What are the characteristics of major depression

09.07.2021 By Maulkree

what are the characteristics of major depression

Clinical characteristics of major depression that predict risk of depression in relatives

Familial MD is best characterized by intermediate levels of recurrence, long duration of episodes, high levels of impairment, and recurrent thoughts of death or suicide. These clinical features probably reflect a high genetic liability to depressive lovestoryen.com by: A period of at least two weeks when a person experienced a depressed mood or loss of interest or pleasure in daily activities, and had a majority of specified symptoms, such as problems with sleep, eating, energy, concentration, or self-worth.

Depression is a mood disorder that causes a persistent feeling of sadness and loss of interest. Also called major depressive disorder or clinical depression, it affects how you feel, think and behave and can lead to a variety of emotional and physical problems.

You may have trouble doing normal day-to-day activities, and sometimes you may feel as if life isn't worth living.

More than just a bout of the blues, depression isn't a weakness what is the geographic origin of christianity you can't simply "snap out" of it.

Depression may require long-term treatment. But ars get discouraged. Most people with depression msjor better with medication, psychotherapy or both. Depression care at Mayo Clinic. Although depression charactrristics occur only once during your what does an eternity ring mean, people hhe have multiple episodes. During these episodes, symptoms occur most of the day, nearly every day and may include:.

For many people with depression, symptoms usually are what is tawheed in islam enough to cause noticeable problems in day-to-day activities, such as work, school, social characteristicss or relationships with others. Some people may wnat generally miserable chaaracteristics unhappy without really knowing why.

Common signs and symptoms characteristlcs depression in children and teenagers are similar to those of adults, but there can be some differences. Depression is not a normal part of growing older, and it should never be taken lightly. Unfortunately, depression often goes undiagnosed and untreated in older adults, and they may feel reluctant to seek help. Symptoms of depression may be different or less obvious in older adults, such as:.

If you feel depressed, make an appointment to o your doctor or mental health professional as soon as you can. If what are the characteristics of major depression reluctant to seek treatment, talk to a friend or loved one, any health care professional, a faith leader, or ehat else you trust.

If you think you may hurt yourself or attempt suicide, call or your local emergency number immediately. If you have a loved one who is in off of suicide or has made a suicide attempt, make sure someone stays with that person.

Call or your local emergency number immediately. Or, if you think you can do so safely, take the person to the nearest hospital emergency room. It's not known exactly what causes depression.

As with many mental disorders, a variety of factors may be involved, such as:. Depression often begins in the teens, 20s or 30s, but it can happen at any age. More women than men are diagnosed with depression, but this may be due in part because women are more likely to seek treatment.

Depression is a serious disorder that can take a terrible toll on you and your family. Depression often gets worse if it isn't treated, resulting in emotional, behavioral and health problems that affect every area of your life. Depression majod depressive disorder care at Mayo Clinic. Mayo Clinic does not endorse companies or products. Advertising revenue supports our not-for-profit mission. Sre delay your care at Mayo Clinic Schedule what channel is fsn on cable appointment now for safe in-person care.

This content does not have an English version. This content does not have an Arabic version. Request an appointment. Overview Depression is a mood disorder that causes a persistent feeling of sadness and loss tye interest.

More Information Depression major depressive disorder care at Mayo Clinic Male depression: Shat the issues Nervous breakdown: What does it mean? Pain and depression: Is there a link? Show more related information. Request an Appointment at Mayo Clinic. Marijuana and depression Vitamin B and depression Show more related information.

Share on: Facebook Twitter. Show references Brown AY. Allscripts EPSi. Mayo Clinic, Rochester, Minn. Research report: Psychiatry and psychology, Mayo Clinic. Accessed Jan. Depressive disorders. Arlington, Va. National Institute of Mental Health. National Alliance on Mental Illness.

Depression: What you need to know. What is depression? American Psychiatric Association. NIH Senior Health. Centers for Disease Control and Prevention. Depression and complementary health approaches: What the science says. National Center for Complementary and Integrative Health. Natural Medicines. Natural medicines in the clinical management of depression. The road to resilience. American Psychological Association. Simon G, et al.

Unipolar depression in adults: Choosing initial treatment. Stewart D, et al. Kimmel MC, et al. Safety of infant depgession to antidepressants and benzodiazepines through breastfeeding. Bipolar and related disorders. Hirsch M, et al. Monoamine oxidase inhibitors MAOIs for what causes plaque in arteries to rupture depressed adults.

Hall-Flavin DK expert opinion. Krieger CA expert opinion. Related Antidepressant withdrawal: Is there such a thing? Antidepressants and alcohol: What's the concern? Antidepressants and weight gain: What causes it? Antidepressants: Can they stop working? Antidepressants: Selecting one that's right for you Antidepressants: Side effects Antidepressants: Which cause the fewest sexual side effects?

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Apr 01,  · MAJOR DEPRESSION (MD) is both etiologically heterogeneous, with a wide range of risk factors, and clinically heterogeneous, presenting with varying patterns of symptoms, ages at onset, severity, duration, and recurrence. This article attempts to clarify further the relationship between etiologic and clinical heterogeneity in lovestoryen.com by:

The hazard ratio for onset of major depression MD vs the co-twin of a twin with 1 lifetime episode of MD. The hazard ratio is presented as a function of the number of episodes of lifetime MD reported by the index twin. The risk for MD in co-twins of index twins with a single lifetime episode of MD is set at unity.

The number of index twins in the various categories is as follows: 1 lifetime episode, ; 2 lifetime episodes, ; 3 to 6 lifetime episodes, ; 7 to 9 lifetime episodes, ; 10 to 15 lifetime episodes, ; and greater than 15 lifetime episodes, Arch Gen Psychiatry. Background Major depression MD is both clinically and etiologically heterogeneous.

We attempt to relate clinical and etiologic heterogeneity by determining those features of MD that reflect a high familial liability to depressive illness. We examine, using Cox proportional hazard models, the clinical features of MD in affected twins that predicted the risk for MD in the co-twin.

Control variables were zygosity, age at interview, and sex of the twin and co-twin. Results The best-fitting model contained 4 significant predictors: number of episodes, duration of longest episode, recurrent thoughts of death or suicide, and level of distress or impairment. These 4 clinical features were similarly predictive of the risk for MD in the co-twins of male and female twins and predicted risk of illness more strongly in monozygotic than in dizygotic twins. Variables that did not uniquely predict risk of MD in the co-twin included age at onset and number of depressive symptoms.

For number of episodes, the best-fitting model indicated an inverted U-shaped function with greatest co-twin risk for MD with 7 to 9 lifetime episodes. Conclusions The clinical features of MD in epidemiologic samples can be meaningfully related to the familial vulnerability to illness. Familial MD is best characterized by intermediate levels of recurrence, long duration of episodes, high levels of impairment, and recurrent thoughts of death or suicide. These clinical features probably reflect a high genetic liability to depressive illness.

This article attempts to clarify further the relationship between etiologic and clinical heterogeneity in MD. Because familial factors consistently influence risk for MD, 5 , 6 , 8 - 12 investigators have identified a range of clinical features of MD related to the risk of illness in relatives, including age at onset, 10 , 13 - 23 recurrence, 10 , 16 , 22 , 24 impairment, 22 , 24 and number or kind of depressive symptoms.

These studies have several potential limitations. First, all but two 22 , 24 ascertained depressed patients in clinical settings, possibly confounding family history of MD and help seeking. Third, many studies relied on family history assessments or only compared depressive probands with or without a positive family history for MD.

Fourth, while some of the sample sizes of depressed probands were reasonably large eg, 75 probands, 16 probands, 15 or probands 10 , larger samples may be needed to resolve the effect of more modest predictors of familial liability.

Fifth, all but 3 of the prior studies 10 , 22 , 23 examined nuclear families and, therefore, could not disentangle the effect of genetic vs familial-environmental effects. Sixth, since the risk for MD differs substantially in men and women, 29 , 30 clinical features of depressive illness that reflect high familial vulnerability may differ by sex.

To our knowledge, this has not been examined previously. In this article, we examine the relationship between a range of clinical features of MD in the affected twin and the hazard rate for MD in the co-twin in a large sample of epidemiologically ascertained and personally interviewed twins from female-female, male-male, and male-female pairs. In this sample, we test for sex differences and examine the degree to which the clinical features reflect the genetic liability to MD.

The twins examined in this article are from 2 interrelated projects that studied white twins ascertained through the population-based Virginia Twin Registry, which was formed from a systematic review of all birth certificates in the Commonwealth of Virginia.

Eighty-eight percent of our sample was first interviewed face-to-face between and and has subsequently been the subject of 3 additional telephone interview waves. From these 2 samples, we formed a total of twin pairs in which both members were personally interviewed. Zygosity was determined by standard questions, 32 photographs, and when necessary in the female-female twins, by DNA testing.

All interviewers were blind to information about the co-twin. First, we assessed last-year and lifetime history for MD prior to the last year in 2 separate sections. Second, SCID questions for MD were modified so that, from the "A criteria" for depression, 35 we independently assessed the presence of the 14 disaggregated symptoms eg, we separately recorded weight loss and weight gain.

Twins with a history of depression were also asked about their age at onset of depression, the number of episodes of depression, length of the longest episode, degree of impairment during the worst episode, level of distress during the worst episode, and depression-related help seeking.

Interviewers had at least a master's degree in social work, psychology, or another mental health—related field, or a bachelor's degree in 1 of these areas plus 2 years' clinical experience. We focused on pairs: a proband twin with MD and the co-twin. Since the onset of MD is age dependent and our sample was variable in age, we used the Cox proportional hazard model, as operationalized in the PHREG procedure in SAS, 36 to predict the hazard rate for MD in the co-twin as a function of clinical characteristics in the proband twin.

To avoid an undue influence from the few twins who reported very large numbers of episodes or long durations, we truncated depressive episodes at and duration at 5 years. The sample comprised twins with a lifetime history of MD chosen from pairs where both members were interviewed. In 26 1. Of the co-twins, The proband sample had a mean age at onset and interview of They endorsed 6. The mean and median duration, in weeks, of the longest episode were Because of the rightward skew in number of episodes and duration of longest episode, we log-transformed these variables for further analyses.

Impairment and level of distress during the worst episode were assessed on 3- and 4-point scales, respectively none, moderate, and severe; and not at all, somewhat, moderately, and very and had mean scores of 2.

Severe impairment was defined as "marked impairment in main life task so that respondent was almost nonfunctional, eg, could not go to job, do any housework. The co-twin's hazard rate for MD was substantially higher when the co-twin was female, younger, and belonged to a monozygotic MZ pair, and was slightly higher when the proband twin was female.

Since prior evidence pointed most strongly to age at onset and recurrence as predictors of risk of illness in relatives, we began with these variables. Model 2 added number of episodes that also significantly predicted risk for MD in the co-twin.

In model 3, we added number of episodes 2 , which was significant and negative, indicating a lower risk for MD with very high and very low numbers of episodes. Adding number of episodes 2 to the model also strengthened the linear effect of number of episodes HR from 1. Adding length of episode 2 , however, produced no improvement in model fit.

We examined the HR for MD in the co-twin as a function of an increasing number of lifetime episodes Figure 1. We examined separately the interaction between the 5 predictor variables in our best model and sex of the proband and zygosity.

Although human recall is of limited reliability in general, 37 and for depressive episodes in particular, 38 , 39 we found 4 retrospectively reported clinical features of MD that significantly discriminated, among people with a lifetime history of depression, those who have a high vs low familial vulnerability to illness. We review these results herein.

Five previous studies have suggested that recurrent episodes of MD are associated with higher familial vulnerability to illness. While the risk of illness in the co-twin increased steadily as the number of reported lifetime episodes increased from 1 to 9, further increases were associated with a decline in risk to the co-twin. Given the importance of the number of episodes in these analyses, we examined its reliability in randomly selected female twins who were interviewed twice, by different interviewers, with a mean interval of 4.

With respect to the number of lifetime episodes, our results suggest that persons with MD can be divided into 3 groups: 1 those with few lifetime episodes where nonfamilial risk factors eg, stressful life events probably play a major role and familial factors play a minor causative role; 2 those with intermediate levels of recurrence with the highest level of familial risk; and 3 those who report very large numbers of episodes who have a low familial risk for depressive illness and may suffer from difficulties with affective modulation that are partially distinct from those that underlie MD.

The Maudsley sample contained twins hospitalized for MD where the mean duration of illness was twice that found in our epidemiologic sample. Consistent with our findings, we observed in our female-female twins that genetic risk for MD was 1 independent predictor of duration of depressive episode. The degree of impairment during the worst episode also significantly predicted risk of depression in the co-twin. We obtained a similar finding in an earlier interview wave with our female-female twins.

We are unaware of a previous precedent for this finding. Both of these symptoms reflect derogatory self-evaluation, a core feature of the cognitive changes that may predispose to and accompany MD. We could not replicate previous findings that early age at onset of MD uniquely predicts increased risk of MD in relatives.

Four reasons for this discrepancy are possible. First, in addition to age at onset, our analyses included other variables such as recurrence and severity. In our own analyses, age at onset significantly predicted risk of illness in the co-twin prior to the inclusion of other predictor variables.

Second, unlike most but not all 15 , 16 studies, we included age at interview as a control variable. If not controlled for, a noncausal association between age at onset and risk in relatives could be induced.

Third, only our study examined a nontreated sample. If both early onset and positive family history commonly produces help seeking eg, a parent with prior depression insisting that a depressed teenager get treatment , the association in treated samples might be artifactual. Fourth, our sample is young, few persons having an onset of MD after age 40 years, a group that may have a particularly low familial loading.

Although differences in the lifetime prevalence of MD in men and women is consistently shown in epidemiologic studies of this condition, 29 , 30 we found no significant differences in the clinical features of MD between the sexes that predicted risk of depression in the co-twin.

High familial liability to illness seems to effect the clinical features of MD similarly in men and women. Because our study contained MZ and DZ twins, who differ in their degree of genetic relatedness, we could assess whether the clinical features of MD that predicted rates of illness in the co-twin were likely to reflect genetic vs familial environmental risk factors.

Of the 5 significant variables, 1 was equally predictive of risk in MZ and DZ co-twins, while the remaining 4 were more predictive in MZ co-twins, 1 nonsignificantly and 3 significantly.

These results suggest that the identified significant predictors are largely indices of a high genetic liability to MD.

This result is consistent with prior evidence in this and other twin samples that the familial aggregation of MD is largely or entirely due to genetic factors. Could the variables found to predict co-twin risk for MD reflect reliability of reporting rather than familial risk? In results from an earlier wave of interviews with the female-female twin pairs in this study, 3 clinical variables uniquely predicted stability of the diagnosis of MD: number of symptoms, treatment-seeking, and number of episodes.

Given the recall and measurement problems inherent in the assessment of lifetime psychopathologic disorders, it is likely that we have underestimated the relationship between these measures and the genetic risk of illness. Most importantly, these results suggest that MD is indeed an etiologically heterogeneous syndrome and that this heterogeneity can be reflected in clinical heterogeneity.

With rapidly increasing interest in linkage studies of MD, the appropriate definition of the highly "familial" or "genetic" forms takes on new urgency. The recent report from the National Institute of Mental Health Genetics Workgroup 47 has declared that "early-onset depression" is the form of depressive illness that should be considered for "large-scale molecular approaches.

We have obtained the lifetime history of mania only in the female-female pairs. When we removed twins with a prior history of mania or hypomania from the sample, virtually no change was seen in the results of the full model model 6 in Table 1. It is unlikely that our findings are substantially skewed by the small subset of affected people with bipolar illness. In these pairs, we use clinical features of twin A to predict risk in twin B and clinical features of twin B to predict risk in twin A.

For our final model we performed replicates of nonparametric bootstrap simulations and thereby obtained empirical SEs.

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