New support of 1985 explanation of Pecking Order and Fight or Flight Mechanism

Copyright 2005, James Michael Howard, Fayetteville, Arkansas, U.S.A.

In 1985 (copyrighted and registered) I first suggested that the adrenal steroids
may be classified into two different systems: the "mineralocorticoid pathway"
and the "dehydroepiandrosterone pathway."  I deduced from this that pecking
order and the fight or flight mechanism are dependent upon the ratio of cortisol
to DHEA.  Here is an excerpt from a treatise I wrote, including this material,
in 2001, entitled "Pecking Order: Support of a Mechanism that Affects Human
Evolution"  (http://www.anthropogeny.com/Pecking%20Order.htm)

"In 1985, I first developed my explanation of "pecking order" or the "fight or
flight" mechanism. Basically, I suggested that the adrenal steroid hormone,
dehydroepiandrosterone (DHEA), activates the brain during consciousness, so DHEA
should be directly involved in activation of behavior. The more DHEA one has,
the more active one is. (DHEA is the major steroid hormone of our bodies.) Also
in 1985, I first suggested that the other major adrenal steroid hormone,
cortisol, evolved to counteract DHEA. When the ratio of DHEA to cortisol is
high, behavior is activated; when the ratio of DHEA to cortisol is low, behavior
is repressed. Depending upon inheritance and experience, this ratio acts as a
"set point," which affects most of our lives.

During fights, if DHEA is high, the individual pursues the fighting impulse. If
cortisol exceeds a certain amount, the effectiveness of the DHEA is overcome and
the individual alters behavior. This produces the advantage of allowing both
individuals in a confrontation to avoid potential harm. This mechanism has
survival advantage for both the dominant individual and the subordinate
individual."

Today, at PubMed, I found the following abstract which supports my hypotheses:

Psychopharmacology (Berl). 2005 Jul 29;:1-8 [Epub ahead of print]

Cortisol and DHEA-S are associated with startle potentiation during aversive
conditioning in humans.

Grillon C, Pine DS, Baas JM, Lawley M, Ellis V, Charney DS.

NIMH/NIH/DHHS, Mood and Anxiety Disorder Program, 15K North Drive, MSC 2670,
Bethesda, MD, 20892-2670, USA

RATIONALE: Fear conditioning reliably increases the startle reflex and stress
hormones, yet very little is known about the effect of stress hormones on
fear-potentiated startle. Cortisol and the sulfate ester of
dehydroepiandrosterone (DHEA-S) are involved in stress and anxiety. Evidence
suggests that low cortisol/DHEA-S ratio has a buffering effect on stress and
anxiety in preclinical and clinical studies, suggesting that there may be a
relationship between fear-potentiated startle and cortisol and DHEA-S activity.
OBJECTIVE: The aim of the study was to examine whether there is a relationship
between cortisol/DHEA-S ratio and fear-potentiated startle. METHODS: Thirty
healthy subjects participated in a differential aversive conditioning experiment
during which one of two stimuli (CS+) was paired with a shock, and the other was
not (CS-). Conditioned responses were assessed with the startle reflex, defined
as startle potentiation during CS+ compared to CS-. DHEA-S and cortisol levels
were assayed from blood samples collected in both a baseline and an aversive
conditioning session. Subjective state anxiety, arousal, and valence were
assessed at various times during testing. RESULTS: Fear-potentiated startle was
larger in individuals with high compared to low cortisol/DHEA-S ratio. Multiple
regression analyses revealed that fear-potentiated startle was positively
associated with cortisol and negatively associated with DHEA-S. There was no
significant correlation between DHEA-S and cortisol levels. CONCLUSION: These
data suggest that cortisol and DHEA-S are involved in fear conditioning.