A new pill to swallow in treating depression

UnknownIt's January in Portland, dark outside more than half the time. The only glimpse of color comes from those Hawaiian Airlines billboards around town, advertising flights to tropical islands that feel financially out of reach.

An antidepressant sounds good right about now. Maybe a few bottles of antidepressants, carried close in a fanny pack and popped like mints until the weather and economy improve. There's a few problems with this pharmaceutical fantasy, though:

* Antidepressants don't work for most people who want them, according to a major new study.

* The risk of taking these pills often outweighs the benefit.

* Antidepressants are already the third-most-prescribed class of drug in the United States. This $10 billion industry doesn't need any more mildly bummed Oregon people as customers to turn a profit.

Drugs typically prescribed to treat depression work no better than placebos in most cases, according to a new analysis published last week in the Journal of the American Medical Association.

The one exception is severe depression: Most people who are depressed enough to feel suicidal or incapacitated, for example, will experience some relief from antidepressants. But the same isn't true for people with mild or moderate depression, who represent the bulk of the antidepressant market.

People who are merely singing the blues rather than drowning in them, it turns out, will find little or no more relief from their Paxil, Lexapro or Prozac than from a sugar pill.

(Why has previous research painted a rosier picture? First, drug companies have a history of downplaying negative clinical trials. Second, patients who participate in trials tend to be more depressed than the average bear, so they see more benefits from drugs. Third, just seeing a doctor can make people feel better, even when the actual medicine is ineffective.)

The new research calls the true power of happy pills into question. It certainly contradicts those drug ads about the instant, painless, magical and restorative nature of antidepressants.

It also has big implications for health care costs -- not to mention medical ethics.

Doctors wrote 164 million prescriptions for antidepressants in 2008, totaling $10 billion in U.S. sales, according to IMS Health. About 27 million Americans now take antidepressants, mostly for problems less acute than severe clinical depression.

In doing so, these patients expose themselves to side effects such as weight gain, agitation, insomnia, loss of sex drive and so on -- which in turn can lead to more health problems, doctor visits and prescriptions. Such patients might be better off exercising or spending time with friends instead.

Again, there's no question that antidepressants can be lifesavers. I've watched friends overcome crippling anxiety and even suicidal feelings while using antidepressants, usually in conjunction with therapy and exercise. When you're hurting and nothing else works, sometimes you've got to throw everything at the wall and see what sticks.

Yet this research does raise serious questions about our reliance on antidepressants and susceptibility to drug marketing. True, it's possible someone will invent a perfect pill that makes a jobless recovery in January feel like a day at the beach, but no one has yet.

Until then, the best strategy may be to bundle up, hold tight and wait for spring.

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New Drug Funded To Help Depression Sufferers

A new drug for people suffering depression who are resistant to other medications is being funded by Pharmac from today.

Mirtazapine (Avanza) would be funded for people who had tried other types of antidepressant without an adequate response, Pharmac's medical director Dr Peter Moodie said.

The Government drug funding agency already funded 16 antidepressant medications, but mirtazapine was a different type so might help people for whom other treatments hadn't worked, he said.

"There are many different causes and facets of depression and it is a major source of concern in the community," Dr Moodie said.

"Our view -- and that of our clinical advisory committees -- is that a wide range of these treatments is needed."

A particular need had been identified by Pharmac's clinical advisory committees for people who suffered severe depression and had not responded well to currently funded treatments, he said.

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New depression drug wins Mich. development funding

Wayne State University and former Pfizer scientists have formed a partnership hoping to expedite a promising new drug for depression while attracting biotech investors to the state.

The drug, which could lead to better treatment of depression and is backed by a $118,000 grant funded by the state's 21st Century Job Fund to commercialize intellectual property in Michigan, was discovered by Aloke Dutta, a WSU professor of pharmaceutical sciences.

It would target dopamine, a chemical in the brain that regulates walking, movement, balance, and two other neurotransmitters in the brain. None of the 38 FDA-approved anti-depressant drugs on the market target dopamine, and they can take weeks to help patients feel better. Dutta's discovery has the potential to offer relief and minimize side effects for 1 in 5 Americans suffering from depression.

"Dopamine has been implicated in depression for quite some time," said Dutta. "Now we are addressing the missing link."

Typically a drug must undergo further development before investors get interested, and that expertise is often based outside Michigan, said Randy Ramharack, WSU technology licensing manager. But research on Dutta's discovery will proceed faster because of the university's partnership with Michigan Technology and Research Institute, an Ann Arbor firm launched by seven former Pfizer scientists after the pharmaceutical company left Michigan in 2007.

The institute will provide the initial development for Dutta's drug and create a business plan for a new company. The institute and Wayne State will approach venture capitalists with the business plan to back the new company as the drug moves into clinical trials.

"The chances of keeping this (drug discovery) in Michigan are greater if we form a company here," said Ramharack.

Scientists at the institute, who have years of experience developing and bringing new drugs to the marketplace, have been providing research consultation to Michigan State University and University of Michigan. This is the first collaborative they have entered to move a new drug into the marketplace.

"It holds a great deal of promise," said David G. Pegg, president of the company's technical center. "Depression is an area of medicine where there is a need for new drugs that are safer and more effective."

Scientists at the institute are excited about the partnership since Dutta's discovery also offers a potential new drug for Parkinson's disease, substance abuse and pain.

The collaborative effort also is a model aimed at driving more technology growth in the state.

"There's a real gap between these early ideas within the university, and somebody willing to take them on," said Mike Bleavins, president of the institute's lab center.

Source : www.detnews.com

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Potential new drug target for depression identified

An acid-sensitive protein in the brain may represent a new target for the treatment of depression, according to animal research in the April 29 issue of The Journal of Neuroscience. The study shows that disrupting acid-sensitive ion channel-1a (ASIC1a) produces antidepressant-like effects in mice. The findings may one day benefit people who do not respond to traditional antidepressants or who cannot tolerate their side effects.

"Depression is one of the most devastating and difficult-to-treat disorders known to man," said John F. Cryan, PhD, at University College Cork in Ireland, who was not affiliated with the study. "Despite much research, all antidepressant medications that are currently prescribed work in much the same way and are of limited efficacy in more than a third of all patients. The development of antidepressants that act on other molecular targets in the brain would be a major breakthrough," Cryan said.

Although animal models cannot reproduce all of the symptoms of human depression, several behavioral tests in rodents are sensitive to antidepressant treatment, suggesting that they address important aspects of the disease. For example, chronically stressed mice lose their normal preference for sugary drinks, and mice repeatedly placed in a pool of water tend to give up and float rather than swim in the hopes of escaping. These mouse behaviors are thought to reflect loss of interest in pleasurable activities and hopelessness or despair. But traditional antidepressants are able to restore the mouse preference for sweet treats and reduce the amount of time that they float rather than swim.

The researchers, led by Matthew Coryell, PhD and senior researcher John Wemmie, MD, PhD, at the University of Iowa, found that mice lacking the ASIC1a gene and normal mice treated with drugs that inhibit ASIC1a showed reduced depression-like behaviors. These mice showed increased sweet taste preference and reduced immobility, consistent with antidepressant treatment.

Mice lacking the ASIC1a gene also failed to show a known biomarker for depression. Chronic stress normally decreases the amount of the BDNF gene in the brain, but mice lacking ASIC1a failed to show this change.

The researchers found that ASIC1a-based treatment works through a different biological pathway than traditional antidepressants, suggesting that it may benefit people who do not respond to traditional therapies.

ASIC1a is located in brain structures associated with mood, including the amygdala, which is critical for so-called negative emotions such as anger, anxiety, and fear. The researchers previously showed reduced amygdala activity in animals that lacked the ASIC1a gene. In the current study, they reversed the antidepressant effect of ASIC1a gene deletion by turning the ASIC1a gene back on only in the amygdala. These findings support the idea that depression could be caused, at least in part, by hyperactivity of the amygdala.

"ASIC1a inhibitors may combat depression by reducing amygdala activity. Because of the importance of the amygdala in negative emotions and fear, we speculate that ASIC1a inhibition increases the brain's resistance to the negative effects of stress, perhaps reducing the likelihood of developing depression," said study author Wemmie.

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