In addition to directly stimulating breast tissue growth, estrogens indirectly decrease secretion of testosterone by suppressing luteinizing hormone secretion, resulting in decreased testicular secretion of testosterone. Estrogen excess
One of the main mechanisms for imbalance between estrogens and androgens is the overproduction of estrogens. A possible cause may be a neoplasm that originates from estrogen-secreting cells. Tumors that produce hCG stimulate production of estradiol while reducing other testicular hormone production. Obesity is another common cause of excess serum estrogens due to the presence of aromatase in peripheral tissue, which is a protein that converts androgens into estrogens. Peutz-Jeghers syndrome is a rare cause of testicular tumors that affect aromatase expression, which results in elevated serum estrogen levels. Aromatase excess syndrome is a rare genetic disorder that leads to increased conversion of androgens to estrogens in the body. Androgen deficiency
Primary hypogonadism (indicating an intrinsic problem with the testes in males) leads to decreased testosterone synthesis and increased conversion of testosterone to estradiol potentially leading to a gynecomastic appearance. Klinefelter syndrome is a notable example of a disorder that causes hypogonadism and gynecomastia, and has a higher risk of breast cancer in males (20–50 times higher than males without the disorder). Secondary hypogonadism (indicating a problem with the brain) leads to decreased production and release of luteinizing hormone (LH, a stimulatory signal for endogenous steroid hormone synthesis) which leads to decreased production of testosterone and estradiol in the testes.
These are:
Parkinsonism - slow, stiff movement, writing becomes small and spidery
Cerebellar dysfunction - difficulty coordinating movement and balance
Autonomic nervous system dysfunction - impaired automatic body functions, including one, some, or all of the following:postural or orthostatic hypotension, resulting in dizziness or fainting upon standing up
urinary incontinence or urinary retention
impotence
constipation
vocal cord paralysis
dry mouth and skin
trouble regulating body temperature due to sweating deficiency in all parts of the body
loud snoring, abnormal breathing or inspiratory stridor during sleep
other sleep disorders including sleep apnea, REM behavior disorder
double vision
muscle twitches
Cognitive impairment

Genetics
One study found a correlation between the deletion of genes in a specific genetic region and the development of MSA in a group of Japanese patients. The region in question includes the SHC2 gene which, in mice and rats, appears to have some function in the nervous system. The authors of this study hypothesized that there may be a link between the deletion of the SHC2 and the development of MSA.A follow-up study was unable to replicate this finding in American MSA patients. The authors of the U.S. study concluded that "Our results indicate that SHC2 gene deletions underlie few, if any, cases of well-characterized MSA in the US population. This is in contrast to the Japanese experience reported by Sasaki et al., likely reflecting heterogeneity of the disease in different genetic backgrounds. "Another study investigated the frequency of RFC1 intronic repeat expansions, a phenomenon implicated in CANVAS; a disease with a diagnostic overlap with MSA.