Statin Drugs Markedly Inhibit Testosterone Production

[Excel Male]

View attachment 532


Statin Drugs Markedly Inhibit Testosterone Production by Rat Leydig Cells in Vitro: Implications for Men

Reproductive Toxicology
Available online 22 January 2014

Highlights

•Statins cause significant reductions in LH-stimulated testosterone production by rat Leydig cells; possible human relevance.

•Statin induced inhibition in testosterone production was bypassed by providing pregnenolone or progesterone.

•Bypassing the site of action with pregnenolone resulted in greater LH stimulated testosterone production than progesterone.

•LH responsiveness of Leydig cells was only maintained when progesterone was used to bypass the site of action.

Abstract

Statin drugs lower blood cholesterol by inhibiting hepatic 3-hydroxy-3-methylglutaryl-Coenzyme-A reductase. Statins are known to inhibit sterol production in the testis, but effect of statins on testosterone production has not been studied critically in vitro and clinical data are controversial. We measured 18-hour testosterone production in vitro, using highly purified rat Leydig cells exposed to atorvastatin, mevastatin, or simvastatin and also determined if statin-induced inhibition of testosterone production could be bypassed with substrate distal to cholesterol. Statins had no effect on testosterone production during culture without LH. However, with 10 ng/mL LH, testosterone production was 12-fold higher and markedly inhibited (-40%) by statin. Leydig cells provided sub-saturating pregnenolone or progesterone to bypass the site of statin action, maintained LH-stimulated testosterone production at or above amounts observed with LH stimulation and no statin. Pregnenolone resulted in greater testosterone production, but LH responsiveness was lost. With progesterone, LH responsiveness was maintained.

 

[jonathanb]

My cholesterol has been running high for most of my life on HIV meds. I don't know if it is the meds, my diet, or just a family history issue. After reading about how these cholesterol lowering drugs affect testosterone and the depletion of CoQ10, I quit taking the medication. I honestly don't know if I am doing the right thing .. I watch what I eat and eat plenty of good fats ..olive oil, avacados, walnuts, fish etc.. my cholesterol always is 230+ and I can't seem to get it below 200 .. any suggestions on what I am doing wrong? I don't drink, nor do I smoke. I exercise regularly and I am in good muscular condition .. I also take testosterone injections 1cc a week. Still I have unaccomplished erections .. and libido is poor.

 

[Nelson Vergel]

If you are on efavirenz or a protease inhibitor switch to an integrase to improve your lipids.

 

[JohnnyQuest]

I have recently learned that my testosterone level was 163. I'm 50, and have been on 10mg Crestor for a few years. I'm wondering if it is the reason for the drop. I have an appointment with an endocrinologist in March.
In the meantime, I had 200 units of depo-testosterone injected, and 2 weeks later I retested, and I was still only at 179. So I got another shot but this time T 400 units. And a week later I started Androgel.

No major libido issues other than nowhere near my youth and could be a little better, but having testosterone levels below the average 85 year old man is very bothersome.

 

[Nelson Vergel]

The effects of statin treatment on adrenal and sexual function and nitric oxide levels in hypercholesterolemic male patients treated with a statin.
Baspnar O, et al. J Clin Lipidol. 2016 Nov - Dec.


Citation
J Clin Lipidol. 2016 Nov - Dec;10(6):1452-1461. doi: 10.1016/j.jacl.2016.09.004. Epub 2016 Sep 13.

Abstract

BACKGROUND: Erectile dysfunction complaints among men treated with a statin are not uncommon.

OBJECTIVES: To evaluate the effect of lowering low-density lipoprotein cholesterol (LDL-C) to target levels using varying doses of atorvastatin therapy in hypercholesterolemic male patients on adrenocortical hormones, sexual functions, and serum nitric oxide (NO) levels.

METHODS: Eleven hypercholesterolemic male patients who had LDL-C levels greater than 160 mg/dL were included in the study and 11 healthy male individuals served as controls. Following basal hormone measurements, 1-and 250-mcg adrenocorticotropic hormone stimulation tests were performed in both groups, and blood sampling was performed at 0, 30, and 60 minutes for the determination of blood levels of cortisol, total testosterone (TT), free testosterone (FT), 11-deoxycortisol, and dehydroepiandrostenedione. Depending on baseline LDL-C concentrations, atorvastatin therapy was given to patients with daily doses of 5 or 10 mg and the study procedures were repeated once patients reached risk stratified goal LDL-C levels. LDL-C values after treatment were classified into 3 groups as LDL-C > 160 mg/dL, LDL-C 100 to 130 mg/dL and LDL-C < 100 mg/dL. NO levels were measured at baseline and after statin therapy. Erectile function was assessed both objectively and subjectively by using penile somatosensory evoked potential (SEP) and the International Index of Erectile Function-5 Questionnaire, respectively, at 3 different LDL-C levels.

RESULTS: With regard to adrenocorticotropic hormone stimulation test (1 or 250 mcg) results, peak cortisol levels before and after statin treatment among 3 LDL-C groups and among controls did not differ significantly. However, peak TT and FT hormone levels decreased in conjunction with decreasing levels of LDL-C among the statin-treated patients, whereas dehydroepiandrostenedione and 11-11-deoxycortisol peak values did not change. N1 latency obtained during SEP, which is the first negative deflection, was prolonged with decreasing levels of LDL-C and a significant decrease in International Index of Erectile Function-5 scores were observed. When LDL-C levels of &#8805; 160 mg/dl was reduced to 100 to 130 mg/dl, maximal NO elevations were noted.

CONCLUSIONS: Our results suggest that decreased LDL-C levels caused by different doses of atorvastatin treatment did not associate with significant changes in adrenal hormone levels. In contrast, there was a significant relationship between attained LDL-C on statin therapy and TT and FT levels. Electrophysiologically, abnormal SEP responses obtained in the patient group with LDL-C levels below 100 indicate a negative impact on the integrity of the somatosensory pathway, which plays a role in erectile function. Reducing LDL-C with a statin was associated with both decreased testosterone levels and erectile dysfunction.

 

[Nelson Vergel]

Do statins affect erections in men?

 

[SoCal Guy]

Statins are not necessarily even good for what they're good for.

Statins stimulate atherosclerosis and heart failure: pharmacological mechanisms

tandfonline.com/doi/full/10.1586/17512433.2015.1011125

 

[Nelson Vergel]

Wow, SoCal...great paper! Scary indeed.

Figure 4. Comparison of skeletal muscle properties in the leg between statin users and statin non-users. As compared with non-users, statin users exhibited higher systolic blood pressure and elevated glycated hemoglobin (HbA1c) level. Levels of CoQ10, anti-peroxidative enzymes, uncoupling protein (UCP), Complex IV, and myosin were lower, oxidative phosphorylation ability was lower and glucose level in glucose tolerance test was higher




"Pharmacological evidence and clinical trial results support the interpretation that statins stimulate atherogenesis by suppressing vitamin K2 synthesis and thereby enhancing artery calcification. Statins cause heart failure by depleting the myocardium of CoQ10, & heme A' and selenoproteins, thereby impairing mitochondrial ATP production. In summary, statins are not only ineffective in preventing CHD events but instead are capable of increasing CHD and heart failure. Physicians who are involved in prescribing cholesterol-lowering medications cannot ignore the moral responsibility of informed consent'. Patients must be informed of all statin adverse effects, including the ability to cause CHD and heart failure, onset of diabetes mellitus, carcinogenicity, teratogenicity and central and peripheral nervous disorders besides the well-known rhabdomyolysis and hepatic injury. Most of these adverse effects of statins become apparent after 6 or more years of statin therapy. Chronic administration could ultimately lead to these statin adverse effects as pharmaceutical and biochemical research has now demonstrated."

 

[molonlabedoc]

I believe there are some growing concerns of statins and Cancers as well. Pun intended.

I would not put a hated and rich in law on them.

 

[Tommy Wall]

Just an input! I´m unfortunate guy since I suffer from Hypercholesterolemia, also called dyslipidemia.
I can basically drink water for weeks and still have high lipid values. My diet doesn´t make a lot of difference in values since my liver produces almost all of the Cholesterol etc.. there is no way in heaven I could lower my values more than some % without statins
I think my problem is really an absorbing problem.
Any way I been on statins since the early -90 and never had any problem. But I can´t really tell what could have been different since I been on Statins all the time.
I supply everyday with Q10.

 

[SoCal Guy]

Just an input! I´m unfortunate guy since I suffer from Hypercholesterolemia, also called dyslipidemia.
I can basically drink water for weeks and still have high lipid values. My diet doesn´t make a lot of difference in values since my liver produces almost all of the Cholesterol etc.. there is no way in heaven I could lower my values more than some % without statins
I think my problem is really an absorbing problem.
Any way I been on statins since the early -90 and never had any problem. But I can´t really tell what could have been different since I been on Statins all the time.
I supply everyday with Q10.

Cutting back on grains, sugars, and seed oils may improve your lipids.

 

[Nelson Vergel]

DO STATINS CAUSE TESTOSTERONE DEFICIENCY IN MEN? SYSTEMATIC REVIEW AND META ANALYSIS​