07/04/2003 - Articles

Low Testosterone Levels Linked to Atherosclerosis

By: Robert W. Griffith, MD

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Introduction

Men get cardiovascular disease (CVD) more often than women, and this has been blamed on the male sex hormone testosterone. Although women have more CVD after the menopause than before it, suggesting a protective influence of female hormones such as estrogen, CVD is still more common in men than in post-menopausal women of the same age.

It's been shown, however, that testosterone may have a good effect on other cardiac risk factors; for instance, low testosterone is linked with high levels of insulin, something that's seen in CVD. Men with low testosterone levels are often more obese, have raised blood pressure and blood glucose levels, as well as raised cholesterol levels. And there's some evidence that low testosterone is associated with an increased risk of CVD and stroke.

Scientists in Japan have now reported their results of comparing serum testosterone levels and signs of atherosclerosis in the carotid arteries of men with diabetes - people who have an increased risk of CVD. The findings in carotid arteries mirror those in other blood vessels, such as the coronary arteries in the heart. This is a summary of their report.

What was done

The investigators measured serum testosterone levels in 254 men who had type 2 diabetes. In 154 of them, carotid artery ultrasound examinations were done to measure how much atherosclerosis was present. All the volunteers had a battery of tests done to assess the severity of their diabetes and their cardiovascular risk factors.

What was found

Low serum testosterone levels were found to be linked with carotid artery atherosclerosis. In addition, links were found with their age, BMI (as a measure of overweight), the duration of their diabetes, and some lipid levels. However, low testosterone was associated with raised total cholesterol levels.

An additional analysis showed that the testosterone link to atherosclerosis was present whatever the blood pressure was.

Comment

Just how low were the testosterone levels in these men? The average was about 10 pg/mL (picograms per milliliter of 'free' or available testosterone). The range in normal men is 14 to 40 pg/mL, so the hormone was clearly reduced in the diabetics. Lower levels were linked to more advanced atherosclerosis in the carotid arteries, although there was no link to the severity of small blood vessel changes often seen in a diabetic's retina or kidneys.

Free testosterone levels below 10 pg/mL in men with symptoms of weakened sexual development (hypogonadism) are generally treated by testosterone replacement therapy. Roughly half the men in this study had levels below this threshold point. Should they receive testosterone replacement? This is still open to question. There still isn't enough good evidence to show that a low testosterone is associated with an increased risk of a heart attack or stroke.

Prescription sales of testosterone have been growing in the USA at an alarming rate - they're 17 times what they were 10 years ago. We've discussed possible reasons for this growth in other articles - see the links below. And there's probably quite a 'black market' in hormone use by body-builders.

It would be wrong, at this stage, to encourage widespread use of testosterone replacement therapy. The side effects can include: sodium and water retention, elevated blood pressure, increased total cholesterol, liver problems (cysts or tumors), and blood clotting problems. Some people may have emotional and behavioral changes, including irritability, aggressiveness, depression, and mood swings.

However, the findings from this and other studies mean that it's time to do some well-planned and well-conducted clinical trials of testosterone replacement therapy in men at risk of heart attack and stroke who have levels of the hormone well below normal.

Source

Association between serum testosterone concentration and carotid atherosclerosis in men with type 2 diabetes.
M. Fukui, Y. Kitagawa, N. Nakamura,  et al., Diabetes Care, 2003, vol. 26, pp. 1869--1873

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Created on: 06/16/2003
Reviewed on: 07/04/2003

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