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Thursday, July 21, 2011

Depression, Anti-Depressants, and Tardive Dysphoria

Depression is diagnosed symptomatically, even when those symptoms are the result of grief instead of physiological abnormalities. This is particularly flagrant when considering the variety of physiological abnormalities which can cause depressive symptoms compared to the dearth of psychiatric treatment methods.

I have read that Lyme disease; hypothyroidism; insufficient synaptic supplies of any of at least three different neurotransmitters (serotonin, dopamine, and norepinephrine), each of which require different nutrients to make; blood sugar abnormalities which may be caused by the consumption of insufficient, excessive, or simply poorly timed glycemic loads or deficiency of glucose-regulating nutrients, especially chromium; Omega-3 deficiency, resulting in inferior formation of synapses and degradation of neurotransmission; brain injuries; post-traumatic stress (a similar condition to grief); substance abuse; giving birth; hormonal imbalances; heavy metal, especially vanadium or mercury, toxicity; chemical toxicity, especially from neurotoxins1 and nutrient-depleting substances; chemical sensitivity2; food allergies, particularly celiac disease; intestinal dysbiosis, especially candidiasis; Circadian irregularities such as seasonal affective disorder; lack of exercise (in studies exercise has a similar success rate to anti-depressants and can relieve symptoms of patients who do not respond to medication)3; and impaired migration of neurotransmitters across synapses.

It is thought that 'tardive dysphoria' results from the impaired migration of neurotransmitters across synapses. The phrase was coined after yet another psychiatrist began to explore the possibility that anti-depressants could induce depression; this time there was not only a sound biological explanation (not just that increasing the flow of serotonin in the brain can deplete certain regions of serotonin because synapses don't form tidy circuits) but statistics as well.4

There are basically two types of anti-depressants prescribed today: neurotransmitter re-uptake inhibitors and mono-amine oxidase inhibitors. A neurotransmitter re-uptake inhibitor causes the originating neuron in a synapse to leave its neurotransmitters in the synaptic cleft indefinitely (instead of re-uptaking those that are not punctually absorbed by the receiving neuron on the other side of the synapse); this causes increased reception of the neurotransmitters by the neuron on the other side of the synapse. But the same way the dopamine re-uptake inhibiting effect of cocaine results in chronic desensitization, the body may adjust to increased reception of neurotransmitters across a synapse, resulting in decreased pre-synaptic (originating neuron) release of neurotransmitters and post-synaptic (receiving neuron) neuroreceptor density. Mono-amine oxidase inhibitors decrease the breakdown of neurotransmitters, increasing not just the flow but also the amount of neurotransmitters in the brain - they have greater physical risks due to an increased potential for causing serotonin syndrome from excessive serotonergic activity.

E(lectro)C(onvulsive)T(herapy), shock therapy, is more often used as a treatment for depression than any other disorder. It is rarely denied that ECT results in impaired working and long-term memories.5


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