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T1 - Serotonin Hypothesis of Autism
Nor does the theory explain why “talk therapies” work in some patients and not in others, and why the combination of talk and antidepressants seems to work consistently better than either alone. It is very unlikely that we can “talk” our brains into growing cells. But perhaps talking alters the way that nerve death is registered by the conscious parts of the brain. Or talking could release other chemicals, opening up parallel pathways of nerve-cell growth.
Other evidence supporting the monoamine hypothesis comes from post-mortem studies of the brains of depressed people who unfortunately committed suicide. Some studies have found abnormally high numbers of serotonin receptors in the prefrontal cortex in suicide cases (Stanley and Mann, 1983; Yates et al., 1990). The significance of increased numbers of serotonin receptors in the brain is that it may enhance neuron to neuron communication when serotonin levels are low, by facilitating the capture of as much of the available serotonin as possible.
The Serotonin Hypothesis of Major Depression will be available on
In the late 1980s, studies examined the effect of Prozac on depressed subjects. Several of these trials showed Prozac reduced the symptoms of depression when compared with a placebo. Depression is usually assessed using a standardized rating scale of different symptoms. In general, some patients reported clinically meaningful improvements, although the effects were often small and varied from trial to trial. In real-world terms, such a change could be profound: a transformation in anxiety, the lifting of the ache of guilt, an end to the desire to commit suicide. But for other patients, the changes were marginal. Perhaps the most important number that emerged from these trials was the most subjective: 74 percent of the patients reported feeling “much” or “very much” better on antidepressants.
Then there is the use of these medications in children as young as 2 years old. How did we ever get the idea that this was a safe and effective treatment for this demographic? Look no further than data like , which cost Glaxo Smith Klein 3 billion dollars for their efforts to promote antidepressants to children. These efforts required ghost-written and manipulated data that suppressed a signal of suicidality, falsely represented Paxil as outperforming placebo, and contributes to an irrepressible done to our children by the field of psychiatry.
These serotonin drugs are used for depression with some success.
I have countless patients in my practice who report new onset of suicidal ideation within weeks of starting an antidepressant. In a population where there are only 2 randomized trials, I have grave concerns about postpartum women who are treated with antidepressants before more benign and such as dietary modification and thyroid treatment. Hold your heart as you read through of women who took their own and their children’s’ lives while treated with medications.
In 1997, a psychologist, Irving Kirsch, currently at the Harvard Medical School, set out to look at the placebo effect in relation to depression. In part, the placebo effect works because the psyche acutely modifies the perception of illness or wellness. Kirsch wondered how powerful this effect might be for drugs that treat depression — where the medical condition itself happens to involve an alteration of the psyche.
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Is this true? If this is what they said, I don't agree.
To Janet above comment re: trans cranial magnetic stimulation. IN our clinic we have offered TMS. But dropped it when the costs to patients was too prohibitive. It is very effective but can be incredibly expensive, hard to find providers – needs daily treatment for 30+ days typically to see results and hard for insurance carriers to pay for. A more affordable alternative and equally rewarding (IMHO) is cranial electric stimulation… you can even have “home units” – with a physician script. easy and affordable and many insurance companies will reimburse you for the cost. Over 40 years of great research supporting the effectiveness of CES for depression, anxiety, insomnia and pain.
This is what happens when you take SSRIS:
Apparently a gluten sensitivity can cause depression, also i have heard that all auto immune disease is caused by a gluten sensitivity. My daughters depression was caused by pyroluria, unfortunately only just found this out, she has been on anti depressants for 7 years now, so i don’t think she will be be to get off them because her brain has been altered/damaged by them. she now has chronic fatigue & i just read that CFS sufferers have low zinc & B6, pyroluria causes a deficiency of these nutrients.
this is exactly what I am finding. Thanks a lot for you kind post,
The SNRIs as an antidepressant class exhibit affinity toward both 5-HT and NE transporter molecules, but their selectivity differs among members of the class, possibly leading to differences in their effects on central and peripheral targets. Recent advances in pharmacogenomics demonstrate that polymorphisms of gene loci involved in monoamine signaling pathways are associated with changes in the efficacy, safety, and tolerability of SNRIs.119,120,122-124,133 As this area of investigation matures, it may be possible to select patients who will be more likely to respond to specific classes of drugs based on the presence of certain genes or biomarkers. Until such time, data suggest that there are theoretical reasons why medications with a broader profile of effects on monoamine systems may have a slight advantage over the more neurotransmitter-selective compounds. PP
Serotonin and depression | The BMJ
Given that the projections and function of the NE and 5-HT systems are not identical, it would be anticipated that SSRIs, NRIs, and SNRIs should have marked differences in the quality of antidepressant response and tolerability, as well as the overall proportion of patients that respond. SNRIs should be effective in a larger number of patients, and patients should have a more complete response to treatment with SNRIs. However, while greater efficacy of SNRIs in MDD has been reported, the magnitude of this effect is significantly smaller than one may have predicted based on the neurobiological data. The more robust magnitude of the relative benefit of SNRIs versus SSRIs for treatment of neuropathic pain136 is closer to what one would have expected for MDD and is likely explained by the dual modulation of pain centers in the brain and spinal cord by NE and 5-HT.
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