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To assess the relationship between food insecurity, sleep quality, and days with mental and physical health issues among college students.
An online survey was administered. Food insecurity was assessed using the ten-item Adult Food Security Survey Module. Sleep was measured using the nineteen-item Pittsburgh Sleep Quality Index (PSQI). Mental health and physical health were measured using three items from the Healthy Days Core Module. Multivariate logistic regression was conducted to assess the relationship between food insecurity, sleep quality, and days with poor mental and physical health.
Twenty-two higher education institutions.
College students (n 17 686) enrolled at one of twenty-two participating universities.
Compared with food-secure students, those classified as food insecure (43·4 %) had higher PSQI scores indicating poorer sleep quality (P < 0·0001) and reported more days with poor mental (P < 0·0001) and physical (P < 0·0001) health as well as days when mental and physical health prevented them from completing daily activities (P < 0·0001). Food-insecure students had higher adjusted odds of having poor sleep quality (adjusted OR (AOR): 1·13; 95 % CI 1·12, 1·14), days with poor physical health (AOR: 1·01; 95 % CI 1·01, 1·02), days with poor mental health (AOR: 1·03; 95 % CI 1·02, 1·03) and days when poor mental or physical health prevented them from completing daily activities (AOR: 1·03; 95 % CI 1·02, 1·04).
College students report high food insecurity which is associated with poor mental and physical health, and sleep quality. Multi-level policy changes and campus wellness programmes are needed to prevent food insecurity and improve student health-related outcomes.
Alcohol intake is known to modulate plasma concentrations of neuroendocrine peptides. However, recent results suggest that the endocrine system may not only respond passively to alcohol intake, but that -vice versa- it also actively modulates alcohol intake behaviour. The most coherent body of data concerns the hypothalamo-pituitary-adrenocortical (HPA) axis, with low corticotropin releasing hormone (CRH) being associated with more intense craving and increased probability of relapse after acute detoxification. It is important to bear in mind that dysregulation of the HPA system, as observed in alcohol dependence, is also a feature of anxiety and depression, two conditions which are frequently linked with alcohol dependence and have been reported to be associated with a poor prognosis. In depression, increased secretion of CRH seems to be one crucial mechanism. It has been found as a marker of depressive symptoms, which normalises when depression is successfully treated. Hypersecretion of CRH is associated with a general hyperactivity of the HPA system, notably elevated plasma levels of ACTH and cortisol, a blunted cortisol stress response and a blunted dexamethasone suppression test. In any case, HPA dysregulation, alcohol dependence, and depression are closely interrelated. Exactly which component of this triad is the driving force behind the various neuroendocrine correlates of drinking behaviour is currently unclear, and will need to be elucidated by future research. This will allow for an enlightened choice of potentially therapeutic agents for the treatment of co-morbid anxiety, depression, and alcohol dependence, acting primarily on the HPA system.
A synopsis of current treatment options shows only moderate effect sizes. They could be improved considerably if individual predictors were available.
Previous attempts to identify predictors for the treatment response in alcoholism have mainly concentrated on social and personality variables. Project MATCH was such an attempt which finally failed. The same holds true for similar attempts in pharmacotherapy. Therefore, we set out for a large oligocentre trial “Project PREDICT”. 432 patients are randomly assigned to treatment with acamprosate, naltrexone or placebo. At baseline patients are assessed with a battery of interviews, questionnaires and biological examinations (e.g. genetics). Specific emphasis is put on patients’ individual pathways into relapse. It is determined whether relapse drinking respresented a positive reinforcer (“reward craving”) or a negative reinforcer (“relief craving”). This is assessed with questionnaires, the startle reflex and fMRI. We hypothesize, that patients who are a priori identified as “positive reinforcers” better respond to naltrexone. Negative reinforcers should benefit most from acamprosate.
All patients have been included by now. Preliminary analyses suggest that it is possible to distinguish between the two craving types. The equivalent of positive reinforcement in the startle reflex correlates with fMRI responses to cues with a positive valence of about 0.7. These methods might offer a platform for a targeted pharmacotherapy in alcoholism.
There has been continued interest in the nature of the association between affective disorders and alcoholism. This may be due to the fact that during the course of alcoholism 30-70% of the patients suffer from mood disturbances meeting the criteria for severe depression, especially in periods of excessive alcohol consumption or during withdrawal. In the course of a prospective multidimensional study, Tiibinger Alkoholismusprojekt (T-ALK Study), symptoms of depression in 31 male alcohol-dependent patients (RDC diagnosis) were assessed using the Beck Depression Inventory (BDI) and the Freiburger Personlichkeitsinventar (FPI-R) at the beginning and at the end of a 6-week inpatient treatment program. There was only a moderate degree of depression (BDI) in 20% of the patients which decreased significantly during the psychotherapeutic treatment under conditions of confirmed abstinence. No correlations between the degree of depression and neuropsychological impairment were found. Although the “satisfaction with life” (FPI-R factor) was still impaired in a third of the patients at the end of that short-term treatment period, our results do not indicate a general nosological overlap between alcoholism and affective disorders in males.
In alcoholism, one relevant mechanism contributing to relapse is the exposure to stimuli that are associated with alcohol intake. Such conditioned cues can elicit conditioned responses like alcohol craving and consumption. In the last decade, considerable progress has been made in identifying basic neuronal mechanisms that underlie cue-induced alcohol craving.
We explored whether functional brain activation during exposure to alcohol-associated stimuli is related to the prospective relapse risk in detoxified alcohol-dependent patients.
46 alcohol-dependent and 46 healthy volunteers participated in a fMRI study using a cue reactivity paradigm, in which visual alcohol-related and control stimuli were presented. Patients were followed for 3 months. Afterwards data was analysed regarding the subsequent relapse, resulting in 16 abstainers and 30 relapsers.
Alcohol-related versus neutral stimuli activated a frontocortical-limbic network including inferior, medial and middle frontal gyrus as well as putamen in the group of patients relative to healthy controls. Moreover, abstainers showed a stronger activation in orbitofrontal cortex as well as midbrain during the presentation of alcohol-related cues whereas relapsers revealed a stronger activation of cingulate gyrus.
This study suggests that cue-induced activation of orbitofrontal cortex and dopaminergic innervated midbrain is negatively associated with the prospective relapse risk in alcohol-dependent patients. This could indicate a more pronounced and conscious processing of alcohol cues which might serve as a warning signal and a behavioural controlling function. In contrast, prospective relapsers showed a stronger activation of cingulate gyrus, a region involved in the attribution of motivational value.
Starting from the hypothesis that alcoholics have a specific semantic network which causes a perceptual-processing bias, we tested 30 male inpatients and 20 healthy male controls. Our modified card version of the Stroop color-naming task consisted of a neutral and critical word condition. The results revealed that alcoholic patients showed a small information processing bias under the critical experimental condition (alcohol-related words); although this was only a trend in the expected direction and statistically not significant. However, neuropsychological impairment of the patients was demonstrated with the “standard Stroop procedure”. The most significant deficits were found in the interference task, which requires cognitive flexibility.
Multiple neurochemical pathways have been identified to be involved in mediating craving and relapse to alcohol and, further, animal models greatly assist in investigating pharmacological interventions of relapse behaviour. Opioidergic and glutamatergic systems play a key role in alcoholism as demonstrated by the clinically effective compounds naltrexone and acamprosate acting through these systems. Although the dopaminergic system has been in the focus of alcohol research for many years, clinical trials interfering with several components of this system displayed rather disappointing results. This situation, however, could change in light of the discovery that dopamine D3 receptor antagonism produces very consistent and robust results in preclinical studies. Corticotropin-releasing factor signalling and the endocannabinoid system integrate stress-related events and thereby mediate relapse behaviour. Thus, many new targets have been identified and several new compounds are currently undergoing clinical testing. However, given the heterogeneity in treatment response, genetic and protein markers as well as endophenotypes are currently characterised for individualised pharmacotherapy.
Pathological gambling and comorbide alcohol dependence are common occuring diseases. Disulfiram is one of the proven drugs for alcohol dependence. It was shown recently, that Disulfiram is also effective in relapse prevention of cocaine addiction. In addition to its inhibiting effect of the acetaldehyde dehydrogenase (ADH), disulfiram inhibits the dopamine β-hydroxylase (DBH) and thereby augments dopamine and depletes norepinephrine concentrations in the CNS. Inhibition of the DBH is suggested to be the responsible mechanism of Disulfiram acting in cocaine addiction. Previous research indicates common neurochemical substrates for pathological gambling and cocaine addiction. This suggests that dopamine substrates may directly govern the reinforcement process in pathological gambling.
In this report we now present the clinical data of a patient who was treated with disulfiram in our outpatient unit for addiction treatment due to existing alcohol dependence. The patient suffered also from severe pathological gambling.
Initialy we started to treat the patient with supervised disulfiram because of his alcohol dependence. During the treatment with disulfiram the patient’ desire for gambling disappeared entirely and he has not gambled anymore since then.
However, the exact mechnism of action by which disulfiram reduces urge to gamble is not fully unterstood, yet. Because craving is a key contributor to relapse, strategies aimed at modulate dopamine increases are likely to be therapeutically beneficial in gambling. Although uncontrolled case observations can only be interpreted with caution disulfiram seems to deserve further investigation and may hold the potential for preventing relapse in gamblers suffering from additional alcohol dependence.
Among abstinent alcohol-dependent patients, sleep disorders are a wide-spread and persistent problem and have been associated with the risk of alcohol relapse. The melatonin-agonist agomelatine has been shown to improve overall sleep quality without daytime sedation.
To examine the effect of agomelatine on sleep quality in abstinent alcohol-dependet patients suffering from chronic sleep disorders.
9 alcohol-dependet patients suffering from chronic sleep disorders received nightly doses between 25 and 50 mg of agomelatine. Sleep quality was assesed using the Pittsburgh Sleep Quality Index prior and following 6 weeks of treatment with agomelatine. Prior and during treatment with agomelatine all patients were monitored for serum levels of liver enzymes.
After 6 weeks of agomelatine treatment, the Pittsburgh Sleep Quality Index global score for all patients had decreased significantly.
The present data suggest that agomelatine may improve the sleep quality of alcohol-dependent patients suffering from chronic sleep disorders.
The reclassification of PG as an addictive disorder is under debate for ICD-11. Data on psychiatric comorbidity and family history might provide the basis for a well-informed decision.
We compared 515 male pathological gamblers from inpatient treatment units with 269 matched controls. Patients were diagnosed by experienced clinicians. In a random sample of 58 patients clinical diagnoses were validated through SKID 1 interviews .
88% had a comorbid diagnosis of substance dependence (nicotine dependence 80%, alcohol dependence 28%). Only 1% of the gamblers had an impulse control disorder diagnosis. Compared with controls first degree relatives were more likely to suffer from alcohol dependence (27.0% vs. 7.4%), PG (8.3% vs. 0.7%) and suicide attempts (2.7% vs. 0.4%).
In addition to recent papers on the neurobiology (Fauth-Bühler et al., 2016) and genetics of gambling [2,3], our findings support the classification of PG as behavioural addiction in the ICD-11 .
Disclosure of interest
The authors have not supplied their declaration of competing interest.
Pathological gambling is a behavioural addiction with negative economic, social, and psychological consequences. Identification of contributing genes and pathways may improve understanding of aetiology and facilitate therapy and prevention. Here, we report the first genome-wide association study of pathological gambling. Our aims were to identify pathways involved in pathological gambling, and examine whether there is a genetic overlap between pathological gambling and alcohol dependence.
Four hundred and forty-five individuals with a diagnosis of pathological gambling according to the Diagnostic and Statistical Manual of Mental Disorders were recruited in Germany, and 986 controls were drawn from a German general population sample. A genome-wide association study of pathological gambling comprising single marker, gene-based, and pathway analyses, was performed. Polygenic risk scores were generated using data from a German genome-wide association study of alcohol dependence.
No genome-wide significant association with pathological gambling was found for single markers or genes. Pathways for Huntington's disease (P-value = 6.63 × 10−3); 5′-adenosine monophosphate-activated protein kinase signalling (P-value = 9.57 × 10−3); and apoptosis (P-value = 1.75 × 10−2) were significant. Polygenic risk score analysis of the alcohol dependence dataset yielded a one-sided nominal significant P-value in subjects with pathological gambling, irrespective of comorbid alcohol dependence status.
The present results accord with previous quantitative formal genetic studies which showed genetic overlap between non-substance- and substance-related addictions. Furthermore, pathway analysis suggests shared pathology between Huntington's disease and pathological gambling. This finding is consistent with previous imaging studies.
While DSM-5 classified pathological gambling as an addictive disorder, there is debate as to whether ICD-11 should follow suit. The debate hinges on scientific evidence such as neurobiological findings, family history of psychiatric disorders, psychiatric comorbidity, and personality variables.
In the “Baden-Württemberg Study of Pathological Gambling”, we compared a group of 515 male pathological gamblers receiving treatment with 269 matched healthy controls. We studied differences in sociodemographic characteristics, gambling-related variables, psychiatric comorbidity (lifetime), family history of psychiatric conditions, as well as personality traits such as impulsivity (Barratt Impulsiveness Scale), sensation seeking (Zuckerman's Sensation Seeking Scale) and the NEO-FFI big five. Personality traits were validated in an age- and ethnicity-matched subsample of “pure” gamblers without any psychiatric comorbidity (including nicotine dependence). Data were analyzed using two-sample t-tests, Chi2 analyses, Fisher's exact test and Pearson correlation analysis, as appropriate. Bonferroni correction was applied to correct for multiple comparisons.
Only 1% of the gamblers had been diagnosed with an impulse control disorder other than gambling (ICD-10). Notably, 88% of the gamblers in our sample had a comorbid diagnosis of substance dependence. The highest axis I comorbidity rate was for nicotine dependence (80%), followed by alcohol dependence (28%). Early age of first gambling experience was correlated with gambling severity. Compared to first-degree relatives of controls, first-degree relatives of pathological gamblers were more likely to suffer from alcohol dependence (27.0% vs. 7.4%), pathological gambling (8.3% vs. 0.7%) and suicide attempts (2.7% vs. 0.4%). Significant group differences were observed for the NEO-FFI factors neuroticism, agreeableness and conscientiousness. Gamblers were also more impulsive than controls, but did not differ from controls in terms of sensation seeking.
Our findings support classifying pathological gambling as a behavioural addiction in the ICD-11. This decision will have a significant impact on the approaches available for prevention (e.g. age limits) and treatment.
Internet gaming disorder appears to be associated with self-concept deficits and increased identification with one's avatar. For increased social network use, the few existing studies suggest striatal-related positive social feedback as an underlying factor. Furthermore, few study findings indicate that internet addicts generally have problems in emotional inhibitory control processing.
Pathological and addicted internet gamers as well as social network users were compared with healthy controls regarding psychometric and neurobiological measures of self-concept-related characteristics, avatar identification and emotional inhibitory control processing.
Results and conclusion
Psychometric results indicated that both subgroups showed higher self-concept deficits compared to healthy controls. Neurobiologically, different brain activation patterns were observed in the subgroups during self-knowledge retrieval and inhibition of emotional stimuli. Furthermore, addicted internet gamers showed a higher identification with the own avatar, mirrored in an increased left angular gyrus activation, a region functionally associated with identification processing and feelings of empathy.
These findings provide a starting point for the deduction of specific psychotherapeutic treatment approaches for addicted internet gamers and social network users.
Disclosure of interest
The authors have not supplied their declaration of competing interest.
Three new tephras have been identified in Southeast Alaska. An 8-cm-thick black basaltic tephra with nine discrete normally graded beds is present in cores from a lake on Baker Island. The estimated age of the tephra is 13,492 ± 237 cal yr BP. Although similar in age to the MEd tephra from the adjacent Mt. Edgecumbe volcanic field, this tephra is geochemically distinct. Black basaltic tephras recovered from two additional sites in Southeast Alaska, Heceta Island and the Gulf of Esquibel, are also geochemically distinct from the MEd tephra. The age of the tephra from Heceta Island is 14,609 ± 343 cal yr BP. Whereas the tephras recovered from Baker Island/Heceta Island/Gulf of Esquibel are geochemically distinct from each other, similarities in the ages of these tephras and the MEd tephra suggest a shared eruptive trigger, possibly crustal unloading caused by retreat of the Cordilleran Ice Sheet. The submerged Addington volcanic field on the continental shelf, which may have been subaerially exposed during the late Pleistocene, is a possible source for the Southeast Alaska tephras.
Cortisol is the primary output of the hypothalamic–pituitary–adrenal (HPA) axis and is central to the biological stress response, with wide-ranging effects on psychiatric health. Despite well-studied biological pathways of glucocorticoid function, little attention has been paid to the role of genetic variation. Conventional salivary, urinary and serum measures are strongly influenced by diurnal variation and transient reactivity. Recently developed technology can be used to measure cortisol accumulation over several months in hair, thus indexing chronic HPA function.
In a socio-economically diverse sample of 1070 twins/multiples (ages 7.80–19.47 years) from the Texas Twin Project, we estimated effects of sex, age and socio-economic status (SES) on hair concentrations of cortisol and its inactive metabolite, cortisone, along with their interactions with genetic and environmental factors. This is the first genetic study of hair neuroendocrine concentrations and the largest twin study of neuroendocrine concentrations in any tissue type.
Glucocorticoid concentrations increased with age for females, but not males. Genetic factors accounted for approximately half of the variation in cortisol and cortisone. Shared environmental effects dissipated over adolescence. Higher SES was related to shallower increases in cortisol with age. SES was unrelated to cortisone, and did not significantly moderate genetic effects on either cortisol or cortisone.
Genetic factors account for sizable proportions of glucocorticoid variation across the entire age range examined, whereas shared environmental influences are modest, and only apparent at earlier ages. Chronic glucocorticoid output appears to be more consistently related to biological sex, age and genotype than to experiential factors that cluster within nuclear families.
Resilience is the capacity of individuals to resist mental disorders despite exposure to stress. Little is known about its neural underpinnings. The putative variation of white-matter microstructure with resilience in adolescence, a critical period for brain maturation and onset of high-prevalence mental disorders, has not been assessed by diffusion tensor imaging (DTI). Lower fractional anisotropy (FA) though, has been reported in the corpus callosum (CC), the brain's largest white-matter structure, in psychiatric and stress-related conditions. We hypothesized that higher FA in the CC would characterize stress-resilient adolescents.
Three groups of adolescents recruited from the community were compared: resilient with low risk of mental disorder despite high exposure to lifetime stress (n = 55), at-risk of mental disorder exposed to the same level of stress (n = 68), and controls (n = 123). Personality was assessed by the NEO-Five Factor Inventory (NEO-FFI). Voxelwise statistics of DTI values in CC were obtained using tract-based spatial statistics. Regional projections were identified by probabilistic tractography.
Higher FA values were detected in the anterior CC of resilient compared to both non-resilient and control adolescents. FA values varied according to resilience capacity. Seed regional changes in anterior CC projected onto anterior cingulate and frontal cortex. Neuroticism and three other NEO-FFI factor scores differentiated non-resilient participants from the other two groups.
High FA was detected in resilient adolescents in an anterior CC region projecting to frontal areas subserving cognitive resources. Psychiatric risk was associated with personality characteristics. Resilience in adolescence may be related to white-matter microstructure.