Alvin Lim

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A former health psychologist turned software engineer, my current interests include the…

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  • Circulating Interleukin-6 concentration covaries inversely with self-reported sleep duration as a function of polymorphic variation in the glucocorticoid receptor.

    Brain Behavior and Immunity

    Growing evidence links extremes of self-reported sleep duration with higher circulating markers of inflammatory disease risk, although not all findings are consistent. Extremes of sleep duration also associate with activation of the hypothalamic-pituitary-adrenocortical (HPA) system and the peripheral release of cortisol, a glucocorticoid (GC) important in downregulating transcription of pro-inflammatory molecules. Polymorphic variation in the gene encoding the GC receptor (GR; NR3C1) modulates…

    Growing evidence links extremes of self-reported sleep duration with higher circulating markers of inflammatory disease risk, although not all findings are consistent. Extremes of sleep duration also associate with activation of the hypothalamic-pituitary-adrenocortical (HPA) system and the peripheral release of cortisol, a glucocorticoid (GC) important in downregulating transcription of pro-inflammatory molecules. Polymorphic variation in the gene encoding the GC receptor (GR; NR3C1) modulates cellular sensitivity to GC-mediated anti-inflammatory signaling, thereby affecting levels of pro-inflammatory molecules. Thus, we hypothesized that extremes of self-reported sleep duration may covary with circulating levels of inflammatory markers as a function of allelic variation in NR3C1. Specifically, we examine the possibility that a single nucleotide polymorphism of the GR gene-(rs6198), the minor (G) allele of which confers reduced GR sensitivity-moderates an association of sleep duration with interleukin (IL)-6 and C-reactive protein (CRP) among a large sample (IL-6: N = 857; CRP: N = 929) of midlife community volunteers of European ancestry. Findings showed that sleep duration varied inversely with IL-6 (β = -0.087, p = .012), and this association was stronger among individuals homozygous for the rs6198 G-allele compared to alternate genotypes (β = -0.071, p = .039). We also found that sleep duration showed a U-shaped association with CRP (polynomial term: β = 0.093, p = .006), which was not moderated by rs6198 genotype. In conclusion, we show that a common genetic variant in the GR moderates an inverse association of self-reported sleep duration with circulating IL-6, possibly contributing to the increased disease risk observed among some short sleepers.

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  • Negative Affectivity and Inflammation: Moderation by the Glucocorticoid Receptor-9beta Polymorphism

    University of Pittsburgh Electronic Theses and Dissertations

    Growing evidence suggests that negative emotions may play a role in the upregulation of innate inflammatory processes and associated disease risk. Although the hypothalamic-adrenal-pituitary (HPA) axis is believed to play a role in these associations, empirical evidence is mixed. We examined whether genotypes of a single nucleotide polymorphism (SNP) in the GR gene—GR-9beta (rs6198), the minor (G) allele of which confers reduced GR sensitivity—moderated associations of negative affectivity (NA)…

    Growing evidence suggests that negative emotions may play a role in the upregulation of innate inflammatory processes and associated disease risk. Although the hypothalamic-adrenal-pituitary (HPA) axis is believed to play a role in these associations, empirical evidence is mixed. We examined whether genotypes of a single nucleotide polymorphism (SNP) in the GR gene—GR-9beta (rs6198), the minor (G) allele of which confers reduced GR sensitivity—moderated associations of negative affectivity (NA) and inflammatory activity. Here, NA was assessed by the neuroticism subscale of the NEO Personality Inventory and by the Positive and Negative Affect Schedule. In bivariate and hierarchical regression analyses adjusted for potential covariates, none of the NA measures predicted any of the inflammatory cytokine levels. However, subjects homozygous for the GR-9β G allele had higher IL-6 levels than those of alternate genotypes after adjustment for age, gender, and years of school (β = .057, p = .045, R2 = .047). Although GR-9β genotype was not associated with any of the stimulated cytokines, the interaction of GR-9β was significant, and showed that greater PANAS NA scores associated with greater IL-1β levels, but only among G allele homozygotes (β = .127, p = .027, ∆R2 = .015). These results raise the possibility that GR-9β G allele homozygotes show increased inflammatory susceptibility to negative emotionality.

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  • Peripheral Inflammation and Cognitive Aging

    Inflammation in Psychiatry. Modern Trends in Pharmacopsychiatry

    Evidence suggests that inflammation, an innate immune response facilitating recovery from injury and pathogenic invasion, is positively associated with age-related cognitive decline and may play a role in risk for dementia. Physiological pathways linking the peripheral immune and central nervous systems are outlined, and studies linking inflammation with neurocognitive function are overviewed. We also present recent studies from our laboratory showing that midlife inflammation is related to…

    Evidence suggests that inflammation, an innate immune response facilitating recovery from injury and pathogenic invasion, is positively associated with age-related cognitive decline and may play a role in risk for dementia. Physiological pathways linking the peripheral immune and central nervous systems are outlined, and studies linking inflammation with neurocognitive function are overviewed. We also present recent studies from our laboratory showing that midlife inflammation is related to cognitive function and brain morphology. Finally, potential implications for treatment, future directions, and limitations are discussed.

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  • Current understanding of the bi-directional relationship of major depression with inflammation.

    Biology of Mood & Anxiety Disorders

    Consistent evidence links major depression and its affective components to negative health outcomes. Although the pathways of these effects are likely complex and multifactorial, recent evidence suggests that innate inflammatory processes may play a role. An overview of current literature suggests that pathways between negative moods and inflammation are bi-directional. Indeed, negative moods activate peripheral physiologic mechanisms that result in an up regulation of systemic levels of…

    Consistent evidence links major depression and its affective components to negative health outcomes. Although the pathways of these effects are likely complex and multifactorial, recent evidence suggests that innate inflammatory processes may play a role. An overview of current literature suggests that pathways between negative moods and inflammation are bi-directional. Indeed, negative moods activate peripheral physiologic mechanisms that result in an up regulation of systemic levels of inflammation. Conversely, peripheral inflammatory mediators signal the brain to affect behavioral, affective and cognitive changes that are consistent with symptoms of major depressive disorder. It is likely that these pathways are part of a complex feedback loop that involves the nervous, endocrine, and immune systems and plays a role in the modulation of peripheral inflammatory responses to central and peripheral stimuli, in central responses to peripheral immune activation and in the maintenance of homeostatic balance. Further research is warranted to fully understand the role of central processes in this feedback loop, which likely contributes to the pathophysiology of mental and physical health.

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  • Low early-life social class leaves a biological residue manifested by decreased glucocorticoid and increased proinflammatory signaling

    Proceedings of the National Academy of Sciences

    Children reared in unfavorable socioeconomic circumstances show increased susceptibility to the chronic diseases of aging when they reach the fifth and sixth decades of life. One mechanistic hypothesis for this phenomenon suggests that social adversity in early life programs biological systems in a manner that persists across decades and thereby accentuates vulnerability to disease. Here we examine the basic tenets of this hypothesis by performing genome-wide transcriptional profiling in…

    Children reared in unfavorable socioeconomic circumstances show increased susceptibility to the chronic diseases of aging when they reach the fifth and sixth decades of life. One mechanistic hypothesis for this phenomenon suggests that social adversity in early life programs biological systems in a manner that persists across decades and thereby accentuates vulnerability to disease. Here we examine the basic tenets of this hypothesis by performing genome-wide transcriptional profiling in healthy adults who were either low or high in socioeconomic status (SES) in early life. Among subjects with low early-life SES, there was significant up-regulation of genes bearing response elements for the CREB/ATF family of transcription factors that conveys adrenergic signals to leukocytes, and significant down-regulation of genes with response elements for the glucocorticoid receptor, which regulates the secretion of cortisol and transduces its antiinflammatory actions in the immune system. Subjects from low-SES backgrounds also showed increased output of cortisol in daily life, heightened expression of transcripts bearing response elements for NF-B, and greater stimulated production of the proinflammatory cytokine interleukin 6. These disparities were independent of subjects’ current SES, lifestyle practices, and perceived stress. Collectively, these data suggest that low early-life SES programs a defensive phenotype characterized by resistance to glucocorticoid signaling, which in turn facilitates exaggerated adrenocortical and inflammatory responses. Although these response patterns could serve adaptive functions during acute threats to well-being, over the long term they might exact an allostatic toll on the body that ultimately contributes to the chronic diseases of aging.

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