Tuesday, May 1, 2018

We find that for men, particularly among younger cohorts, the physically stronger are more likely to be married (no relation for women), consistent with a hypothesis that women increasingly have selected male marital partners based on preferred individual traits

Women’s Spousal Choices and a Man’s Handshake: Evidence from a Norwegian Study of Cohort Differences. Vegard Skirbekk, Melissa Hardy, Bjørn Heine Strand. SSM - Population Health, https://doi.org/10.1016/j.ssmph.2018.04.004

Abstract: Both high grip strength and being married independently relate to better functional capacity and health at older ages, but the combined effect of marital status and strength have not been investigated. Especially at older ages, declining strength can have adverse health and social consequences, where having a spouse could potentially help with everyday support and alleviate some of the negative effects of sarcopenia. We investigate how grip strength relates to being married among two cohorts of 59–71 year olds (born 1923-35 and 1936-48) in the Norwegian city of Tromsø, controlling for a broad set of health variables and sociodemographic characteristics. The baseline included N=5009 participants of whom 649 died during follow-up. We find that for men, particularly among younger cohorts, the physically stronger are more likely to be married, but no relation is found for women. This is consistent with a hypothesis that women increasingly have selected male marital partners based on preferred individual traits, whereas men do not emphasize strength when selecting women. We find that both marital status and grip strength independently affect mortality, but there is no significant joint effect. However, the distribution of strength and marital status implies that more men than women and increasing shares of later born cohorts have a “double-burden” of low strength and a lack of support from a spouse.

Keywords: Sarcopenia, Marriage, Gender Differences, Older Adults

Why Hate the Good Guy? Antisocial Punishment of High Cooperators Is Greater When People Compete to Be Chosen

Why Hate the Good Guy? Antisocial Punishment of High Cooperators Is Greater When People Compete to Be Chosen. Aleta Pleasant, Pat Barclay. Psychological Science, https://doi.org/10.1177/0956797617752642

Abstract: When choosing social partners, people prefer good cooperators (all else being equal). Given this preference, people wishing to be chosen can either increase their own cooperation to become more desirable or suppress others’ cooperation to make them less desirable. Previous research shows that very cooperative people sometimes get punished (“antisocial punishment”) or criticized (“do-gooder derogation”) in many cultures. Here, we used a public-goods game with punishment to test whether antisocial punishment is used as a means of competing to be chosen by suppressing others’ cooperation. As predicted, there was more antisocial punishment when participants were competing to be chosen for a subsequent cooperative task (a trust game) than without a subsequent task. This difference in antisocial punishment cannot be explained by differences in contributions, moralistic punishment, or confusion. This suggests that antisocial punishment is a social strategy that low cooperators use to avoid looking bad when high cooperators escalate cooperation.

Keywords: public-goods games, biological markets, partner choice, competitive altruism, do-gooder derogation, open data, open materials

Identity prediction errors in the human midbrain update reward-identity expectations in the orbitofrontal cortex

Identity prediction errors in the human midbrain update reward-identity expectations in the orbitofrontal cortex. James D. Howard & Thorsten Kahnt. Nature Communications, volume 9, Article number: 1611 (2018), doi 10.1038/s41467-018-04055-5

Abstract: There is general consensus that dopaminergic midbrain neurons signal reward prediction errors, computed as the difference between expected and received reward value. However, recent work in rodents shows that these neurons also respond to errors related to inferred value and sensory features, indicating an expanded role for dopamine beyond learning cached values. Here we utilize a transreinforcer reversal learning task and functional magnetic resonance imaging (fMRI) to test whether prediction error signals in the human midbrain are evoked when the expected identity of an appetitive food odor reward is violated, while leaving value matched. We found that midbrain fMRI responses to identity and value errors are correlated, suggesting a common neural origin for these error signals. Moreover, changes in reward-identity expectations, encoded in the orbitofrontal cortex (OFC), are directly related to midbrain activity, demonstrating that identity-based error signals in the midbrain support the formation of outcome identity expectations in OFC.

h/t: Sadashiva Pai

Antidepressant Use Prospectively Relates to a Poorer Long-Term Outcome of Depression: Results from a Prospective Community Cohort Study over 30 Years

Antidepressant Use Prospectively Relates to a Poorer Long-Term Outcome of Depression: Results from a Prospective Community Cohort Study over 30 Years. Michael P. Hengartner, Jules Angst, Wulf Rössler. Psychotherapy and Psychosomatics, doi 10.1159/000488802

Despite marked increases in antidepressant drug prescriptions over the last 3 decades, the burden and disability attributed to major depression are still on the rise. This calls into question the sustainable clinical benefits attributed to antidepressants. The efficacy of antidepressants based on mostly industry-funded short-term trials has been challenged due to selective reporting and systematic method biases (e.g., unblinding of outcome assessors), and the long-term benefits of antidepressants have also been debated [1, 2]. Two long-term effectiveness trials of 1 year duration found no clinically important effect in terms of sustained remission for long-term antidepressant use (the sustained remission rate was < 6% [3, 4]), and a meta-analysis of long-term parallel-arm efficacy trials of 6–8 months treatment duration found no significant difference between antidepressants and placebo with respect to both remission and premature treatment discontinuation [5]. Some prospective observational studies with 1- to 9-year follow-ups even reported a poorer outcome in antidepressant users relative to non-users [6–8]. In contrast to these findings, discontinuation trials of commonly 6–18 months duration suggest that long-term antidepressant use may prevent relapses (reviewed in Hengartner [1]). However, the validity of these trials has been questioned, because they include only participants who respond well to the drugs and randomise some of them to have the drug withdrawn rapidly and replaced by placebo, which can cause severe withdrawal syndromes that mimic depression relapse [1, 2]. Since extended observation periods of 10 years and more are not feasible within a randomised placebo-controlled trial design, the aim of the present work was to test in a representative community cohort study over 30 years whether antidepressant use, relative to non-use, would relate to a poorer long-term outcome of depression.

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In this community cohort of 591 adults followed from the age of 20/21 to 49/50 years, we found that, independently of illness severity and distress at baseline, antidepressant use prospectively relates to a poorer long-term outcome in depression. These findings are in line with a growing body of evidence from several naturalistic observational studies suggesting that (long-term) antidepresant use may produce a poor long-term outcome in people with depression [6–8]. A neurobiological mechanism that may causally explain these findings is the oppositional model of tolerance by Fava [10], which proposes that continued antidepressant use may recruit pharmacodynamic processes such as receptor sensitization that results in loss of clinical effect and in some patients even in an increased vulnerability to depression relapse.

The present work is not without limitations. Most importantly, participants were not randomised to antidepressant use, which precludes causal conclusions. Antidepressant use relied on self-report, and we do not have data on the specific drug prescribed, its dosage, and on the duration of medication. Considering these limitations, our findings raise the possibility that antidepressants may worsen the long-term course of depression. It remains to be established whether this effect is causally related to antidepressant use or to uncontrolled aetiological factors differentiating antidepressant users from non-users, such as for instance coping skills, social support, or personality characteristics.