Ruth M. Benca

Putative contributors to the secular increase in obesity: exploring the roads less traveled

Objective:To investigate plausible contributors to the obesity epidemic beyond the two most commonly suggested factors, reduced physical activity and food marketing practices.Design:A narrative review of data and published materials that provide evidence of the role of additional putative factors in contributing to the increasing prevalence of obesity.Data:Information was drawn from ecological and epidemiological studies of humans, animal studies and studies addressing physiological mechanisms, when available.Results:For at least 10 putative additional explanations for the increased prevalence of obesity over the recent decades, we found supportive (although not conclusive) evidence that in many cases is as compelling as the evidence for more commonly discussed putative explanations.Conclusion:Undue attention has been devoted to reduced physical activity and food marketing practices as postulated causes for increases in the prevalence of obesity, leading to neglect of other plausible mechanisms and well-intentioned, but potentially ill-founded proposals for reducing obesity rates.

Ten Putative Contributors to the Obesity Epidemic

The obesity epidemic is a global issue and shows no signs of abating, while the cause of this epidemic remains unclear. Marketing practices of energy-dense foods and institutionally-driven declines in physical activity are the alleged perpetrators for the epidemic, despite a lack of solid evidence to demonstrate their causal role. While both may contribute to obesity, we call attention to their unquestioned dominance in program funding and public efforts to reduce obesity, and propose several alternative putative contributors that would benefit from equal consideration and attention. Evidence for microorganisms, epigenetics, increasing maternal age, greater fecundity among people with higher adiposity, assortative mating, sleep debt, endocrine disruptors, pharmaceutical iatrogenesis, reduction in variability of ambient temperatures, and intrauterine and intergenerational effects as contributing factors to the obesity epidemic are reviewed herein. While the evidence is strong for some contributors such as pharmaceutical-induced weight gain, it is still emerging for other reviewed factors. Considering the role of such putative etiological factors of obesity may lead to comprehensive, cause specific, and effective strategies for prevention and treatment of this global epidemic.

Sleep and Behavior Problems in School-Aged Children

Objectives. The primary purposes of the present study were to survey the prevalence of sleep problems in school-aged children and to examine these associations with parental perception of sleep problems, medical history, and childhood psychopathology. Methods. Sleep and medical history questionnaires and the Child Behavior Checklist were administered to the parents of 472 children between ages 4 and 12 years receiving routine pediatric care from urban, rural, and suburban pediatric practices. Results. Although sleep problems were reported for 10.8% of the sample during the past 6 months, less than one half of the parents who identified sleep problems reported that they had discussed sleep with their childs pediatrician. The best predictor of current sleep problems was a history of sleep problems before age 2 years. Sleep problems such as snoring, tiredness during the day, and taking excessive time to fall asleep were very common, occurring at least 1 night per week in over 20% of the total sample. Factor analysis of the sleep problems questionnaire resulted in 5 sleep problem factors that accounted for 58.7% of the variance. Specific sleep problem factors include: parasomnias, enuresis/gags, tiredness, noisy sleep, and insomnia. Sleep problem factor scores were differentially associated with medical history variables and measures of childhood psychopathology. Children rated highly on parasomnias were more likely to have frequent falls and to display pica. Parasomnias and noisy sleep were inversely associated with socioeconomic status (SES). Children from lower SES families were rated higher on these factors than children from higher SES families. Enuresis/gags was the only sleep problem factor associated with age. Younger children scored higher on this factor. Duration of naps was highly correlated with age and with bed times during the week and weekends. As expected, younger children were more likely to nap for longer periods and to have earlier bed times. In addition, higher tiredness factor scores were associated with napping and with later bed times during the week and weekend. Boys were much more likely than were girls to have higher scores on enuresis/gags, and higher enuresis/gags scores were associated with an increased prevalence of trauma and falls. Bed times were not associated with any other sleep problem factor score. Children rated highly on tiredness were more likely to have a history of hospitalizations. Tiredness factor scores were strongly associated with the sleep practice of sharing a bed but not with sharing a room. Sharing a room was not associated with any sleep problem factor score. High scores on noisy sleep were associated with allergies, falls frequently, and with sharing a bed. Children with high scores on the insomnias were also more likely to display an increased prevalence of allergies. Conclusions. Parental perception of global sleep problems was surprisingly common in school-aged children receiving routine pediatric care. Parental reports of their childrens sleep problems may be a red flag for specific sleep problems and psychiatric, social, or medical problems. Sleep problems should be queried about during pediatric visits for school-aged children.

Functional but not structural subgenual prefrontal cortex abnormalities in melancholia

Major depression is a heterogeneous condition, and the search for neural correlates specific to clinically defined subtypes has been inconclusive. Theoretical considerations implicate frontostriatal, particularly subgenual prefrontal cortex (PFC), dysfunction in the pathophysiology of melancholia—a subtype of depression characterized by anhedonia—but no empirical evidence has been found yet for such a link. To test the hypothesis that melancholic, but not nonmelancholic depression, is associated with the subgenual PFC impairment, concurrent measurement of brain electrical (electroencephalogram, EEG) and metabolic (positron emission tomography, PET) activity were obtained in 38 unmedicated subjects with DSM-IV major depressive disorder (20 melancholic, 18 nonmelancholic subjects), and 18 comparison subjects. EEG data were analyzed with a tomographic source localization method that computed the cortical three-dimensional distribution of current density for standard frequency bands, allowing voxelwise correlations between the EEG and PET data. Voxel-based morphometry analyses of structural magnetic resonance imaging (MRI) data were performed to assess potential structural abnormalities in melancholia. Melancholia was associated with reduced activity in the subgenual PFC (Brodmann area 25), manifested by increased inhibitory delta activity (1.5–6.0 Hz) and decreased glucose metabolism, which themselves were inversely correlated. Following antidepressant treatment, depressed subjects with the largest reductions in depression severity showed the lowest post-treatment subgenual PFC delta activity. Analyses of structural MRI revealed no group differences in the subgenual PFC, but in melancholic subjects, a negative correlation between gray matter density and age emerged. Based on preclinical evidence, we suggest that subgenual PFC dysfunction in melancholia may be associated with blunted hedonic response and exaggerated stress responsiveness.

Thalamic dysfunction in schizophrenia suggested by whole-night deficits in slow and fast spindles

OBJECTIVE Slow waves and sleep spindles are the two main oscillations occurring during non-REM sleep. While slow oscillations are primarily generated and modulated by the cortex, sleep spindles are initiated by the thalamic reticular nucleus and regulated by thalamo-reticular and thalamo-cortical circuits. In a recent high-density EEG study, the authors found that 18 medicated schizophrenia patients had reduced sleep spindles, compared with healthy and depressed subjects, during the first non-REM episode. In the present study, the authors investigated whether spindle deficits were present in a larger sample of schizophrenia patients, were consistent across the night, were related to antipsychotic medications, and were suggestive of impairments in specific neuronal circuits. METHOD Whole-night high-density EEG recordings were performed in 49 schizophrenia patients, 20 nonschizophrenia patients receiving antipsychotic medication, and 44 healthy subjects. In addition to sleep spindles, several parameters of slow waves were assessed. RESULTS Schizophrenia patients had whole-night deficits in spindle power (12-16 Hz) and in slow (12-14 Hz) and fast (14-16 Hz) spindle amplitude, duration, number, and integrated activity in the prefrontal, centroparietal, and temporal regions. Integrated spindle activity and spindle number had the largest effect sizes (effect size: ≥ 2.21). In contrast, no slow wave deficits were found in schizophrenia patients. CONCLUSIONS These results indicate that spindle deficits can be reliably established in schizophrenia, are stable across the night, are unlikely to be due to antipsychotic medications, and point to deficits in the thalamic reticular nucleus and thalamo-reticular circuits.

A multisite randomized trial of portable sleep studies and positive airway pressure autotitration versus laboratory-based polysomnography for the diagnosis and treatment of obstructive sleep apnea: The HomePAP study

STUDY OBJECTIVES To test the utility of an integrated clinical pathway for obstructive sleep apnea (OSA) diagnosis and continuous positive airway pressure (CPAP) treatment using portable monitoring devices. DESIGN Randomized, open-label, parallel group, unblinded, multicenter clinical trial comparing home-based, unattended portable monitoring for diagnosis and autotitrating CPAP (autoPAP) compared with in-laboratory polysomnography (PSG) and CPAP titration. SETTING Seven American Academy of Sleep Medicine (AASM) accredited sleep centers. PARTICIPANTS Consecutive new referrals, age 18 yr or older with high probability of moderate to severe OSA (apnea-hypopnea index [AHI] ≥ 15) identified by clinical algorithm and Epworth Sleepiness Scale (ESS) score ≥ 12. INTERVENTIONS Home-based level 3 testing followed by 1 wk of autoPAP with a fixed pressure CPAP prescription based on the 90% pressure from autotitration of PAP therapy (autoPAP) device (HOME) compared with attended, in-laboratory studies (LAB). MEASUREMENTS CPAP acceptance, time to treatment, adherence at 1 and 3 mo; changes in ESS, and functional outcomes. RESULTS Of 373 participants, approximately one-half in each study arm remained eligible (AHI ≥ 15) to continue in the study. At 3 mo, PAP usage (nightly time at pressure) was 1 hr greater: 4.7 ± 2.1 hr (HOME) compared with 3.7 ± 2.4 hr (LAB). Adherence (percentage of night used ≥ 4 hr) was 12.6% higher: 62.8 ± 29.2% compared with 49.4 ± 36.1% in the HOME versus LAB. Acceptance of PAP therapy, titration pressures, effective titrations, time to treatment, and ESS score change did not differ between arms. CONCLUSIONS A home-based strategy for diagnosis and treatment compared with in-laboratory PSG was not inferior in terms of acceptance, adherence, time to treatment, and functional improvements. TRIAL REGISTRATION http://www.ClinicalTrials.gov; Identifier: NCT: 00642486.

Migratory sleeplessness in the white-crowned sparrow (Zonotrichia leucophrys gambelii)

Twice a year, normally diurnal songbirds engage in long-distance nocturnal migrations between their wintering and breeding grounds. If and how songbirds sleep during these periods of increased activity has remained a mystery. We used a combination of electrophysiological recording and neurobehavioral testing to characterize seasonal changes in sleep and cognition in captive white-crowned sparrows (Zonotrichia leucophrys gambelii) across nonmigratory and migratory seasons. Compared to sparrows in a nonmigratory state, migratory sparrows spent approximately two-thirds less time sleeping. Despite reducing sleep during migration, accuracy and responding on a repeated-acquisition task remained at a high level in sparrows in a migratory state. This resistance to sleep loss during the prolonged migratory season is in direct contrast to the decline in accuracy and responding observed following as little as one night of experimenter-induced sleep restriction in the same birds during the nonmigratory season. Our results suggest that despite being adversely affected by sleep loss during the nonmigratory season, songbirds exhibit an unprecedented capacity to reduce sleep during migration for long periods of time without associated deficits in cognitive function. Understanding the mechanisms that mediate migratory sleeplessness may provide insights into the etiology of changes in sleep and behavior in seasonal mood disorders, as well as into the functions of sleep itself.

SLEEP IN PSYCHIATRIC DISORDERS

Psychiatric disorders are some of the most common causes of sleep-related complaints, particularly insomnia. Sleep abnormalities may be caused by CNS abnormalities associated with psychiatric illnesses as well as by accompanying behavioral disturbances. Although sleep patterns are not necessarily diagnostic of particular psychiatric disorders, there are relationships between certain sleep abnormalities and categories of psychiatric disorders. Sleep disturbances associated with psychiatric disorders and general approaches to treatment are reviewed.

Brain electrical tomography in depression: the importance of symptom severity, anxiety, and melancholic features

BACKGROUND The frontal lobe has been crucially involved in the neurobiology of major depression, but inconsistencies among studies exist, in part due to a failure of considering modulatory variables such as symptom severity, comorbidity with anxiety, and distinct subtypes, as codeterminants for patterns of brain activation in depression. METHODS Resting electroencephalogram was recorded in 38 unmedicated subjects with major depressive disorder and 18 normal comparison subjects, and analyzed with a tomographic source localization method that computes the cortical three-dimensional distribution of current density for standard electroencephalogram frequency bands. Symptom severity and anxiety were measured via self-report and melancholic features via clinical interview. RESULTS Depressed subjects showed more excitatory (beta3, 21.5-30.0 Hz) activity in the right superior and inferior frontal lobe (Brodmanns area 9/10/11) than comparison subjects. In melancholic subjects, this effect was particularly pronounced for severe depression, and right frontal activity correlated positively with anxiety. Depressed subjects showed posterior cingulate and precuneus hypoactivity. CONCLUSIONS While confirming prior results implicating right frontal and posterior cingulate regions, this study highlights the importance of depression severity, anxiety, and melancholic features in patterns of brain activity accompanying depression.

Insomnia and depression

It is clear that insomnia and depression are intimately related, which may suggest an overlapping neurobiology. Although much progress has been made toward understanding how these disorders relate to each other, the exact neurobiological mechanisms that link them remain elusive. Sleep changes in depression may be associated with abnormal neurotransmission, genetic polymorphisms, HPA overactivity, impaired plasticity, or most likely a combination of factors. It is therefore crucial that sleep assessments go beyond traditional polysomnography to include a more expanded set of objective measures in the hope that these will uncover the common neurobiology that is thought to underlie insomnia and depression.