The Relationship Between Alcohol and Glycohemoglobin: A Biopsychosocial Perspective.
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ABSTRACT:
SUBMITTER: Wiss DA
PROVIDER: S-EPMC6776959 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Many factors appear to be related to physical activity after stroke, yet it is unclear how these factors interact and which ones might be the best predictors. Therefore, the purpose of this study was twofold: (1) to examine the relationship between walking capacity and walking activity, and (2) to investigate how biopsychosocial factors and self-efficacy relate to walking activity, above and beyond walking capacity impairment poststroke.Individuals greater than 3 months poststroke (n = 55) completed the Yesavage Geriatric Depression Scale (GDS), Fatigue Severity Scale (FSS), Modified Cumulative Illness Rating (MCIR) Scale, Walk 12, Activities-Specific Balance Confidence (ABC) Scale, Functional Gait Assessment (FGA), and oxygen consumption testing. Walking activity data were collected via a StepWatch Activity Monitor. Predictors were grouped into 3 constructs: (1) walking capacity: oxygen consumption and FGA; (2) biopsychosocial: GDS, FSS, and MCIR; (3) self-efficacy: Walk 12 and ABC. Moderated sequential regression models were used to examine what factors best predicted walking activity.Walking capacity explained 35.9% (P < 0.001) of the variance in walking activity. Self-efficacy (?R = 0.15, P < 0.001) and the interaction between the FGA×ABC (?R = 0.047, P < 0.001) significantly increased the variability explained. The FGA (? = 0.37, P = 0.01), MCIR (? = -0.26, P = 0.01), and Walk 12 (? = -0.45, P = 0.00) were each individually significantly associated with walking activity.Although measures of walking capacity and self-efficacy significantly contributed to "real-world" walking activity, balance self-efficacy moderated the relationship between walking capacity and walking activity. Improving balance self-efficacy may augment walking capacity and translate to improved walking activity poststroke.Video Abstract available for more insights from the authors (see Supplemental Digital Content 1, http://links.lww.com/JNPT/A139).
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Project description:Alcohol consumption is typically correlated with the alcohol use behaviors of one's peers. Previous research has suggested that this positive relationship could be due to social selection, social influence, or a combination of both processes. However, few studies have considered the role of shared genetic and environmental influences in conjunction with causal processes.This study uses data from a sample of male twins (N = 1,790) who provided retrospective reports of their own alcohol consumption and their peers' alcohol-related behaviors, from adolescence into young adulthood (ages 12 to 25). Structural equation modeling was employed to compare 3 plausible models of genetic and environmental influences on the relationship between phenotypes over time.Model fitting indicated that one's own alcohol consumption and the alcohol use of one's peers are related through both genetic and shared environmental factors and through unique environmental causal influences. The relative magnitude of these factors, and their contribution to covariation, changed over time, with genetic factors becoming more meaningful later in development.Peers' alcohol use behaviors and one's own alcohol consumption are related through a complex combination of genetic and environmental factors that act via correlated factors and the complementary causal mechanisms of social selection and influence. Understanding these processes can inform risk assessment as well as improve our ability to model the development of alcohol use.
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Project description:A few studies have suggested a relationship between thyroid hormones and alcohol dependence (AD) such as a blunted increase of thyroid stimulating hormone (TSH) in response to thyrotropin-releasing hormone (TRH), lower levels of circulating free triiodothyronine (fT3) and free thyroxine (fT4) levels and down regulation of the TRH receptors. The current study aimed to explore the relationship between the hormones of the thyroid axis and alcohol-seeking behaviors in a sample of alcohol-dependent patients.Forty-two treatment-seeking alcohol-dependent individuals enrolled in a 12-week treatment study were considered. The Timeline Follow Back (TLFB) was used to assess the number of drinks consumed during the 12-week period. Blood levels of thyroid hormones (TSH, fT3 and fT4) were measured prior to and at the end of treatment. Questionnaires were administered to evaluate craving for alcohol [Penn Alcohol Craving Scale (PACS) and the Obsessive Compulsive Drinking Scale (OCDS) and its two subscales ODS for obsessions and CDS for compulsions] as well as anxiety [State and Trait Inventory (STAI)], depression [the Zung Self-Rating Depression Scale (Zung)] and aggression [the Aggressive Questionnaire (AQ)].At baseline, we found significant positive correlations between fT3 and OCDS (r = 0.358, P = 0.029) and CDS (r = 0.405, P = 0.013) and negative correlations between TSH levels and STAI (r = -0.342, P = 0.031), and AQ (r = -0.35, P = 0.027). At the end of the 12-week study period, abstinent patients had a greater change in TSH than those who relapsed (-0.4 vs. -0.25, F(1,24) = 5.4, P = 0.029).If confirmed in larger samples, these findings could suggest that the thyroid axis might represent a biomarker of alcohol craving and drinking.
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Project description:BACKGROUND:Physical activity behavior is a complex and multidimensional phenomenon. For its analysis, transdisciplinary biopsychosocial approaches yield great potential. In health research, the biopsychosocial model has experienced a renaissance. Researchers have tried to grasp the complex interplay of biological, psychological, and social factors. With this scoping review, we aimed to examine how the 'biopsychosocial' has been conceptualized in scientific work related to physical activity behavior. METHODS:The scoping review was informed by the PRISMA guidelines for scoping reviews (PRISMA-ScR). A systematic literature search was conducted in Web of Science, SportDiscus, PsycArticles, PsycInfo, and PubMed. Only articles published in peer-reviewed journals that contained all three components of a biopsychosocial approach (e.g., bio/physio/genetic, psycho/mental, and socio/cultural/environmental) were included. We only included articles in our narrative synthesis that integrated physical activity behavior into a biopsychosocial model, or investigated or described physical activity behavior on the basis of such a model. RESULTS:Thirteen studies met the inclusion criteria; eight articles pursued a biopsychosocial approach in the tradition of Engel, five employed a socio-ecological approach. The models in the analyzed articles referred to either correlates of physical activity behavior, or the influence of physical activity on health or aging. Only a minority of the articles, however, referred to interactions between biological, psychological, and social factors. CONCLUSIONS:The included articles were quite heterogeneous in their approach to physical activity from a biopsychosocial perspective. The included articles illustrate that the adoption of a biopsychosocial perspective may assist to capture and understand the complex phenomenon of physical activity behavior and might inform future transdisciplinary physical activity research.
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Project description:Background and aimsWhile epidemiological studies support a role for heavy, high-potency cannabis use on first-episode psychosis, genetic models of causation suggest reverse causal effects of schizophrenia on cannabis use liability. We estimated the genetic relationship between cannabis use disorder (CUD) and schizophrenia (SCZ) and tested whether liability for CUD is causally associated with increased liability to SCZ while adjusting for tobacco smoking.DesignThis study used summary statistics from published genome-wide association studies (GWAS). We used genomic structural equation modeling, latent causal variable analysis, and multivariable Mendelian randomization to examine genetic relationships between CUD, cannabis ever-use, ever-smoked tobacco regularly, nicotine dependence and SCZ, and to test for a causal relationship between liability to CUD and liability to SCZ.SettingGenome-wide association studies were published previously as part of international consortia.ParticipantsSample sizes of the GWAS summary statistics used in this study ranged from 161 405 to 357 806 individuals of European ancestry.MeasurementsGenome-wide summary statistics for CUD and SCZ were the primary measurements, while summary statistics for cannabis ever-use, ever-smoked tobacco regularly and nicotine dependence were included as additional variables in the genomic structural equation models and the multivariable Mendelian randomization analyses.FindingsGenetic liability to CUD was significantly associated with SCZ [β = 0.29, 95% confidence interval (CI) = 0.11, 0.46, P = 0.001], even when accounting for cannabis ever-use, ever-smoked tobacco regularly and nicotine dependence as simultaneous predictors. We found mixed evidence of a causal relationship, with the latent causal variable analysis finding no evidence of causality (genetic causality proportion = -0.08, 95% CI = -0.40, 0.23, P = 0.87) but the multivariable Mendelian randomization analyses suggesting a significant, risk-increasing effect of CUD on liability to SCZ (β = 0.10, 95% CI = 0.02, 0.18, P = 0.02), accounting for the additional risk factors (cannabis ever-use, ever-smoked tobacco regularly and nicotine dependence).ConclusionsGenetic liability for cannabis use disorder appears to be robustly associated with schizophrenia, above and beyond tobacco smoking and cannabis ever-use, with mixed evidence to support a causal relationship between cannabis use disorder and schizophrenia.
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Project description:BackgroundDecision-making deficits in obesity and alcohol use disorder (AUD) may contribute to the choice of immediate rewards despite their long-term deleterious consequences.MethodsGambling task functional MRI in Human connectome project (HCP) dataset was used to investigate neural activation differences associated with reward or punishment (a key component of decision-making behavior) in 418 individuals with obesity (high BMI) and without obesity (lean BMI) and either at high (HR) or low (LR) risk of AUD based on their alcohol drinking levels.ResultsInteraction between BMI and alcohol drinking was seen in regions of the default mode network (DMN) and those implicated in self-related processing, memory, and salience attribution. ObesityHR relative to obesityLR also recruited DMN along with primary motor and regions implicated in inattention, negative perception, and uncertain choices, which might facilitate impulsive choices in obesityHR. Furthermore, obesityHR compared to leanHR/leanLR also demonstrated heightened activation in DMN and regions implicated in uncertain decisions.ConclusionsThese results suggest that BMI is an independent variable from that of alcohol drinking levels in neural processing of gambling tasks. Moreover, leanLR relative to leanHR, showed increased activation in motor regions [precentral and superior frontal gyrus] suggestive of worse executive function from excessive alcohol use. Delayed discounting measures failed to distinguish between obesity and high alcohol drinking levels, which as for gambling task results suggests independent negative effects of obesity and chronic alcohol drinking on decision-making. These findings highlight distinct associations of obesity and high-risk alcohol drinking with two key constituents of decision-making behavior.
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Project description:The role of childhood trauma in the development of borderline personality disorder (BPD) in young age has long been studied. The most accurate theoretical models are multifactorial, taking into account a range of factors, including early trauma, to explain evolutionary pathways of BPD. We reviewed studies published on PubMed in the last 20 years to evaluate whether different types of childhood trauma, like sexual and physical abuse and neglect, increase the risk and shape the clinical picture of BPD. BPD as a sequela of childhood traumas often occurs with multiple comorbidities (e.g. mood, anxiety, obsessive-compulsive, eating, dissociative, addictive, psychotic, and somatoform disorders). In such cases it tends to have a prolonged course, to be severe, and treatment-refractory. In comparison with subjects who suffer from other personality disorders, patients with BPD experience childhood abuse more frequently. Adverse childhood experiences affect different biological systems (HPA axis, neurotransmission mechanisms, endogenous opioid systems, gray matter volume, white matter connectivity), with changes persisting into adulthood. A growing body of evidence is emerging about interaction between genes (e.g. FKBP5 polymorphisms and CRHR2 variants) and environment (physical and sexual abuse, emotional neglect).
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Project description:OBJECTIVE:A single nucleotide variation in the alcohol dehydrogenase 1B (ADH1B) gene, rs1229984, produces an ADH1B enzyme with faster acetaldehyde production. This protective variant is associated with lower alcohol consumption and lower risk for alcohol use disorders (AUDs). Based on the premise that faster ADH1B kinetics decreases alcohol consumption, we formally tested if the association between ADH1B variant rs1229984 and AUDs occurs through consumption. We also tested whether the association between rs1229984 and each of the 11 Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV), AUD criteria occurs through consumption. METHOD:A total of 1,130 lifetime drinkers from an Israeli household sample were assessed with a structured interview and genotyped for rs1229984 (protective allele frequency = 0.28). Logistic regression evaluated the association between rs1229984 and each phenotype (AUDs, 11 individual DSM-IV criteria). For phenotypes significantly related to rs1229984, the effect through consumption was tested with logistic regression and bootstrapping. RESULTS:ADH1B rs1229984 was significantly associated with AUDs and six criteria, with odds ratios ranging from 1.32 to 1.96. The effect through consumption was significant for these relationships, explaining 23%-74% of the total ADH1B effect. CONCLUSIONS:This is the first study to show that ADH1B rs1229984 is related to 6 of the 11 DSM-IV AUD criteria and that alcohol consumption explained a significant proportion of these associations and the association of ADH1B with AUDs. Better understanding of the relationship between ADH1B and the DSM-IV AUD criteria, including effects through consumption, will enhance our understanding of the etiologic model through which AUDs can occur.
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Project description:ObjectiveTo systematically review studies that have assessed the mediating role of internalised weight stigma on the relationship between experienced/perceived weight stigma and any biopsychosocial outcomes.MethodsPsycINFO, PsycExtra, Web of Science, CINAHL, Medline and Embase were systematically searched. Identified studies were double screened (HB and XPG).ResultsSeventeen studies (across 16 articles) met our inclusion criteria (N = 21,172), and almost all studies measured only psychological outcomes (n = 15). Eight studies found consistent evidence for internalised weight stigma as a mediator of the relationship between experienced/perceived weight stigma and disordered eating outcomes. Preliminary evidence was found for the mediating role of internalised weight stigma on the relationship between experienced/perceived weight stigma and body shame, body dissatisfaction, exercise behaviour, healthcare experiences and behaviours, bodily pain and parental weight talk. However, the findings were inconsistent for depression and anxiety, although only two studies reported these.ConclusionThis review provides preliminary evidence for internalised weight stigma as an intervening variable in the relationship between experienced/perceived weight stigma and adverse health outcomes. Results suggest that there are potential benefits of interventions addressing internalised weight stigma to improve health outcomes. However, these findings must be considered in the context of the psychometric limitations of the Weight Bias Internalisation Scale, which was used in all but one study.
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