According to the National Institute on Drug Abuse, the active element in beer, wine, and liquor is ethyl alcohol, or ethanol, which is known colloquially as alcohol.
In 2013, the National Survey on Drug Use and Health has shown that 52.2% people over 12 years of age in America were current alcohol users, 6.3% of the population over 12 are a heavy drinker and 10.9% had driven a car under influence of alcohol (1). Alcohol is a central nervous system depressant. It is highly lipid soluble and can cross the blood-brain-barrier. After that, it acts on the receptor level, particularly the GABA and Glutamate. Here it acts by slowing down the movement and speech. But the pleasurable effects produced by alcohol are brought about by its action at a Dopamine receptor level. A casual drinker may suffer from a loss of memory even after a few drinks (1).
Parkinson's disease is a progressive neurodegenerative disease that is associated with impaired Dopaminergic discharge in the nigro-striatal pathway in the brain. It has both motor and non-motor symptoms, of the non-motor symptoms depression, apathy, cognitive impairment, sleep disturbances, pain, and autonomic dysfunction are most prevalent (2). 83% of patients having cognitive impairment will lead to dementia within the next 20 years (3). Patients with concurrent alcoholism will certainly increase their non-motor symptoms, particularly depression and dementia. These are major adverse effects of moderate alcoholism, which may be complicated with sudden blackout, recklessness, and impaired decision making (1).
There was extensive research on Parkinson's disease and alcoholism. So far it has been documented that moderate alcoholism is associated with reduced risk of Parkinson's disease (4, 5, 6). Various types of alcohol have been studied in relation to causation of the disease. One study shows low to moderate beer consumption may be associated with lower PD risk; heavy liquor consumption was associated with higher PD risk and wine consumption did not appear to be associated (5). The mechanism behind this lower risk may be linked to Urate. One of the researchers (Dr. Chen) of this study has elaborated "unlike wine or liquor, beer contains a large amount of purine, which may work synergically with ethanol to augment urate production. Uric acid is a potent free radical scavenger, and accumulating epidemiologic evidence has linked higher plasma urate with a reduced risk of Parkinson's disease and slower clinical progression among Parkinson's disease patients" (5).
One study has shown that heavy drinking contributes to involuntary body movements such as akathisia (7). Several other studies have demonstrated that acute alcohol intoxication and withdrawal may provoke transient Parkinsonian movements particularly, akathisia, dystonia, cogwheeling, tremor, wide-based gait and bradykinesia. These symptoms were diminished following abstinence from alcohol (8,9). Animal studies have demonstrated impaired striatal dopaminergic function during severe ethanol intoxication or withdrawal. Thus chronic alcoholism may exacerbate or uncover the sign-symptoms of latent Parkinson's disease (9).
Experimental clinical studies are less common regarding the relationship of alcoholism and dopaminergic activity in the brain. But an animal-based study has demonstrated that a sub-hypnotic dose of alcohol reduces the dopaminergic turnover in the substantia nigra and caudate nucleus of basal ganglia.
Whatever alcohol is related to the causation of Parkinson's syndrome or not, the side effects of alcohol and its withdrawal will exacerbate or uncover the motor symptoms of Parkinson's disease. Moreover, the side effects of alcohol are related to the non-motor symptoms of Parkinson's disease that's why masking of the symptoms of PD may occur and mistakenly may be described as the symptoms of alcohol.
You can record data and discover patterns to identify the effects of alcohol on your symptoms. This information can then be shared with your specialist.