Waist circumference and risk of Parkinson’s disease

Abstract

Although many studies support the association of obesity with neurodegenerative diseases, such as Parkinson’s disease (PD), there are limited data regarding the association between abdominal obesity and PD, with mixed findings. The aim of this study was to examine the association of waist circumference (WC) with the risk of PD incidence. We retrospectively analyzed a large-scale nationwide cohort of 6,925,646 individuals aged ≥40 years who underwent the Korean National Health Screening during 2009. We performed multivariable Cox proportional hazards regression to evaluate the association of WC and abdominal obesity with PD risk and calculated hazard ratios (HRs) with 95% confidence intervals (CIs) of PD incidence. During a median follow-up period of 8.35 years, 33,300 cases of PD developed. PD incidence was positively associated with increases in WC (P for trend < 0.001). The risk of PD incidence tended to elevate as WC increased (P for trend < 0.001), indicating that the adjusted HRs of PD incidence in the highest WC group versus the reference group was 1.16 (95% CI, 1.10–1.23), whereas it was 0.91 (95% CI 0.84–0.98) in the lowest WC group. Individuals with abdominal obesity were significantly associated with an increased PD risk (HR 1.10, 95% CI: 1.07–1.13). These associations persisted even after adjustment for body mass index and stratification by sex. Even among non-obese individuals, abdominal obesity was associated with a higher PD risk (adjusted HR 1.13, 95% CI: 1.09–1.18). Taken together, higher WC and abdominal obesity were associated with increased PD risk. Even in non-obese individuals, abdominal obesity was associated with an increased PD risk.

Association Between Body Composition Patterns, Cardiovascular Disease, and Risk of Neurodegenerative Disease in the UK Biobank

“…The robust association of "central obesity" and "muscle strength" patterns with both neurodegenerative diseases and MRIbased brain aging biomarkers aligned with previous evidence from Mendelian randomization 9 and observational studies. 6,7,24,25 The inverse associations of "bone density" 12 (high vs low) and "fat-to-lean mass" 26 (moderate vs low) patterns with the clinical onset of neurodegenerative diseases partly collaborated with previous studies yet showed inconsistency or even contradiction with the subclinical outcomes of brain aging biomarkers. Such discrepancies suggest potential reverse causation in clinical outcomes, even after incorporating a 5-year or 10-year lag time.…”

Western diet-induced obesity results in brain mitochondrial dysfunction in female Ossabaw swine

“…Collectively, the data implicate diet-induced obesity as a contributing factor to mitochondrial Complex I dysfunction in the brain, and that early compensatory responses may include enhanced antioxidant defense as well as increased mitochondrial biogenesis signaling. These findings are critical, as they provide mechanistic insight into the clinical link between obesity and mitochondrial Complex I related neurodegenerative disorders (Picone et al, 2020;Park et al, 2022).…”

“…Lack of mitochondrial Complex I protein or function is a feature observed in an array of neurodegenerative disorders (Schapira et al, 1990;Navarro et al, 2009;Adav et al, 2019;Holper et al, 2019), including those associated with increased adiposity (Picone et al, 2020;Park et al, 2022). Yet, the cause of Complex I dysfunction has yet to be elucidated (Wang et al, 2022).…”

“…Lack of mitochondrial Complex I protein or function, also known as Complex I syndrome, is a key feature commonly observed in neurodegenerative disorders (Schapira et al, 1990;Navarro et al, 2009;Adav et al, 2019;Holper et al, 2019). The cause of Complex I dysfunction remains unknown; however, epidemiological evidence indicates obesity may serve a role (Picone et al, 2020;Park et al, 2022). Using a mouse model, Cavaliere et al (2019) demonstrated diet-induced obesity causes brain mitochondrial dysfunction, possibly related to dyslipidemia and increased oxidative stress.…”