Month: September 2015

Depression: Causes, Symptoms and Treatments

Sadness, feeling down, having a loss of interest or pleasure in daily activities – these are symptoms of depression familiar to all of us.

Depression is a mental health disorder, a psychiatric condition. Specifically, it is a mood disorder characterized by persistently low mood in which there is a feeling of sadness and loss of interest.

Depression is known by different medical terms, some of which signify a particular diagnosis:

Depression can affect appetite.
  • Clinical depression
  • Major depression
  • Major depressive disorder
  • Persistent depressive disorder
  • Dysthymia
  • Dysphoric disorder.

Depression is a persistent problem, not a passing one – the average length of a depressive episode is 6 to 8 months.

Depression is different from the fluctuations in mood that we all experience as a part of a normal and healthy life. Temporary emotional responses to the challenges of everyday life do not constitute depression.

Likewise, even the feeling of grief resulting from the death of someone close or other kind of loss is not itself depression if it does not persist.5 Depression can, however, be related to bereavement – when depression follows a loss, psychologists call it a “complicated bereavement.

Similarly, discouraged mood that results from the disappointment of a life event such as a financial problem, a serious illness, or even involvement in a natural disaster, does not necessarily mean depression.

Unipolar versus bipolar depression

A separate condition may be diagnosed if it is characterized by both manic and depressive episodes separated by periods of normal mood, in which case the mood disorder is not depression but bipolar disorder, which used to be known as manic depression or manic-depressive illness.

Unipolar or major depressive disorder is estimated to be 3.5 times more prevalent than bipolar spectrum disorders.

Unipolar depression may be described as mild, moderate, or severe, and can involve anxiety and other symptoms – but no manic episodes. However, nearly 40% of the time over a 13-year period, individuals with bipolar disorder are depressed, making the two conditions difficult, and important, to distinguish.

Psychotic depression

Depression brought on by the birth of a baby is a separate diagnosis.

This diagnosis is characterized by depression accompanied by psychosis.

Psychosis can involve delusions – false beliefs and detachment from reality – or hallucinations – sensing things that do not exist.

Postpartum depression

Women often experience the “baby blues” with a newborn, but postpartum depression – also known as postnatal depression – is more severe and estimated to affect about 1 in 10 women who have given birth.

Seasonal effective disorder

Often abbreviated to SAD, seasonal effective disorder is related to the reduced daylight of winter – the depression occurs during this season but lifts for the rest of the year and in response to light therapy.

Countries with long or severe winters seem to be affected more by SAD.

Causes of depression

The causes of depression are not fully understood and may not be down to a single source. Depression is likely to be caused by a complex combination of factors:3,5,6,9

  • Genetic
  • Biological – with changes in noradrenergic, dopaminergic and serotonergic neurotransmitter levels theorized
  • Environmental
  • Psychological and social/psychosocial.

Some people are at higher risk of depression than others – risk factors, which play into the above causes, include:

  • Life events – for example, unemployment, divorce, poverty, although these events lead to lasting, severe depression usually only in people predisposed to it
  • Personality. Failure of adaptive mechanisms/coping strategies to stressors
  • Genetic factors. First-degree relatives of depressed patients are themselves at higher risk, and occurrence of depression between identical twins is high. Genetic factors may influence individual responses to events that trigger depression
  • Childhood trauma can cause long-term brain changes affecting responses to fear and stress. Other history also raises the risk, including a suicide attempt, or any form of abuse – sexual, physical or substance
  • Some prescription drugs – including corticosteroids, some beta-blockers, interferon, and reserpine – can lead to depression.
  • Abuse of recreational drugs – including alcohol, amphetamines – can accompany depression or result in it. There is a high level of comorbidity between drug abuse and depression
  • A past head injury
  • Past diagnosis of depression – people who have had an episode of major depression are at higher risk of a subsequent one
  • Chronic pain syndromes in particular, but also other chronic conditions, such as diabetes, chronic obstructive pulmonary disease, cardiovascular disease.

Symptoms of depression

The criteria used to make a diagnosis of depression are based on the symptoms that are present, so the list of possible symptoms is similar:3,5,10

  • Depressed mood – feeling sad or low
  • Reduced interest or pleasure in activities previously enjoyed, loss of sexual desire
  • Unintentional weight loss (without dieting) or low appetite
  • Insomnia (difficulty sleeping) or hypersomnia (excessive sleeping)
  • Psychomotor agitation (for example, restlessness, pacing up and down), or psychomotor retardation (slowed movements and speech)
  • Fatigue or loss of energy
  • Feelings of worthlessness or guilt
  • Worsened ability to think, concentrate or make decisions
  • Recurrent thoughts of death or suicide, or attempt at suicide.

Signs are the features that may be noticed by the doctor and others – as opposed to the symptoms that patients can describe themselves. Signs of a person with depression include:5

  • Appearing miserable, tearful eyes, furrowed brows, down-turned corners of the mouth
  • Slumped posture, lack of eye contact and facial expression
  • Little body movement, and speech changes (for example, soft voice, use of monosyllabic words)
  • Gloomy, pessimistic, humorless, passive, lethargic, introverted, hypercritical of self and others, complaining.

New Research into Anxiety Disorders

Nearly one in five Americans have been diagnosed with some form of anxiety disorder. These range from panic attacks and post-traumatic stress disorder to social phobias and obsessive-compulsive disorders.

Anti-anxiety drugs or antidepressants can curb symptoms that interfere with day-to-day life. And these drugs are big business. In 2013, Americans filled 48 million prescriptions for the benzodiazepine drug alprazolam (Xanax). Patients also picked up 27 million prescriptions for sertraline (Zoloft), an antidepressant drug that also helps some people with anxiety.

Yet, while many people do find relief in these drugs, they don’t work for everyone. Benzodiazepines can interfere with normal thinking and induce drowsiness. They also can be highly addictive, so doctors are reluctant to prescribe them for people with a history of substance abuse. Zoloft and other selective serotonin reuptake inhibitors (SSRIs) also don’t work for everyone. They can cause nausea, jitters, insomnia, suicidal thoughts, and loss of libido.

However, researchers are teasing out another option for reducing anxiety. When stress kicks in, so would this experimental drug.

“By targeting specific enzymes,” said neuroscientist J. Megan Gray, “we can minimize side effects.”

Researchers from Calgary to Southern California are investigating the inner struggle between one brain chemical that keeps stress in check and another that is part of the body’s fight or flight response. Many of these investigators talked about their latest findings during the November 2014 Society for Neuroscience conference in Washington, D.C.

The brains of humans and some animals naturally synthesize endocannabinoids, molecules that help regulate functions including appetite, mood and response to stress. An ample supply of endocannabinoids keeps anxiety under control, and this is the function that Gray and her colleagues at the Hotchkiss Brain Institute at the University of Calgary want to boost.

When something stressful happens — a deadline approaches or travel plans go awry — the fight or flight response floods the brain with corticotropin-releasing hormone (CRH). It degrades endocannabinoids and turns anxiety on. That’s like releasing the parking brake when a car is parked on a hill. The new drug would boost the level of endocannabinoids in the brain, creating a buffer against CRH’s action.

Endocannabinoids and the active compounds in marijuana both bind to the same brain receptors, which is why some people self-medicate by smoking marijuana.

“Often, if you go to a medical marijuana place and tell them you have anxiety, they’ll give you marijuana,” said James Lim, a neuroscientist at the University of California-Irvine. The problem is that cannabis also contains many other chemicals, including harmful tars, that complicate the reaction. If researchers can design an endocannabinoid-boosting compound that is simpler, said Gray, “we can better understand what people are exposing themselves to.”

Previously, researchers assumed that the stress “parking brake” system acted the same in everyone. But new research during the November conference points to a different model — that some people’s brains synthesize more endocannabinoids than others, and that people with higher levels can handle more stress.

Researchers have long known that some people can take more metaphorical heat than others. “Some kids can undergo a lot of traumatic events in early life and turn out just fine,” said University of Michigan researcher Pam Maras. “Some undergo relatively minor things and turn out to have severe anxiety and depression.”

Numerous researcher teams are using rat models to try to understand how stress responses can be manipulated, and they reported their findings at the conference.

In separate experiments, Gray and Lim tinkered with endocannabinoid levels in rats. Both found that rats with higher levels acted less anxious after being exposed to stress. Lim made part of a maze scary by tainting it with the scent of a fox’s feces. Rats with more stress-braking power would explore the tainted regions of the maze. More timid rats avoided it for as long as seven days after the scent was laid down.

Two other research groups, working independently in Ohio and Colorado, manipulated CRH levels in different ways but arrived at complementary results.

At Kent State University, neuroscientist Lee Gilman blocked CRH receptors in mice, shutting out the stress-inducing peptide and enabling them to approach other, unfamiliar mice.

At the University of Colorado-Boulder, Christopher Lowery is interested in how the brain responds to repeated social defeat. For example, what happens when a child is repeatedly bullied? He mimicked this by putting a male rat into the home cage of another male rat, where the newcomer would be forced to surrender to the more dominant native. In his study, rats that faced social defeat over and over produced more CRH each time, and were more quickly immobilized by fear during later encounters.

However, as Lim and Gilman both observed, some animals can put the brake on anxiety longer than others. Clinicians know this is true for humans; what the laboratory scientists are probing is when and how those differences manifest in the brain.

Michigan researcher Pam Maras sees evidence that these differences begin early in development. Her more nervous rats began displaying excessive anxiety as early as 11 days after birth, which corresponds to the fifth week of life for an infant. Animals that did not manifest anxiety at that point grew up to be more resilient to stress, though Maras can’t say why.

“We don’t have an answer for that right now,” said Maras. “It’s exciting sometimes when you don’t have an answer, because that means that there’s more to do.”

Some people are probably born more vulnerable to anxiety disorders than others. And although they might benefit greatly from a medication that puts a brake on runaway anxiety, scientists have a lot to learn before such a drug will be ready for clinical use.

References

Ammerman, S. Marijuana. Adolesc Med State Art Rev. 2014 Apr;25(1):70-88.

J. Megan Gray, PhD, Hotchkiss Brain Institute, University of Calgary.

Christopher Lowery, PhD, University of Colorado, Boulder.

Bayer, S.A., Altman, J., Russo, R.J. et al. Timetables of Neurogenesis in the Human Brain Based on Experimentally Determined Patterns in the Rat.NeuroToxicology 1993 14(1): 83-144.

Kedzior, K.K. and Laeber, L.T. A positive association between anxiety disorders and cannabis use or cannabis use disorders in the general population – a meta-analysis of 31 studies. BMC Psychiatry 2014, 14:136http://www.biomedcentral.com/1471-244X/14/136

Pam Maras, PhD, post-doctoral. University of Michigan.

James Lim, PhD. University of California-Irvine.

Lee Gilman. Kent State University.

Scaini, S., Belotti, R., Ogliari, A. Genetic and environmental contributions to social anxiety across different ages: a meta-analytic approach to twin data. J Anxiety Disord 2014 Oct;28(7):650-6. doi: 10.1016/j.janxdis.2014.07.002. Epub
2014 Jul 12.

Grohol, J.M. “Top 25 Psychiatric Medication Prescriptions for 2013”. PsychCentral. http://psychcentral.com/lib/top-25-psychiatric-medication-prescriptions-for-2013/00019543

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