Why are people so quick to assume the motivations of others for a basic comment?
Posting form this position - Psychopharmacology and neuroscience research to post graduate level. I'm not keen to see a genetic explanation, i'm keen to see the results of research into this area because then we can discuss the extent biology plays a role in relation to socio-economical factors.
There is some research suggesting opiate addicts could be compensating for a dysregualted endogenous opiate system through substance abuse. There is similar work for dopamine with smoking. Looking at things this way could change the way interventions are offered and also potentially reduce stigma for some of those who have addictions.
Some interesting links that have likely already been shared on HN for both socio-economical and biological theories:
Would there not be value in pre-screening patients for SCN9A mutations to predict an increased risk of pain killer addiction? Socioeconomic factors play as role as well, but it doesn't to be so black and white.
> Would there not be value in pre-screening patients for SCN9A mutations to predict an increased risk of pain killer addiction?
Dangers, too. Legitimate pain patients already frequently have to drop through an onerous set of hoops for opiates, and the medical system isn't always good at teasing out "increased risk" from "unacceptable risk". (For example: https://en.wikipedia.org/wiki/Rofecoxib, aka Vioxx)
SCN9A variants have certainly been linked to changes in pain sensitivity (in both directions), but where have they been linked to changes in risk for opiate addiction? Even for the variant identified in this paper, the fact that it was linked to increased pain doesn't necessarily mean that it would put one at an increased risk for opiate addiction; in fact, you could easily imagine the opposite.
Furthermore, in spite of the strong genetic evidence, especially for the cases for congenital pain insensitivity, it has also been hard for the industry to develop Nav1.7 inhibitors, but that could mostly be due to targeting specificity.
As a follow-up for those that have said genetic studies have been fruitful, here's excerpts from the most recent genetic study [1]. This study looked at a link in the μ-opioid receptor gene, which was the only gene that barely reached genome-wide significance in their meta-analysis of 8529 individuals with opioid use disorder (OUD). In contrast, smoking, alcohol use, and education status showed clear effects on OUD.
"Understanding the genetic architecture of OUD might provide clinically useful clues about its biology. However, to our knowledge, only a few risk variants have been identified by GWAS so far, and none has had clear external replication. Several factors contribute to this situation: (1) OUD is a complex psychiatric disease with relatively low heritability, and there is no single variant with a large effect size that can be detected in small cohorts"
Because "genetic causes" will be abused (and arguably is pretty much just a dogwhistle) for racial stereotyping and Untermensch classifications, so you better be damn sure about the accuracy and impact magnitude before talking about it.
Yes. We live in a kind of reflexive terror of a regime that has been dead for the better part of a century and we must not look at certain parts of reality, lest they be true, because those people did something terrible related to that field of inquiry. There comes a time when crouching in silence waiting for a dogwhistle to be blown that nobody else can hear becomes paranoia.
It would be more reasonable and compassionate to identify genetic risk factors so that the people in question could make more informed choices in their lives, but instead we must keep them (and ourselves) ignorant lest, somewhere in the dark, a reel of Triumph of the Will begins spinning all on its own.
> That is hardly a good explanation to avoid scientific research.
I agree it's not, because it's not about research, but rather about science and "science" reporting as well as what ends up in the "news" ("researchers find the addiction gene"). That's why I said it is important to consider the magnitude before talking about it, not before researching it, because obviously you don't know the impact before the research is done.
Yeah it's very tricky given that being able to identify genetic causes could make it easier to identify and help people who may have a higher probability of suffering from some specific issue, such as opt-in screening for Tay-Sachs for people of Ashkenazi Jewish heritage.
I think the line to draw is that for it to be positive it should always be private, voluntary, independent from public policy and strictly for the purposes of improving medical outcomes.
Both are valid searches IMHO. Acknowledging the results of the search is also important.
If we replace the DNA in a human OVA with different DNA we get a different person. I conclude therefore, that DNA plays a role in who and what we are, the extent of which requires honest study.
We like elegant single-variable explanations for observed phenomenon.
See whatever that effect is called where a hundred thousand people collaborate to make something great, and the single person at the top of the organization is given 100% of the credit.
Posting form this position - Psychopharmacology and neuroscience research to post graduate level. I'm not keen to see a genetic explanation, i'm keen to see the results of research into this area because then we can discuss the extent biology plays a role in relation to socio-economical factors.
There is some research suggesting opiate addicts could be compensating for a dysregualted endogenous opiate system through substance abuse. There is similar work for dopamine with smoking. Looking at things this way could change the way interventions are offered and also potentially reduce stigma for some of those who have addictions.
Some interesting links that have likely already been shared on HN for both socio-economical and biological theories:
https://en.wikipedia.org/wiki/Rat_Park
https://www.nature.com/articles/s41380-018-0117-2