People suffering depression have an enlarged amygdala, a structure deep in the brain, which produces amongst other things stress hormones. An enlarged, overactive amygdala may produce too much cortizol, a fight-or-flight stress hormone. Too much cortizol can whittle away neural structures - especially in the hippocampus which is the cortizol shut off valve. In depressed people, this structure can be 15% smaller than the statistical average.
With the hippocampus function reduced and the amygdala enlarged and in overdrive, a damaging positive feedback loop gets established and eventually other neural structures such as the prefrontal cortex get damaged - the dentrites (the connections) get sheared away, leading to a tragic reduction of the full potential of a person.
Thus, depression is both a somatic and psychologically self-reinforcing cycle that requires intervention on several levels. The commonly persued course of action is via anti-depressants such as SSRI’s which increase serotonin.
The old theory for administering selective serotonin reuptake Inhibitors is that the brain is suffering from a lack of available serotonin, and that Prozac and other drugs in its class help by increasing the amount of serotonin circulating in the brain by reducing their uptake. However, it is well known such drugs take weeks to take effect, despite the fact that serotonin levels are boosted straight away.
Scientists are discovering that the mechanism is a lot more complicated than a simple lack of serotonin, but is rather enmeshed in the damage rendered by cortizol and related stress hormones, and impeded function of the hippocampus.
Serotonin can promote neurogenesis, the birth of new brain cells, and Prozac seems to work by promoting neurogenesis in the hippocampus. And not only SSRIs, but other antidepression treatments affect a type of protein that is involved in neurogenesis. It is established that SSRI’s help to increase levels of brain-derived neurotrophic factor (BDNF) in the hippocampus. A neurotrophic factor is a protein, such as nerve growth factor, that promotes nerve cell growth and survival.
BDNF is a growth, sustainer and protector factor in the brain ; a neurogenesis hormone. Antidepressants apparently help keep hippocampal cells alive by boosting BDNF levels, inducing neurogenesis. Raising serotonin ups a protein known as CREB inside nerve cells, which also give rise to neurogenesis. This means that SSRI’s help to regenerate the hippocampus thus keeping the amygdala in balance.
This path of action restores the neurological balance which contributes (or else, determines) a healthy emotional life.
Banisteriopsis caapi, the Ayahuaca vine, is regarded by many that use it as an antidepressant. The mono-amine oxidase inhibiting beta-carbolines in the vine reduce the clearing of serotonin from the synaptic cleft : i.e MAOI is another angle from which serotonin can be boosted, which qualifies the use of MAOI in the treatment of depression back in the mid twentieth century.
It has been indicated that one of the constituents of the vine, THH, actually causes an increase in the density of platelet serotonin uptake sites in long-term users. It is likely that the increase of density of serotonin uptake sites in longterm users be an adaption to more monoamines in the system. . Increases in serotonin transporters could well be an adaptation to increased serotonin levels caused by MAO inhibition.
The additional power of Ayahuasca over commonly prescribed SSRI’s is that it allows people to experientially approach the early causal factors to their depression and work to symbolically resolve them, and cathart the primal pain and energies bound up in those repressed early experiences. After all, whilst we can address the run-away neurological consequences of deep trauma or chronic stress, the experiential gestalts themselves must be catharted and integrated. Ayahuasca allows conscious realization of how those experiences effect ones constitution and patterns of behaviour, giving beneficial insights into how the effects of the damaging influences on ones life can be greatly negated by changes of attitude and lifestyle.