Adherence to Mediterranean-type diet (MeDi) may delay onset of Alzheimer's and Parkinson's disease. Whether adherence to MeDi affects time to phenoconversion in Huntington’s Disease (HD), a highly penetrant, single gene disorder, is unknown.
To determine if MeDi modifies the time to clinical onset of HD ('phenoconversion') in premanifest carriers participating in Prospective Huntington At Risk Observational Study (PHAROS), and to examine the effects of BMI and caloric intake on time to phenoconversion.
A prospective cohort study.
41 Huntington Study Group sites in the US and Canada.
1001 participants were enrolled in PHAROS between July 1999 and January 2004, and were followed every 9 months until 2010. A total of 211 participants aged 26–57 with an expanded CAG repeat (≥37) were included in the current study.
A semi-quantitative food frequency questionnaire (FFQ) was administered 33 months after baseline. We calculated daily gram intake for dairy, meat, fruit, vegetables, legumes, cereals, fish, monounsaturated and saturated fatty-acids, and alcohol, and constructed MeDi scores (0–9); higher scores indicate higher adherence. Demographics, medical history, BMI, and Unified Huntington's Disease Rating Scale (UHDRS) were collected.
Main Outcome Measure
Cox proportional hazards models to determine the association of MeDi and phenoconversion.
Age, caloric intake, gender, education, and UHDRS motor scores did not differ among MeDi tertiles (0–3, 4–5, 6–9). The highest BMI was associated with lowest adherence to MeDi. 31 participants phenoconverted. In a model adjusted for age, CAG, and caloric intake, MeDi was not associated with phenoconversion (p for trend=0.14 for tertile of MeDi, and p=0.22 for continuous MeDi). When individual diet components of MeDi were analyzed, higher dairy consumption (hazard ratio 2.36; 1.0–5.57; p=0.051) and higher caloric intake (p=0.035) were associated with risk of phenoconversion.
Conclusion and Relevance
MeDi was not associated with phenoconversion, however higher consumption of dairy products had a two-fold increased risk, and may be a surrogate for lower urate levels (associated with faster progression in manifest HD). Studies of diet and energy expenditure in premanifest HD may provide data for interventions to modify specific components of diet that may delay the onset of HD.