On 2014 Dec 04, David Keller commented:

Cause and effect cannot be distinguished in the observed associations

Dopamine levels are reduced in the brains of patients with Parkinson's disease (PD). Dopamine inhibits the secretion of prolactin, and prolactin, in turn, reduces the activity of the steroid sex hormones (estrogen, testosterone, etc.) Thus, untreated PD patients should have low brain dopamine levels, high prolactin levels and thus low sex steroid hormone levels. These hormone actions are well-documented in physiology texts.

The next clinical scenario to consider is the effect of treating PD with levodopa, which is metabolized to dopamine in the brain. Clearly, brain dopamine levels will rise, driving down prolactin levels, which, in turn, allows an increase in sex steroid levels, ameliorating, to a variable degree, the hypogonadism caused by untreated PD.

To what degree does the dose of levodopa, taken in amounts sufficient to control the movement disorder symptoms of PD, also treat the hypogonadism caused by PD? This question is not addressed in the abstract.

The authors conclude that lower sex steroid levels and higher prolactin levels "may result in a bigger susceptibility to the disease in men." This observational study cannot possibly prove the cause-and-effect mechanism implied in that statement. The observed associations are explained equally well by the opposite conclusion: that PD causes men to have lower dopamine levels, higher prolactin levels and consequently lower sex steroid levels (hypogonadism), in other words, that hypogonadism is an effect of PD, not a cause. It would require a randomized, controlled interventional study in which hypogonadal PD patients were repleted with administered exogenous sex steroids to prove that hypogonadism is a cause, rather than just an effect, of PD.

On 2014 Dec 04, David Keller commented:

Cause and effect cannot be distinguished in the observed associations

Dopamine levels are reduced in the brains of patients with Parkinson's disease (PD). Dopamine inhibits the secretion of prolactin, and prolactin, in turn, reduces the activity of the steroid sex hormones (estrogen, testosterone, etc.) Thus, untreated PD patients should have low brain dopamine levels, high prolactin levels and thus low sex steroid hormone levels. These hormone actions are well-documented in physiology texts.

The next clinical scenario to consider is the effect of treating PD with levodopa, which is metabolized to dopamine in the brain. Clearly, brain dopamine levels will rise, driving down prolactin levels, which, in turn, allows an increase in sex steroid levels, ameliorating, to a variable degree, the hypogonadism caused by untreated PD.

To what degree does the dose of levodopa, taken in amounts sufficient to control the movement disorder symptoms of PD, also treat the hypogonadism caused by PD? This question is not addressed in the abstract.

The authors conclude that lower sex steroid levels and higher prolactin levels "may result in a bigger susceptibility to the disease in men." This observational study cannot possibly prove the cause-and-effect mechanism implied in that statement. The observed associations are explained equally well by the opposite conclusion: that PD causes men to have lower dopamine levels, higher prolactin levels and consequently lower sex steroid levels (hypogonadism), in other words, that hypogonadism is an effect of PD, not a cause. It would require a randomized, controlled interventional study in which hypogonadal PD patients were repleted with administered exogenous sex steroids to prove that hypogonadism is a cause, rather than just an effect, of PD.