Cocaine Overdose Mortality Increased During Hot Days

James Howard jmhoward at sprynet.com
Fri Jun 12 14:12:51 EST 1998


Cocaine Overdose Mortality Increased During Hot Days

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

It was recently reported that deaths from cocaine overdose are higher on hot
days. “High ambient temperature is associated with a significant increase in
mortality from cocaine overdose. Based on our comparison groups, the
increase is not explained by changes in cocaine use among the general
population. Although cocaine use is dangerous on all days, it appears to be
even more dangerous on hot days.”  Journal of the American Medical
Association 1998: 279: 1795-1800.  My work may explain this.  I suggest the
reason cocaine is abused is to increase the supply of the major adrenal
hormone, dehydroepiandrosterone (DHEA) for the brain.  No one else has
considered a connection of cocaine and DHEA, but a number of investigators
have examined the connection of cocaine and cortisol, the second major
adrenal hormone.  The effects of cortisol and DHEA may explain the JAMA
findings.

I suggest a person who produces sufficient DHEA to maintain a DHEA response
to cocaine use will not be prone to death during hot days.  DHEA is proven
to protect animals from heat stress.  Rats “reared from day 21 of life at
temperatures of 23, 34 or 37 degrees C. While the rats survived for
unlimited periods at 23 and 34 degrees C, the animals reared at 37 degrees C
succumbed within 5 days to heat stress. [37 degrees C is normal human
temperature.] The latter group, when injected s.c. or i.p. with 50 mg
dehydroepiandrosterone (DHA)/kg/day were no longer affected by the heat.”
(J Endocrinol 1975; 67: 99).  What this means is that DHEA is higher in some
people, and some cocaine users, than in others.  It is well known that heat
stress in humans occurs mainly in the young and the very old.  DHEA is at
low levels in the young and the very old.  You can see my chart on this in
my article on human evolution at my internet page at
http://www.naples.net/~nfn03605 .  I suggest it is the low DHEA in these two
groups that makes them vulnerable to heat and why some cocaine users are
vulnerable on hot days.  The mechanism involves the negative effects of the
other adrenal hormone, cortisol.

In 1985, I copyrighted my explanation of how the “fight or flight” mechanism
works.  Based on my hypothesis that all tissues rely on DHEA for proper
growth and development  and maintenance in adult tissues, I concluded that
the known negative effects of cortisol evolved to counteract the effects of
DHEA.  Since I think DHEA is necessary for proper brain function, then DHEA
is involved in motivation.  When an animal confronts another, DHEA is
involved in this brain function.  If two animals are properly motivated, a
fight usually ensues with death or damage most likely occurring.  This would
soon remove the most fierce animals; they would not leave many offspring.
Since the stress hormone is known to be cortisol, I deduced that this
evolved to counteract the motivation.  Some animals will still fight for the
“alpha male” position, but most conflicts end before, or early into, the
fight.  I suggest this is due to the ratio of DHEA to cortisol.  High DHEA
types will engage in the high stress activity, they will fight; high
cortisol types will refrain.  (A study of first time parachutists discovered
that these individuals, who can jump out of an airplane, actually experience
an increase in DHEA, compared to cortisol.  (J Endocrinol Invest 1998; 21:
148).  I suggest most risk seekers are of this type.)  Many more males who
refrain from fighting to the death produce more offspring than the few who
will.  This is why and how I think the DHEA – cortisol ratio became a part
of us.  The problem is that prolonged, or excess, cortisol will also
negatively affect every tissue as DHEA will positively affect every tissue.

DHEA and cortisol are usually produced in a combination; in the parachutists
mentioned above, cortisol and DHEA were both produced during the jump.  The
hormone ACTH stimulates both DHEA and cortisol.  It is known that cocaine
stimulates ACTH.  “ACTH increases were significantly correlated with
increases in plasma cocaine levels.”  (J Clin Endocrinol Metab 1998;  83:
966)  As would be expected, another study demonstrated that cocaine
increased both ACTH and cortisol.  “In summary, cocaine stimulated the
pulsatile ACTH and cortisol release by increasing the amplitude of secretory
episodes in behaviorally responsive monkeys.”  (J Pharmacol Exp Ther 1996;
277: 225)  Cocaine increases levels of norepinephrine (NE) and epinephrine
(E) and exaggerates these levels during exercise (Metabolism 1991; 40:
1043).  Very hot exercise increases both catecholamines (NE and E) and
cortisol (Int J Sports Med 1998; 19: 130).  Heat and cocaine produce similar
stress responses, i.e., increases in catecholamines and cortisol.

 “Many of the known actions of cortisol and catecholamines are atherogenic,
cardiotoxic and arrhythmogenic. Emotional stress can produce sudden cardiac
death in experimental animals, as can the administration of exogenous
catecholamines. Previous studies have found that emotional stress is a
common precursor to sudden cardiac death.” (J Am Coll Cardiol 1985; 5 (6
Suppl): 95B). Since it is known, from above, that DHEA increases resistance
to heat stress, and that “DHEAS [the serum precursor of DHEA] at
physiological concentration of human serum significantly inhibited the
release of NE…” (Neurosci Lett 1996; 204: 181), sufficient levels of DHEA
may reduce the impact of cocaine-induced stimulation of catecholamines and
cortisol.  I suggest the reason that “High ambient temperature is associated
with a significant increase in mortality from cocaine overdose.” is due to a
low DHEA to cortisol ratio in these individuals.  Now, this could happen in
new users of cocaine or in those who have exhausted their DHEA supply due to
repeated use of cocaine.






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