Previous studies have established that scores on Major Depressive Disorder scales are correlated with measures of impairment of psychosocial functioning. It remains unclear, however, whether ...individual depressive symptoms vary in their effect on impairment, and if so, what the magnitude of these differences might be. We analyzed data from 3,703 depressed outpatients in the first treatment stage of the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) study. Participants reported on the severity of 14 depressive symptoms, and stated to what degree their depression impaired psychosocial functioning (in general, and in the five domains work, home management, social activities, private activities, and close relationships). We tested whether symptoms differed in their associations with impairment, estimated unique shared variances of each symptom with impairment to assess the degree of difference, and examined whether symptoms had variable impacts across impairment domains. Our results show that symptoms varied substantially in their associations with impairment, and contributed to the total explained variance in a range from 0.7% (hypersomnia) to 20.9% (sad mood). Furthermore, symptoms had significantly different impacts on the five impairment domains. Overall, sad mood and concentration problems had the highest unique associations with impairment and were among the most debilitating symptoms in all five domains. Our findings are in line with a growing chorus of voices suggesting that symptom sum-scores obfuscate relevant differences between depressed patients and that substantial rewards will come from close attention to individual depression symptoms.
Abstract Background The DSM-5 encompasses a wide range of symptoms for Major Depressive Disorder (MDD). Symptoms are commonly added up to sum-scores, and thresholds differentiate between healthy and ...depressed individuals. The underlying assumption is that all patients diagnosed with MDD have a similar condition, and that sum-scores accurately reflect the severity of this condition. To test this assumption, we examined the number of DSM-5 depression symptom patterns in the “Sequenced Treatment Alternatives to Relieve Depression” (STAR*D) study. Methods We investigated the number of unique symptom profiles reported by 3703 depressed outpatients at the beginning of the first treatment stage of STAR*D. Results Overall, we identified 1030 unique symptom profiles. Of these profiles, 864 profiles (83.9%) were endorsed by five or fewer subjects, and 501 profiles (48.6%) were endorsed by only one individual. The most common symptom profile exhibited a frequency of only 1.8%. Controlling for overall depression severity did not reduce the amount of observed heterogeneity. Limitations Symptoms were dichotomized to construct symptom profiles. Many subjects enrolled in STAR*D reported medical conditions for which prescribed medications may have affected symptom presentation. Conclusions The substantial symptom variation among individuals who all qualify for one diagnosis calls into question the status of MDD as a specific consistent syndrome and offers a potential explanation for the difficulty in documenting treatment efficacy. We suggest that the analysis of individual symptoms, their patterns, and their causal associations will provide insights that could not be discovered in studies relying on only sum-scores.
Evolutionary biology provides a crucial foundation for medicine and behavioral science that has been missing from psychiatry. Its absence helps to explain slow progress; its advent promises major ...advances. Instead of offering a new kind of treatment, evolutionary psychiatry provides a scientific foundation useful for all kinds of treatment. It expands the search for causes from mechanistic explanations for disease in some individuals to evolutionary explanations for traits that make all members of a species vulnerable to disease. For instance, capacities for symptoms such as pain, cough, anxiety and low mood are universal because they are useful in certain situations. Failing to recognize the utility of anxiety and low mood is at the root of many problems in psychiatry. Determining if an emotion is normal and if it is useful requires understanding an individual's life situation. Conducting a review of social systems, parallel to the review of systems in the rest of medicine, can help achieve that understanding. Coping with substance abuse is advanced by acknowledging how substances available in modern environments hijack chemically mediated learning mechanisms. Understanding why eating spirals out of control in modern environments is aided by recognizing the motivations for caloric restriction and how it arouses famine protection mechanisms that induce binge eating. Finally, explaining the persistence of alleles that cause serious mental disorders requires evolutionary explanations of why some systems are intrinsically vulnerable to failure. The thrill of finding functions for apparent diseases is evolutionary psychiatry's greatest strength and weakness. Recognizing bad feelings as evolved adaptations corrects psychiatry's pervasive mistake of viewing all symptoms as if they were disease manifestations. However, viewing diseases such as panic disorder, melancholia and schizophrenia as if they are adaptations is an equally serious mistake in evolutionary psychiatry. Progress will come from framing and testing specific hypotheses about why natural selection left us vulnerable to mental disorders. The efforts of many people over many years will be needed before we will know if evolutionary biology can provide a new paradigm for understanding and treating mental disorders.
Abstract Background The symptoms for Major Depression (MD) defined in the DSM-5 differ markedly from symptoms assessed in common rating scales, and the empirical question about core depression ...symptoms is unresolved. Here we conceptualize depression as a complex dynamic system of interacting symptoms to examine what symptoms are most central to driving depressive processes. Methods We constructed a network of 28 depression symptoms assessed via the Inventory of Depressive Symptomatology (IDS-30) in 3,463 depressed outpatients from the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) study. We estimated the centrality of all IDS-30 symptoms, and compared the centrality of DSM and non-DSM symptoms; centrality reflects the connectedness of each symptom with all other symptoms. Results A network with 28 intertwined symptoms emerged, and symptoms differed substantially in their centrality values. Both DSM symptoms (e.g., sad mood) and non-DSM symptoms (e.g., anxiety) were among the most central symptoms, and DSM criteria were not more central than non-DSM symptoms. Limitations Many subjects enrolled in STAR*D reported comorbid medical and psychiatric conditions which may have affected symptom presentation. Conclusion The network perspective neither supports the standard psychometric notion that depression symptoms are equivalent indicators of MD, nor the common assumption that DSM symptoms of depression are of higher clinical relevance than non-DSM depression symptoms. The findings suggest the value of research focusing on especially central symptoms to increase the accuracy of predicting outcomes such as the course of illness, probability of relapse, and treatment response.
Most measures of depression severity are based on the number of reported symptoms, and threshold scores are often used to classify individuals as healthy or depressed. This method--and research ...results based on it--are valid if depression is a single condition, and all symptoms are equally good severity indicators. Here, we review a host of studies documenting that specific depressive symptoms like sad mood, insomnia, concentration problems, and suicidal ideation are distinct phenomena that differ from each other in important dimensions such as underlying biology, impact on impairment, and risk factors. Furthermore, specific life events predict increases in particular depression symptoms, and there is evidence for direct causal links among symptoms. We suggest that the pervasive use of sum-scores to estimate depression severity has obfuscated crucial insights and contributed to the lack of progress in key research areas such as identifying biomarkers and more efficacious antidepressants. The analysis of individual symptoms and their causal associations offers a way forward. We offer specific suggestions with practical implications for future research.
Enormous progress in understanding the mechanisms that mediate pain can be augmented by an evolutionary medicine perspective on how the capacity for pain gives selective advantages, the trade-offs ...that shaped the mechanisms, and evolutionary explanations for the system's vulnerability to excessive and chronic pain. Syndromes of deficient pain document tragically the utility of pain to motivate escape from and avoidance of situations causing tissue damage. Much apparently excessive pain is actually normal because the cost of more pain is often vastly less than the cost of too little pain (the smoke detector principle). Vulnerability to pathological pain may be explained in part because natural selection has shaped mechanisms that respond adaptively to repeated tissue damage by decreasing the pain threshold and increasing pain salience. The other half of an evolutionary approach describes the phylogeny of pain mechanisms; the apparent independence of different kinds of pain is of special interest. Painful mental states such as anxiety, guilt and low mood may have evolved from physical pain precursors. Preliminary evidence for this is found in anatomic and genetic data. Such insights from evolutionary medicine may help in understanding vulnerability to chronic pain. This article is part of the Theo Murphy meeting issue 'Evolution of mechanisms and behaviour important for pain'.
Emotions research is now routinely grounded in evolution, but explicit evolutionary analyses of emotions remain rare. This article considers the implications of natural selection for several classic ...questions about emotions and emotional disorders. Emotions are special modes of operation shaped by natural selection. They adjust multiple response parameters in ways that have increased fitness in adaptively challenging situations that recurred over the course of evolution. They are valenced because selection shapes special processes for situations that have influenced fitness in the past. In situations that decrease fitness, negative emotions are useful and positive emotions are harmful. Selection has partially differentiated subtypes of emotions from generic precursor states to deal with specialized situations. This has resulted in untidy emotions that blur into each other on dozens of dimensions, rendering the quest for simple categorically distinct emotions futile. Selection has shaped flexible mechanisms that control the expression of emotions on the basis of an individual's appraisal of the meaning of events for his or her ability to reach personal goals. The prevalence of emotional disorders can be attributed to several evolutionary factors.
The emerging discipline of evolutionary medicine is breaking new ground in understanding why people become ill. However, the value of evolutionary analyses of human physiology and behaviour is only ...beginning to be recognised in the field of public health. Core principles come from life history theory, which analyses the allocation of finite amounts of energy between four competing functions—maintenance, growth, reproduction, and defence. A central tenet of evolutionary theory is that organisms are selected to allocate energy and time to maximise reproductive success, rather than health or longevity. Ecological interactions that influence mortality risk, nutrient availability, and pathogen burden shape energy allocation strategies throughout the life course, thereby affecting diverse health outcomes. Public health interventions could improve their own effectiveness by incorporating an evolutionary perspective. In particular, evolutionary approaches offer new opportunities to address the complex challenges of global health, in which populations are differentially exposed to the metabolic consequences of poverty, high fertility, infectious diseases, and rapid changes in nutrition and lifestyle. The effect of specific interventions is predicted to depend on broader factors shaping life expectancy. Among the important tools in this approach are mathematical models, which can explore probable benefits and limitations of interventions in silico, before their implementation in human populations.
Psychiatric nosology is widely criticized, but solutions are proving elusive. Planned revisions of diagnostic criteria will not resolve heterogeneity, comorbidity, fuzzy boundaries between normal and ...pathological, and lack of specific biomarkers. Concern about these difficulties reflects a narrow model that assumes most mental disorders should be defined by their etiologies. A more genuinely medical model uses understanding of normal function to categorize pathologies. For instance, understanding the function of a cough guides the search for problems causing it, and decisions about when it is expressed abnormally. Understanding the functions of emotions is a foundation missing from decisions about emotional disorders. The broader medical model used by the rest of medicine also recognizes syndromes defined by failures of functional systems or failures of feedback control. Such medical syndromes are similar to many mental diagnoses in their multiple causes, blurry boundaries, and nonspecific biomarkers. Dissatisfaction with psychiatric nosology may best be alleviated, not by new diagnostic criteria and categories, but by more realistic acknowledgment of the untidy landscape of mental and other medical disorders.
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