
otherwise would, so it would reduce conversion rate by 50%. But if the
amount of substrate is increased 10 times while the amount of inhibitor
remains the same, then the inhibitor would be outcompeted by the more
numerous substrate molecules. It would therefore be rather ineffective.
For example, with more testosterone molecules available, and similar
binding strengths, the enzyme will mostly bind testosterone. It will
then mostly be working to produce estrogen. To obtain the 50% reduction
we had before, then the amount of inhibitor would also have to be
increased 10 times.
To be really effective, the inhibitor must either be present in higher
concentration than the normal substrate, or must bind more tightly.
With Cytadren or Proviron, it takes quite a lot of inhibitor to
outcompete high testosterone levels. With Arimidex, rather little, even
1 mg/day, can be sufficient because it binds so strongly.
The other general approach is estrogen receptor antagonism. If a
molecule binds strongly to a hormone receptor, but does not activate
that receptor and makes it unresponsive to the normal hormone, then it
is a receptor antagonist. Clomid (clomiphene) and Nolvadex (tamoxifen)
follow this approach. These drugs are very similar structurally. They
are both what are called triphenylethylenes, and are not steroids. The
differences are relatively minor, but seem to affect an important
characteristic of these compounds: drug metabolism.
Both tamoxifen and clomiphene are metabolized to other related compounds
which can be estrogenic or anti-estrogenic. Both act as estrogens in
bone tissue, perhaps after metabolism, which is a very useful property
for female patients, for whom these drugs are usually intended.
(Otherwise, an anti-estrogen could lead to osteoporosis.) Tamoxifen
seems particularly prone to acting as an estrogen in the liver, which
may account for reduced IGF-1 levels seen when this drug is taken.
Users generally seem to agree that when tamoxifen is used, gains are a
little less than what otherwise would be expected. (Let’s not take
this too far though: many people have made great gains while using
tamoxifen as an anti-estrogen. And it’s always hard to say what
"would" have been the case if a drug had not been included.)
I’ve heard nothing but good about clomiphene, though.
Proviron, an anabolic steroid, is particularly interesting. I suspect
that it not only acts as an antiaromatase but in an unknown DHT-like
anti-estrogenic manner. This might involve estrogen receptor
downregulation for example. In any case, aromatase inhibition and/or
Clomid don’t seem to give the same effect on appearance and muscle
hardness as when Proviron is included.
How much of these agents is needed for effective estrogen suppression?
Again, it depends on the dose of anabolic/androgenic steroids (AAS) and
it depends what type of AAS is being used.
With Primobolan or trenbolone there is no need for these drugs.
With nandrolone, an aromatase inhibitor will be of no use, because
aromatase is not used in the aromatization of nandrolone. A rather small
amount of estrogen receptor antagonist can be useful. 12.5 to 25 mg
Clomid would be plenty for 400 mg/week Deca.
With testosterone, stacking of an aromatase inhibitor and an estrogen
receptor antagonist will give the best results. Cytadren use should not
exceed 250 mg/day in my opinion. This alone would not be sufficient for
say 1 g/week or more of testosterone. With such a dose, ideally one
would add in 50 mg/day Clomid. Proviron at 100 mg/day could substitute
for the Cytadren. Or Cytadren and Proviron can be used in combination,
125/50 or higher, together with 50 mg/day Clomid.
For lower doses of testosterone, proportionally less antiestrogens can
be used.
Arimidex is very effective but extremely expensive. 1 mg/day of this is
at least as effective as 250 mg/day Cytadren. If a milligram per day
cannot be afforded, use of half a milligram would allow Cytadren use to
be cut in half, which may be desirable.
How does Clomid "stimulate" testosterone production at the end
of the cycle?
It really doesn’t. Rather, by acting as an estrogen receptor
antagonist, it reduces the inhibition that results from elevated
estradiol levels. This helps return LH to normal levels, which helps
testosterone to return to normal levels (if the testicles have not
atrophied).
How does hCG help?
Acts as an LH receptor agonist, thus substituing for LH. It does nothing
to help the hypothalamus and pituitary. Thus, it can be effective during
the cycle to help avoid testicular atrophy, but is not best used in the
taper when one is attempting to restore LH production. Increases in
natural testosterone, stimulated by the hCG, will act to inhibit LH
production. Thus, you can see where hCG use is counterproductive in the
taper itself.
Can Clomid, taken throughout a cycle, completely eliminate inhibition?
I do not believe so. There is also androgenic inhibition mediated by the
androgen receptor, which has nothing to do with the estrogen receptor.
Androgenic inhibition is unavoidable and cannot be helped by estrogen
receptor antagonists. However, use of Clomid throughout a cycle can
definitely reduce the degree of the inhibition and allow a speedier
recovery at the end of the cycle.
Is it safe to take Clomid for so many weeks? I heard it should only be
taken for 2 weeks.
The two week idea comes from the fact that medically its main use is to
help women with fertility problems. Because of the menstrual cycle,
there are only certain times of the month when there is any chance of
ovulation. It is pointless, then, for these women to take the drug for
more than two weeks at a time. Some have misconstrued this to apply to
males.
Men have taken the drug in clinical studies for a year continuously. It
is a rather safe drug.
Why do you say not to use more than 250 mg/day of Cytadren?
Cytadren has two main therapeutic activities. At high doses, such as a
gram per day, it is a very effective inhibitor of the enzyme desmolase,
which is required for all steroid production, and is rate limiting for
the production of cortisol. So the drug is very useful for treating
patients with Cushing’s Syndrome, who produce abnormally high levels
of cortisol.
It is also an inhibitor of aromatase, and it is a better aromatase
inhibitor than a desmolase inhibitor. About 250 mg/day is sufficient for
fairly good inhibition of aromatase, resulting in only fairly low levels
of desmolase inhibition.
As dosage increases, aromatase inhibition does not improve much, but
desmolase inhibition increases greatly.
Even at 250 mg day, there is still significant desmolase inhibition.
Other side effects, such as lethargy, may bother some individuals even
at this dose.
Why is desmolase inhibition bad? I have read that cortisol is the enemy
of our muscles, and we want to reduce it.
Those articles are written by people trying to sell you alleged cortisol-reducing
supplements.
While abnormally high levels of cortisol are indeed muscle wasting,
abnormally low levels of cortisol do not result in extra muscle growth,
and cause joint problems.
You’ve talked about tapering off Cytadren. Why?
There is a feedback mechanism for production of cortisol. Low levels of
cortisol enhance release of corticotropin releasing hormone from the
hypothalamus, and ACTH from the pituitary. Both will result in higher
production of cortisol.
So moderate inhibition of desmolase will temporarily reduce cortisol,
but soon it will be back to normal as this feedback mechanism
compensates.
If you then suddenly discontinue the drug, then these elevated ACTH
levels will result in abnormally high cortisol for a time, until the
body adjusts again. This can be avoided simply by tapering down over
about a week.
Should Cytadren be taken all at once, or in divided doses?
Because the half life is only 6 or 8 hours, if the drug is taken only
once, then through part of the day there will be little drug in the
system, and little anti-aromatase activity.
I think the best approach is to use half the dose on arising (or an hour
or two afterwards) to get blood levels from a somewhat low level up to
the desired maintenance level. This would then be followed by quarters
of the dose at 7 or 8 hour intervals twice after that.
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