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Key Sununaries

l. Sexual function in the male is governed by


endocrine influences such as testosterone, together
with psychological inputs such as body image and
mood. Because all of these can be adversely
affected by obesity, it is not surprising that obese
men suffer from a higher incidence of sexual
difficulties (erectile dysfunction, reduced sexual
desire).
2. Obesity, especially abdominal obesity associated
with an increased WC, has been definitively
associated with reduced testosterone by several
investigators. It is estimated that at least 50% of

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Key Sununaries
obese men aged 45 years or older will have
suboptimal testosterone levels, with age-associated
increases in BMI being the primary cause for the
observed drop in testosterone with advancing age.
3. Testosterone levels are lowered in obese men by several
interacting mechanisms originating at the 'level of the
hypothalamic—pituitary (HP) axis, the testis, and the liver (sex
hormone- binding globulin 'ISHBGI production), First, increased
conversion of testosterone to estrogen by aromatase action in
adipose tissue results in negative feedback on the HP axis,
reducing luteinizing hormone and folliclestimulating hormone-
driven testosterone production. Elevated levels of insulin, leptilli
and inflammatory cytokines have also been implicated in the
inhibition of testosterone production. Second, insulin, cortisol,

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Key Sununaries
and leptin, all increased in obese men, act directly on the Leydig
cells in the testis and inhibit testosterone biosynthesis. Finally,
hyperinsulinemia associated with obesity and metabolic syndrome
suppresses hepatic production of SHBG, resulting in reduced
binding of testosterone to this carrier, which subsequently
decreases circulating testosterone and delivery of testosterone to
peripheral tissues.

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4. The relationship between obesity and male
hypogonadism is bidirectional, each exacerbating
the other. Low testosterone promotes visceral fat
accumulation at the expense of lean muscle mass,
while also exacerbating insulin resistance, thereby
creating a vicious cycle positive feedback loop.
5. The impact of macronutrient intake on testosterone production
is currently uncertain owing to conflicting results of human and
animal studies and difficulties controlling for the effects of
macronutrient intake from calorie (energy) restriction. However,
it appears that a diet high in saturated fats (e.g., animal fats)
appears to increase testosterone levels, whereas animal studies
suggest that omega-3 polyunsaturated fatty acids (PUFAs; e.g.,
fish) tend to reduce circulating testosterone, Conversely, omega-
6 PUFAs (meat, vegetable oils) and monounsaturated fatty acids

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(MUFAs) such as those found in olive oil both increase
testosterone production. Increasing the percentage of protein in
energy intake reduces testosterone levels while increasing
carbohydrate intake increases testosterone in healthy men.
However, it should be noted that acute high carbohydrate loads
in obese glucoseintolerant men does result in a fall in
testosterone levels.
6. Inadequate intake of the micronutrients zinc and
selenium are associated with hypogonadism, with
testosterone levels normalizing on adequate
replacement of these micronutrients. Vitamin D
deficiency is also associated with hypogonadism in
men that can be reversed with dietary
supplementation. Light alcohol intake is associated
with small increases in testosterone production;

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however, consumption of 40 g (four standard drinks)
or more of alcohol per week results in a drop in
testosterone. This fall in testosterone becomes
pronounced in alcoholic cirrhosis.
7. Erectile dysfunction (ED) is present in approximately 40%
of obese men, with the underlying pathophysiology being
multifactorial. First, obesity-related low testosterone impairs
normal neural and penile vascular endothelial nitric oxide
(NO) synthesis necessary for initiation and maintenance of
an erection. Second, obesity-related systemic inflammation
and oxidative stress impairs endothelial function and
vascular responses. Third, obesity- related hypertension and
adverse lipid profiles predispose to atherosclerotic reduction
in pelvic arterial blood supply, impeding normal penile

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vascular erectile responses. Finally, poor personal body
image associated with obesity, together with lethargy and
negative mood from sleep fragmentation and hypoxia
associated with obstructive sleep apnea, all combine to add
a psychological element to ED and decreased sexual desire,
8. Both animal and human studies suggest that modification of
diet can improve obesity-related sexual dysfunction. A
Mediterranean diet (low saturated fat, high MUFA such as
olive oil, moderate alcohol intake, abundant fruits and nuts
with high antioxidant content, plus fish abundant in anti
inflammatory omega-3 PUFAs) has been shown to reduce
the incidence and severity of ED in obese men. Weight loss
through either bariatric surgery or diet and exercise has been
shown to improve testosterone levels and erectile function,
To maintain long-term weight loss and improved sexual

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function, studies suggest obese men should adopt a diet with
increased protein (30% of calories) and reduced fat (20%).
Furthermore, human and animal studies have provided some
preliminary evidence sup- porting the use of antioxidant and
I-arginine (nitric oxide donor) supplements to boost erectile
function.
9. Underweight males also experience hypogonadism,
triggered by the relative deficiency of adipose-
derived leptin that results in impaired HP axis drive
of testosterone production. Restoration of normal
body weight will result in normalization of
testosterone levels.

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