Obesity, a condition linked to heart disease and diabetes, now
appears to be associated with another health problem, but one that
affects men only—low testosterone levels.
Results of a study conducted by UB endocrinologists—and
published online ahead of print in the journal Diabetes
Care—showed that 40 percent of obese participants involved in
the Hypogonadism in Males (HIM) study had lower-than-normal
testosterone readings.
The percentage rose to 50 percent among obese men with diabetes.
Results also revealed that as body mass index (BMI)—a
relationship of weight–to-height—increased,
testosterone levels fell.
“The effect of diabetes on lowering testosterone levels
was similar to that of a weight gain of approximately 20
pounds,” says Sandeep Dhindsa, MD, an endocrinology
specialist in the Department of Medicine and first author on the
study.
“In view of the fact that almost one-third of the U.S. is
obese, these observations have profound pathophysiological,
clinical, epidemiological and public-health
implications.”
This is the largest analysis of the association between obesity
and low testosterone, and the first to compare prevalence of low
testosterone with obesity and diabetes separately and together. The
study shows that obesity and diabetes may exert independent
influences on testosterone concentrations.
“We published a report in 2004 on the high prevalence of
low testosterone levels in men with type 2 diabetes, and multiple
studies all over the world have confirmed the association of low
testosterone with diabetes,” Dhindsa notes.
“The Endocrine Society now recommends that all men with
type 2 diabetes should have their testosterone levels measured. Our
new study shows that obese men also have a very high prevalence of
low testosterone levels, so physicians should consider screening
obese non-diabetic men, as well, for low testosterone.”
The HIM study was funded by Solvay Pharmaceuticals Inc., and was
conducted from November 2003 to February 2004 in 95 primary care
practices throughout the U.S. The study involved 2,165 men 45 years
or older who provided blood samples for analysis of testosterone
concentrations.
UB researchers excluded participants from the full study who had
no BMI data or were on certain drugs that can affect testosterone
levels, providing a study population of 1,849 men—398 with
diabetes and 1,451 non-diabetics.
“With the rising prevalence of obesity in the U.S. and the
rest of the world,” says Paresh Dandona, MD, head of the
Division of Endocrinology, Diabetes and Metabolism at UB and
Kaleida Health, and senior author of the study, “it is
imperative that the prevalence of low testosterone levels in obese
men be defined. In addition, the magnitude of the contribution of
obesity to subnormal testosterone needs to be quantified.
“We hypothesized that obese men are more likely to have
low testosterone than non-obese men, and that we would find more
low testosterone levels in men with diabetes than in men without
diabetes, both obese and non-obese.”
Results confirmed these hypotheses, showing a 40 percent higher
prevalence of low testosterone in obese men compared to the
non-obese participants. Men with diabetes, whether obese or not,
showed lower levels of testosterone than non-diabetic men across
all weight categories. Testosterone levels decreased significantly
in both diabetic and non-diabetic men as BMI increased.
“In view of the increasing prevalence of obesity, even in
younger populations, it would be important to conduct a similar
study in the men at the prime of their reproductive years,”
he says.
UB endocrinologists published a study in Diabetes Care in 2008
showing that more than 50 percent of men between 18 and 35 years
old with type 2 diabetes had lower than normal testosterone
levels.
“In view of the high rates of subnormal testosterone in
patients with obesity or diabetes, testosterone concentrations
should be measured regularly in these populations, especially when
these conditions occur together,” says Dandona.
Contributors to this study from UB, in addition to Dhindsa and
Dandona, are Donald E. Mager, PharmD, PhD, Husam Ghanim, PhD, and
Ajay Chaudhuri, MD. Cecilia L. McWhirter and Michael G. Miller,
PharmD, both from Solvay Pharmaceuticals Inc., also contributed to
the study.
This was an unfunded analysis of HIM data. Dandona and Dhindsa
are supported by grants from The American Diabetes Association and
Dandona’s work also is supported by the NIH.