Relationship of Mediterranean diet and caloric intake to phenoconversion in Huntington disease
- PMID: 24000094
- PMCID: PMC4040231
- DOI: 10.1001/jamaneurol.2013.3487
Relationship of Mediterranean diet and caloric intake to phenoconversion in Huntington disease
Abstract
Importance: Adherence to Mediterranean-type diet (MeDi) may delay onset of Alzheimer and Parkinson diseases. Whether adherence to MeDi affects time to phenoconversion in Huntington disease (HD), a highly penetrant, single-gene disorder, is unknown.
Objectives: 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 body mass index and caloric intake on time to phenoconversion.
Design, setting, and participants: A prospective cohort study of 41 Huntington study group sites in the United States and Canada involving 1001 participants enrolled in PHAROS between July 1999 and January 2004 who were followed up every 9 months until 2010. A total of 211 participants aged 26 to 57 years had an expanded CAG repeat length (≥ 37).
Exposure: A semiquantitative food frequency questionnaire 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, body mass index, and Unified Huntington's Disease Rating Scale (UHDRS) score were collected.
Main outcome and measure: Cox proportional hazards regression models to determine the association of MeDi and phenoconversion. RESULTS Age, sex, caloric intake, education status, and UHDRS motor scores did not differ among MeDi tertiles (0-3, 4-5, and 6-9). The highest body mass index was associated with the lowest adherence to MeDi. Thirty-one participants phenoconverted. In a model adjusted for age, CAG repeat length, and caloric intake, MeDi was not associated with phenoconversion (P for trend = 0.14 for tertile of MeDi, and P = .22 for continuous MeDi). When individual components of MeDi were analyzed, higher dairy consumption (hazard ratio, 2.36; 95% CI, 1.0-5.57; P = .05) and higher caloric intake (P = .04) were associated with risk of phenoconversion.
Conclusions and relevance: MeDi was not associated with phenoconversion; however, higher consumption of dairy products had a 2-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.
Conflict of interest statement
Disclosures: The authors report no conflict of interest
Similar articles
-
Dietary intake in adults at risk for Huntington disease: analysis of PHAROS research participants.Neurology. 2009 Aug 4;73(5):385-92. doi: 10.1212/WNL.0b013e3181b04aa2. Neurology. 2009. PMID: 19652143 Free PMC article.
-
Factors associated with Mediterranean diet adherence in Huntington's disease.Clin Nutr ESPEN. 2016 Apr;12:e7-e13. doi: 10.1016/j.clnesp.2016.01.001. Epub 2016 Mar 5. Clin Nutr ESPEN. 2016. PMID: 28531758
-
Clinical-Genetic Associations in the Prospective Huntington at Risk Observational Study (PHAROS): Implications for Clinical Trials.JAMA Neurol. 2016 Jan;73(1):102-10. doi: 10.1001/jamaneurol.2015.2736. JAMA Neurol. 2016. PMID: 26569098
-
Dietary Intake, Mediterranean Diet Adherence and Caloric Intake in Huntington's Disease: A Review.Nutrients. 2020 Sep 25;12(10):2946. doi: 10.3390/nu12102946. Nutrients. 2020. PMID: 32992896 Free PMC article. Review.
-
Exploring the correlates of intermediate CAG repeats in Huntington disease.Postgrad Med. 2011 Sep;123(5):116-21. doi: 10.3810/pgm.2011.09.2466. Postgrad Med. 2011. PMID: 21904093 Review.
Cited by
-
Is Dysregulation of the HPA-Axis a Core Pathophysiology Mediating Co-Morbid Depression in Neurodegenerative Diseases?Front Psychiatry. 2015 Mar 9;6:32. doi: 10.3389/fpsyt.2015.00032. eCollection 2015. Front Psychiatry. 2015. PMID: 25806005 Free PMC article. Review.
-
Mediterranean Diet in Preventing Neurodegenerative Diseases.Curr Nutr Rep. 2018 Mar;7(1):10-20. doi: 10.1007/s13668-018-0222-5. Curr Nutr Rep. 2018. PMID: 29892785 Free PMC article. Review.
-
IKKβ signaling mediates metabolic changes in the hypothalamus of a Huntington disease mouse model.iScience. 2022 Jan 19;25(2):103771. doi: 10.1016/j.isci.2022.103771. eCollection 2022 Feb 18. iScience. 2022. PMID: 35146388 Free PMC article.
-
Neurodegenerative Diseases: New Hopes and Perspectives.Curr Mol Med. 2024;24(8):1004-1032. doi: 10.2174/1566524023666230907093451. Curr Mol Med. 2024. PMID: 37691199 Review.
-
New directions in therapeutics for Huntington disease.Future Neurol. 2018 May;13(2):101-121. doi: 10.2217/fnl-2017-0035. Epub 2018 May 29. Future Neurol. 2018. PMID: 30800004 Free PMC article. Review.
References
-
- Petersen A, Bjorkqvist M. Hypothalamic-endocrine aspects in Huntington's disease. Eur J Neurosci. 2006;24:961–967. - PubMed
-
- Underwood BR, Broadhurst D, Dunn WB, et al. Huntington disease patients and transgenic mice have similar pro-catabolic serum metabolite profiles. Brain. 2006;129:877–886. - PubMed
-
- Morales LM, Estevez J, Suarez H, Villalobos R, Chacin de Bonilla L, Bonilla E. Nutritional evaluation of Huntington disease patients. Am J Clin Nutr. 1989;50:145–150. - PubMed
Publication types
MeSH terms
Grants and funding
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical