Recent revelations have discredited this class of drug as both dangerous (it can cause suicide, violence, dependency, impotence, anorexia and, ironically, depression) and no more effective than its predecessors.
However, the latest revelation concerns Effexor (venlafaxine), one of the second generation of anti-depressants. A new study has revealed that this drug causes a higher rate of suicide than Prozac (fluoxetine) and the other first-generation selective serotonin-reuptake inhibitors (SSRIs).
Effexor is what is termed a 'serotonin-norepinephrine reuptake inhibitor' (SNRI). This second-generation Prozac, like the 'nor-adrenergic and selective serotonergic antidepressant' (NaSSA), is designed to be a more specific manipulator
of brain chemicals than the SSRIs. Pharmaceutical researchers assume that depression is caused by a deficiency of two chemicals in the brain-norepinephrine (noradrena-line) and serotonin, which bind to two different receptor sites on brain nerve cells. SNRIs supposedly work by selectively blocking these receptor sites-unlike SSRIs, which are not so selective. In theory, at least, the two brain chemicals, if allowed to circulate for longer, help to elevate mood.
At least, it looked good on paper. However, researchers from RTI Health Solutions at Manchester Science Park recently analyzed the medical records of 219,088 patients who were on the UK's General Practice Research Database, and taking antidepressants between 1995 and 2005, and compared the number of suicides among users of venlafaxine with those of citalo-pram and fluoxetine. Those given venlafaxine were found to have nearly three times the risk of committing suicide as those who took either of the two other drugs.
Nevertheless, as the researchers pointed out, the venlafaxine users were considered at higher risk than the other patients in the first place. Yet, when other factors (such asan increased risk of suicide) were accounted for, those taking venla-faxine still evidenced a 30 to 70 per cent increased risk of committing suicide (BMJ, 2007; 334: 242-5).
Now, the patients themselves have banded together to petition Wyeth-Ayerst Laboratories, which manu-factures Effexor, to publicize the fact that the drug causes such serious dependence that it is virtually impossible even to reduce the dosage, not to mention quit the drug. According to the petition, "The rapid onset of severe withdrawal-like symptoms . . . often initiates before a patient begins dose reduction due to the short half-life of Effexor."
The petition, signed by thousands of patients, claims that Wyeth-Ayerst "misleadingly advertises" that only drug abusers are at risk of physical and psychological dependence when trying to taper off or abruptly discontinue the drug.
Most damning of all, the petitioners allege that the drug giant knew all along that all pa-tients would experience withdrawal symptoms, but only gradually dribbled out the information over the course of the eight years that the drug has been licensed. Among the patient community, the drug is also known as one of the hardest of all antidepressants to tolerate. Indeed, the petition enumerates a litany of nightmarish side-effects-including sexual dys-function, hypomania, weight gain, high blood pressure, insomnia, bizarre vivid nightmares, deteriora-tion of eyesight and thyroid disorders that cause depression.
The petition also alleges that Wyeth, cognizant of these side-effects, co-prescribed the antianxiety medication benzodiazepine during clinical trials of Effexor to minimize the agitation and anxiety brought about by the drug. According to the petitioners, many patients are not forewarned that using Effexor would make it necessary for them to also have to take drugs to help them sleep, lower their blood pressureand calm their anxiety.
The purpose of the petition is simply to alert the public to the adverse effects and addictive nature of the drug, and to highlight web-sites for further information.
New evidence suggests why it may be so difficult to stop taking the drug. Israeli psychiatrists speculate that the new antidepressants, such as venlafaxine and mirtazapine, involve the brain's opioid system in their mechanism of action. Cruel studies using mice and rats that were given the drugs after having a paw burned on a hot-plate revealed a dose-dependent 'antinociceptive' and 'analgesic' effect-that is, the drug inhibited the perception of pain. Apparently, the higher the dose, the more numb were the animals to the pain (J Mol Neurosci, 2002; 18: 143-9; Yakugaku Zasshi, 2006; 126: 117-21).
Other animal studies have dem-onstrated that the effect is even more complicated (Prog Neuropsycho-pharmacol Biol Psychiatry, 2006; 30: 873-80). While it doesn't involve the body's opioids, there is a clear painkilling effect (Neurosci Lett, 2003; 342: 105-8).
Nevertheless, other research involving cocaine abusers (some who were opioid-free and some taking methadone, an opioid) dis-covered that the antidepressant significantly decreased subjective feelings of being 'high' in both groups. This would be consistent with a drug that has an opioid effect (Exp Clin Psychopharmacol, 2003; 11: 123-30). The drug also shares many molecular and pharmacological characteristics with the new opioid tramadol (Med Hypoth, 1998; 51: 167-8).