Interesting paper out in JAMA, Coffee, CYP1A2 genotype, and risk of myocardial infarction:
The association between coffee intake and risk of myocardial infarction (MI) remains controversial. Coffee is a major source of caffeine, which is metabolized by the polymorphic cytochrome P450 1A2 (CYP1A2) enzyme. Individuals who are homozygous for the CYP1A2*1A allele are "rapid" caffeine metabolizers, whereas carriers of the variant CYP1A2*1F are "slow" caffeine metabolizers....Intake of coffee was associated with an increased risk of nonfatal MI only among individuals with slow caffeine metabolism, suggesting that caffeine plays a role in this association.
Imagine when insurance companies get their hands on this sort of information, they'll give you your lowest risk lifestyle dependent on your genotypic predispositions. This sort of trait indicates the contextual response of genes and subsequent development. Genes don't "determine" anything, they are important (or not) parameters in concert with a host of other variables.
Here is a popular press review of this paper.
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This is junk science.
if the hypothetical "one" is very sensitive to caffeine, does that make him/her a slow or fast metabolizer?
it is an interesting breakdown, supplating my much more crude initial reaction: "Yea, no shit it plays with some people's hearts. Caffeine is a friggin' CNS stimulant; that's what stimulants do."
This is junk science.
care to elaborate?
kevin, i think slow metabolizers are hit harder.
no CYP1A2 alleles are sufficient for coffee-related MI susceptibility, but I think it's pretty clear from this data that they are a causal determinant
"genes don't "determine" anything, they are important(or not) parameters in concert with a host of other variables."
According to the bell curve, low SES combined with high cognitive ability is not a barrier to higher education. Genes, probably more than anything else, are what constrains a dullard from becoming an elite professor, or what keeps a cow from holding a conversation. The coming singularity will allow our genes to be less deterministic in our lives, or maybe not. Maybe our cyborg personalities will only be extensions of our genetically determined personalities. There's no escaping the hegemony of the gene.
Coffee Time
No one knows exactly when and where humans first discovered the uses of the coffee plant, though legend generally attributes it to an Arabian goat herder named Kaldi. However,. "Recent botanical evidence indicates that Coffea arabica ...
Genes don't "determine" anything, they are important (or not) parameters in concert with a host of other variables.
Hmmm, I am male. SRY seems to have done a very good job of determining that. I know, lots of other things had to happen along the way. Many genes had to work in concert for that to happen, and, of course, my mother had to offer a womb for it to occur in and she had to provide the initial environment, and so on.
Similarly, I am only 5'7" in height. I note that recent studies have shown that something like 80% of the variation in height is due to genes. That seemed pretty obvious to me just by looking at the heights of parents and offspring in my family.
It seems pretty clear to me that our genomes are repositories of knowledge about the average environments they are likely to turn up in, and they have some pretty neat methods for ensuring that their reactions to variable environments is appropriate to their goals ...
Indeed, it seems to me that we can think of the environment as being divied into two classes:
- The passive envionment, like climate, soil, day/night etc around us.
- The active environment, ie that part of the environment that is composed of other replicators like ourselves. Some of those, of course, are more important to worry about than others. Eg, bacteria and viruses. They change so quickly that we need quick acting defences against them. Then there are members of our own species who make up our social envionment. They change very quickly, and are very deceptive. They might pretend to help us when in reality they want us to help them at our expense.
Well, I can attest to that. I started consuming large amounts of veggies(and quercitin heavy veggies like grapes, raisins, etc, something that supposedly slows the liver's detox met functions.) for breakfast and my heart started behaving funny after a few weeks. I simply had to stop taking my coffee(thick black, very concentrated's the way I like it), Got rid of the coffee and lo and behold back to normal.
Bok,
Okay, but raise the would-be MIT math professor in an African village, malnourished and carrying lots of parasites for his whole childhood, and there's a reasonable chance he won't arrive at college age with the same potential that he might have had if raised in a US middle class home. It's an interaction.
Interesting that the CYP1A2*1F variant appears to be dominant. Wouldn't someone who is homozygous for *that* variant be an even slower metabolizer, most likely? Why did they choose to split their population into CYP1A2*1A homozygotes and 'others' when they could have done a finer partitioning? Does the full text address that at all?
Also, their statistics seem to show that moderate coffee consumption actually decreases the risk of MI for rapid metabolizers, especially those younger than 59 years of age. Or am I misreading the odds ratios?