Commonly prescribed anti-depressants appear to be doing patients more harm than good, say researchers who have published a paper examining the impact of the medications on the entire body.
“It’s important because millions of people are prescribed anti-depressants each year, and the conventional wisdom about these drugs is that they’re safe and effective.”
“We need to be much more cautious about the widespread use of these drugs,” says Paul Andrews, an evolutionary biologist at McMaster University and lead author of the article, published today in the online journal Frontiers in Psychology.
Andrews and his colleagues examined previous patient studies into the effects of anti-depressants and determined that the benefits of most anti-depressants, even taken at their best, compare poorly to the risks, which include premature death in elderly patients.
Anti-depressants are designed to relieve the symptoms of depression by increasing the levels of serotonin in the brain, where it regulates mood. The vast majority of serotonin that the body produces, though, is used for other purposes, including digestion, forming blood clots at wound sites, reproduction and development.
What the researchers found is that anti-depressants have negative health effects on all processes normally regulated by serotonin.
The findings include these elevated risks:
developmental problems in infants
problems with sexual stimulation and function and sperm development in adults
digestive problems such as diarrhea, constipation, indigestion and bloating
Serotonin is a brain chemical that carries signals across the synapse, or gap between nerve cells. The supply of serotonin is regulated by the serotonin transporter (SERT).
In 2005, a team of researchers from Vanderbilt University led by Randy Blakely and James Sutcliffe identified rare genetic variations in children with ASD that disrupt SERT function.
In a new study published this week in the Proceedings of the National Academy of Sciences (PNAS), the researchers report the creation of a mouse model that expressed the most common of these variations.
The change is a very small one in biochemical terms, yet it appears to cause SERT in the brain to go into overdrive and restrict the availability of serotonin at synapses.
“The SERT protein in the brain of our mice appears to exhibit the exaggerated function and lack of regulation we saw using cell models,” said Blakely, director of the Vanderbilt Silvio O. Conte Center for Neuroscience Research.
“Remarkably, these mice show changes in social behavior and communication from early life that may parallel aspects of ASD,” noted first author Jeremy Veenstra-VanderWeele, assistant professor of psychiatry, pediatrics and pharmacology.
The researchers conclude that a lack of serotonin during development may lead to long-standing changes in the way the brain is wired. [continue reading…]
Many psychiatric conditions are caused by aberrant metabolism of the neurotransmitter serotonin. Researchers in the Department of Pharmacy at LMU have now developed a new screening method, which will facilitate the search for new drugs that modulate the biological activity of serotonin.
Psychiatric ailments such as depression, obsessive-compulsive disorder or anxiety states are often associated with disturbances in the metabolism of the neurotransmitter serotonin. Neurotransmitters are compounds that are released from the synapses at nerve cell endings and activate the firing of neighboring neurons. Thus, as their name suggests, they mediate the transmission of nerve impulses. The serotonin transporter (SERT) is responsible for reuptake of the transmitter into neurons, terminating its action. SERT is a major target for drugs that are used to treat many mood disorders, and the search for new SERT inhibitors is of continuing therapeutic relevance.
A research team led by Professor Klaus Wanner of the Department of Pharmacy in the Center for Pharmaceutical Research at Ludwig-Maximilians Univeristät München (LMU) has now developed a novel binding assay, based on the use of mass spectrometry (MS), which promises to simplify the search for potential SERT inhibitors very significantly. The major advantage of the technique is that, unlike conventional binding assays, it avoids the need to use radiolabeled substances.
A paper that describes the new assay will appear in the journal ChemMedChem on 4. October. The article has been rated as a “very important paper” and is featured on the cover of the upcoming issue of the journal. [continue reading…]
University of Michigan Health System researchers have found new evidence that our genes help determine our susceptibility to depression.
Their findings, published online today in the Archives of General Psychiatry, challenge a 2009 study that called the genetic link into question and add new support to earlier research hailed as a medical breakthrough.
In the summer of 2003, scientists announced they had discovered a connection between a gene that regulates the neurotransmitter serotonin and an individual’s ability to rebound from serious emotional trauma, such as childhood physical or sexual abuse. [continue reading…]
