Bupropion, Smoking, Melatonin and DHEA

James Howard phis at sprynet.com
Sun Dec 15 15:03:45 EST 1996

Bupropion, Smoking, Melatonin and DHEA
James Howard

It has just been announced that the antidepressant, bupropion, will be
marketed as "the first smoking-cessation therapy that doesn’t contain
nicotine."  (Buproprion is also known as "wellbutrin.")  The maker of
bupropion, Glaxo Wellcome, says its studies show bupropion is more
effective than the nicotine patch.  "In one study of 843 patients, 49 percent
who took bupropion quit smoking after four weeks, compared with 36
percent of the patients who used [nicotine] patches."  Well, I developed an
explanation for why people smoke that also explained why kids are
increasingly beginning to smoke.  This idea is based on my theory of DHEA
and melatonin.  When I read about bupropion, I immediately decided to see
if the drug had any effects on DHEA or melatonin.  I found a direct
connection of bupropion and melatonin that directly fits my explanation of
smoking.  The article containing the quotations included in this paragraph
also said: "Glaxo, which is the U.S. unit of British pharmaceutical giant
Glaxo Wellcome Plc, reported sales of $50.5 million for its Wellbutrin
antidepressant in the first six months of this year."  Perhaps, there is a cheap
alternative to bupropion that is also a natural product of your body, rather
than a product of chemical manufacturing.  I intend to show you that the
effect of bupropion in inhibiting smoking is simply that it stimulates our
natural hormone, melatonin.  Melatonin is freely available and cheap.

To explain this to you, I am including the following "letter to the editor,"
that I had published in "The Morning News of Northwest Arkansas," October 8,
1995.  This is a good summary of my explanation of smoking.  "In 1985, I
copyrighted a mechanism of sleep in which the hormone melatonin and the
hormone DHEA cycle to produce sleep and consciousness.  [You can read
this in detail at http://www.naples.net/~nfn03605 on the internet.]  My work
directly links them; one affects production of the other.  DHEA is used during
the day to maintain consciousness and is literally ‘used up.’  We get tired at
the end of the day.  This loss of DHEA stimulation allows the pineal gland
(where melatonin is made) to release melatonin.  This large release of
melatonin starts the first, very important slow wave sleep by slowing release
(not production) of prolactin, which is known to specifically stimulate DHEA.
During the night, melatonin is also used up; then, a large release of prolactin
triggers the large morning release of DHEA that triggers awakening.  this
completes the cycle.  I think it is necessary for growth and development.  To
understand how nicotine works, remember that melatonin first inhibits
DHEA, then participates in DHEA release when melatonin declines.

Nicotine mimics melatonin.  The structure of nicotine is very similar to
melatonin; so are caffeine, cocaine, methamphetamine and, seemingly
contradictory, so are narcotics.  I think all of these attach to melatonin’s
‘doorways’ (receptors) in the brain, and I think they all, ultimately, stimulate
DHEA.  They are better at this than melatonin.  Nicotine is proven to
stimulate DHEA ("The New England Journal of Medicine" 318: 1705).  In
the case of nicotine, I suggest people first use it like melatonin, to block the
stimulatory effects of DHEA.  They use it to relax.  I suggest the pleasure
centers deliver pleasure when the are temporarily relaxed or inhibited, e.g.
at the end of sex.  Therefore, nicotine relaxes the pleasure center, which
then leads to further DHEA stimulation, which then resets the pleasure
center by stimulating it.  The smoker then seeks relaxation again.  This
relaxation and stimulation become so connected in time, by frequent
smoking, that relaxation, i.e., pleasure and stimulation become
simultaneous.  As this mechanism is continued DHEA production increases;
this requires increased nicotine to relax the pleasure center.  This is
addiction.  other drugs have differing times of attachment to, and
activity at, the melatonin receptor and, therefore, differing effects on the
amount of DHEA production.  Addiction looks different, but the mechanism
is the same.

Near puberty, melatonin production declines, and DHEA production rises,
both dramatically.  Because of this, DHEA is then used by the brain for
stimulation, not growth and development.  This begins puberty and is the
reason teen-agers are so full of energy.  This is the time most people start
smoking and become addicted.  I suggest it is due to the decline in
melatonin and increase in DHEA.  Kids are reaching puberty earlier now
than in the past, and smoking among our youth is also increasing in the face
of a very expensive and well-directed anti-smoking campaign."

Again, I suggested it is the loss of melatonin that triggers the appetite for
nicotine.  It is proven that bupropion increases melatonin production.  That
is, not only bupropion, but other antidepressants, increase melatonin
production.  "Twenty-four-hour urinary excretion of 6-hydroxymelatonin and
‘whole body norepinephrine (NE) turnover,’ ie, 24-hour urinary ouput of NE
and its major metabolites 3-methoxy-4-hydroxphenylglycol,
vanillylmandelic acid, and normetanephrine, were measured before and
after treatment with the tricyclic desipramine hydrochloride, the aminoketone
bupropion hydrochloride, the nonselective monoamine oxidase
(MAO) inhibitor tranylcypromine sulfate, and the specific MAO type A
inhibitor clorgiline.  6-Hydroymelatonin excretion increased following
antidepressant treatment, while at the same time whole-body NE turnover
was reduced."  (Archives of General Psychiatry 1988; 45: 150).    Urinary
excretion of 6-hydroxymelatonin is considered a convincing measurement of
melatonin production.  "This study validates the comparison of plasma
levels of the hormone [melatonin] or urinary levels of its metabolite [6-
hydroxymelatonin] to assess pineal gland production of melatonin in
humans." ("Clin. Chim. Acta 1985; 150: 221).  The connection of bupropion
and melatonin has been reported as late as 1995: Ascher, JA, et al.,
"Burpropion: A Review of its Mechanism of Antidepressant Activity,"  Journal
of Clinical Psychiatry 1995 (Sept.); 56: 395.  The review reports that "The
mechanism of action of the novel antidepressant bupropion remains unclear
after many years of study."  One of the five listings of known findings about
bupropion in "Results" is: "5) Clinical studies indicate that bupropion
enhances noradrenergic functional activity as reflected by an increased
excretion of the hydroxy metabolite of melatonin..."

I think bupropion helped some smokers quit by increasing melatonin.
Because of the mechanism I advance to explain smoking, I see two kinds of
potential smokers.  I think some smoke because of too much DHEA, in other
words, to relax.  This kind of smoker seeks to decrease DHEA.  I think some
smoke to increase DHEA, that is, to stimulate themselves.  The same
mechanism will satisfy both of these needs.  It just happens that both kinds
of smokers become addicted.  If I am correct that bupropion helps smokers
quite by stimulating melatonin, then it should only help about half.  Look
back at the percentage helped by bupropion, mentioned in the first
paragraph; bupropion helped 49 percent.  I think it would be far more
appropriate to take a small amount of melatonin than either nicotine or
bupropion, and the cost of melatonin is far below that of either nicotine or
bupropion.  I did the experiment.  I took a small amount of melatonin, along
with my regular DHEA, during the day.  Of course, it may be my expectation,
but I perceived an increase in awareness and activity.
James Howard

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