1. Iceland Tops Worldwide Antidepressant Consumption

    December 20, 2013

    Iceland Tops Worldwide Antidepressant Consumption

    by Niall McCarthy


    Over the course of the past ten years, the consumption of anti-depressants has skyrocketed across much of the developed world. According to the OECD, rich countries are consuming at least 10 percent more antidepressants than they were a decade ago.

    Even though rates of depression have not risen globally, more people are being diagnosed with the illness all over the world. Awareness levels about depression have proven an important factor when it comes to greater drug consumption – greater awareness leads to greater social acceptance of medication.

    The OECD also stated that the financial crisis may have been a factor in recent spikes in antidepressant prescriptions. In Spain and Portugal, consumption has increased by a whopping 20 percent over the past five years. What country is actually on top when it comes to taking this type of medication?


    Iceland is way ahead at almost twice the OECD average. An early casualty of the global financial crisis, it has the highest prescribing rate at 105.8 doses per day per 1,000 inhabitants. In 2000, this figure was 70.9 per 1,000.  Back in 1989, it was just 14.9. These consumption levels can be attributed to the catastrophic failure of Iceland’s three primary banks, as well as the fact that alternative treatments for depression, such as psychotherapy, are deeply unpopular.

    When compared with those alternative treatments, antidepressant drugs were viewed as being more effective by the Icelandic population. However, research suggests that the prescription of this medication has still had little impact on depression levels in the country. On the contrary, percentage of people seeking psychiatric consultations have actually increased.

    After Iceland, Australia, Canada, Denmark and Sweden round off the top five countries for the consumption of antidepressant medication. Drugs are now being used in milder cases and this is heightening concerns about their appropriateness as a first resort for sufferers. The majority of psychiatrists agree that medication works well on people suffering from severe cases of depression – they should not be used in milder instances.

    More than one in 10 people in developing nations are taking antidepressant medication. In the United States for instance, 10 percent of adults take antidepressants. In China, the market has grown by 20 percent for each of the past three years. This begs the question. Why are doctors freely prescribing these drugs to so many people?

    Though there have been cases of people trying to commit suicide, antidepressants are not addictive and side-effects are kept to a minimum. As it stands antidepressants are overprescribed in a desperate attempt to combat growing life dissatisfaction and unhappiness. It seems like they are the “quick and easy solution”.

    There are depression treatments that can be administered non-pharmacologically – psychotherapy methods (e.g. cognitive behaviour therapy) are widely regarded as being as effective as antidepressants in the long term. Doctors need to start correctly identifying the symptoms of milder depression and start realising that drugs are not always the answer.


    Image Credit: Jeff Schmaltz/Wikimedia


  2. The End of Anti-Depressants as We Know Them

    November 26, 2013


    How the future of antidepressants is diverging from its scattershot past


    The End of Anti-Depressants as We Know Them

    by Amy Maxmen

    Sixty-one years ago, in a Staten Island hospital complex, doctors testing a new drug on tuberculosis patients observed a strange side effect: While the drug, known as an MAO inhibitor, was no miracle cure

    for the hospital’s debilitated residents, it seemed to have an energizing, almost magical effect on their mood. One report noted that patients were “dancing in the halls tho’ there were holes in their lungs.’

    The early history of what would come to be known as antidepressants is dominated by such stories of serendipity, and many pharmaceuticals prescribed for depression today are, by and large, descendents of these decades-old happy accidents. Newer drugs replaced old ones because they were safer, not more effective, explains William Potter, senior advisor to the director of the National Institute of Mental Health.

    Now, as psychiatry inches toward a more refined understanding of the neurochemistry of depression, the course of drug discovery is changing. Roughly half of all clinically depressed patients fail to respond to available antidepressants-all of which target one neurotransmitter or another-and the lack of relief provides an important clue: Depression is not a monolithic disease, but a set of symptoms that can spring from a variety of causes. A treatment may work, scientists are finding, only when it is tailored to the type of depression found in a particular patient. “Today’s antidepressants seem to change the brain only slowly and indirectly,” explains Olivier Berton, a neuroscientist at the University of Pennsylvania.

    How the future of antidepressants is diverging from its scattershot past

    Because doctors knew that some early antidepressants boosted serotonin, they hypothesized that the neurotransmitter may be linked to depression. But a person’s outlook doesn’t start to shift until a month after beginning serotonin-altering drugs like Prozac, even when they work. The delay suggests another process is involved. Enter neural plasticity. Researchers have long observed the growth of new brain cells following antidepressant use. It may be that the sluggishness and stunted outlook that characterize depression at bottom  reflect a failure to generate  new nerve cells, and yet the role of serotonin in neurogenesis is indirect, at best. The chain of reactions that link them remains largely unknown.

    Recently, however, new research has begun to point to substances in the brain that act closer to the scene of neurogenesis, suggesting  more logical drug targets.  In June, researchers reported one important step in Nature Medicine. After mice took Prozac-Iike antidepressants, the levels of a fat molecule in the brain called ceramide plummeted.  Ceramide normally stalls brain cell growth;  by blocking ceramide, the drugs presumably  jump-started  neural regeneration.  New drugs that inhibit ceramide  could  work  faster than  drugs that  act on serotonin   because  they  are more directly linked to neurogenesis, the authors suggest.

    Others   are  entirely    abandoning approaches related to serotonin. Researchers know that individuals who are obese or who take immune-altering   medications may not respond to antidepressants. What such people have in common  is chronic inflammation,  explains Emory University psychiatrist  Andrew  Miller. He believes that inflammation   is a particular  path to depression  that  stems from  a beneficial adaptation. Depression is often characterized by what are called sickness behaviors – withdrawal  from others, loss of appetite, lethargy.  These are typical  responses  to physical  injury  and infection, and, in the short term, may foster recovery. Such responses become a problem, Miller says, only when the inflammation   is chronic. Then the depressive behavior endures.

    Earlier this year, Miller investigated whether a drug  currently used to tame inflammation in rheumatoid arthritis might  help people  who found  no relief in antidepressants   and failed to respond to talk therapy. The drug indeed  helped depressed patients with excess inflammation and did little for those without.

    Depression  that stems from trauma can  also be especially resistant   to conventional    antidepressants. Scientists believe that trauma  may cause epigenetic changes-lastingly modifying molecules that  turn  mood-  and  behavior-related genes on or off. The upshot  may be that those who experience trauma early in life may be unable to bounce back from later hardship the way other people can.

    Penn’s   Berton  recently studied trauma-induced depression in  mice. Bullying – one type  of trauma, easily modeled  in animals – typically causes a meeker mouse to act asocial, refrain from favored foods, and scare easily-behaviors analogous to those of depressed humans. But when Berton blocked a particular protein in the bullied  mice, they showed no such symptoms.  Berton  is now collaborating  with  a pharmaceutical  company to develop  a drug  that  blocks  the same protein. Other researchers are also experimenting  with drugs that block different proteins that may act as on/off switches for the genes affected by trauma.

    “For  a long  time,  people  focused only  on serotonin,   and  that  inhibited new avenues  of investigation,” Berton says.  Now that the variety of mechanisms underlying depression is becoming clearer, a one-size-fits-all approach may soon be a thing of the past.

    (article originally published at Psychology Today – Nov/Dec 2013)