A recent Aging and Disease study reports that adults with obesity have reduced circulating choline levels alongside multiple biochemical markers associated with metabolic dysfunction and early neurodegenerative risk. The findings may be relevant for laboratories assessing metabolic health and for those monitoring biomarkers linked to Alzheimer’s disease.
The research compared fasting blood measures from 30 adults with either healthy or obese body mass index (BMI) classifications. Individuals with obesity had significantly lower plasma choline levels than healthy-weight participants. Choline also showed strong negative correlations with BMI, percentage body fat, fasting insulin, and HOMA-IR, indicating close association with insulin resistance metrics.
Inflammatory profiling revealed that all 11 measured cytokines – including IFN-γ, IL-6, IL-1β, IL-8, and TNF-α – were elevated in obesity. Each cytokine was negatively correlated with circulating choline, suggesting that lower choline levels aligned with heightened systemic inflammation.
Liver-associated enzymes were also altered. Aldolase B and sorbitol dehydrogenase, both linked to hepatic carbohydrate metabolism, were significantly higher in participants with obesity. Both enzymes showed strong inverse relationships with plasma choline levels. These findings are consistent with the role of choline in supporting liver function and its depletion in metabolic stress.
The study further assessed neurofilament light chain (NfL), a biomarker of axonal injury used in diagnostic testing for neurodegenerative disorders. NfL levels were elevated in participants with obesity and negatively correlated with choline. To validate this relationship, the researchers examined post-mortem serum from individuals with mild cognitive impairment or Alzheimer’s disease. NfL increased with disease severity, while choline decreased, mirroring the pattern observed in the obesity cohort.
These results highlight the potential value of panels that include choline alongside metabolic, inflammatory, hepatic, and neurodegenerative markers. Although the study does not determine causality, the consistent associations suggest choline could serve as an indicator of broader metabolic and neuronal changes.
The authors note limitations, including small sample size and absence of dietary intake data. However, the findings indicate that reduced circulating choline may accompany states of insulin resistance, inflammation, liver dysfunction, and elevated NfL – biomarkers relevant to both metabolic disease progression and Alzheimer’s-related pathology.
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