TESTS AND EXPECTATIONS
There are a couple of problems, though. First, drug effects and placebo effects may not be “additive.” In other words, even if it’s possible to reproduce 80 percent of a drug’s effect with a placebo, that doesn’t mean the people taking the drug derive 80 percent of their benefit from the placebo response. If people received the drug without their knowledge, would they get only 20 percent of the effect? The question is worth asking, but it’s difficult to answer, because researchers can’t study drugs by slipping them into people’s coffee. Drug trials require informed consent—and once participants know what’s going on in a study, expectations rise. But suppose 80 percent of the antidepressant effect is just placebo. Is there a practical way to tap that benefit in the absence of an actual drug? If clinicians stopped prescribing antidepressants, patients wouldn’t lose only the two-point advantage that treatment offers over placebo, they would lose the whole 10-point improvement. And no one is suggesting that drugmakers start bottling sugar pills.
Even Kirsch admits that the real problem may be figuring out the best way to measure the power of the drugs. For the millions who owe their peace of mind to the antidepressants they take, the point may be irrelevant. In the end, anything that lightens the days of those who suffer depression is a good thing.
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Dopamine, Acetylcholine, GABA and Serotonin are probably the most important brain neurotransmitters, with dopamine being the "precursor" for norepinephrine and epinephrine
People with neurotransmitter deficiency disorder can suffer from one or more of the following conditions: obesity, depression, anxiety, fibromyalgia, chronic fatigue, insomnia, attention deficit, learning disorders, panic attacks, migraines, pms, menopausal symptoms, digestive complaints and many more.
Selective serotonin re-uptake inhibitors (SSRIs) such as Prozac, Zoloft, Effexor, Celexa, etc. are currently some of the most commonly prescribed drugs. They work by artificially increasing the amount of serotonin in the synapse of the nerve which allows a temporary improvement in the chemical messaging system.
The problem with this approach is that these drugs DO NOT increase serotonin levels; in fact they deplete reserves of the NT. This occurs because the SSRI class drugs cause an increase in an enzyme called MAO. It is common for people to experience only temporary improvement due to this effect.
The natural treatment for optimizing the neurotransmitter levels is to provide the basic amino acid precursors, or building blocks, so the body can replenish the inadequate neurotransmitter levels.