Co-morbid depression

Treat comorbid depression, substance abuse disorders simultaneously

Co-morbid depression

SAN DIEGO – Adolescents with substance abuse and depression should be simultaneously treated for both conditions – and preferably by the same provider or clinical team, said Dr. Paula Riggs, professor of psychiatry and director of the division of substance dependence at the University of Colorado at Denver, Aurora.

“It’s hard to be successful in drug treatment under the best of circumstances. If you have an untreated Axis I mental health disorder, it’s not going to go well,” said Dr. Riggs, who is an expert in treating comorbid adolescent substance abuse and psychiatric disorders.

“Adolescent depressions usually do not remit with abstinence” from drugs and alcohol, Dr. Riggs said at the annual meeting of the American Academy of Child and Adolescent Psychiatry.

“If you have a kid walk through your door with depression and SUD [substance abuse disorder], treating the SUD won’t make the depression go away.

Once you’ve got both, you’ve got two things you’ve got to address – and preferably in an integrated fashion.”

Successful treatment of childhood depression does reduce the risk of later substance abuse, especially if the depression remits within 12 weeks of starting treatment, said Dr. Riggs. “But the converse is not true,” she said.

About 25%-50% of adolescents who present for mental health treatment meet criteria for SUDs, Dr. Riggs said.

And more than half of preteens with mental health problems are at risk for developing a SUD by the time they reach adolescence, she said.

“By and large, psychiatric problems are pediatric-onset illnesses, and we know from ample research that most adults who suffer from addiction started using when they were adolescents,” she added.

But all too often, teens with comorbid SUD and Axis I disorders go without treatment, said Dr. Riggs.

In a recent pooled analysis of 2,111 adolescents with comorbid major depression and SUD, 48% were treated for depression and 10% received help for substance abuse, she noted.

Furthermore, being in the juvenile justice system was the strongest predictor of dual treatment. “I don’t know why people aren’t up in arms about that,” she said.

“We kind of require kids to fall in the hole to get treatment.”

In 2013, the Substance Abuse and Mental Health Services Administration recommended that adolescents with comorbid SUD and depression receive integrated, simultaneous treatment for both disorders, Dr. Riggs noted. No matter which problem arose first, “recovery depends on treating both the addiction and the mental health problem,” she said.

Currently, the best treatment for adolescent SUD is motivational enhancement, “totally integrated with cognitive behavioral therapy,” Dr. Riggs said. Motivational incentives should encourage attendance, abstinence, and alternative activities that do not involve drugs, she added.

Individual therapy is more effective than group therapy for treating comorbid substance abuse and psychiatric disorders. But studies also suggest that the patient’s family should be involved in treatment, Dr. Riggs said.

Furthermore, coordinating mental health care, substance abuse treatment, and family therapy has been shown to significantly alleviate symptoms in patients with SUDs who also have Axis I major depressive disorder, attention-deficit/hyperactivity disorder, or an anxiety disorder, she said.

Data support the judicious use of antidepressants for adolescents who have major depressive disorder with comorbid SUD, Dr. Riggs said.

In her randomized controlled trial of fluoxetine versus placebo in teens with major depression and SUD, fluoxetine showed “about the same safety profile as in kids who were not using drugs, despite nonabstinence.” And overall treatment gains lasted for a year after treatment, she said.

“If you don’t see remission in the first month of substance abuse treatment, I would not hesitate to use fluoxetine,” she added. “You have got to do a comprehensive diagnostic assessment at baseline, and get a really good longitudinal history to map symptom onset.

The bottom line is, if you are carefully monitoring the substance, and if the kid is in substance treatment, continue the fluoxetine.”

Clinicians and parents should not look the other way when the substance in question is cannabis, Dr. Riggs emphasized.

“Prenatal exposure to marijuana can cause irritable babies, deficits in abstract reasoning and memory, symptoms that look ADHD, and executive functioning deficits,” she said.

“Marijuana use in adolescence doubles your risk of developing depression or an anxiety disorder in your twenties. And all of it adds up to poor academic achievement and underachievement in adulthood.”

Dr. Riggs reported receiving research support from the National Institute on Drug Abuse and the ENCOMPASS substance abuse treatment program.

Source: https://www.mdedge.com/psychiatry/article/88516/addiction-medicine/treat-comorbid-depression-substance-abuse-disorders

Many People With Depression Also Have Comorbidity

Co-morbid depression

Comorbidity means having more than one diagnosis.

Getty / DrAfter123

The term comorbidity was coined in the 1970s by A.R. Feinstein, a renowned American doctor, and epidemiologist.

Feinstein demonstrated comorbidity through the example of how people who suffered from rheumatic fever also usually suffered from multiple other diseases.

 Since that time, comorbidity has come to be associated with the presence of multiple mental or physical illnesses in the same person.

It's not uncommon for people to suffer from two disorders or illnesses at once. Comorbidity in mental illness can include a situation where a person receives a medical diagnosis that is followed by the diagnosis of a mental disorder (or vice versa), or it can involve the diagnosis of a mental disorder that is followed by the diagnosis of another mental disorder.

A 2009 large cross-sectional national epidemiological study of comorbidity of mental disorders in primary care in Spain published in the Journal of Affective Disorders showed that among a sample of 7936 adult patients, about half had more than one psychiatric disorder.

Furthermore, in the U.S. National Comorbidity Survey, 51% of patients with a diagnosis of major depression also had at least one anxiety disorder and only 26% of them had no other mental disorder.

However, in the Early Developmental Stages of Psychopathology Study, 48.6% of patients with a diagnosis of major depression also had at least one anxiety disorder and 34.

8% of them had no other mental disorder.

Overlap of medical conditions with psychiatric conditions is a significant challenge for healthcare professionals and creates additional costs for the healthcare system.

 For example, a person diagnosed with both diabetes and depression would be treated for both conditions, but consideration for overlap between medications and symptoms would need to be coordinated by the various health care professionals offering treatment.

If you live with multiple conditions or disorders, it is important that your doctor is aware of all medications and over-the-counter drugs you are taking, to ensure the risk of medication interactions is reduced.

Healthcare professionals also play a role in the prevention of comorbidity. For example, if social anxiety disorder is left untreated for a long period of time, a person may also develop depression and/or substance abuse in response to the anxiety symptoms.

At a broader level, coordination between primary doctors and mental health professionals is key to preventing comorbid conditions. If you've been diagnosed with a physical and/or mental health condition, keep good records of the care that you receive from various professionals, so that each can be aware of the various treatments you are receiving.

If you feel that you have symptoms of more than one mental disorder or those of a physical health condition in addition to a mental disorder, it is important to consult with your primary care physician or mental health professional to determine the best course of action. The unique combination of symptoms that you experience will determine whether medication and/or therapy is best for your situation.

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  1. Koyuncu A, İnce E, Ertekin E, Tükel R. Comorbidity in social anxiety disorder: diagnostic and therapeutic challenges. Drugs Context. 2019;8:212573. doi:10.7573/dic.212573

  2. He VY, Condon JR, Ralph AP, et al. Long-Term Outcomes From Acute Rheumatic Fever and Rheumatic Heart Disease: A Data-Linkage and Survival Analysis Approach. Circulation. 2016;134(3):222-232. doi:10.1161/CIRCULATIONAHA.115.020966

  3. Vaidyanathan U, Patrick CJ, Iacono WG. Patterns of comorbidity among mental disorders: a person-centered approach. Compr Psychiatry. 2011;52(5):527-535. doi:10.1016/j.comppsych.2010.10.006

  4. Roca M, Gili M, Garcia-Garcia M, et al. Prevalence and comorbidity of common mental disorders in primary care. J Affect Disord. 2009;119(1-3):52-58. doi:10.1016/j.jad.2009.03.014

  5. Starcevic, V. Psychiatric Comorbidity: Concepts, Controversies and Alternatives. Australasian Psychiatry. The British Journal of Psychiatry. 2005:13(4):375.

  6. Sartorious N. Comorbidity of mental and physical diseases: a main challenge for medicine of the 21st century. Shanghai Arch Psychiatry. 2013;25(2):68-69. doi:10.3969/j.issn.1002-0829.2013.02.002

  7. McHugh RK. Treatment of Co-Occurring Anxiety Disorders and Substance Use Disorders. Harv Rev Psychiatry. 2015;23(2):99-111. doi:10.1097/HRP.0000000000000058

Additional Reading

  • Maj M. “Psychiatric comorbidity”: an artefact of current diagnostic systems? Br J Psychiatry. 2005 Mar;186:182–4.
  • Trivedi RB, Post EP, Sun H, Pomerantz A, Saxon AJ, Piette JD, et al. Prevalence, Comorbidity, and Prognosis of Mental Health Among US Veterans. Am J Public Health. 2015 Dec;105(12):2564–9.
  • U.S National Library of Medicine, World Psychiatry. 2004 Feb; 3(1): 18–23.

Source: https://www.verywellmind.com/what-is-comorbidity-3024480

Self-Esteem Instability in Current, Remitted, Recovered, and Comorbid Depression and Anxiety

Co-morbid depression

  1. Aiken, L. S., & West, S. G. (1991). Multiple regression: Testing and interpreting interactions. Thousand Oaks, CA: SAGE. Retrieved from http://search.ebscohost.com/login.aspx?direct=true&db=psyh&AN=1991-97932-000&site=ehost-live&scope=site.

  2. Baird, B. M., Le, K., & Lucas, R. E. (2006). On the nature of intraindividual personality variability: Reliability, validity, and associations with well-being. Journal of Personality and Social Psychology, 90(3), 512–527. https://doi.org/10.1037/0022-3514.90.3.512.

    • Article
    • PubMed
    • Google Scholar
  3. Beck, A. T. (2002). Cognitive models of depression. In R. L. Leahy & E. T. Dowd (Eds.), Clinical advances in cognitive psychotherapy: Theory and application (pp. 29–61). New York, NY: Springer Publishing Co.

  4. Beck, A. T., Epstein, N., Brown, G., & Steer, R. A. (1988). An inventory for measuring clinical anxiety: Psychometric properties. Journal of Consulting and Clinical Psychology, 56(6), 893–897. https://doi.org/10.1037/0022-006X.56.6.893.

    • CAS
    • Article
    • PubMed
    • Google Scholar
  5. Clasen, P. C., Fisher, A. J., & Beevers, C. G. (2015). Mood-reactive self-esteem and depression vulnerability: Person-specific symptom dynamics via smart phone assessment. PLoS ONE. https://doi.org/10.1371/journal.pone.0129774.

    • Article
    • PubMed
    • PubMed Central
    • Google Scholar
  6. Dawson, J. F. (2014). Moderation in management research: What, why, when, and how. Journal of Business and Psychology, 29(1), 1–19. https://doi.org/10.1007/s10869-013-9308-7.

  7. de Man, A. F., Gutiérrez, B. I. B., & Sterk, N. (2001). Stability of self-esteem as moderator of the relationship between level of self-esteem and depression. North American Journal of Psychology, 3(2), 303–308.

  8. Farmer, A. S., & Kashdan, T. B. (2014). Affective and self-esteem instability in the daily lives of people with generalized social anxiety disorder. Clinical Psychological Science, 2(2), 187–201. https://doi.org/10.1177/2167702613495200.

    • Article
    • PubMed
    • PubMed Central
    • Google Scholar
  9. Ford, M. B., & Collins, N. L. (2010). Self-esteem moderates neuroendocrine and psychological responses to interpersonal rejection. Journal of Personality and Social Psychology, 98(3), 405–419. https://doi.org/10.1037/a0017345.

    • Article
    • PubMed
    • Google Scholar
  10. Franck, E., & De Raedt, R. (2007). Self-esteem reconsidered: Unstable self-esteem outperforms level of self-esteem as vulnerability marker for depression. Behaviour Research and Therapy, 45(7), 1531–1541. https://doi.org/10.1016/j.brat.2007.01.003.

    • Article
    • PubMed
    • Google Scholar
  11. Frank, E., Prien, R. F., Jarrett, R. B., Keller, M. B., Kupfer, D. J., Lavori, P. W., … Weissman, M. M. (1991). Conceptualization and rationale for consensus definitions of terms in major depressive disorder: Remission, recovery, relapse, and recurrence. Archives of General Psychiatry, 48(9), 851–855. https://doi.org/10.1001/archpsyc.1991.01810330075011.

    • CAS
    • Article
    • PubMed
    • Google Scholar
  12. Gemar, M. C., Segal, Z. V., Sagrati, S., & Kennedy, S. J. (2001). Mood-induced changes on the implicit association test in recovered depressed patients. Journal of Abnormal Psychology, 110(2), 282–289. https://doi.org/10.1037/0021-843X.110.2.282.

    • CAS
    • Article
    • PubMed
    • Google Scholar
  13. Herche, J., & Engelland, B. (1996). Reversed-polarity items and scale unidimensionality. Journal of the Academy of Marketing Science, 24(4), 366–374. https://doi.org/10.1177/0092070396244007.

  14. Kernis, M. H., Grannemann, B. D., & Mathis, L. C. (1991). Stability of self-esteem as a moderator of the relation between level of self-esteem and depression. Journal of Personality and Social Psychology, 61(1), 80–84. https://doi.org/10.1037/0022-3514.61.1.80.

    • CAS
    • Article
    • PubMed
    • Google Scholar
  15. Kleiman, E. M., & Riskind, J. H. (2012). Cognitive vulnerability to comorbidity: Looming cognitive style and depressive cognitive style as synergistic predictors of anxiety and depression symptoms. Journal of Behavior Therapy and Experimental Psychiatry, 43(4), 1109–1114. https://doi.org/10.1016/j.jbtep.2012.05.008.

    • Article
    • PubMed
    • Google Scholar
  16. Leary, M. R., & Baumeister, R. F. (2000). The nature and function of self-esteem: Sociometer theory. In M. P. Zanna (Ed.), Advances in experimental social psychology (Vol. 32, pp. 1–62). San Diego, CA: Academic Press. https://doi.org/10.1016/S0065-2601(00)80003-9.

  17. Lewinsohn, P. M., Steinmetz, J. L., Larson, D. W., & Franklin, J. (1981). Depression-related cognitions: Antecedent or consequence? Journal of Abnormal Psychology, 90(3), 213–219. https://doi.org/10.1037/0021-843X.90.3.213.

    • CAS
    • Article
    • PubMed
    • Google Scholar
  18. Okada, R. (2010). A meta-analytic review of the relation between self-esteem level and self-esteem instability. Personality and Individual Differences, 48(2), 243–246. https://doi.org/10.1016/j.paid.2009.10.012.

  19. Orth, U., & Robins, R. W. (2014). The development of self-esteem. Current Directions in Psychological Science, 23(5), 381–387. https://doi.org/10.1177/0963721414547414.

  20. Penninx, B. W. J. H., Beekman, A. T. F., Johannes, H. S., Zitman, F. G., Nolen, W. A., et al. (2008). The Netherlands Study of Depression and Anxiety (NESDA): Rationale, objectives and methods. International Journal of Methods in Psychiatric Research, 17(3), 121–140. https://doi.org/10.1002/mpr.256.

    • Article
    • PubMed
    • Google Scholar
  21. Penninx, B. W. J. H., Nolen, W. A., Lamers, F., Zitman, F. G., Smit, J. H., et al. (2011). Two-year course of depressive and anxiety disorders: Results from the Netherlands Study of Depression and Anxiety (NESDA). Journal of Affective Disorders, 133(1–2), 76–85. https://doi.org/10.1016/j.jad.2011.03.027.

    • Article
    • PubMed
    • Google Scholar
  22. Raes, F., & Gucht, D. V. (2009). Paranoia and instability of self-esteem in adolescents. Personality and Individual Differences, 47(8), 928–932.

  23. Richardson, T., Stallard, P., & Velleman, S. (2010). Computerised cognitive behavioural therapy for the prevention and treatment of depression and anxiety in children and adolescents: A systematic review. Clinical Child and Family Psychology Review, 13(3), 275–290.

  24. Roberts, J. E., Kassel, J. D., & Gotlib, I. H. (1995). Level and stability of self-esteem as predictors of depressive symptoms. Personality and Individual Differences, 19(2), 217–224. https://doi.org/10.1016/0191-8869(95)00049-C.

  25. Roberts, J. E., & Monroe, S. M. (1992). Vulnerable self-esteem and depressive symptoms: Prospective findings comparing three alternative conceptualizations. Journal of Personality and Social Psychology, 62(5), 804–812. https://doi.org/10.1037/0022-3514.62.5.804.

    • CAS
    • Article
    • PubMed
    • Google Scholar
  26. Roberts, J. E., & Monroe, S. M. (1994). A multidimensional model of self-esteem in depression. Clinical Psychology Review, 14(3), 161–181. https://doi.org/10.1016/0272-7358(94)90006-X.

  27. Roberts, J. E., Shapiro, A. M., & Gamble, S. A. (1999). Level and perceived stability of self-esteem prospectively predict depressive symptoms during psychoeducational group treatment. British Journal of Clinical Psychology, 38(4), 425–429. https://doi.org/10.1348/014466599162917.

    • Article
    • PubMed
    • Google Scholar
  28. Robins, L. N., Wing, J., Wittchen, H. U., Helzer, J. E., Babor, T. F., Burke, J., … Regier, D. A. (1988). The composite international diagnostic interview: An epidemiologic instrument suitable for use in conjunction with different diagnostic systems and in different cultures. Archives of General Psychiatry, 45(12), 1069–1077.

    • CAS
    • Article
    • Google Scholar
  29. Rosenberg, M. (1989). Society and the adolescent self-image (revised edition). Middletown: Wesleyan University Press.

  30. Rush, A. J., Giles, D. E., Schlesser, M. A., Fulton, C. L., Weissenburger, J., & Burns, C. (1986). The inventory for depressive symptomatology (IDS): Preliminary findings. Psychiatry Research, 18(1), 65–87. https://doi.org/10.1016/0165-1781(86)90060-0.

    • CAS
    • Article
    • PubMed
    • Google Scholar
  31. Rush, A. J., Gullion, C. M., Basco, M. R., Jarrett, R. B., & Trivedi, M. H. (1996). The inventory of depressive symptomatology (IDS): Psychometric properties. Psychological Medicine, 26(3), 477–486. https://doi.org/10.1017/S0033291700035558.

    • CAS
    • Article
    • PubMed
    • Google Scholar
  32. Segal, Z. V., Gemar, M., & Williams, S. (1999). Differential cognitive response to a mood challenge following successful cognitive therapy or pharmacotherapy for unipolar depression. Journal of Abnormal Psychology, 108(1), 3–10.

    • CAS
    • Article
    • Google Scholar
  33. Sowislo, J. F., & Orth, U. (2013). Does low self-esteem predict depression and anxiety? A meta-analysis of longitudinal studies. Psychological Bulletin, 139(1), 213–240. https://doi.org/10.1037/a0028931.

    • Article
    • PubMed
    • Google Scholar
  34. van Tuijl, L. A., Glashouwer, K. A., Bockting, C. L. H., Tendeiro, J. N., Penninx, B. W., et al. (2016). Implicit and explicit self-esteem in current, remitted, recovered, and comorbid depression and anxiety disorders: The NESDA study. PLoS ONE, 11(11), e0166116. https://doi.org/10.1371/journal.pone.0166116.

    • CAS
    • Article
    • PubMed
    • PubMed Central
    • Google Scholar
  35. Wittchen, H.-U. (1994). Reliability and validity studies of the WHO-composite international diagnostic interview (CIDI): A critical review. Journal of Psychiatric Research, 28(1), 57–84.

    • CAS
    • Article
    • Google Scholar
  36. Zuckerman, M. (1999). Vulnerability to psychopathology: A biosocial model. Washington, DC: American Psychological Association.

Source: https://link.springer.com/article/10.1007/s10608-018-9926-5

Understanding Comorbid Depression and Anxiety

Co-morbid depression

Comorbidity of psychiatric syndromes is quite common—in a 12-month period, almost 50% of adults in the United States with any psychiatric disorder had 2 or more disorders.1 The prevalence of comorbid anxiety disorder and major depressive disorder (MDD) is frequent and perhaps as high as 60%.

2 It may be higher if significant but subsyndromal symptoms are included in analyses.3 This is far greater than the 2% or less co-occurrence that would be expected by chance.

Although panic disorder (PD) and generalized anxiety disorder (GAD) have been most studied as part of an anxiety-depression comorbid state, all or almost all of the anxiety disorders appear to show comorbidity with at least depressive symptoms if not full MDD.

The National Comorbidity Survey Replication1 reported that in a 12-month period, the prevalence for an anxiety disorder was about 18%, and for a mood disorder it was 9.5%.

Lifetime prevalences for any anxiety disorder and MDD were approximately 29% and 16.6%, respectively.

4 Assuming a (perhaps conservative) 50% comorbidity rate, between 5% and 9% of the adult population has comorbid depression-anxiety in a 12-month period.

The impact of comorbid depression and anxiety is substantial. As demonstrated by the Global Burden of Disease study, neuropsychiatric disorders accounted for more than 13% of all medical disability worldwide and for more than 27% of all noncommunicable disease in 2005.

5 Depression alone produced 10% to 12% of all disability from noncommunicable disease and approximately 5% of all disability (noncommunicable, communicable, injury). Thus, comorbid anxiety and depression may account for as much as 2% to 4% of all medical disability worldwide.

In addition, depression (and, thus, comorbid depression and anxiety) is associated with other psychiatric and nonpsychiatric medical conditions (eg, cardiovascular disease, diabetes, HIV/AIDS, maternal and reproductive-related syndromes, and psychosomatic illnesses), with their resulting socioeconomic costs.5

Risk factors and prognoses

There has been little research on risk factors that predict the development of comorbid anxiety and depression compared with risk factors for either disorder alone.

However, the high rate of comorbidity indicates that the simple occurrence of one disease state should be considered a predisposing factor for the development of the other.

Psychosocial and situational difficulties also appear to be risk factors for the development of comorbid anxiety and depression.6 Familial/genetic studies reported different results, partly determined by the anxiety disorder under consideration.

6 For example, MDD and GAD appear to be related to the same genetic factors, while MDD and PD are familially independent.7-9 Gender may also play a role, because women have a higher risk than men for both disorders.4

Age is another consideration. Patients with anxiety disorders have a much earlier median age at onset than do those with mood disorders (age 11 years vs age 30 years).4 As would be expected, onset of anxiety usually predates onset of depression in patients with this comorbidity.6,10 However, the earlier onset of anxiety disorders does not necessarily infer causality.

The expected prognosis for patients with comorbid anxiety and depressive disorders is poorer than that for either disorder alone.

These patients have greater severity of symptoms, increased risk of suicidality, a more chronic and persistent course, and more functional impairment.

This syndrome is also more difficult to treat, with longer time to remission and need for increased medication.6,11,12

Biological studies

There are several possible explanations for this high rate of comorbidity.13 First, the present DSM-IV diagnostic criteria tend to overlap, raising the lihood that a person meeting criteria for one disorder has an increased probability of having the other.

For example, depressive ruminations are similar to the obsessional thinking/worry seen in GAD; poor sleep quality and difficulty in concentrating occur in both depression and posttraumatic stress disorder; and phobic avoidance can be mistaken for depressive loss of energy or fatigue.

A second possibility is that the disorders are etiologically different, but symptom episodes are provoked by related environmental events (ie, stressors), such as threat (anxiety) and loss (depression).

14 The third possibility is that the underlying biologies of the disorders are the same or are highly overlapping; this is related to the first possible explanation. An understanding of the pathophysiology of depressive and anxiety disorders is necessary to address the first and third reasons.

A number of potential biological markers have been studied in people with comorbid depression and anxiety.13 Several markers have assessed noradrenergic or hypothalamic-pituitary-adrenocortical (HPA) axis function.

Serotonergic (along with noradrenergic) function has also been of interest, because many medications with serotonergic and/or noradrenergic effects are beneficial for individuals with depression and/or anxiety.

15 Other markers studied include sleep (which is abnormal in both types of disorders), thyroid axis activity (abnormal in depression), lactate infusion (abnormal in anxiety), and cardiovascular function (abnormal in both depression and anxiety). (Abnormality associated with sleep and cardiovascular functions presents differently in anxiety versus depression.)

Earlier studies have not included nonpathological controls, patients with depression only, patients with anxiety only, and patients with both disorders. Interpretation of results has been somewhat hampered by the lack of inclusion of all 4 groups. Therefore, we recently designed and completed a study of HPA axis function and CNS noradrenergic function that included these 4 groups.16-19

In order to determine the roles of each disorder as well as the comorbid state, we compared “pure” participants —those with anxiety only (social anxiety disorder or PD) or MDD only—with individuals who had comorbidity; these participants were also matched with controls. We used the Trier Social Stress Test (a reliable activator of the HPA axis) and the growth hormone response to the a2-adrenoreceptor agonist clonidine.

As can be seen in the Table, anxiety was associated with a noradrenergic abnormality; depression was associated with a disruption of the normal negative correlation between the 2 systems.

Most notably, hyperactivity of the HPA axis was uniquely associated with the comorbid state, indicating that there is something qualitatively (not just quantitatively) distinctly biological about the comorbid state.

In other words, comorbid anxiety and depression might be a distinct disorder.

TABLEBiological changes in anxiety, depression,and comorbid anxiety and depression
Diagnostic group HPA axis Noradrenergic function Association of markers
Anxiety Blunted GH response*
Depression No negative correlation‡
Comorbid Hyperactive† Blunted GH response* No negative correlation‡

References

1. Kessler RC, Chiu WT, Demler O, et al. Prevalence, severity, and comorbidity of 12-month DSM-IV disorders in the National Comorbidity Survey Replication. Arch Gen Psychiatry. 2005;62:617-627.

2. Kaufman J, Charney D. Comorbidity of mood and anxiety disorders. Depress Anxiety. 2000;12:69-76.
3. Gorman JM. Comorbid depression and anxiety spectrum disorders. Depress Anxiety. 1996/7;4:160-168.
4. Kessler RC, Berglund P, Demler O, et al. Lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the National Comorbidity Survey Replication. Arch Gen Psychiatry. 2005;62:593-602.
5. Prince M, Patel V, Saxena S, et al. No health without mental health. Lancet. 2007;370:859-877.
6. Pollack MH. Comorbid anxiety and depression. J Clin Psychiatry. 2005;66:22-29.
7. Kendler KS, Neale MD, Kessler RC, et al. Major depression and generalized anxiety disorder: (partly) different environments? Arch Gen Psychiatry. 1992;48:716-722.
8. Weissman MM. Family genetic studies of panic disorder. J Psychiatr Res. 1993;27(suppl 1):69-78.
9. Kendler KS, Walters EE, Neale MC, et al. The structure of the genetic and environmental risk factors for six major psychiatric disorders in women: phobia, generalized anxiety disorder, panic disorder, bulimia, major depression, and alcoholism. Arch Gen Psychiatry. 1995;52:374-383.
10. Wittchen HU, Kessler RC, Pfister RC, Lieb M. Why do people with anxiety disorders become depressed? A prospective-longitudinal community study. Acta Psychiatr Scand. 2000;406:14-23.
11. Roy-Byrne PP, Stang P, Wittchen HU, et al. Lifetime panic-depression comorbidity in the National Comorbidity Survey. Association with symptoms, impairment, course, and help-seeking. Br J Psychiatry. 2000;176: 229-235.
12. Belzer K, Schneier FR. Comorbidity of anxiety and depressive disorders: issues of conceptualization, assessment, and treatment. J Psychiatr Pract. 2004;10:296-306.
13. Cameron OG. Anxious-depressive comorbidity: effects on HPA axis and CNS noradrenergic functions. Essent Psychopharmacol. 2006;7:24-34.
14. Finley-Jones R, Brown GW. Types of stressful life event and the onset of anxiety and depressive disorders. Psychol Med. 1981;11:803-815.
15. Baldwin DS, Evans DL, Hirschfeld RM, Kasper S. Can we distinguish anxiety from depression? Psychopharmacol Bull. 2002;36(suppl 2):158-165.
16. Young EA, Abelson JL, Cameron OG. Effect of comorbid anxiety disorders on the hypothalamic-pituitary-adrenal axis response to a social stressor in major depression. Biol Psychiatry. 2004;56:113-120.
17. Cameron OG, Abelson JL, Young EA. Anxious and depressive disorders and their comorbidity: effect on central nervous system noradrenergic function. Biol Psychiatry. 2004;56:875-883.
18. Young EA, Abelson JL, Cameron OG. Interaction of brain noradrenergic system and the hypothalamic-pituitary adrenal (HPA) axis in man. Psychoneuroendocrinology. 2005;30:807-814.
19. Boerner RJ, Moller HJ. The importance of new antidepressants in the treatment of anxiety/depressive disorders. Pharmacopsychiatry. 1999;32:119-126.
20. Borkovec TD, Ruscio AM. Psychotherapy for generalized anxiety disorder. J Clin Psychiatry. 2001;62:37-42.
21. Kapczinski F, Lima MS, Souza JS, et al. Antidepressants for generalized anxiety disorder. Cochrane Database Syst Rev. 2003;(2):CD003592..
22. Panzer MJ. Are SSRIs really more effective for anxious depression? Ann Clin Psychiatry. 2005;17:23-29.
23. Furukawa TA, Streiner DL, Young LT, Konoshita Y. Antidepressants plus benzodiazepines for major depression. Cochrane Database Syst Rev. 2001;(3):CD001026.
24. Grunhaus L, Harel Y, Krugler T, et al. Major depressive order and panic disorder. Effects of comorbidity on treatment outcome with antidepressant medications. Clin Neuropharmacol. 1988;11:454-461.
25. Tollefson GD, Greist JH, Jefferson JW, et al. Is baseline agitation a relative contraindication for a selective serotonin reuptake inhibitor? A comparative trial of fluoxetine versus imipramine. J Clin Psychopharmacol. 1994;14:385-391.
26. Pini S, Amador XF, Dell'Osso L, et al. Treatment of depression with comorbid anxiety disorders: differential efficacy of paroxetine versus moclobemide. Int Clin Psychopharmacol. 2003;18:15-21.
27. Trivedi MH, Rush AJ, Carmody TJ, et al. Do bupropion SR and sertraline differ in their effects on anxiety in depressed patients? J Clin Psychiatry. 2001;62:776-781.
28. Nutt DJ. Efficacy of mirtazapine in clinically relevant subgroups of depressed patients. Depress Anxiety. 1998;7:7-10.
29. Silverstone PH, Salinas E. Efficacy of venlafaxine extended release in patients with major depressive disorder and comorbid generalized anxiety. J Clin Psychiatry. 2001;62:523-529.
30. Davidson JR, Meoni P, Haudiquet V, et al. Achieving remission with venlafaxine and fluoxetine in major depression: its relationship to anxiety symptoms. Depress Anxiety. 2002;16:4-13.

Source: https://www.psychiatrictimes.com/anxiety/understanding-comorbid-depression-and-anxiety

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Co-morbid depression

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Co-morbid depression

Co-morbid depression

Co-morbid depression refers to depression that occurs in the presence of another illness.

People with chronic (long-term) physical illnesses, especially those with conditions that produce a lot of pain, restriction of activity or a poor outlook are all prone to developing depression on top of their existing illness.

Physical illnesses that are commonly associated with co-morbid depression include:

  • cancer;
  • heart disease;
  • stroke;
  • chronic obstructive pulmonary disease (COPD);
  • diabetes;
  • epilepsy; and
  • Parkinson’s disease.

Depression also commonly affects people with other mental health problems, such as anxiety or drug and alcohol problems.

Symptoms of depression

For people with chronic or serious illnesses it can sometimes be hard to tell the difference between ‘understandable unhappiness’ and depression.

Typical features of depression include:

  • a prolonged period of low mood that is uncharacteristic for the person;
  • a loss of interest in everyday things such as hobbies and family;
  • an inability to look forward to things;
  • an inability to find pleasure in things they used to enjoy;
  • a loss of self esteem;
  • negative thoughts and feelings;
  • feelings of guilt;
  • sleep disturbance; and
  • a change in appetite.

Treatment

Treating depression helps relieve the symptoms of depression, but can also help treat symptoms associated with your medical condition, improve physical functioning and increase your quality of life.

Treatment of depression involves psychological treatments, antidepressant medicines, lifestyle changes and sometimes a combination of all three. For some people with physical illnesses, modifications to the usual treatment approach are necessary. Your doctor will be able to assess your situation and create a treatment plan to fit your needs.

Your doctor will also review any treatments you are using for your medical condition to ensure none of them are associated with depressed mood.

Getting sufficient sleep, eating healthily, getting some physical activity (depending on your physical limitations) and joining a support group can also help treat depression and improve mood.

References

1. Olver JS, Hopwood MJ. Depression and physical illness. MJA Open 2012; 1 Suppl 4: 9-12. https://www.mja.com.au/open/2012/1/4/depression-and-physical-illness (accessed Jan 2013).2. Beyondblue. Chronic physical illness and depression – Fact sheet 23 (updated 26 April 2012). http://www.

beyondblue.org.au/index.aspx?link_id=7.980&http://www.beyondblue.org.au/index.aspx?link_id=6.1068&tmp=FileDownload&fid=773 (accessed Jan 2013).

3. MayoClinic.com. Depression (major depression) (updated10 Feb 2012). http://www.mayoclinic.com/health/depression/DS00175/ (accessed Jan 2013).

Source: https://www.mydr.com.au/mental-health/co-morbid-depression

Comorbid Depression May Boost Neurocognition in Schizophrenia

Co-morbid depression

Patients with first-episode schizophrenia spectrum and comorbid depressive disorder showed better neurocognitive performance compared with patients without comorbidity, according to findings published in the Journal of Affective Disorders.

Researchers conducted a secondary analysis of data from a single blind, randomized controlled trial of vocational intervention for individuals age 15 to 25 years with first-episode schizophrenia spectrum (n=82).

They sought to compare the neurocognitive profiles of people with first-episode schizophrenia spectrum with and without comorbid depressive disorder and to determine whether there is a relationship between severity of depressive symptoms and neurocognitive performance.

Of the 82 participants, 24 had comorbid full-threshold depressive disorder: 11 had major depressive disorder, 12 had depressive disorder not otherwise specified, and 1 had dysthymia.

The researchers used scores from 18 tests to examine 4 neurocognitive domains: verbal comprehension and working memory, verbal learning and memory, information processing speed, and visual organization and memory.

The 18 neurocognitive raw test scores included the following: Wechsler Adult Intelligence Scale-Third Edition subtests (Digit Span, Letter-Number Sequencing, Similarities, Information and Picture Completion), the Trail Making Test A and B, Symbol Digit Modalities Test’s Letter Cancellation Task, Rey Auditory Verbal Learning Test, Rey-Osterrieth Complex Figure Test, Controlled Oral Word Association Test, and the Animal Fluency test.

After controlling for premorbid intelligence quotient and positive and negative psychotic symptoms, the researchers found that participants with comorbid depressive disorder showed significantly better information processing speed compared with those without depressive disorders. In addition, the severity of depressive symptoms was associated with better information processing speed.

There were no significant differences between those with and without comorbid depression in other neurocognitive domains.

Up to 80% of patients with first-episode schizophrenia spectrum have comorbid depressive disorder, which usually appears during the prodrome or first psychotic episode. However, medical professionals often overlook depressive disorder when researching and treating first-episode schizophrenia spectrum, instead focusing on treating psychotic symptoms.

“This is the first study to examine the influence of depressive disorder on neurocognitive performance in a sample of individuals free from the long-term effects of psychotic illness and other potentially confounding variables,” the researchers wrote. “Such novel findings are therefore more ly to accurately reflect the influence of depressive disorder during the post-psychotic phase on neurocognitive performance in this population and thus uniquely add to the current knowledge base.”

Reference

Herniman SE, Cotton SM, Killackey E, Hester R, Allott KA. Co-morbid depressive disorder is associated with better neurocognitive performance in first episode schizophrenia spectrum. J Affect Disord. 2018;229:498-505.

Source: https://www.psychiatryadvisor.com/home/schizophrenia-advisor/comorbid-depression-may-boost-neurocognition-in-schizophrenia/

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