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There is increasing evidence that smoking is a risk factor for severe mental illness, including bipolar disorder. Conversely, patients with bipolar disorder might smoke more (often) as a result of the psychiatric disorder.
We conducted a bidirectional Mendelian randomisation (MR) study to investigate the direction and evidence for a causal nature of the relationship between smoking and bipolar disorder.
We used publicly available summary statistics from genome-wide association studies on bipolar disorder, smoking initiation, smoking heaviness, smoking cessation and lifetime smoking (i.e. a compound measure of heaviness, duration and cessation). We applied analytical methods with different, orthogonal assumptions to triangulate results, including inverse-variance weighted (IVW), MR-Egger, MR-Egger SIMEX, weighted-median, weighted-mode and Steiger-filtered analyses.
Across different methods of MR, consistent evidence was found for a positive effect of smoking on the odds of bipolar disorder (smoking initiation ORIVW = 1.46, 95% CI 1.28–1.66, P = 1.44 × 10−8, lifetime smoking ORIVW = 1.72, 95% CI 1.29–2.28, P = 1.8 × 10−4). The MR analyses of the effect of liability to bipolar disorder on smoking provided no clear evidence of a strong causal effect (smoking heaviness betaIVW = 0.028, 95% CI 0.003–0.053, P = 2.9 × 10−2).
These findings suggest that smoking initiation and lifetime smoking are likely to be a causal risk factor for developing bipolar disorder. We found some evidence that liability to bipolar disorder increased smoking heaviness. Given that smoking is a modifiable risk factor, these findings further support investment into smoking prevention and treatment in order to reduce mental health problems in future generations.
Declaration of interest
W.v.d.B received fees in the past 3 years from Indivior, C&A Pharma, Opiant and Angelini. G.M.G. is a National Institute for Health Research (NIHR) Emeritus Senior Investigator, holds shares in P1vital and has served as consultant, advisor or CME speaker in the past 3 years for Allergan, Angelini, Compass Pathways, MSD, Lundbeck (/Otsuka and /Takeda), Medscape, Minervra, P1Vital, Pfizer, Sage, Servier, Shire and Sun Pharma.
Long-term care facilities have partly taken over the traditional asylum function of psychiatric hospitals and house an increasing group of patients with mental–physical multimorbidity (MPM). Little is known about the characteristics, behavior, and care dependency of these patients. This paper aims to describe these aspects.
Explorative, descriptive study among patients with MPM without dementia (n = 142), living in 17 geronto-psychiatric nursing home (NH) units across the Netherlands, stratified by those referred from mental healthcare services (MHS) and other healthcare services (OHS). Data collection consisted of chart review, semi-structured interviews, (brief) neuropsychological testing, and self-report questionnaires. Patients referred from MHS (n = 58) and from OHS (n = 84) were compared by descriptive statistics.
Despite exclusion of patients with dementia, the majority of participants had cognitive impairment. Prevalence and severity of frontal impairment were high, as well as the number of patients with clinically relevant neuropsychiatric symptoms. MHS patients were younger, had more chronic psychiatric disorders, and more often used antipsychotics. Neuropsychiatric symptoms, domains of care dependency, physical conditions and concomitant medication use differed not significantly between the subgroups.
Both groups of patients with MPM showed heterogeneity in various aspects but differed not significantly regarding the consequences of their multimorbidity. In a variety of characteristics, this group seems to be different from other NH patient groups, which requires extra knowledge and skills of the staff. To uncover which knowledge and skills are necessary, the next step should be to investigate the specific care needs of NH patients with MPM without dementia.
Poor recovery from depressive disorder has been shown to be related to low perceived social support and loneliness, but not to social network size or frequency of social interactions. Some studies suggest that the significance of social relationships for depression course may be greater in younger than in older patients, and may differ between men and women. None of the studies examined to what extent the different aspects of social relationships have unique or overlapping predictive values for depression course. It is the aim of the present study to examine the differential predictive values of social network characteristics, social support and loneliness for the course of depressive disorder, and to test whether these predictive associations are modified by gender or age.
Two naturalistic cohort studies with the same design and overlapping instruments were combined to obtain a study sample of 1474 patients with a major depressive disorder, of whom 1181 (80.1%) could be studied over a 2-year period. Social relational variables were assessed at baseline. Two aspects of depression course were studied: remission at 2-year follow-up and change in depression severity over the follow-up period. By means of logistic regression and random coefficient analysis, the individual and combined predictive values of the different social relational variables for depression course were studied, controlling for potential confounders and checking for effect modification by age (below 60 v. 60 years or older) and gender.
Multiple aspects of the social network, social support and loneliness were related to depression course, independent of potential confounders – including depression severity – but when combined, their predictive values were found to overlap to a large extent. Only the social network characteristic of living in a larger household, the social support characteristic of few negative experiences with the support from a partner or close friend, and limited feelings of loneliness proved to have unique predictive value for a favourable course of depression. Little evidence was found for effect modification by gender or age.
If depressed persons experience difficulties in their social relationships, this may impede their recovery. Special attention for interpersonal problems, social isolation and feelings of loneliness seems warranted in depression treatment and relapse prevention. It will be of great interest to test whether social relational interventions can contribute to better recovery and relapse prevention of depressive disorder.
HII galaxies are dwarf galaxies which are currently actively forming stars. We speculated that an interaction with an optically faint, but gas-rich object might be responsible for their enhanced star formation. This prompted us to search for companions with the VLA in the 21–cm line of HI. This has several advantages over optical searches (Campos–Aguilar et al. 1991, AJ, 106, 1784; Telles & Terlevich 1995, MNRAS, 275, 1), e.g., the direct availability of redshifts.
We present the first results from multi-site observations of the δ Scuti star XX Pyx (CD–24°7599). The observations were carried out as the 17th run of the Delta Scuti Network. We collected 583 hr of B, V time-series photometry, resulting in a detection level (4σ) in the amplitude spectrum of 0.5 mmag. We detect 6 new pulsation frequencies, bringing the total number of frequencies known in this star up 19.
Endothelial dysfunction (ED) and low-grade inflammation (LGI) have a role in the development of CVD. The two studies reported here explored the effects of dietary proteins and carbohydrates on markers of ED and LGI in overweight/obese individuals with untreated elevated blood pressure. In the first study, fifty-two participants consumed a protein mix or maltodextrin (3×20 g/d) for 4 weeks. Fasting levels and 12 h postprandial responses of markers of ED (soluble intercellular adhesion molecule 1 (sICAM), soluble vascular cell adhesion molecule 1 (sVCAM), soluble endothelial selectin and von Willebrand factor) and markers of LGI (serum amyloid A, C-reactive protein and sICAM) were evaluated before and after intervention. Biomarkers were also combined into mean Z-scores of ED and LGI. The second study compared 4 h postprandial responses of ED and LGI markers in forty-eight participants after ingestion of 0·6 g/kg pea protein, milk protein and egg-white protein. In addition, postprandial responses after maltodextrin intake were compared with a protein mix and sucrose. The first study showed significantly lower fasting ED Z-scores and sICAM after 4 weeks on the high-protein diet (P≤0·02). The postprandial studies found no clear differences of ED and LGI between test meals. However, postprandial sVCAM decreased more after the protein mix compared with maltodextrin in both studies (P≤0·04). In conclusion, dietary protein is beneficial for fasting ED, but not for fasting LGI, after 4 weeks of supplementation. On the basis of Z-scores, postprandial ED and LGI were not differentially affected by protein sources or carbohydrates.
Costanza and Finkelstein (2015) question whether there really are generational differences in the workplace. They argue that the generation construct is not properly operationalized (often confounding age, period, and cohort factors) and that generational research is atheoretical and plagued by methodological problems. We agree that generational research is largely guilty as charged. We also share their concern regarding the generationally based interventions that are being sold to, and adopted by, managers—interventions that are often little more than fads based on popular myths and folklore. We are also in full agreement with the potential significant harm that can be associated with stereotyping groups of individuals.
Although exact figures are lacking, many studies show that mental–physical multimorbidity is common in older people (van den Brink et al., 2013). Particularly, older patients with a chronic disease often have psychiatric disorders (Verdurmen et al., 2006). Conversely, medical comorbidity is common in psychiatric patients, especially cardiovascular, pulmonary, and neurological disorders and diabetes (Lyketsos et al., 2002).
Diet composition may affect blood pressure (BP), but the mechanisms are unclear. The aim of the present study was to compare postprandial BP-related responses to the ingestion of pea protein, milk protein and egg-white protein. In addition, postprandial BP-related responses to the ingestion of maltodextrin were compared with those to the ingestion of sucrose and a protein mix. We hypothesised that lower postprandial total peripheral resistance (TPR) and BP levels would be accompanied by higher plasma concentrations of nitric oxide, insulin, glucagon-like peptide 1 (GLP-1) and glucagon. On separate occasions, six meals were tested in a randomised order in forty-eight overweight or obese adults with untreated elevated BP. Postprandial responses of TPR, BP and plasma concentrations of insulin, glucagon, GLP-1 and nitrite, nitroso compounds (RXNO) and S-nitrosothiols (NOx) were measured for 4 h. No differences were observed in TPR responses. Postprandial BP levels were higher after the ingestion of the egg-white-protein meal than after that of meals containing the other two proteins (P≤ 0·01). The ingestion of the pea-protein meal induced the highest NOx response (P≤ 0·006). Insulin and glucagon concentrations were lowest after the ingestion of the egg-white-protein meal (P≤ 0·009). Postprandial BP levels were lower after the ingestion of the maltodextrin meal than after that of the protein mix and sucrose meals (P≤ 0·004), while postprandial insulin concentrations were higher after the ingestion of the maltodextrin meal than after that of the sucrose and protein mix meals after 1–2 h (P≤ 0·0001). Postprandial NOx, GLP-1 and glucagon concentrations were lower after the ingestion of the maltodextrin meal than after that of the protein mix meal (P≤ 0·008). In conclusion, different protein and carbohydrate sources induce different postprandial BP-related responses, which may be important for BP management. Lower postprandial BP levels are not necessarily accompanied by higher NOx, insulin, glucagon or GLP-1 responses.
Impulsivity is a multidimensional construct, including impulsive decision-making and impulsive action, representing relatively independent neurocircuitries. ADHD is treated with methylphenidate, a drug that binds to dopamine transporters. This study in 24 adult male patients with ADHD shows that dopamine transporter occupancy by methylphenidate in the putamen correlates with improvements in cognitive but not in motor impulsivity.
Impulsive decision making is a hallmark of frequently occurring addiction disorders including alcohol dependence (AD). Therefore, ameliorating impulsive decision making is a promising target for the treatment of AD. Previous studies have shown that modafinil enhances cognitive control functions in various psychiatric disorders. However, the effects of modafinil on delay discounting and its underlying neural correlates have not been investigated as yet. The aim of the current study was to investigate the effects of modafinil on neural correlates of impulsive decision making in abstinent AD patients and healthy control (HC) subjects.
A randomized, double-blind, placebo-controlled, within-subjects cross-over study using functional magnetic resonance imaging (fMRI) was conducted in 14 AD patients and 16 HC subjects. All subjects participated in two fMRI sessions in which they either received a single dose of placebo or 200 mg of modafinil 2 h before the session. During fMRI, subjects completed a delay-discounting task to measure impulsive decision making.
Modafinil improved impulsive decision making in AD pateints, which was accompanied by enhanced recruitment of frontoparietal regions and reduced activation of the ventromedial prefrontal cortex. Moreover, modafinil-induced enhancement of functional connectivity between the superior frontal gyrus and ventral striatum was specifically associated with improvement in impulsive decision making.
These findings indicate that modafinil can improve impulsive decision making in AD patients through an enhanced coupling of prefrontal control regions and brain regions coding the subjective value of rewards. Therefore, the current study supports the implementation of modafinil in future clinical trials for AD.
In the present controlled, randomised, multiple cross-over dietary intervention study, we aimed to identify potential biomarkers for dietary protein from dairy products, meat and grain, which could be useful to estimate intake of these protein types in epidemiological studies. After 9 d run-in, thirty men and seventeen women (22 (sd 4) years) received three high-protein diets (aimed at approximately 18 % of energy (en%)) in random order for 1 week each, with approximately 14 en% originating from either meat, dairy products or grain. We used a two-step approach to identify biomarkers in urine and plasma. With principal component discriminant analysis, we identified amino acids (AA) from the plasma or urinary AA profile that were distinctive between diets. Subsequently, after pooling total study data, we applied mixed models to estimate the predictive value of those AA for intake of protein types. A very good prediction could be made for the intake of meat protein by a regression model that included urinary carnosine, 1-methylhistidine and 3-methylhistidine (98 % of variation in intake explained). Furthermore, for dietary grain protein, a model that included seven AA (plasma lysine, valine, threonine, α-aminobutyric acid, proline, ornithine and arginine) made a good prediction (75 % of variation explained). We could not identify biomarkers for dairy protein intake. In conclusion, specific combinations of urinary and plasma AA may be potentially useful biomarkers for meat and grain protein intake, respectively. These findings need to be cross-validated in other dietary intervention studies.
Background: Aging societies will be confronted with increased numbers of long-term care (LTC) residents with multimorbidity of physical and mental disorders other than dementia. Knowledge about the prevalence rates, medical and psychosocial characteristics, and care needs of this particular group of residents is mandatory for providing high-quality and evidence-based care. The purpose of this paper was to review the literature regarding these features.
Methods: A systematic literature search was conducted in PubMed, EMBASE, PsycINFO, and CINAHL from January 1, 1988 to August 16, 2011. Two reviewers independently assessed eligibility of studies on pre-established inclusion criteria as well as methodological quality using standardized checklists.
Results: Seventeen articles were included. Only one small study describes multimorbidity of a wide range of chronic psychiatric and somatic conditions in LTC residents and suggests that physical–mental multimorbidity is rather rule than exception. All other studies show prevalence rates of comorbid physical and mental illnesses (range, 0.5%–64.7%), roughly in line with reported prevalence rates among community-dwelling older people. LTC residents with mental–physical multimorbidity were younger than other LTC residents and had more cognitive impairment, no dementia, and problem behaviors. Care needs of these residents were not described.
Conclusions: Although exact figures are lacking, mental–physical multimorbidity is common in LTC residents. Given the specific characteristics of the pertaining residents, more knowledge of their specific care needs is essential. The first step now should be to perform research on symptoms and behavior, which seem more informative than diagnostic labels as well as care needs of LTC residents with mental–physical multimorbidity.
Much is still unclear about the role of personality in the structure of common psychiatric disorders such as depressive/anxiety disorders and alcohol dependence. This study will therefore examine whether various traits of negative emotionality and impulsivity showed shared or specific associations with these disorders.
Cross-sectional data were used from the Netherlands Study of Depression and Anxiety (NESDA), including individuals with no DSM-IV psychiatric disorder (n = 460), depressive/anxiety disorder only (i.e. depressive and/or anxiety disorder; n = 1398), alcohol dependence only (n = 32) and co-morbid depressive/anxiety disorder plus alcohol dependence (n = 358). Aspects of negative emotionality were neuroticism, hopelessness, rumination, worry and anxiety sensitivity, whereas aspects of impulsivity included disinhibition, thrill/adventure seeking, experience seeking and boredom susceptibility.
Aspects of negative emotionality formed a homogeneous dimension, which was unrelated to the more heterogeneous construct of impulsivity. Although all aspects of negative emotionality were associated with alcohol dependence only, associations were much stronger for depressive/anxiety disorder only and co-morbid depressive/anxiety disorder with alcohol dependence. The results for impulsivity traits were less profound and more variable, with disinhibition and boredom susceptibility showing modest associations with both depressive/anxiety disorder and alcohol dependence, whereas low thrill/adventure seeking and high disinhibition were more strongly related with the first and the latter, respectively.
Our results suggest that depressive/anxiety disorder and alcohol dependence result from shared as well as specific aetiological pathways as they showed the same associations with all aspects of negative emotionality, disinhibition and boredom susceptibility as well as specific associations with thrill/adventure seeking and disinhibition.
The rise in interdisciplinary scholarship between philosophy and theology has produced a number of critiques of historical biblical criticism (HBC) by philosophers of religion. Some dialogue has resulted, but these critiques have gone largely unnoticed by historical critical scholars. This article argues that two such critiques of HBC, offered by Plantinga and Stump, are undermined by faulty presuppositions on the philosophers' part regarding the nature and value of HBC and misunderstandings of the nature of the ancient texts on which the discipline of HBC focuses.
Hypertension is highly prevalent among renal transplant recipients (RTR) and a risk factor for graft failure and cardiovascular events. Protein intake has been claimed to affect blood pressure (BP) in the general population and may affect renal function. We examined the association of dietary protein with BP and renal function in RTR. We included 625 RTR (age 53 (sd 13) years; 57 % male). Protein intake was assessed with a FFQ, differentiating between animal and plant protein. BP was measured according to a strict protocol. Creatinine clearance and albuminuria were measured as renal parameters. Protein intake was 83 (sd 12) g/d, of which 63 % derived from animal sources. BP was 136 (sd 17) mmHg systolic (SBP) and 83 (sd 11) mmHg diastolic (DBP). Creatinine clearance was 66 (sd 26) ml/min; albuminuria 41 (10–178) mg/24 h. An inverse, though statistically insignificant, association was found between the total protein intake and both SBP (β = − 2·22 mmHg per sd, P= 0·07) and DBP (β = − 0·48 mmHg per sd, P= 0·5). Protein intake was not associated with creatinine clearance. Although albuminuria was slightly higher in the highest tertile of animal protein intake compared with the lowest tertile (66 v. 33 mg/d, respectively, P= 0·03), linear regression analyses did not reveal significant associations between dietary protein and albuminuria. Protein intake exceeded the current recommendations. Nevertheless, within the range of protein intake in our RTR population, we found no evidence for an association of dietary protein with BP and renal function. Intervention studies focusing on different protein types are warranted to clarify their effect on BP and renal function in RTR.