Zpol
Member
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- Apr 14, 2013
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- 45
More on the GRIN2A genotype that was briefly mentioned in the study...
Caffeine, creatine, GRIN2A and Parkinson's disease progression
I would like to learn more about this GRIN2A thing but I don't want to purchase the full text of this study, so if anyone has some links or info they could share, that'd be awesome.
I don't have PD but I would think that anything that would increase the rate of progression of this terrible disease would not be good for disease prevention either.
Before reading about the GRIN2A issue, it sounded like the problem was more from the Levdopa interaction or possibly the participants in the high caffeine+creatine group were drinking dangerous sports drinks and doing high-stress inducing workouts and that's what caused increased progression. Now I'm not so sure. Or maybe those factors are what caused the gene variant.
Would those of us taking dopaminergic supplements along with creatine and coffee be at the same risk (of having spare methyl groups)?
So much to consider.
Caffeine, creatine, GRIN2A and Parkinson's disease progression
Abstract
Caffeine is neuroprotective in animal models of Parkinson's disease (PD) and caffeine intake is inversely associated with the risk of PD. This association may be influenced by the genotype of GRIN2A, which encodes an NMDA-glutamate-receptor subunit. In two placebo-controlled studies, we detected no association of caffeine intake with the rate of clinical progression of PD, except among subjects taking creatine, for whom higher caffeine intake was associated with more rapid progression. We now have analyzed data from 420 subjects for whom DNA samples and caffeine intake data were available from a placebo-controlled study of creatine in PD. The GRIN2A genotype was not associated with the rate of clinical progression of PD in the placebo group. However, there was a 4-way interaction between GRIN2A genotype, caffeine, creatine and the time since baseline. Among subjects in the creatine group with high levels of caffeine intake, but not among those with low caffeine intake, the GRIN2A T allele was associated with more rapid progression (p = 0.03). These data indicate that the deleterious interaction between caffeine and creatine with respect to rate of progression of PD is influenced by GRIN2A genotype. This example of a genetic factor interacting with environmental factors illustrates the complexity of gene-environment interactions in the progression of PD.
Caffeine is neuroprotective in animal models of Parkinson's disease (PD) and caffeine intake is inversely associated with the risk of PD. This association may be influenced by the genotype of GRIN2A, which encodes an NMDA-glutamate-receptor subunit. In two placebo-controlled studies, we detected no association of caffeine intake with the rate of clinical progression of PD, except among subjects taking creatine, for whom higher caffeine intake was associated with more rapid progression. We now have analyzed data from 420 subjects for whom DNA samples and caffeine intake data were available from a placebo-controlled study of creatine in PD. The GRIN2A genotype was not associated with the rate of clinical progression of PD in the placebo group. However, there was a 4-way interaction between GRIN2A genotype, caffeine, creatine and the time since baseline. Among subjects in the creatine group with high levels of caffeine intake, but not among those with low caffeine intake, the GRIN2A T allele was associated with more rapid progression (p = 0.03). These data indicate that the deleterious interaction between caffeine and creatine with respect to rate of progression of PD is influenced by GRIN2A genotype. This example of a genetic factor interacting with environmental factors illustrates the complexity of gene-environment interactions in the progression of PD.
I would like to learn more about this GRIN2A thing but I don't want to purchase the full text of this study, so if anyone has some links or info they could share, that'd be awesome.
I don't have PD but I would think that anything that would increase the rate of progression of this terrible disease would not be good for disease prevention either.
Before reading about the GRIN2A issue, it sounded like the problem was more from the Levdopa interaction or possibly the participants in the high caffeine+creatine group were drinking dangerous sports drinks and doing high-stress inducing workouts and that's what caused increased progression. Now I'm not so sure. Or maybe those factors are what caused the gene variant.
Would those of us taking dopaminergic supplements along with creatine and coffee be at the same risk (of having spare methyl groups)?
So much to consider.