Short communication : Lameness impairs feeding behavior of dairy cows

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Patterns of diagnostic transition in eating disorders: A longitudinal population study in Sweden

Background Transition across eating disorder diagnoses is common, reflecting instability of specific eating disorder presentations. Previous studies have examined temporal stability of diagnoses in adult treatment-seeking samples but have not uniformly captured initial presentation for treatment. The current study examines transitions across eating disorder diagnostic categories in a large, treatment-seeking sample of individuals born in Sweden and compares these transitions across two birth cohorts and from initial diagnosis.Methods Data from Swedish eating disorders quality registers were extracted in 2013, including 9622 individuals who were seen at least twice from 1999 to 2013. Patterns of remission were examined in the entire sample and subsequently compared across initial diagnoses. An older (born prior to 1990) and younger birth cohort were also identified, and analyses compared these cohorts on patterns of diagnostic transition.Results Although diagnostic instability was common, transition between threshold eating disorder diagnoses was infrequent. For all diagnoses, transition to remission was likely to occur following a diagnosis state that matched initial diagnosis, or through a subthreshold diagnostic state. Individuals in the younger cohort were more likely to transition to a state of remission than those in the older cohort.Conclusions Results indicate more temporal continuity in eating disorder presentations than suggested by previous research and highlight the importance of early detection and intervention in achieving remission

Risk of being convicted of theft and other crimes in anorexia nervosa and bulimia nervosa: A prospective cohort study in a Swedish female population

Objective: We examined epidemiological associations between anorexia nervosa (AN) and bulimia nervosa (BN) and risks of committing theft and other crimes in a nationwide female population. Method: Females born in Sweden during 1979–1998 (N = 957,106) were followed from age 15 for up to 20 years using information on clinically diagnosed AN and BN (exposures), convictions of theft and other crimes (outcomes), psychiatric comorbidities, and familial relatedness from Swedish national registers. We estimated hazard ratios (HRs) of criminality in exposed versus unexposed females using Cox proportional hazards regressions and explored how comorbidities and unmeasured familial factors explained the associations. Results: The cumulative incidence of convictions of theft (primarily petty theft) and other crimes was higher in exposed females (AN: 11.60% theft, 7.39% other convictions; BN: 17.97% theft, 13.17% other convictions) than in unexposed females (∼5% theft, ∼6% other convictions). The significantly increased risk of being convicted of theft in exposed females (AN: HR = 2.51, 95% confidence interval = [2.29, 2.74], BN: 4.31 [3.68, 5.05]) was partially explained by comorbidities; unmeasured familial factors partially explained the association with convictions of theft in BN but not in AN. Females with BN had a doubled risk of convictions of other crimes, which was partially explained by comorbidities. Discussion: Individuals with eating disorders had increased risk for convictions of theft and potentially other crimes. Results underscore the importance of regular forensic screening and encourage research on mechanisms underlying the relation between crime and eating disorder psychopathology and efforts to determine how best to address such relation in treatment

Bidirectional relationship between eating disorders and autoimmune diseases

Background: Immune system dysfunction may be associated with eating disorders (ED) and could have implications for detection, risk assessment, and treatment of both autoimmune diseases and EDs. However, questions regarding the nature of the relationship between these two disease entities remain. We evaluated the strength of associations for the bidirectional relationships between EDs and autoimmune diseases. Methods: In this nationwide population-based study, Swedish registers were linked to establish a cohort of more than 2.5 million individuals born in Sweden between January 1, 1979 and December 31, 2005 and followed up until December 2013. Cox proportional hazard regression models were used to investigate: (a) subsequent risk of EDs in individuals with autoimmune diseases; and (b) subsequent risk of autoimmune diseases in individuals with EDs. Results: We observed a strong, bidirectional relationship between the two illness classes indicating that diagnosis in one illness class increased the risk of the other. In women, the diagnoses of autoimmune disease increased subsequent hazards of anorexia nervosa (AN), bulimia nervosa (BN), and other eating disorders (OED). Similarly, AN, BN, and OED increased subsequent hazards of autoimmune diseases. Gastrointestinal-related autoimmune diseases such as, celiac disease and Crohn's disease showed a bidirectional relationship with AN and OED. Psoriasis showed a bidirectional relationship with OED. The previous occurence of type 1 diabetes increased the risk for AN, BN, and OED. In men, we did not observe a bidirectional pattern, but prior autoimmune arthritis increased the risk for OED. Conclusions: The interactions between EDs and autoimmune diseases support the previously reported associations. The bidirectional risk pattern observed in women suggests either a shared mechanism or a third mediating variable contributing to the association of these illnesses

Paternal age at childbirth and eating disorders in offspring

Background. Advanced paternal age at childbirth is associated with psychiatric disorders in offspring, including schizophrenia, bipolar disorder and autism. However, few studies have investigated paternal age’s relationship with eating disorders in offspring. In a large, population-based cohort, we examined the association between paternal age and offspring eating disorders, and whether that association remains after adjustment for potential confounders (e.g. parental education level) that may be related to late/early selection into fatherhood and to eating disorder incidence. Method. Data for 2 276 809 individuals born in Sweden 1979–2001 were extracted from Swedish population and healthcare registers. The authors used Cox proportional hazards models to examine the effect of paternal age on the first incidence of healthcare-recorded anorexia nervosa (AN) and all eating disorders (AED) occurring 1987–2009. Models were adjusted for sex, birth order, maternal age at childbirth, and maternal and paternal covariates including country of birth, highest education level, and lifetime psychiatric and criminal history. Results. Even after adjustment for covariates including maternal age, advanced paternal age was associated with increased risk, and younger paternal age with decreased risk, of AN and AED. For example, the fully adjusted hazard ratio for the 45+ years (v. the 25–29 years) paternal age category was 1.32 [95% confidence interval (CI) 1.14–1.53] for AN and 1.26 (95% CI 1.13–1.40) for AED. Conclusions. In this large, population-based cohort, paternal age at childbirth was positively associated with eating disorders in offspring, even after adjustment for potential confounders. Future research should further explore potential explanations for the association, including de novo mutations in the paternal germline.NonePublishe

A register-based case-control study of health care utilization and costs in binge-eating disorder

Objective: Capturing trends in healthcare utilization may help to improve efficiencies in the detection and diagnosis of illness, to plan service delivery, and to forecast future health expenditures. For binge-eating disorder (BED), issues include lengthy delays in detection and diagnosis, missed opportunities for recognition and treatment, and morbidity. The study objective was to compare healthcare utilization and expenditure in people with and without BED. Methods: A case-control design and nationwide registers were used. All individuals diagnosed with BED at eating disorder clinics in Sweden between 2005 and 2009 were included (N = 319, 97% female, M age = 22 years). Ten controls (N = 3190) were matched to each case on age-, sex-, and location of birth. Inpatient, hospital-based outpatient, and prescription medication utilization and expenditure were analyzed up to eight years before and four years after the index date (i.e., date of diagnosis of the BED case). Results: Cases had significantly higher inpatient, hospital-based outpatient, and prescription medication utilization and expenditure compared with controls many years prior to and after diagnosis of BED. Utilization and expenditure for controls was relatively stable over time, but for cases followed an inverted U-shape and peaked at the index year. Care for somatic conditions normalized after the index year, but care for psychiatric conditions remained significantly higher. Conclusion: Individuals with BED had substantially higher healthcare utilization and costs in the years prior to and after diagnosis of BED. Since previous research shows a delay in diagnosis, findings indicate clear opportunities for earlier detection and clinical management. Training of providers in detection, diagnosis, and management may help curtail morbidity. A reduction in healthcare utilization was observed after BED diagnosis. This suggests that earlier diagnosis and treatment could improve long-term health outcomes and reduce the economic burden associated with BED

Paternal age at childbirth and eating disorders in offspring

Background. Advanced paternal age at childbirth is associated with psychiatric disorders in offspring, including schizophrenia, bipolar disorder and autism. However, few studies have investigated paternal age’s relationship with eating disorders in offspring. In a large, population-based cohort, we examined the association between paternal age and offspring eating disorders, and whether that association remains after adjustment for potential confounders (e.g. parental education level) that may be related to late/early selection into fatherhood and to eating disorder incidence. Method. Data for 2 276 809 individuals born in Sweden 1979–2001 were extracted from Swedish population and healthcare registers. The authors used Cox proportional hazards models to examine the effect of paternal age on the first incidence of healthcare-recorded anorexia nervosa (AN) and all eating disorders (AED) occurring 1987–2009. Models were adjusted for sex, birth order, maternal age at childbirth, and maternal and paternal covariates including country of birth, highest education level, and lifetime psychiatric and criminal history. Results. Even after adjustment for covariates including maternal age, advanced paternal age was associated with increased risk, and younger paternal age with decreased risk, of AN and AED. For example, the fully adjusted hazard ratio for the 45+ years (v. the 25–29 years) paternal age category was 1.32 [95% confidence interval (CI) 1.14–1.53] for AN and 1.26 (95% CI 1.13–1.40) for AED. Conclusions. In this large, population-based cohort, paternal age at childbirth was positively associated with eating disorders in offspring, even after adjustment for potential confounders. Future research should further explore potential explanations for the association, including de novo mutations in the paternal germline.NonePublishe

Plasma neurofilament light chain concentration is increased in anorexia nervosa

Anorexia nervosa (AN) is a severe psychiatric disorder with high mortality and, to a large extent, unknown pathophysiology. Structural brain differences, such as global or focal reductions in grey or white matter volumes, as well as enlargement of the sulci and the ventricles, have repeatedly been observed in individuals with AN. However, many of the documented aberrances normalize with weight recovery, even though some studies show enduring changes. To further explore whether AN is associated with neuronal damage, we analysed the levels of neurofilament light chain (NfL), a marker reflecting ongoing neuronal injury, in plasma samples from females with AN, females recovered from AN (AN-REC) and normal-weight age-matched female controls (CTRLS). We detected significantly increased plasma levels of NfL in AN vs CTRLS (medianAN = 15.6 pg/ml, IQRAN = 12.1-21.3, medianCTRL = 9.3 pg/ml, IQRCTRL = 6.4-12.9, and p < 0.0001), AN vs AN-REC (medianAN-REC = 11.1 pg/ml, IQRAN-REC = 8.6-15.5, and p < 0.0001), and AN-REC vs CTRLS (p = 0.004). The plasma levels of NfL are negatively associated with BMI overall samples (β (±se) = -0.62 ± 0.087 and p = 6.9‧10-12). This indicates that AN is associated with neuronal damage that partially normalizes with weight recovery. Further studies are needed to determine which brain areas are affected, and potential long-term sequelae

Low body condition predisposes cattle to lameness: An 8-year study of one dairy herd

Lameness in dairy cows is a multifactorial and progressive disease with complex interactions between risk factors contributing to its occurrence. Detailed records were obtained from one United Kingdom dairy herd over an 8-yr period. Weekly locomotion scores were used to classify cows as not lame (score 1 to 2), mildly lame (score 3) and severely lame (score 4 to 5). These outcomes were used to investigate the hypothesis that low body condition score (BCS) is associated with an increased risk of lameness in dairy cows. Mixed effect multinomial logistic regression models were used to investigate the association between prior BCS and repeat lameness events during the longitudinal period of the study. Discrete time survival models were used to explore the relationship between prior BCS and first lifetime lameness events. In total, 79,565 cow weeks at risk were obtained for 724 cows. The number of lameness events was 17,114, of which 8,799 were categorized as mildly lame and 8,315 as severely lame. The median BCS was 2.25 (range, 0.75 to 4.25) and the mean body weight (BW) and age at first calving were 619.5 kg (range, 355.6 to 956.4 kg) and 25.8 mo (range, 20.5 to 37.8 mo), respectively. Subsets of the data were used in the discrete time survival models: 333 mild and 211 severe first lifetime lameness events in heifers (first lactation cows), and 81 mild and 49 severe first lifetime lameness events in cows second lactation or greater. Low BCS 3 wk before a repeated lameness event was associated with a significantly increased risk of lameness. Cows with BCS <2 were at greatest risk of mild or severe lameness, and an increased BCS above 2 was associated with a reduced risk of mild or severe lameness. Low BCS 16 or 8 wk before a first mild or severe lifetime lameness event, respectively, also had a positive association with risk of lameness in cows second lactation or greater. This provides evidence to support targeting management toward maintaining BCS to minimize the risk of lameness. Low BW (independent of BCS) and increased age at first calving above 24 mo were also associated with increased long-term risk of repeated lameness events. Overall, the model explained 62 and 60% of the variability for mild and severe lameness, respectively, highlighting the importance of these variables as risk factors and hence where management could be targeted to significantly affect reducing the risk of lameness