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Dyslipidemia, Other Metabolic Syndrome Factors May Raise Parkinson’s Disease Risk

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According to investigators, individuals with 3 or more risk factors for metabolic syndrome have a 40% greater risk of developing Parkinson’s.

A larger waistline and higher blood pressure, among other factors connected to metabolic syndrome, may be connected to a steep increase in Parkinson’s disease risk, according to a new study.1

Concerns about metabolic syndrome and its relation to several chronic diseases have been increasing globally. Research has highlighted insulin resistance, central obesity, glucose intolerance, dyslipidemia with elevated triglycerides, microalbuminuria, hypertension, and high waist circumference, among other conditions, as risk factors for metabolic syndrome.2

Additionally, Parkinson’s disease and its potential endpoint of dementia have become critical focuses of neurology. A growing body of evidence has spotlighted many of the same components of metabolic syndrome as potential contributors to the pathophysiology of Parkinson’s disease.2

A previous study from 2024 evaluated the correlation through the computation of aggregated relative risks. During this analysis, investigators identified elevated blood pressure, elevated serum triglyceride, elevated plasma fasting glucose levels, and central obesity as potentially indicative of a greater risk of Parkinson’s disease.3

Investigators defined metabolic syndrome as the presence of ≥3 of the following risk factors: excess belly fat, high blood pressure, high blood sugar, low high-density lipoprotein cholesterol, and a higher number of triglycerides than normal.1

“Parkinson’s disease is the second most common neurodegenerative disorder among older adults after Alzheimer’s disease, and metabolic syndrome affects an estimated 1 in 4 adults and is highly modifiable,” said Weili Xu, PhD, department of neurobiology, care sciences and society, Karolinska Institutet, and lead author of the study. “Our findings suggest that metabolic syndrome may be a modifiable risk factor for Parkinson’s disease. Future studies are needed to see whether working to control metabolic syndrome could help prevent Parkinson’s disease.”1

Investigators included 467,200 individuals in the study, with an average age of 57 years. Of these, 38% of participants had metabolic syndrome. The team then followed participants for a median of 15 years, during which time 3,222 patients developed Parkinson’s disease. Those without metabolic syndrome exhibited an incidence rate of 4.87 per 10,000 person-years, compared to 5.21 cases per 10,000 person-years for people with metabolic syndrome.1

Xu and colleagues then adjusted for age, smoking status, physical activity, and genes that increase the risk of Parkinson’s. They found a 40% greater likelihood of Parkinson’s development in patients with metabolic syndrome than without.1

“We also found a higher risk of Parkinson’s disease for people with both metabolic syndrome and a genetic susceptibility for Parkinson’s disease,” Xu said. “This suggests that maintaining metabolic health may be especially important for people who have genes that increase their risk for Parkinson’s disease.”1

The team did note, however, that most included participants were white, potentially limiting the applicability of these results to broader groups. Additionally, they pointed out that the study did not show a definitive correlation; it only highlighted an association. More research is required to cement a connection between the 2 conditions.1

References
  1. American Academy of Neurology. Parkinson’s disease risk increases with metabolic syndrome. Eurekalert! August 20, 2025. Accessed August 20, 2025. https://www.eurekalert.org/news-releases/1095206?
  2. Zhang P, Tian B. Metabolic syndrome: an important risk factor for Parkinson's disease. Oxid Med Cell Longev. 2014;2014:729194. doi:10.1155/2014/729194
  3. Zhong Y, Wang TH, Huang LJ, Hua YS. Association between metabolic syndrome and the risk of Parkinson's disease: a meta-analysis. BMC Neurol. 2024;24(1):313. Published 2024 Sep 4. doi:10.1186/s12883-024-03820-y

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