Over the years there have been a few studies regarding the risks of substance abuse with tobacco, alcohol or other drugs in Huntington's disease (HD). Does using -- or abusing these substances cause an earlier onset of disease or faster rate of progression in Huntington's disease?
Although "common sense" and anecdotal experience suggest that these substances are likely harmful in both the short and long term in HD, what can we learn from the scientific literature?
Alcohol use/misuse: Does it affect symptoms of HD? Short term effects of alcohol on cognition and behavior in healthy individuals are well known. Just one or two drinks can cause decrease in inhibition, and impairments in judgement, memory, motor coordination, concentration, reaction times, balance, etc. For those with HD, these are problems already present that alcohol makes more severe. It is more problematic for women, who are more susceptible to alcohol than men, because higher blood levels of alcohol occur in women than men for an equal amount of alcohol consumed. And for unknown reasons, similar amounts of alcohol will cause more medical injury to brain, liver and heart in women than men.
An early small study done in Baltimore suggested that alcohol abuse was not more common in HD than the local community[King M 1985].
Whether HD or not, greater consumption of alcohol leads to more aggressive behaviors, particularly in men. In fact, the majority of criminal acts in the general population occur in those under the influence of alcohol. It is not surprising that this is also true for those with HD. In a study of prevalence of criminal behavior in HD, those individuals affected by HD had more associated criminal acts than in non HD-affected siblings. These crimes in HD -- though of relative minor severity -- correlated with alcohol misuse [Jensen P 1998]. Further, psychiatric problems [Ehret JC 2007] and suicidal ideation [Wetzel HH 2011] occur more commonly in those HD individuals who abuse alcohol or other drugs.
Substance abuse: Does it affect age of onset? In a recent publication with Dr. Peg Nopoulos as lead author, results of a study of Iowa-based patients suggested that "life-time substance abuse may be a risk factor for earlier onset of HD" [Byars JA 2012]. In this study, risk for earlier onset was much greater for women with substance abuse (more so for alcohol than other drugs) than men. Tobacco use also had a trend for causing earlier onset in women, but not men. Using information not published yet, but obtained (with permission) from an abstract accepted for the 2013 Huntington Study Group Symposium, lead author Dr. Clement Loy and others report that alcohol abuse was associated with earlier age of onset of HD symptoms. In this larger study of 792 COHORT participants, tobacco use was not associated with earlier onset. Detailed information about this study will be presented at the November 2013 Huntington Study Group Symposium in Raleigh, North Carolina.
Substance abuse: Does it affect rate of progression in HD? in an early small study of 42 patients no correlation was seen regarding tobacco or alcohol use (not abuse) with rate of disease progression [Myers RH 1991]. However in other study (the abstract mentioned above) that analyzed data from almost 800 individuals, authors report that alcohol abuse was associated with an increase in the rate of disease progression. Detailed information will be reported in a Key Note presentation at the November 2013 Huntington Study Group Symposium.
Marijuana use: Does it affect HD? In the general population, acute and chronic use of marijuana impairs attention, learning and memory, though in adults impairment appears to disappear 4 weeks after stopping the drug [White KG 2002]. More lasting cognitive defects occur if abuse starts in adolescence. In HD use of this drug acutely or chronically adds to cognitive problems and apathy or lack of motivation already present in HD. In a small study of oral cannabis given for 6 weeks in HD patients, there appeared to be no improvement in chorea [Consroe P 1991]. No long term study has addressed marijuana use specifically in regards to age of onset or disease progression.
Is marijuana neuroprotective? Marihuana, obtained from cannabis plants contains several different cannabinoid chemicals, some of which are psychoactive like tetrahydrocannabinol (THC). Others cannabinoid chemicals have antioxidant and anti-inflammatory properties. These latter chemicals, in purified form and at high dosages are those that have been used in animal studies reporting potential neuroprotective properties. A similar dose of THC or other psychoactive marijuana chemical is toxic.
Author's comments: Substance abuse is bad for your body and brain health whether you have HD or not. Further, because substance abuse often leads to aggression and violence, it also is bad for the health of others. Even small amounts of alcohol or other recreational drugs interfere with cognition and motor coordination, so should be used with caution --or not at all -- in healthy individuals and especially in those with HD where pre-existing impairment will be magnified.
However, we should not go overboard: For instance, an occasional drink at a celebration is reasonable for most individuals, except for recovering alcoholics. Just how much is okay for other individuals is an unknown, but it is probably best to err on the low side. Regarding tobacco and recreational drug use, because of the greater risk of addiction, it really is best not to start.
King M. Alcohol abuse in Huntington's disease. Psychol Med. 1985 Nov;15(4):815-9. PubMed abstract
Jensen P, Fenger K, Bolwig TG, Sørensen SA. Crime in Huntington's disease: a study of registered offences among patients, relatives, and controls. J Neurol Neurosurg Psychiatry. 1998 Oct;65(4):467-71. PubMed abstract
Ehret JC, Day PS, Wiegand R, Wojcieszek J, Chambers RA. Huntington disease as a dual diagnosis disorder: data from the National Research Roster for Huntington disease patients and families. Drug Alcohol Depend. 2007 Jan 12;86(2-3):283-6. Epub 2006 Aug 22. PubMed abstract
Wetzel HH, Gehl CR, Dellefave-Castillo L, Schiffman JF, Shannon KM, Paulsen JS; Huntington Study Group. Suicidal ideation in Huntington disease: the role of comorbidity. Psychiatry Res. 2011 Aug 15;188(3):372-6. doi: 10.1016/j.psychres.2011.05.006. Epub 2011 May 24. PubMed abstract
Byars JA, Beglinger LJ, Moser DJ, Gonzalez-Alegre P, Nopoulos P. Substance abuse may be a risk factor for earlier onset of Huntington disease. J Neurol. 2012 Sep;259(9):1824-31. doi: 10.1007/s00415-012-6415-8. Epub 2012 Jan 25. PubMed abstract
Myers RH, Sax DS, Koroshetz WJ, Mastromauro C, Cupples LA, Kiely DK, Pettengill FK, Bird ED. Factors associated with slow progression in Huntington's disease. Arch Neurol. 1991 Aug;48(8):800-4. PubMed abstract
White KG, Ruske AC. Memory deficits in Alzheimer's disease: the encoding hypothesis and cholinergic function. Psychon Bull Rev. 2002 Sep;9(3):426-37. PubMed abstract
Consroe P, Laguna J, Allender J, Snider S, Stern L, Sandyk R, Kennedy K, Schram K. Controlled clinical trial of cannabidiol in Huntington's disease. Pharmacol Biochem Behav. 1991 Nov;40(3):701-8. PubMed abstract