Type 2 diabetes may promote Parkinson development

Type 2 diabetes mellitus may be associated with an increased risk of Parkinson’s disease, according to a large retrospective cohort study published online June 13 in Neurology.

Researchers accessed the linked English national Hospital Episode Statistics and mortality data from 1999-2011 to compare data from 2,017,115 individuals admitted to hospital who had a diagnostic code for type 2 diabetes with data from a reference cohort of 6,173,208 individuals admitted for a range of other minor procedures.

They found a significant 32% higher incidence of Parkinson’s disease among individuals with type 2 diabetes, compared with the reference cohort (95% confidence interval, 1.29-1.35; P less than .001).

The incidence was particularly high among younger individuals with type 2 diabetes; those aged 25-44 years at the time of admission had a 3.8-fold higher rate of Parkinson’s disease, compared with the reference group (P less than .001). Individuals aged 45-64 years with type 2 diabetes had 71% greater rate of Parkinson, those aged 65-74 years had a 40% higher incidence, and those aged 75 years or over had an 18% higher rate.

Individuals with complicated type 2 diabetes, defined as the presence of diabetic neuropathy, nephropathy, or retinopathy, had a 49% higher incidence of Parkinson disease than did the reference cohort.

Eduardo De Pablo-Fernandez, MD, from the University College London Institute of Neurology, and his coauthors suggested that the interaction between the two, apparently unconnected, diseases may be a function of both genetics and shared pathogenic pathways.

“The magnitude of risk in our study was greater in younger individuals, whereby genetic factors may relatively exert more of an effect, and more than 400 genes, previously identified through genome-wide association studies, have been closely linked to both conditions using integrative network analysis,” the authors wrote.

“However, the association in elderly patients may be the consequence of disrupted insulin signaling secondary to additional lifestyle and environmental factors causing cumulative pathogenic brain changes.”

They proposed that disrupted brain insulin signaling could lead to neuroinflammation, mitochondrial dysfunction, and increased oxidative stress that could contribute to the development of Parkinson’s disease.

The findings were similar to those seen in a previous meta-analysis of five studies, although the authors commented that there was significant heterogeneity among the studies included in that analysis.

The authors of this study also noted that their study did not adjust for potential confounders such as smoking or antidiabetic medication use.

The study was supported by the National Institute for Health Research Biomedical Research Centre at the University of Oxford, England, and the NIHR Biomedical Research Centre at University College London. Two authors declared funding and payments from private industry outside the submitted work, but no other conflicts of interest were declared.

SOURCE: De Pablo Fernandez E et al. Neurology. 2018 June 13. doi: 10.1212/WNL.0000000000005771.

Type 2 diabetes mellitus may be associated with an increased risk of Parkinson’s disease, according to a large retrospective cohort study published online June 13 in Neurology.

Researchers accessed the linked English national Hospital Episode Statistics and mortality data from 1999-2011 to compare data from 2,017,115 individuals admitted to hospital who had a diagnostic code for type 2 diabetes with data from a reference cohort of 6,173,208 individuals admitted for a range of other minor procedures.

They found a significant 32% higher incidence of Parkinson’s disease among individuals with type 2 diabetes, compared with the reference cohort (95% confidence interval, 1.29-1.35; P less than .001).

The incidence was particularly high among younger individuals with type 2 diabetes; those aged 25-44 years at the time of admission had a 3.8-fold higher rate of Parkinson’s disease, compared with the reference group (P less than .001). Individuals aged 45-64 years with type 2 diabetes had 71% greater rate of Parkinson, those aged 65-74 years had a 40% higher incidence, and those aged 75 years or over had an 18% higher rate.

Individuals with complicated type 2 diabetes, defined as the presence of diabetic neuropathy, nephropathy, or retinopathy, had a 49% higher incidence of Parkinson disease than did the reference cohort.

Eduardo De Pablo-Fernandez, MD, from the University College London Institute of Neurology, and his coauthors suggested that the interaction between the two, apparently unconnected, diseases may be a function of both genetics and shared pathogenic pathways.

“The magnitude of risk in our study was greater in younger individuals, whereby genetic factors may relatively exert more of an effect, and more than 400 genes, previously identified through genome-wide association studies, have been closely linked to both conditions using integrative network analysis,” the authors wrote.

“However, the association in elderly patients may be the consequence of disrupted insulin signaling secondary to additional lifestyle and environmental factors causing cumulative pathogenic brain changes.”

They proposed that disrupted brain insulin signaling could lead to neuroinflammation, mitochondrial dysfunction, and increased oxidative stress that could contribute to the development of Parkinson’s disease.

The findings were similar to those seen in a previous meta-analysis of five studies, although the authors commented that there was significant heterogeneity among the studies included in that analysis.

The authors of this study also noted that their study did not adjust for potential confounders such as smoking or antidiabetic medication use.

The study was supported by the National Institute for Health Research Biomedical Research Centre at the University of Oxford, England, and the NIHR Biomedical Research Centre at University College London. Two authors declared funding and payments from private industry outside the submitted work, but no other conflicts of interest were declared.

SOURCE: De Pablo Fernandez E et al. Neurology. 2018 June 13. doi: 10.1212/WNL.0000000000005771.

Type 2 diabetes mellitus may be associated with an increased risk of Parkinson’s disease, according to a large retrospective cohort study published online June 13 in Neurology.

Researchers accessed the linked English national Hospital Episode Statistics and mortality data from 1999-2011 to compare data from 2,017,115 individuals admitted to hospital who had a diagnostic code for type 2 diabetes with data from a reference cohort of 6,173,208 individuals admitted for a range of other minor procedures.

They found a significant 32% higher incidence of Parkinson’s disease among individuals with type 2 diabetes, compared with the reference cohort (95% confidence interval, 1.29-1.35; P less than .001).

The incidence was particularly high among younger individuals with type 2 diabetes; those aged 25-44 years at the time of admission had a 3.8-fold higher rate of Parkinson’s disease, compared with the reference group (P less than .001). Individuals aged 45-64 years with type 2 diabetes had 71% greater rate of Parkinson, those aged 65-74 years had a 40% higher incidence, and those aged 75 years or over had an 18% higher rate.

Individuals with complicated type 2 diabetes, defined as the presence of diabetic neuropathy, nephropathy, or retinopathy, had a 49% higher incidence of Parkinson disease than did the reference cohort.

Eduardo De Pablo-Fernandez, MD, from the University College London Institute of Neurology, and his coauthors suggested that the interaction between the two, apparently unconnected, diseases may be a function of both genetics and shared pathogenic pathways.

“The magnitude of risk in our study was greater in younger individuals, whereby genetic factors may relatively exert more of an effect, and more than 400 genes, previously identified through genome-wide association studies, have been closely linked to both conditions using integrative network analysis,” the authors wrote.

“However, the association in elderly patients may be the consequence of disrupted insulin signaling secondary to additional lifestyle and environmental factors causing cumulative pathogenic brain changes.”

They proposed that disrupted brain insulin signaling could lead to neuroinflammation, mitochondrial dysfunction, and increased oxidative stress that could contribute to the development of Parkinson’s disease.

The findings were similar to those seen in a previous meta-analysis of five studies, although the authors commented that there was significant heterogeneity among the studies included in that analysis.

The authors of this study also noted that their study did not adjust for potential confounders such as smoking or antidiabetic medication use.

The study was supported by the National Institute for Health Research Biomedical Research Centre at the University of Oxford, England, and the NIHR Biomedical Research Centre at University College London. Two authors declared funding and payments from private industry outside the submitted work, but no other conflicts of interest were declared.

SOURCE: De Pablo Fernandez E et al. Neurology. 2018 June 13. doi: 10.1212/WNL.0000000000005771.