Onset Of Depressive Episode Research Articles

Efficacy and Harms of Second-generation Antidepressants for the Prevention of Seasonal Affective Disorder: a Systematic Review

Introduction Seasonal Affective Disorder (SAD) is a seasonal pattern of recurrent major depressive episodes that most commonly occur during autumn or winter and remit in spring. Second-generation antidepressants (SGAs) are established interventions to treat acute episodes of SAD. However, little is known about the efficacy and potential harms of these interventions for preventing SAD. Objectives To assess the efficacy and safety of SGAs to prevent SAD and improve patient–centered outcomes in adults with a history of SAD. Methods We searched the Cochrane Depression, Anxiety and Neuorosis Review Group's specialised register, EMBASE, MEDLINE, PsycINFO and the Cochrane Central Register of Controlled Trials. In addition, we searched pharmaceutical industry trials registers via the Internet to identify unpublished trial data. We also conducted grey literature searches and handsearches of pertinent reference lists. Two authors reviewed the evidence, abstracted data, and assessed risk of bias. We pooled data for meta-analysis when participant groups were similar and the studies assessed the same treatments with the same comparator. Results We did not find eligible studies for most comparisons. We included three RCTs comparing bupropion XL with placebo. Statistically significantly fewer patients treated with bupropion experienced the onset of a major depressive episode during winter months. The overall risk of adverse events was similar between treatment groups. However, bupropionn-treated patients had significantly higher risk for headache, insomnia, and nausea. Conclusion The evidence base on SGA treatment to prevent SAD is limited. Future studies are needed to provide a sufficient evidence base for clinical decisionmaking.

What students do schools allocate to a cognitive-behavioural intervention? Characteristics of adolescent participants in Northern Sweden

BackgroundAdolescents are a vulnerable group when it comes to the risk of developing depression. Preventing the onset of depressive episodes in this group is therefore a major public health priority. In the last decades, school-based cognitive-behavioural interventions have been a common primary prevention approach. However, evidence on what girls actually are allocated to such interventions when no researchers are involved is scarce.ObjectiveTo explore how a selective cognitive-behavioural program (Depression In Swedish Adolescents) developed to prevent depression in adolescents, was implemented in a naturalistic setting in schools in northern part of Sweden. The focus was on characteristics of participants allocated to the intervention.DesignCross-sectional baseline data on depressive symptoms, school environment and socio-economic factors were collected in 2011 by means of questionnaires in schools in a municipality in the northern part of Sweden. Intervention participants were identified in a follow-up questionnaire in 2012. Students (n=288) included in the analyses were in the ages of 14–15.ResultsSixty-six girls and no boys were identified as intervention participants. They reported higher levels of depressive symptoms, lower personal relative affluence, more sexual harassment victimization and less peer support compared to female non-participants (n=222). Intervention participants were more likely to attend schools with a higher proportion of low parental education levels and a lower proportion of students graduating with a diploma.ConclusionsThe developers of the intervention originally intended the program to be universal or selective, but it was implemented as targeted in these schools. It is important for school administrations to adhere to program fidelity when it comes to what students it is aimed for. Implications for effectivenss trials of cognitive-behavioural interventions in the school setting is discussed.

Association of Speed of Onset and Speed of Recovery of Depressive Episodes in Patients with Major Depression

Background: Depressive episodes show large interindividual differences concerning their speed of onset and speed of recovery, which might suggest differences in underlying pathophysiological processes. The aim of the present study was to assess whether there is a relationship between the speed of onset and the speed of recovery from depressive episodes. Methods: The speed of onset and the speed of recovery from depression were assessed using a structured patient interview, the Onset of Depression Inventory (ODI). In total, 28 patients with bipolar depression and 91 patients with unipolar depression were included. Results: The mean speed of onset of depression was significantly faster than the mean speed of recovery from depression (35.25, range 0-360 days vs. 59.60, range 0.13-720 days; Z = -3.40; p = 0.001). The correlation between these variables was positive, but numerically low (ρ = 0.22; p = 0.016). The speed of onset of the previous episode and that of the present episode were significantly correlated (ρ = 0.45; p < 0.001). Limitations: Data are based on retrospective patient reports within a naturalistic study. Conclusions: While the speed of onset of depressive episodes has been found to show large interindividual variability and some intraindividual stability, the data of this study do not indicate that the neurobiological processes involved in the onset of and in the recovery from depressive episodes are closely linked.

Illness Progression, Recent Stress, and Morphometry of Hippocampal Subfields and Medial Prefrontal Cortex in Major Depression

BackgroundLongitudinal studies of illness progression in patients with major depressive disorder (MDD) indicate that the onset of subsequent depressive episodes becomes increasingly decoupled from external stressors. A possible mechanism underlying this phenomenon is that multiple episodes induce long-lasting neurobiological changes that confer increased risk for recurrence. Prior morphometric studies have frequently reported volumetric reductions in patients with MDD—especially in medial prefrontal cortex (mPFC) and the hippocampus—but few studies have investigated whether these changes are exacerbated by prior episodes. MethodsIn a sample of 103 medication-free patients with depression and control subjects with no history of depression, structural magnetic resonance imaging was performed to examine relationships between number of prior episodes, current stress, hippocampal subfield volume and cortical thickness. Volumetric analyses of the hippocampus were performed using a recently validated subfield segmentation approach, and cortical thickness estimates were obtained using vertex-based methods. Participants were grouped on the basis of the number of prior depressive episodes and current depressive diagnosis. ResultsNumber of prior episodes was associated with both lower reported stress levels and reduced volume in the dentate gyrus. Cortical thinning of the left mPFC was associated with a greater number of prior depressive episodes but not current depressive diagnosis. ConclusionsCollectively, these findings are consistent with preclinical models suggesting that the dentate gyrus and mPFC are especially vulnerable to stress exposure and provide evidence for morphometric changes that are consistent with stress-sensitization models of recurrence in MDD.

Cannabis use in first-treatment bipolar I disorder: relations to clinical characteristics.

The aim of this study was to investigate the associations between recent cannabis use, current symptomatology and age at onset of first manic, depressive and psychotic episodes in a large sample with first-treatment bipolar I disorder (BD I). One hundred one patients with first-treatment Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) bipolar I disorder were included as part of the Thematically Organized Psychosis study. The Structural Clinical Interview for DSM-IV was used for DSM-IV diagnosis and identification of episodes of illness. Earlier suicide attempts were recorded. Manic, depressive and psychotic symptoms were rated using the Young Mania Rating Scale, Inventory of Depressive Symptoms and Positive and Negative Syndrome Scale correspondingly. Cannabis use within the six last months was recorded. After controlling for confounders, recent cannabis use was significantly associated with lower age at onset of first manic and psychotic episode, but not with onset of first depressive episode (both P < 0.05). Recent use was also associated with more lifetime suicide attempts (P < 0.01). No group differences were found on symptom levels. The present study confirms earlier findings of an association between cannabis use and a lower age at onset. Recent cannabis use was also associated with more lifetime suicide attempts. The current findings suggest that recent cannabis use is associated with a more severe course of illness in the early phase of BD I.

The GoodNight study--online CBT for insomnia for the indicated prevention of depression: study protocol for a randomised controlled trial.

BackgroundCognitive Behaviour Therapy for Insomnia (CBT-I) delivered through the Internet is effective as a treatment in reducing insomnia in individuals seeking help for insomnia. CBT-I also lowers levels of depression in this group. However, it is not known if targeting insomnia using CBT-I will lower depressive symptoms, and thus reduce the risk of major depressive episode onset, in those specifically at risk for depression. Therefore, this study aims to examine whether Internet delivery of fully automated self-help CBT-I designed to reduce insomnia will prevent depression.Method/designA sample of 1,600 community-dwelling adults (aged 18–64), who screen positive for both subclinical levels of depressive symptoms and insomnia, will be recruited via various media and randomised to either a 9-week online insomnia treatment programme, Sleep Healthy Using The internet (SHUTi), or an online attention-matched control group (HealthWatch). The primary outcome variable will be depression symptom levels at the 6-month post-intervention on the Patient Heath Questionnaire-9 (PHQ-9). A secondary outcome will be onset of major depressive episodes assessed at the 6-month post-intervention using ‘current’ and ‘time from intervention’ criteria from the Mini International Neuropsychiatric Interview.DiscussionThis trial is the first randomised controlled trial of an Internet-based insomnia intervention as an indicated preventative programme for depression. If effective, online provision of a depression prevention programme will facilitate dissemination.Trial registrationAustralian New Zealand Clinical Trials Registry (ANZCTR), Registration number: ACTRN12611000121965.

FUNCTIONAL POLYMORPHISM IN THE BRAIN-DERIVED NEUROTROPHIC FACTOR GENE INTERACTS WITH STRESSFUL LIFE EVENTS BUT NOT CHILDHOOD MALTREATMENT IN THE ETIOLOGY OF DEPRESSION

We test the hypothesis that the functional Val66Met polymorphism of BDNF interacts with recent life events to produce onset of new depressive episodes. We also explore the possibility that the Met allele of this polymorphism interacts with childhood maltreatment to increase the risk of chronic depression. In a risk-enriched combined sample of unrelated women, childhood maltreatment and current life events were measured with the Childhood Experience of Care and Abuse, and Life Events and Difficulties Schedule interviews. Chronic episodes of depression (12 months or longer) during adulthood and onset of a major depressive episode during a 12-month follow-up were established with the Schedules for Clinical Assessment in Neuropsychiatry interview. Met alleles of BDNF moderated the relationship between recent life events and adult onsets of depression in a significant gene-environment interaction (interaction risk difference 0.216, 95% CI 0.090-0.342; P =.0008). BDNF did not significantly influence the effect of childhood maltreatment on chronic depression in the present sample. The Met allele of BDNF increases the risk of a new depressive episode following a severe life event. The BDNF and the serotonin transporter gene length polymorphism (5-HTTLPR) and BDNF may contribute to depression through distinct mechanisms involving interactions with childhood and adulthood adversity respectively, which may, in combination, be responsible for a substantial proportion of depression burden in the general population.

Gene–environment interactions in common mental disorders: an update and strategy for a genome-wide search

A decade of research has demonstrated the explanatory potential of interplay between genetic variants and environmental factors in the development of common mental disorders. Initial findings have undergone tests of replicability and specificity. Some gene-environment interactions have been confirmed, some have not replicated and yet other turned out to be more specific than initially thought. Specific and complementary roles of genetic factors have been delineated: a common functional length polymorphism in the serotonin transporter gene (5-HTTLPR) moderated the effect of childhood maltreatment on chronic depression in adulthood, but did not substantially influence the effects of adult stressful life events on the onset of new depressive episodes; in contrast, a common functional polymorphism in the brain-derived neurotrophic factor gene (BDNF) moderated the effect of stressful life events in adulthood in triggering new depressive episodes, but did not influence the effects of childhood maltreatment. Molecular mechanisms underlying gene-environment interactions are being uncovered, including DNA methylation and other epigenetic modifications. New gene-environment interactions continue to be reported, still largely from hypothesis-driven research. Statistical and biological prioritization strategies are proposed to facilitate a systematic discovery of novel gene-environment interactions in genome-wide analyses.

Changes in neighborhood characteristics and depression among sexual minority young adults.

Using the National Longitudinal Study of Adolescent Health, this study examined the relationship between changes in neighborhood characteristics during the transition from adolescence to young adulthood and depression among sexual minority young adults. Previous research has found that neighborhood characteristics influence sexual minority mental health and that sexual minorities are more likely to move to more urban and politically liberal locations. No study to date, however, has examined the impact of changes in neighborhood characteristics on sexual minority depression. The results from this study show that decreases in the percent urban was associated with increased risk of depression and decreases in the percent Republican voters in sexual minority's neighborhood was associated with decreases in risk of depression. The results suggest that clinicians may want to screen sexual minority youth for recent changes in their neighborhoods to assess if these changes may be related to the onset or exacerbation of depressive episodes.

Prevention of Depression in At-Risk Adolescents

Adolescent offspring of depressed parents are at high risk for experiencing depressive disorders themselves. To determine whether the positive effects of a group cognitive-behavioral prevention (CBP) program extended to longer-term (multiyear) follow-up. A 4-site randomized clinical trial with 33 months of follow-up was conducted. Recruitment of participants was from August 2003 through February 2006. The study settings included a health maintenance organization, university medical centers, and a community mental health center. Three hundred sixteen adolescent (aged 13-17 years) offspring of parents with current and/or prior depressive disorders; adolescents had histories of depression, current elevated depressive symptoms, or both but did not currently meet criteria for a depressive disorder. The CBP program consisted of 8 weekly 90-minute group sessions followed by 6 monthly continuation sessions. Adolescents were randomly assigned to either the CBP program or usual care (UC). The primary outcome was a probable or definite episode of depression (Depression Symptom Rating score ≥4) for at least 2 weeks through the month 33 follow-up evaluation. Over the 33-month follow-up period, youths in the CBP condition had significantly fewer onsets of depressive episodes compared with those in UC. Parental depression at baseline significantly moderated the intervention effect. When parents were not depressed at intake, CBP was superior to UC (number needed to treat, 6), whereas when parents were actively depressed at baseline, average onset rates between CBP and UC were not significantly different. A 3-way interaction among intervention, baseline parental depression, and site indicated that the impact of parental depression on intervention effectiveness varied across sites. The CBP program showed significant sustained effects compared with UC in preventing the onset of depressive episodes in at-risk youth over a nearly 3-year period. Important next steps will be to strengthen the CBP intervention to further enhance its preventive effects, improve intervention outcomes when parents are currently depressed, and conduct larger implementation trials to test the broader public health impact of the CBP program for preventing depression in youth. clinicaltrials.gov Identifier: NCT00073671.

Treatment Challenges of Atypical Depression: A Case Report

Symptoms such as mood reactivity, hyperphagia, hypersomnia, leaden paralysis, and interpersonal rejection sensitivity are classified as atypical features of a major depressive episode. If these symptoms are concurrent with an episode of hypomania, the patient would be diagnosed with having a depressive episode in the continuum of bipolar II disorder. Because patients may have subsequent depressive episodes for years without any symptoms of hypomania, and because they can function unequivocally within the community due to the nature of the disorder, the diagnosis of a bipolar disorder often gets misclassified as one of a unipolar etiol ogy. Most evidence-based literature states the complexity of this diagnosis due to the subtlety of the presenting symptoms, and it is usually only with a thorough patient history that a clinician can diagnose a patient with bipolar II disorder when the chief complaint is atypical depression. An integrative approach to classifying the depression in terms of polarity requires the clinician to consider the longitudinal course of the patient’s illness; the tendency for depression to recur; the onset, prominence, and severity of depressive episodes; and whether there is a family history of bipolar disorder. It is essential to distinguish between unipolar and bipolar depression in order to treat current episodes and prevent further depressive episodes. The firstline treatment for unipolar depression with atypical features is monoamine oxidase inhibitors (MAOIs), whereas first-line treatment for bipolar depres sion is a mood stabilizer that may be augmented with an antidepressant. CASE

Assessment of the speed of onset of depressive episodes by using onset of depression inventory (ODI)

Assessment of the speed of onset of depressive episodes by using onset of depression inventory (ODI)

Physical activity and onset of depression in adolescents: A prospective study in the general population cohort TRAILS

Although it has often been suggested that physical activity and depression are intertwined, only few studies have investigated whether specific aspects of physical activity predict the incidence of major depression in adolescents from the general population. Therefore the aim of this study was to investigate the effects of nature, frequency, duration and intensity of physical activity during early adolescence on the onset of a major depressive episode in early adulthood. In a population sample of adolescents (N = 1396), various aspects of physical activity were assessed at early adolescence (mean age 13.02, SD = 0.61). Major depressive episode onset was assessed using the Composite International Diagnostic Interview. A Cox regression model was performed to investigate whether physical activity characteristics and their interactions with gender predicted a major depressive episode onset up until mean age 18.5 (SD = 0.61). The individual characteristics of physical activity (nature, frequency, duration and intensity) or their interactions with gender did not predict a major depressive episode onset (p values >0.05). So far, there is no prospective evidence that physical activity protects against the development of adolescent depressive episodes in either boys or girls.

Metacognitive Beliefs and Rumination: A Longitudinal Study

High prevalence and costs of depression underline the importance of understanding and treating vulnerability factors of depression such as rumination. Given the role of rumination in predicting the onset of new depressive episodes, it is important to learn why previously healthy people start to ruminate. One explanation is provided by the metacognitive model of depression, which assumes that positive beliefs about rumination initiate rumination. However previous research has been predominantly cross-sectional in nature. We investigated the effect of positive beliefs about rumination on engagement in rumination in a longitudinal design and tested the indirect effect of positive beliefs about rumination on depressive symptoms in 60 healthy university students. A hierarchical regression revealed a significant effect of Time 1 (T1) positive beliefs about rumination on Time 2 rumination, even after controlling for T1 rumination. Additionally, an indirect effect of positive beliefs about rumination on depressive symptoms via rumination was confirmed using a multiple regression and a Sobel test.

State Rumination: Associations with Emotional Stress Reactivity and Attention Biases.

Within dysphoria, rumination has been identified as a particularly maladaptive emotion regulation strategy linked to prolonged negative affect and the onset of depressive episodes. Until now, the majority of research assessing naturally occurring rumination has utilized trait rumination measures; however, additional information may be obtained by assessing state rumination. The current study examined the association between state rumination and participants' emotional recovery from stress. In addition, biased attention toward emotional information was investigated as a mechanism that might underlie state rumination. Participants completed the exogenous cuing task to assess attentional engagement and disengagement from emotional facial expressions followed by a psychosocial stressor. State rumination and self-reported sadness were measured during the recovery period. As expected, state rumination was associated with less recovery in sadness scores, even after controlling for trait rumination and depressive symptoms. Moreover, within the high dysphoria group, participants who had more difficulty disengaging from emotional expressions reported higher levels of rumination in response to the stressor. Results highlight an important association between state rumination and individuals' recovery from stress, and suggest that difficulty disengaging attention from emotional expressions might be one mechanism underlying state rumination in dysphoria.

Test-Retest Stability of the Onset of Depression Inventory

Background: The ‘Onset of Depression Inventory' (ODI) is a patient interview developed for systematically registering the speed of onset of depression. The ODI might contribute to the detection of hidden bipolarity because in previous studies a more rapid depression onset was found in patients with bipolar compared to unipolar depression. The aim of this study was to evaluate the test-retest stability of the ODI. Patients were asked concerning the speed of onset at the time of hospitalization and again before discharge. Sampling and Methods: Test-retest stability of the ODI was investigated in 37 patients with a depressive episode. Each patient was interviewed concerning his present depressive episode by the same person at two different time points. Severity of depression at the different time points was assessed using the Hamilton Depression Rating Scale (HAMD-17) and the Inventory of Depressive Symptomatology (IDS-C). Results: The speed of onset as assessed with the ODI showed good test-retest stability (rho = 0.83, p < 0.001). This parameter was not influenced by changes in depression severity. Conclusions: The ODI allows reliable assessment of the speed of onset of depressive episodes. The instrument might be useful for the detection of hidden bipolarity.

A Case of Valproate Induced Hyperammonemic Encephalopathy in an Elderly Bipolar Patient Under Treatment With Sulphonylureas

Valproic acid induced hyperammonaemic encephalopathy (VPA-VHE) is a rare side effect of valproic acid. It is characterized by impaired consciousness and lethargy, focal neurological signs or symptoms with a serum level of ammonia above 40 mmol/L. This syndrome is often misdiagnosed, especially in psychiatricsetting.Wepresentthe case of a bipolar patient who developed VPA-VHE. He assumed also sulphonylureas to manage mild hyperglycemia. After three months of treatment with valproic acid patient had a depressive episode and acute onset of headache, disorientation, consciousness impairment, and psychomotor slowing. This presentation induced to make investigation and we have discovered hyperammonaemia with EEG alteration; a diagnosis of valproate induced hyperammonemic encephalopathy (VHE) was made. The patient recovered quickly after discontinuing valproic acid therapy. Valproic acid is a frequent treatment in psychiatricsetting and a betterknowledge of possibleadverseeffectsisimportant to prevent and manage rare conditions like VHE. J Med Cases. 2013;4(8):540-543 doi : http://dx.doi.org/10.4021/jmc1313w

1214 – Emptiness in a life full of experiences: major depression in a 66-year-old man

Introduction Depression is a common, recurrent, often underdiagnosed and undertreated disorder in older people. 10-15% of the elderly present depressive symptoms and 3% of that same population meet criteria for a major depressive episode. Several factors, such as psychosocial changes, may be related to the onset of depressive episodes. Retirement (often accompanied with feelings of loss of status, both in the family and in the society), the decrease of social contacts with a tendency to isolation, and the difficulties to adapt to new activities and routines, all lead to feelings of inadequacy, worthlessness and a poor self-esteem. Objectives/aims The aim of this poster is to show and discuss the importance in recognizing some psychosocial factors that can predict the onset of depressive symptoms in the elderly. Methods We report a case of a 66-year-old man, without previous psychiatric history, who presented a major depressive episode with psychotic features, after an important life event (retirement). Results/conclusion Depression in older people has severe consequences, afflicting not only patients but also the caregivers. The amplification of previous disabilities associated with medical and cognitive disorders, the increased rate of mortality by suicide and the increased costs to the health care system are common consequences. To reduce such threats we propose a clinical and social approach that evaluates and regards the different stages of the life cycle and valorize the achieved experiences of older patients.

Interaction between the BDNF gene Val/66/Met polymorphism and morning cortisol levels as a predictor of depression in adult women

Common genetic variants, such as the brain-derived neurotrophic factor (BDNF) Val/66/Met polymorphism (rs6265), are known to interact with environmental factors such as early adversity to increase the risk of subsequent major depression. Much less is known about how they interact with individual differences in cortisol, although these also represent a risk for major depression. To determine whether this BDNF variant moderated the risk represented by higher levels of morning salivary cortisol in adult women. We recruited 279 premenopausal women who were at high risk of major depressive disorder because of either negative self-evaluation, unsupportive core relationship or chronic subclinical symptoms of depression or anxiety. Morning salivary cortisol was measured daily for up to 10 days at entry. Participants were followed up for about 12 months by telephone calls at 3-4 monthly intervals. Major depression and severe life events were assessed through interviews at baseline and follow-up; DNA was obtained from the saliva. There were 53 onsets (19%) of depressive episodes during follow-up. There was a significant U-shaped relationship between adjusted morning cortisol levels at baseline and the probability of depression onset during follow-up. In total, 51% experienced at least one severe life event/difficulty, and this strongly predicted subsequent onsets of depressive episodes. The BDNF Val/66/Met genotype was not directly associated with onsets of depression or with cortisol levels, but there was significant interaction between Val/66/Met and cortisol: the association between baseline cortisol and depression was limited to those with the Val/66/Val variant. There was no interaction between life events and either this BDNF polymorphism or cortisol levels. Morning salivary cortisol interacts with the BDNF Val/66/Met polymorphism in predicting new depressive episodes. This paper adds to the evidence that single gene polymorphisms interact with endogenous factors to predict depression.

Distinguishing subclinical (subthreshold) depression from the residual symptoms of major depression.

The terms ‘sub-clinical’ or ‘subthreshold’ are widely used in medicine to label individuals who are in the early stages of a disease process (e.g., cancer, hypertension, etc.) and to identify high-risk populations that need to be monitored or provided with specific preventative interventions or treatments. Because the pathophysiological changes that occur in the sub-clinical stages of a condition are similar to those that occur during the full-blown disease, sub-clinical states are usually considered prodromal versions of the disease under consideration. Based on this usage, subclinical or subthreshold depression should refer to an individual who has not previously met full criteria for major depression who currently experiences depressive symptoms that are not severe enough or persistent enough to merit a diagnosis of major depression. Using this concept, a recent two-year follow-up study found that subthreshold depression can predict the subsequent occurrence of depressive disorders (OR=6.23, 95% CI=3.31-11.74) or anxiety disorders (OR=3.47, 95% CI= 1.78-6.78).[1] Unlike other medical disciplines, in clinical psychiatry the sub-clinical and subthreshold labels are also used to describe residual clinical states after the partial remission of a full episode of a condition. For example, ‘sub-clinical depression’ is often used to describe the clinical state of a patient who has not entered full remission and still has residual symptoms after treatment with antidepressants.[2],[3] I believe it important to distinguish these two situations. Prodromal depressive symptoms prior to the onset of a full-criteria major depression and the residual depressive symptoms after the partial resolution of a major depressive episode may be symptomatically similar but they are clinically distinct conditions that require different interventions so it is inappropriate to combine them under a single label. Residuals symptoms following a major depressive illness require continued pharmacological and/or psychotherapeutic treatment but sub-clinical depressive symptoms prior to the first occurrence of a major depressive illness usually only require observation and follow-up. More active treatment for sub-clinical depressive symptoms is usually only justified if they persist for two years or longer (in which case the diagnosis of Dysthymic Disorder is usually applied) or if the individual has had full-criteria major depressive illness in the past and thus is at a high risk of progressing to a full-criteria episode of illness. Collapsing these different situations under a single rubric is both inaccurate and could potentially lead to inappropriate treatment. I recommend that persistent depressive symptoms following a major depressive illness that do not meet the full criteria of the disorder be labeled ‘residual symptoms’ (not sub-clinical or subthreshold symptoms) and that the ‘sub-clinical depression’ or ‘subthreshold depression’ labels be limited to depressive symptoms that occur prior to the first onset of a full depressive episode. But depressive affect is part of the normal human condition so we must also avoid the inappropriate overuse of the sub-clinical and subthreshold labels by, for example, labeling the depressive symptoms identified in screening programs of healthy community members as ‘subthreshold depression’. Depressive symptoms in individuals without prior episodes of full-criteria depressive illness should only be given the sub-clinical or subthreshold labels if the symptoms are ‘clinically significant’, that is, when they result in significant distress or significant social or occupational dysfunction.