Hypogonadism and Weight Gain: What Can We Learn from It?
Hypogonadism has been linked with weight gain. In addition to predisposing to obesity, the condition also predisposes to other diseases that normally fall under the constellation of metabolic syndrome (a.k.a. Syndrome X), such as insulin resistance, hypercholesterolemia, and impaired glycemic control. So what can this tell us? And how might this information relate back to the debate about public health and nutrition?
The traditional view about obesity -- as enshrined in the Caloric Balance Hypothesis -- tells us that excess calories make us fat. When we overeat or don't get enough regular exercise, calories somehow get dumped into our fat tissue. Caloric Balance tells us that hypogonadism must somehow change eating behavior or change the way in which the body burns calories.
The Lipophilia Hypothesis, the alternative hypothesis, tells us that our fat tissue is not a garbage bag for excess calories – it's a metabolically active endocrine organ that plays a key role in regulating "Calories In" and "Calories Out." When we gain fat in the fat tissue, this makes us hungry and makes it harder to burn off calories. Lipophilia tells us that hypogonadism must somehow change fat tissue metabolism – most likely by doing something to our insulin levels and/or blood sugar levels.
Both hypotheses try to explain why hypogonadism is linked with obesity and other diseases of civilization.
So let's look at some articles to see whether we can assess these theories.
1. Here is one article: "Testosterone replacement therapy improves insulin resistance, glycemic control, visceral adiposity, and hypercholesterolemia, and hypogonadal man, type 2 diabetes."
"investigated the effect of testosterone treatment on insulin resistance and glycemic control in a hypogonadal man with type 2 diabetes... [The therapy] "improved fasting insulin sensitivity... [and] resulted in reduction of visceral adiposity."
This would seem to provide support for Lipophilia's prediction.
2. Here is another article that also seems to support the alternative hypothesis, albeit in an indirect way: "Chronic administration of neuropeptide y in lateral ventricle C57BL/6J male mice produces an obesity syndrome including hyperphagia, hyperleptinemia, insulin resistance, and hypogonadism."
This study links hypogonadism with obesity and insulin resistance and hyperphagia – suggesting that what causes one symptom might cause the rest. Again, the Lipophilia Hypothesis seems better equipped to explain these results.
3. Here is another study: "Relationship between testosterone levels, insulin sensitivity, and mitochondrial function in men."
The authors found data that:
"indicate that low serum testosterone levels are associated with an adverse metabolic profile and suggest a novel unifying mechanism for the previously independent observation that low testosterone levels and impaired mitochondrial function promote insulin resistance in men."
For more information about how our body's hormonal ensemble can regulate weight gain and sexual characteristics, please see:
4. Good Calories Bad Calories by journalist Gary Taubes.