Sensation seeking traits may explain the low PD risk in smokers and drinkers
The inverse relation between smoking and caffeine intake and Parkinson's disease risk may not be a direct protective effect, but the result of low sensation seeking traits in the individual.Investigators in London found that individuals with PD had lower sensation seeking scores than healthy controls and there was a positive relation between impulsive sensation seeking (ISS) and smoking, caffeine and alcohol intake. Using conditional logistic regression analysis, they also found that low sensation seeking traits explained some of the apparent effect of caffeine and alcohol intake (but little of the effect of smoking) on PD risk, whereas sensation seeking scores appeared to independently predict PD after adjusting for either smoking or caffeine and alcohol intake. The authors acknowledge that their data does not prove a pattern of causation, and that an alternative argument could be that sensation seeking scores are reduced by the development of PD. However, they found that sensation seeking scores did not relate to PD disease duration or severity.Patients with PD also had higher depression and anxiety scores, and sensation seeking in both PD patients and controls was inversely correlated with depression. The authors say this may be because low sensation seeking traits predispose PD patients to depression. Alternatively, depression, reduced sensation seeking traits and susceptibility to PD may all share a common neurobiological substrate. The authors conclude, "This study raises the possibility that there is a neurobiological link between low sensation seeking traits-which might underlie the parkinsonian personality-and the hypothetical protective effect of cigarette smoking and caffeine consumption on PD."They provide a schematic diagram illustrating how reduced sensation seeking may interact with behaviour and environmental factors to influence PD risk and explain, "The reduced sensation seeking model offers one possible explanation through which endogenously determined factors, such as individual variations in brain function, might interact with environmental exposures and lead to disease susceptibility."Reference...
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