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Posts Tagged ‘23andMe’

rs1800955 survives meta-analytical scrutiny of links between DRD4 and personality

Posted in DRD4, tagged , , on February 28, 2008| 1 Comment »

The publication of positive genetic association results is always something to cheer about although most of us know that on a different day, with a different sample, the results could just as easily been flat. So when a meta-analytical paper appears that actually supports a previous finding, you have to savor the sweet joy of it. So it is that Marcus Munafo and colleagues under the leadership of Jonathan Flint – one of the best meta-analytical assessors in the biz – report that the “C” allele of rs1800955 in the dopamine d4 receptor (DRD4) gene (doi: 10.1016/j.biopsych.2007.04.006) survives an analysis of several dozen studies on genetics and personality. Although small, “The evidence from our final meta-analysis indicatest hat the true effect size of the C-521T polymorphism on novelty seeking and impulsivity traits, if genuine, may account for up to 3%o of phenotypic variance.” I, perhaps due to my “C” allele am excited !

MUNAFO, M. (2008). Association of the Dopamine D4 Receptor (DRD4) Gene and Approach-Related Personality Traits: Meta-Analysis and New Data. Biological Psychiatry, 63(2), 197-206. DOI: 10.1016/j.biopsych.2007.04.006

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Sweets now, sweets later: rs165688 makes my holidays hell

Posted in COMT, DLPFC, Dopamine, Frontal cortex, Orbitofrontal cortex, Parahippocampal gyrus, Posterior parietal cortex, tagged , , , on January 1, 2008| Leave a Comment »

Holiday time is full of all things delicious and fattening. Should I have a little chocolate now, or wait till later and have a bigger dessert ? Of course, this is not a real forced choice (in my case, the answer too often seems – alas – “I’ll have both!”), but there are many times in life when we are forced to decide between ‘a little now’ or ‘more later’. Sometimes, its clear that the extra $20 in your pocket now would be better utilized later on, after a few years of compound interest. Other times, its not so clear. Consider the recent ruling by the Equal Employment Opportunity Commission, which allows employers to drop retirees’ health coverage once they turn 65 and become eligible for Medicare. Do I save my resources now to provide for my geezerdom healthcare spending, or do I enjoy (spend) my resources now while I’m young and able ? How do I make these decisions ? How does my life experience and genome interact to influence the brain systems that support these computations ? Boettiger and company provide some insight to these questions in their paper, “Immediate Reward Bias in Humans: Fronto-Parietal Networks and a Role for the Catechol-O-Methyltransferase 158Val/Val Genotype” (DOI). The authors utilize an assay that measures a subject’s preference for rewards now or later and use functional brain imaging to seek out brain regions where activity is correlated to preferences for immediate rewards. Dopamine rich brain regions such as the posterior parietal cortex, dorsal prefrontal cortex and rostral parahippocampal gyrus showed (+) correlations while the lateral orbitofrontal cortex showed a (-) correlation. Variation in the dopaminergic enzyme COMT at the rs165688 SNP also showed a correlation with preferences for immediate reward as well as with brain activation. The authors’ results suggest that improving one’s ability to weigh long-term outcomes is a likely therapeutic avenue for helping impulsive folks (like me) optimize our resource allocation. I have not yet had my genome deCODEd or Google-ed, but strongly suspect I am a valine/valine homozygote.

Indeed it seems I am a GG (Valine/Valine) at this site according to 23andMe !

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I carry genetic risk for mental illness

Posted in DTNBP1, tagged , , , , on December 21, 2007| Leave a Comment »

Joan of ArcImage by dbking via Flickr Amidst the excitement of new personalized genome services, the Economist reports on fraudsters found peddling ‘personalized supplements’ based on bogus genetic testing results. This is an extreme, tragicomic example to be sure, but highlights some of the issues that can arise when confronting one’s genetic blueprint. A recent paper by Stephanis et al., “Impact of Schizophrenia Candidate Genes on Schizotypy and Cognitive Endophenotypes at the Population Level” (DOI) shows that in a population of healthy individuals, those that carry common variants (such as rs760761, rs1018381, rs2619522) located in the dysbindin (DTNBP1) gene, a risk factor for schizophrenia, show minor cognitive impairments such as decreased attentional capacity, worse performance on memory tasks, and alterations in schizotypal beliefs and experiences. Thus, it would seem that, common genetic variation associated with a complex psychiatric disorder can confer minor cognitive impairment in healthy individuals. As personalized genome services proliferate, healthy individuals will begin to recognize that they carry genetic risk for all kinds of ailments – mental illness included. I admit to having cringed somewhat when typing out the blunt title of this post – fraudsters notwithstanding.

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rs6265 (A) is my bodyguard

Posted in BDNF, Nucleus accumbens, Striatum, Ventral tegmental area, tagged , , on November 19, 2007| Leave a Comment »

It’s generally not fun to be browbeaten, bullied, bulldozed or downright oppressed – by the schoolyard bully or perhaps the micromanaging boss – in any form. While we’ve all been there – sometimes with initial feelings of sorrow, mopiness, lethargy, etc. – all part of the normal adaptive response to just pack-it-in and withdraw, the effects of social stress in some individuals can be quite profound and serious. The recent paper, “Molecular Adaptations Underlying Susceptibility and Resistance to Social Defeat in Brain Reward Regions” by Krishnan and company (DOI) provides some insight into mechanisms of social stress and how several genetic factors are implicated in the regulation of activity of a particular synapse linking the ventral tegmental area (VTA) and nucleus accumbens (NAc). Of particular interest is the protective effect of a single G to A nucleotide change (rs6265) in the brain derived neurotrophic factor (BDNF) that leads to a valine to methionine amino acid substitution at position 66, a portion of the protein thought to play a role in cytoplasmic trafficking. As reported, transgenic mice that carry the human form of the poorly secreted Met/Met form of BDNF did not suffer a typical withdrawl, depression-like syndrome when subjected to a paradigm of chronic social defeat as compared to defeated Val/Val (highly secreted form) mice. In correspondence with this finding, higher levels of BDNF were found in the NAc in human cases of human depression. The authors’ work provides a new mechanistic model for regulation of VTA-NAc synaptic activity that makes testable predictions about complex behaviors and avenues for prevention and remediation of one of life’s unpleasant, but inevitable, tribulations.

…darn-it !  my 23andMe profile shws that I am a C/C valine/valine … how depressing 😦

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