Certain dietary choices may change the course of Huntington’s disease (HD), a new study suggests.
Although the research showed that the healthy Mediterranean diet as a whole is not associated with slowing the clinical onset of Huntington’s in people at risk, researchers found that higher consumption of dairy products more than doubled the risk for onset, known as phenoconversion.
Dairy may be a surrogate for lower urate levels, which are associated with faster progression in Huntington’s, the authors speculate.
In addition to being low in dairy products and in red meat and poultry, the Mediterranean diet (MeDi) is rich in plant foods (eg, fruits, nuts, legumes, and cereals) and fish, has few saturated fats (with olive oil being the primary source of monounsaturated fat), and includes moderate consumption of wine. Previous research has shown that higher adherence to the MeDi may delay onset of Alzheimer’s disease and Parkinson’s disease.
The suggestion that dietary factors may modify onset of HD is promising, according the study’s lead author Karen Marder, MD MPH, professor, neurology, and chief, Division of Aging and Dementia, Department of Neurology, Columbia University, New York, New York.
“Although we didn’t see a major effect from the Mediterranean diet, the dairy component being high might suggest an association with low urate. Urate is a potential antioxidant. We thought this is a way of potentially looking at modifiable risk factors for even something as purely genetic as Huntington’s disease.”
The study was published online September 2 in JAMA Neurology.
Modifiable Risk Factor?
The study included 1001 participants in the Prospective Huntington at Risk Observational Study (PHAROS) at 41 centers in the United States and Canada who were at genetic risk for HD because they had an affected parent or sibling, but had not yet themselves undergone genetic testing for CAG expansion.
Researchers performed genetic testing at baseline, with investigators and participants remaining blinded to gene status for the duration of the trial. Participants were therefore unlikely to have changed their diet because they knew their genetic risk.
The first time a rating of 4 on the Unified Huntington’s Disease Rating Scale (UHDRS) was given, it was considered motor phenoconversion (diagnosis of HD). Only the 211 participants who had an expanded CAG repeat length (CAG ≥ 37) and who did not have a diagnostic confidence rating of 4 at enrollment were included in the analyses.
PHAROS participants completed food-frequency questionnaires 33 months after baseline. Researchers arrived at a MeDi score for study participants by calculating the daily gram intake for 7 categories of food — dairy, meat, fruits, vegetables, legumes, cereals, and fish — and assigning values to foods and dietary habits according to whether they were beneficial or detrimental. The MeDi score could theoretically range from 0 to 9, with 0 indicating the least adherence to the MeDi and 9 the strictest adherence.
The researchers divided MeDi scores into tertiles: 0 to 3 (n = 67), 4 to 5 (n = 94), and 6 to 9 (n = 50).
The study found that age, sex, caloric intake, educational status, UHDRS motor score, and chorea subscore did not differ among the MeDi tertiles. The highest body mass index was associated with the lowest adherence to MeDi (P = .02) before adjustments.
During the study period (patients were enrolled between July 1999 and January 2004 and followed every 9 months until 2010), 31 of the 211 participants phenoconverted. The mean time to phenoconversion was 2.5 years.
A fully adjusted model found that age and CAG repeat length were associated with phenoconversion, but adherence to the MeDi diet was not (P for trend = .14 for tertile of MeDi and .22 for continuous MeDi).
When individual components of the MeDi were analyzed, only higher consumption of dairy products was associated with an increased risk for phenoconversion (hazard ratio, 2.36; 95% confidence interval, 1.0 to 5.57; P = .05).
Possible explanations for this include the presence of low levels of pesticides in milk or the fact that higher dairy consumption is related to lower circulating levels of urate; high dairy consumption could be a surrogate marker for a low urate level, they speculate.
It’s impossible to determine at this point the impact that lowering consumption of dairy products, such as milk, yogurt, and cheese, might have on delaying the onset of HD.
“We have absolutely no idea,” said Dr. Marder. “This is suggesting perhaps that one may want to consider additional dietary modification studies in individuals at risk for Huntington’s disease. Dietary interventions are difficult to do, but it does give you a suggestion that this might be a modifiable risk factor.”
The study also showed that higher caloric intake was associated with increased risk for phenoconversion (P = .04), but body mass index was not. There are numerous possible explanations for this, said Dr. Marder. For example, it could be that people who are developing HD need more calories to maintain their weight.
“In other degenerative diseases, we see weight loss with disease progression, so at certain point you do lose weight, but in the premanifest state, people are eating more, not consciously,” she said. “To maintain their weight, they require more calories.”
A limitation of the study is that it’s possible that presymptomatic carriers of an expanded CAG repeat length might have changed their dietary preference as they approached phenoconversion.
Dr. Marder hopes to further explore the role of diet in HD. “We have additional dietary interviews with participants in the PHAROS study, so we want to look at the longitudinal progression to see if people’s diet changes over time. We don’t know how urate levels in premanifest HD compare to population norms. Then ultimately we would like to consider a dietary intervention to see if we can delay disease onset.”
Source: Medscape Medical News
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