Not so fast.
What sounds great often isn't. For one thing, increasing LH also means increasing estrogen. I'll get back to this is a second.
Allow me to digress a bit into manipulating LH naturally.
The fact that LH secretion increases estrogen is the reason why tribulus was such a bust in older guys and those supressed from cycles. Yes, it slightly increased LH but if the body is unable to make enough testosterone, an increase in LH will send the T/e balance out of whack. There are natural supps that increase LH much better than trib (i.e. MyogenX) but that's why I suggest taking something along with it that increases "free testosterone." Of course I believe the best supp for that is "Unleashed" but you can also use the ingredients seperately. Using a natural free T booster along with a natural LH booster is not only a nice thing for "natties" but it can enhance a cycle as well.
Okay, back to HMG.
First off, by increasing LH, you need an anti e (which can hinder gains). Secondly, since HMG decreases cholesterol it may also decrease testosterone, since T is made form cholesterol. More e, less T. Ain't sounding so great now is it? Below is a study where the use of HMG killed libido in its subjects.
Maybe if you asked macro he'd tell you AF is coming out with a homebrew version of HMG made by god knows who with god knows what. Hell, if it's hot and people are interested there's money to be made. Fortunately not everybody operates that way.
Hate to be the bearer of bad news. But it's better than perpetuating harmful information or capitalizing on misinformation.
Br J Clin Pharmacol
58
:3 326–328 326 © 2004 Blackwell Publishing Ltd
British Journal of Clinical Pharmacology
DOI:10.1111/j.1365-2125.2004.02128.x
Is decreased libido associated with the use of
HMG-CoA-reductase inhibitors?
L. de Graaf, A. H. P. M. Brouwers
Eight patients were identified as having decreased libido during use of statins. In two
of these cases testosterone levels were determined and appeared to be decreased.
Conclusion
Decreased libido is a probable adverse drug reaction of HMG-CoA-reductase-inhibitors
and is reversible. The ADR may be caused by low serum testosterone levels, mainly
due to intracellular cholesterol depletion.
Introduction
Hydroxymethylglutaryl-coenzyme-A-reductase (HMGCoA-
reductase) inhibitors, or statins, are widely used
for the treatment of hypercholesterolaemia. The
most severe adverse drug reactions associated with
HMG-CoA-reductase inhibitors are myopathy and
disturbances in hepatic function. Meanwhile, there is
increasing evidence in the literature that sexual disorders
may also occur during therapy with these drugs
[1].
The Netherlands Pharmacovigilance Centre Lareb,
which maintains the spontaneous reporting system for
adverse drug reactions in the Netherlands, received
eight reports of decreased libido during the use of
statins.
Reports
Patient A is a 46-year-old male with symptomatic familial
hypercholesterolaemia (increased
a
lipoprotein),
with a serum cholesterol of 7.1 mmol l
-
). At this time his cholesterol level had
decreased to 5.9 mmol l
-
1
. Fluvastatin was withdrawn
and 5 days later testosterone had increased to
13.2 nmol l
-
1
(morning value). The patient’s libido had
also returned to normal. The man concomitantly used
aspirin 80 mg daily.
Patient B, a 54-year-old male, started treatment with
pravastatin for nonfamilial hypercholesterolaemia
(cholesterol 6.1 mmol l
-
1
). Within days after initiation
of this therapy, he experienced a decrease in his libido.
His testosterone level was determined at 5.8 nmol l
-
1
(morning value), while his total cholesterol level had
decreased to 4.5 mmol l
-
1
. Pravastatin was discontinued
7 months later, and after a few days his libido
returned to normal. Four months later, testosterone
level was determined again and had risen to
22.8 nmol l
-
1
(morning value). The patient used concomitantly
aspirin 80 mg daily, diltiazem 200 mg
daily, ramipril 1.25 mg daily and isosorbidemononitrate
60 mg daily.
Lareb received six more reports concerning a
decreased libido in association with the use of statins,
one of them concerning a woman (Table 1). In none of
the reports on men were testosterone levels determined.
In three cases the outcome is known: two patients recovered
after withdrawal of the suspected drug and one
recovered after switching to another HMG-CoAreductase
inhibitor.
Discussion
Libido is related to serum testosterone levels: lower
testosterone levels decrease male libido [2]. Testosterone
in males is produced mainly in the Leydig cells,
where cholesterol is the main substrate. The Leydig cells
can absorb cholesterol from the blood via the LDLreceptor,
but are also capable of
de novo
cholesterol
synthesis [3]. Statins may interfere with the synthesis of
testosterone in three ways.
First, by decreasing plasma LDL-cholesterol, HMGCoA-
reductase inhibitors lower the total amount of cholesterol
offered to the Leydig cell. Taking into account
the amount of cholesterol in the blood, it is unlikely that
this decrease will have a significant effect. In familial
hypercholesterolaemia (patient A), the LDL-receptor is
malfunctioning [4, 5], which makes the Leydig cell
more dependent on
de novo
synthesis of cholesterol.
Statins are rather liver selective, but are found in small
quantities in the testes, where they can inhibit the
de
novo
synthesis of cholesterol out of acetate by HMGCoA-
reductase [6].
Finally, high-dose simvastatin, and possibly other
statins, directly suppress testosterone synthesis by
inhibiting the 17-ketosteroid-oxidoreductase catalysed
conversion from dehydroepiandrosterone and dehydroandrostenedione
to androstenediol and testosterone,
respectively [7].
Since cholesterol is necessary for the synthesis of
testosterone, the effects of statins on testosterone levels
have been the subject of several investigations. Most of
these studies could not demonstrate a significant decrease
Table 1
Characteristics of reports of decreased libido in association with the use of HMG-CoA-reductase inhibitors in the Lareb database
of adverse drug reactions
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