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ARTICLES: G. Hu, P. Jousilahti, A. Nissinen, R. Antikainen, M. Kivipelto, and J. Tuomilehto Body mass index and the risk of Parkinson disease Neurology 2006; 67: 1955-1959 [Abstract] [Full text] [PDF]

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Body mass index and the risk of Parkinson disease

Ken Ikeda, Hidetoshi Kashihara, Masaki Tamura, Osamu Kano, Konosuke Iwamoto, and Yasuo Iwasaki.   (13 February 2007)

Reply from the Authors

Gang Hu, Department of Health Promotion and Chronic Diseases Prevention   (13 February 2007)

Body mass index and the risk of Parkinson disease 13 February 2007
Ken Ikeda, Department of Neurology, PL Tokyo Health Care Center 16-1, Kamiyamacho, Shibuyaku, Tokyo, 150-0047, Japan, Hidetoshi Kashihara, Masaki Tamura, Osamu Kano, Konosuke Iwamoto, and Yasuo Iwasaki. Send Correspondence to journal: Re: Body mass index and the risk of Parkinson disease keni{at}pl-tokyo-kenkan.gr.jp Ken Ikeda, et al.	We read with great interest the article by Hu et al concerning body mass index (BMI) and the incidence of Parkinson disease (PD). [1] We studied BMI changes before and after the onset of PD and considered the possible mechanism between excess body weight and the risk of PD. During the past ten years, we conducted an annual physical check-up in approximately 20,000 adults (12,000 men and 8,000 women) in PL Tokyo Health Care Center. Their mean age (SD) was 52.1 (11.5) years. Twenty-four patients (14 men and 10 women) developed PD. The mean age of the patients was 75.3 (6.4) years. In twenty PD patients (14 men and 6 women), BMI (kg/m2) was measured for 2 years before and after the disease onset. Mean BMI (SD) was 22.3 (3.1) at two years and 22.1 (3.2) at one year before the onset of PD. The number of patients was 11, 3, 4, 2 and 0 at different BMI levels (<23, 23-24.9, 25-26.9, 27-29.9 and ��30), respectively. The percentage of BMI �� 25 was higher in PD patients (30%) than age- and sex-matched 200 controls (10 %). Compared to BMI before the onset of PD, BMI was significantly reduced to 21.6 (3.6) at 2 years after the onset. However, three patients remained obese without weight loss. Those patients had a history of type II diabetes mellitus (DM) for more than 10 years before the onset of PD. DM was seen in 3 of our 24 patients (12.5 %). In general, prevalence of DM is lower in PD patients than controls. [2] We would like to know the frequency of DM at different levels of BMI in the study of Hu et al; does the risk of PD depend on DM in obese populations? Leptin plays a role of the pathogenesis of feeding, obesity and DM. A previous study shows that serum leptin concentrations is not changed between PD patients with and without weight loss. [3] A more recent study discloses that the midbrain dopamine neuron expresses leptin receptors, and this hormone suppresses firing of dopamine neurons. [4] Thus, the function of leptin could contribute to a putative mechanism between obesity and the onset of PD. Our data suggest that being overweight may increase the risk of PD in the Japanese similar to the Finnish population. [1] Further studies are needed to elucidate the common mechanism between excess weight and incident PD. References 1. Hu G, Jousilahti P, Nissinen A, Antikainen R, Kivipelto M, Tuomilehto J. Body mass index and the risk of Parkinson disease. Neurology 2006; 67: 1955-1959. 2. Scigliano G, Musicco M, Soliveri P, Piccolo I, Ronchetti G, Girotti F. Reduced risk factors for vascular disorders in Parkinson disease patients: a case- control study. Stroke 2006; 37: 1184-1188. 3. Evidente VGH, Caviness JN, Adler CH, Gwinn-Hardy KA, Pratley RE. Serum leptin concentrations and satiety in Parkinson�fs disease patients with and without weight loss. Mov Disord 2001, 16: 924-927. 4. Hommel JD, Trinko R, Sears RM, et al. Leptin receptor signaling in midbrain dopamine neurons regulates feeding. Neuron 2006; 51: 801-810. Disclosure: The authors report no conflicts of interest.
Reply from the Authors 13 February 2007
Gang Hu, National Public Health Institute Mannerheimintie 166, FIN-00300 Helsinki, Finland, Department of Health Promotion and Chronic Diseases Prevention Send Correspondence to journal: Re: Reply from the Authors hu.gang{at}ktl.fi Gang Hu, et al.	We thank Ikeda et al for their comments for our results of body mass index (BMI) and the risk of Parkinson�s disease (PD). [1] We agree with their comments that a history of type 2 diabetes may be a confounding factor for the association between BMI and the risk of PD. We have re-checked our data and found that the multivariate-adjusted direct association between BMI and the risk of PD did not change after further adjustment for the history of type 2 diabetes. The multivariate-adjusted (age, study years, systolic blood pressure, total cholesterol, education, leisure-time physical activity, smoking, alcohol consumption, coffee consumption, tea consumption, and history of type 2 diabetes) hazard ratios of PD at different levels of BMI (<23, 23-24.9, 25-26.9, 27-29.9, and >=30 kg/m2) were 1.00, 1.98 (95% CI 1.22-3.24), 1.84 (95% CI 1.12-3.01), 2.34 (95% CI 1.45-3.78), and 2.42 (95% CI 1.42-4.10) in men, and 1.00, 1.50 (95% CI 0.95-2.37), 1.66 (95% CI 1.06-2.61), 1.80 (95% CI 1.15-2.81), and 1.76 (95% CI 1.11-2.77) in women, and 1.00, 1.71 (95% CI 1.23-2.38), 1.71 (95% CI 1.23-2.38), 2.02 (95% CI 1.47-2.79), and 2.01 (95% CI 1.43-2.83) in men and women combined (adjusted also for sex). We also agree with their comments that the function of leptin could contribute to a putative mechanism between obesity and the onset of PD but further studies are needed to test this hypothesis since we do not have data on leptin. Disclosure: The authors report no conflicts of interest.