Hi John.
Because what's referred to as "depression" is an
engineered-in learning cul-de-sac handling
mechanism, it's necessary that =myriad= molecular
dynamics must become modified during 'depression'.
The nervous system is 'shifting into reverse', after all.
The external observables - the 'quieting' of behavior -
occurs to 'mask' what is a high-TD E/I condition,
thereby checking' the spread of the high-TD E/I through
populations of interacting folks.
[The high-TD E/I occurs be-cause former learning
is, in fact, being dis-integrated.]
These things are discussed in AoK, Ap8 ["mourning
behavior".
It's at once sad and 'hilarious' that folks want to
'treat' stuff that is built-right-into nervous systems
at a fundamental, life-sustaining, and group-sus-
taining 'level'. [Might as well 'treat' the fact that
folks have a nose - or two arms and legs.]
That's what's 'pathalogical', not the information-
processing dynamics that are referred to as
"depression".
As is discussed in AoK, that 'depression' kills
stems from the way that 'treatment' stigmatizes
folks by inducing them to buy-into a belief that
dynamics that are innate within nervous system
function, and necessary for survival, are, sup-
posedly, 'pathalogical'. This results in an internal
'war' between the TD E/I-minimization dynamics
corresponding to these erroneous suppositions
and the innate dynamics of the mechanism of
'depression'. It's the resulting artificially-induced
[by absence-of-understanding] interminable
elevated TD E/I that is deadly - the mechanism
of 'depression', trampled-down by absence-of-
understanding, which leaves the individual
exposed and vulnerable to the TD E/I(up) that
always accompanies "rendering useless" [the
dynamics of unlearning].
Cheers, John,
ken [k. p. collins]
"John H." <johnh at faraway.> wrote in message
news:3fe6804d at dnews.tpgi.com.au...
>>> Stress and cytokine levels underpin a provocative theory of depression
>http://www.the-scientist.com/yr2003/aug/feature_030825.html> ...
> Maes helped to establish the notion that overexpression of proinflammatory
> cytokines, in particular, can disrupt the stress response system's primary
> elements: the hypothalamic-pituitary-adrenal (HPA) axis and the
> monoaminergic system, including the hormones serotonin and norepinephrine.
> Among the stressors that can overstimulate these proinflammatory cytokines
> are infections and melancholy. Although the pathophysiology of depression
> remains unclear, Maes is among those researchers who assert that it is a
> psychoneuroimmunological disorder.
> ....
>>