What is the difference between being very sad and being depressed?
Is there a difference in the brain when being sad and when being depressed?

ANSWER: There are many differences between normal sadness and clinical depression.  Normal sadness is an appropriate response to a sad event, and it dissipates after some time.  Normal sadness does not interfere with a person's ability to function personally and professionally.

Depression is a sense of hopelessness, despair and inability to feel joy that lasts for months or years.  Depression interferes with a person's ability to function normally - they may stop eating and sleep constantly, or sleep during the day and be unable to sleep at night.  Depression also causes aches and pain, a feeling of lethargy and an irrational feeling that the person will never feel "good" again. Depressed patients also have poor memory and cognitive function, usually have a decreased libido.

Research has shown that depression is associated with changes in dopamine, norepinephrine and particularly serotonin, which are neurotransmitters in the brain.  Brain imaging and function studies have shown that limbic structures, deep in the brain are underactive in depressed patients.  These structures are responsible for regulating emotion, memory and biological drives such as sex and eating.  These structures interact with the hormonal system and stress responses.  Many people with depression have very high levels of cortisol, which is a hormone that is released in response to stress.

---------- FOLLOW-UP ----------

Your answer is very interesting and good but there is still one question:
You say that "Normal sadness is an appropriate response to a sad event, and it dissipates after some time.  Normal sadness does not interfere with a person's ability to function personally and professionally".

If I understand you correctly depression is not a response to a sad event but rather something else. Is that correct?
I personally understand that people can experience normal sadness for years without it really dissapearing. They can still experience joy during the time the sadness is still there due to the fact that the joy doesn't take away the sadness.
What do you say?

Clinical depression is not a healthy response to a sad event. Stressors, such as a loss may be a precipitating event for an episode of depression, but depression can occur (as often does) in the absence of a sad event.   You can be sad for the rest of your life that someone you love has died, but if you are mentally healthy, that sadness will not interfere with your life function.  You will still be able to experience joy, eat normally, have a normal sleeping pattern, etc.


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Katherine ONeill


I can answer academic questions about psychology. I am not a clinician (therapist), I am a research psychologist with expertise in biopsychology, general psychology, cognitive psychology, research methods and psychopharmacology.


I have 25 years experience as a researcher in health behavior, biopsychology and psychopharmacology.

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Applications of Market Research for Small Business UMBC Activate Program, March 2008 HIV/AIDS: An assessment of Need in the Continuum of Care. Optum Health Education., 12/2008 Maximizing the online medium for market research: Best practices. Market Research for Pharmaceuticals Conference, 12/06/2006 O誰eill, K.A. APD, ADD, ADHD and AD/HD: Personal and scientific reflections. Audiology Online, 6/6/2005. O誰eill, K.A. et al, Hyperactivity induced by NMDA injections into the nucleus accumbens. Pharmacology, Biochemistry and Behavior 34(4), Dec 1989, 739-745. O誰eill, K.A. and Liebman, J.M. Unique behavioral effects of the NMDA antagonist, CPP, upon injection into the medial prefrontal cortex of rats. Brain Research, 435(1-2), Dec 1987, 371-376. O誰eill, K.A. and Gertner, S.B. Effects of centally administered H2 antagonists on motor activity. Pharmacology, Biochemistry and Behavior. 264, 1987, 683-686. O誰eill, K.A. and Gertner, S.B. Effects of centrally administered H2 antagonists in the behavioral despair test. 90(2), 1986, 190-192. O誰eill, K.A. Chronic desipramine attenuates morphine analgesia. Pharmacology, Biochemistry and Behavior. 24(1), Jan 1986, 155 158. O誰eill, K.A. and Valentino, D. Escapability and generalization: Effect on 礎ehavioral despair. European Journal of Pharmacology 78(3), March 1982, 379-80. O誰eill, K.A. et al, An automated high capacity method for measuring jumping latencies on a hot plate. Journal of Pharmacological Methods, 10(1), Aug 1983, 13-18. O誰eill, K.A., Scott, C. and Weissman, A. Naloxone enhances nociceptive responding. Society for Neuroscience, Abstract 9: 274, 1983.

Ph.D. Experimental Psychology, University of Rhode Island, 1983. Post doctoral fellow dept of psychiatry, New York University Medical Center, 1983-1984. Post doctoral fellow, dept of pharmacology, University of Medicine and Dentistry of New Jersey, 1984-1985.

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