Lipitor and other Statin Drugs Markedly Decrease Your Testosterone

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 ≥0.3 μM 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.

 

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.

 

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

 

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.

 

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

Authors
Baspınar O1, Bayram F2, Korkmaz S3, Aksu M4, Kocer D5, Dizdar OS6, Simsek Y2, Toth PP7.
Author information
1Department of Internal Medicine, Erciyes University Medical School, Kayseri, Turkey.
2Department of Endocrinology and Metabolism, Erciyes University Medical School, Kayseri, Turkey.
3Department of Neurology, Acıbadem University Medical Faculty, Acibadem Kayseri Hospital, Kayseri, Turkey.
4Department of Neurology, Erciyes University Medical School, Kayseri, Turkey.
5Department of Biochemistry, Kayseri Training and Research Hospital, Kayseri, Turkey.
6Department of Internal Medicine, Kayseri Training and Research Hospital, Kayseri, Turkey.
7Department of Preventive Cardiology, CGH Medical Center, Sterling, IL, USA; Ciccarone Center for the Prevention of Cardiovascular Disease, Johns Hopkins University School of Medicine, Baltimore, MD, USA. E
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 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.

 

Do statins affect erections in men?

 

Muscle Damage From Statins May Evade Blood Test

 

Strongest Statin-Diabetes Link Yet? Not so Fast, Say Some Experts

 

Nelson,

My dad took statins for 10+years. Is there any way to recover from them?

 

Nelson,

My dad took statins for 10+years. Is there any way to recover from them?

Unless he can control his lipids by weight loss, exercise and a good diet, it would be risky to get him off. But if he has to, taking 400 mg of coenzyme Q-10 and 200 mg selenium per day may be a good idea to improve his mitochondria.

I would have him check his testosterone blood level.

Full Paper:


http://tandfonline.com/doi/full/10.1586/17512433.2015.1011125



"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 CoQ1' 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.

 

Unless he can control his lipids by weight loss, exercise and a good diet, it would be risky to get him off. But if he has to, taking 400 mg of coenzyme Q-10 and 200 mg selenium per day may be a good idea to improve his mitochondria.

I would have him check his testosterone blood level.

Full Paper:


http://tandfonline.com/doi/full/10.1586/17512433.2015.1011125



"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, &#8216;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 &#8216;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.

I should have clarified, He quit the statins probably about a year ago, he was a complete zombie on them. He's recovered some of his cognitive function. He hits the gym 3-4 days a week, cardio and weight machines. He's 60yr old.

I've no doubt he has low T. Can only lead a horse to water though Nelson....

 

Shameless plug:

Buy him a certificate for $27.55 ($29 minus 5% off) to get a testosterone (free and total) test:


http://www.discountedlabs.com/giftcertificates.php

 

Shameless plug:

Buy him a certificate for $27.55 ($29 minus 5% off) to get a testosterone (free and total) test:


http://www.discountedlabs.com/giftcertificates.php

Thanks Nelson, Unfortunately, my closest labCorp is 6hrs away. He's had it tested before but he lets the doc get by with saying its "normal" He's never been given an actual number AFAIK.

 

Ive also read statin increases heart attack risk or something along those lines and even possibily diabetes.

 

Atorvastatin use is associated with decreased testosterone levels in type 2 diabetes men | ECE2023 | 25th European Congress of Endocrinology | Endocrine Abstracts

www.endocrine-abstracts.org

 

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 &#8805;12-fold higher and markedly inhibited (-40%) by &#8805;0.3 &#956;M 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.

The paper above is Klinefelter, G.R.; Laskey, J.W.; Amann, R.P. Statin drugs markedly inhibit testosterone production by rat Leydig cells in vitro: implications for men. Reprod Toxicol 2014, 45, 52-58, doi:10.1016/j.reprotox.2013.12.010

There are other peer-reviewed papers involving humans:
Stanworth, R.D.; Kapoor, D.; Channer, K.S.; Jones, T.H. Statin therapy is associated with lower total but not bioavailable or free testosterone in men with type 2 diabetes. Diabetes Care 2009, 32, 541-546, doi:10.2337/dc08-1183.

Corona, G.; Boddi, V.; Balercia, G.; Rastrelli, G.; De Vita, G.; Sforza, A.; Forti, G.; Mannucci, E.; Maggi, M. The effect of statin therapy on testosterone levels in subjects consulting for erectile dysfunction. J Sex Med 2010, 7, 1547-1556, doi:10.1111/j.1743-6109.2009.01698.x

In the Stanworth article, the abstract is shown below:
OBJECTIVE: There is a high prevalence of hypogonadism in men with type 2 diabetes. This will lead to an increase in assessments of hypogonadism. Statins could potentially decrease testosterone levels by reducing the availability of cholesterol for androgen synthesis. We compared testosterone levels and hypogonadal symptoms with statin use in a cross-sectional study of 355 men with type 2 diabetes. RESEARCH DESIGN AND METHODS: Total testosterone, sex hormone-binding globulin (SHBG), and estradiol were measured by an enzyme-linked immunosorbent assay. Bioavailable testosterone was measured by the modified ammonium sulfate precipitation method. Free testosterone was calculated using Vermeulen's formula. Symptoms of hypogonadism were assessed using the Androgen Deficiency in the Aging Male questionnaire. RESULTS: Statins were associated with lower total testosterone (11.9 vs. 13.4 nmol/l, P = 0.006) and a trend toward lower SHBG (29.4 vs. 35.3 nmol/l, P = 0.034) compared with no treatment.

11.9x 28.85= 343 ng/dl
13.4 x 28.85= 387 ng/dl

My comment inserted: This may be significant but doubt it has clinical relevance.
Bioavailable testosterone, free testosterone, estradiol, and hypogonadal symptoms were not affected. Subanalysis showed that atorvastatin was associated with reduced total testosterone (11.4 vs. 13.4 nmol/l, P = 0.006) and a trend toward reduced SHBG (27.6 vs. 35.3 nmol/l, P = 0.022) compared with no treatment, and there was an apparent dose-response effect with the lowest levels of total testosterone seen in men treated with >or=20 mg atorvastatin (9.6 nmol/l, P = 0.017). Simvastatin use was not associated with significant reductions in testosterone or SHBG levels. CONCLUSIONS: Assessing androgen status using total testosterone in men with type 2 diabetes treated with statins, particularly atorvastatin, may potentially lead to diagnostic error. Levels of bioavailable testosterone or free testosterone are recommended for the assessment of hypogonadism in this group if total testosterone levels are borderline.

I showed the calculations above and do not think these results would be noticeable by men on statins. The Stanworth article is attached.

 

Happened to me, my T dropped while on statins, which came with long term muscle damage, impaired exercise tolerance and liver signs and symptoms. This picture is too clear in my mind for this to be co-incidental as reason to discount statins being the cause.

The T did not rebound after discontinuing the statin which is why I started TRT.

N=1

 

For 40 years I have monitored serum testosterone using DPC equipment which is of high quality. I monitor my patients lipid status with a test that quantifies lipid fractions such as small LDL and large HDL as well as insulin resistance. Therefore, many of my patients wtih prostate cancer are on statins. Always use CoQ10 prior to initiating a statin. A dose of 300 mg/d is sufficient for most patients but if high dose of statins do not hesitate to go higher to 400 mg/d to prevent muscle cramps. Also, when starting a statin it is a must to check creatine kinase (CK) and LFTs (liver function tests) about 10-14 days after starting or ↑ the dose. It sounds like no one monitored you closely or treated you up-front with CoQ10. Let me know.

The file I attached in my prior email did not show a major drop in testosterone 2° statin treatment. The T not responding is bizarre. If you were carefully documented with baseline studies, your medical story justifies a case report in the peer-reviewed literature.

 

For 40 years I have monitored serum testosterone using DPC equipment which is of high quality. I monitor my patients lipid status with a test that quantifies lipid fractions such as small LDL and large HDL as well as insulin resistance. Therefore, many of my patients wtih prostate cancer are on statins. Always use CoQ10 prior to initiating a statin. A dose of 300 mg/d is sufficient for most patients but if high dose of statins do not hesitate to go higher to 400 mg/d to prevent muscle cramps. Also, when starting a statin it is a must to check creatine kinase (CK) and LFTs (liver function tests) about 10-14 days after starting or ↑ the dose. It sounds like no one monitored you closely or treated you up-front with CoQ10. Let me know.

The file I attached in my prior email did not show a major drop in testosterone 2° statin treatment. The T not responding is bizarre. If you were carefully documented with baseline studies, your medical story justifies a case report in the peer-reviewed literature.

I was monitored for liver enzymes at first. I discovered the possible cause for my symptoms while traveling and decided to stop taking lipitor. That was after a year taking it. AST, ALT and CPK were elevated three weeks after discontinuing, My cardiologist confirmed that my decision to stop the statin was the right thing to do.

MDs have varying outlooks on statin use and cholesterol lowering strategies, and varying opinions over it occur here frequently. You are in a tough room in this regard. Still, glad to have you here!