From the CR Soc. Archives: Appetite Suppressants
Date: Tue, 4 Apr 1995 13:06:49 -0500
From: Brian M. Delaney
Message-Id: <199504041806.NAA21021@ellis.uchicago.edu>
To: crsociety@chunks.csn.net
Subject: Dealing w/hunger.
This is my first post to this list. First: thanks to Stephen
for getting this up and running. It should be a great
resource for us all.
There are a million things to say about CR, but for now I
just want to comment on Steve's earlier points about dealing
w/appetite.
(Note -- I'll be extremely busy until ~mid-June, so if I
drop out of sight for a while, no offense to anyone.)
Steve M. wrote:
>
..I have expended a considerable amount of time looking
through Medline for substances that would aid in appetite
control. Unforetunately, it's a very sharp double edged
sword. While you might get the benifits of caloric
reduction, you certainly run very high risks just because
insufficient time has elasped to discern the risks of drug
interdiction in appetatite. Currently I haven't come across
anything I would risk using.
<
I've looked into this too. The only thing I've been tempted
by are the SSRIs (Prozac, Zoloft, etc.). These are actually
prescribed to some people solely to help them lose weight.
But I'm still uncertain about side-effects. I spent some
time trying to work through the effect of these drugs on
melatonin-production. There's reason to believe that they
might actually increase m-prod., by increasing the pool of
serotonin (which is a precursor to mel.). But the studies
that addressed this Q have yielded conflicting results.
INcreased mel., of course, might be a GOOD thing, given all
the studies about mel. as an anti-aging drug. But the timing
of mel. increase appears to be critical to its anti-aging
effect, and the SSRIs might not alter the diurnal pattern of
mel-prod. in the right way. And , as Steve says about the
other drugs that suppress appetite, we don't know what the
(other) effects are of long-term use.
So, for now, I'm working on psychological tricks to deal
w/the hunger. The most effective, for me, is limiting the
hunger to particular parts of the day. As I went down the
"caloric-descent," I mostly just trimmed food from my
lunches to the point where now, my lunches are just snacks.
That way I can eat a fairly big breakfast (essential, for
me), and eat enough at dinner that I'm not starving by the
time I have to go to sleep.
In the afternoon, when I'm the most hungry, I try to psych
myself into thinking that the hunger is giving me energy,
that I'm not "loaded down" w/the burden of a heavy lunch,
like I was in my pre-CR days. It doesn't require much
"pscyhing-out," since this is pretty much true (tho' there
are times when the blood sugar gets mighty low i n the hour
or so before dinner, and I get a little wiped out -- not too
often tho').
Plus, the more frustrated drives we have, the more
sublimated energy we have to do great things!....
Chow/Ciao,
Brian.
or
P.O. Box 378891
Chicago, IL 60637
312-324-4443
From: John Josephson
Date: Wed, 5 Apr 1995 02:15:24 -0400
Message-Id: <199504050615.CAA08621@columbus.cis.ohio-state.edu>
CC: crsociety@chunks.csn.net
Subject: Re: Dealing w/hunger.
Rather than Prozac or some other SSRI's why not boost serotonin by
taking the nutritional or endogenous precursors? I.E. L-Tryptophan or
5-hydroxytryptophan? True, L-Tryp is a bit hard to get, what with the
FDA ban and all, but 5-HT seems to work better (it's later in the
pathway and apparently you can't use it to make protein) and you can
get 5-HT lately.
.. jj
Date: Wed, 5 Apr 1995 09:42:34 -0500
From: Brian M. Delaney
Message-Id: <199504051442.JAA21889@ellis.uchicago.edu>
To: crsociety@chunks.csn.net
Subject: Re: Dealing w/Hunger.
John Josephson wrote:
>Rather than Prozac or some other SSRI's why not boost
>serotonin by taking the nutritional or endogenous
>precursors?
Because we don't know if the appetite-suppressing effects of
the SSRI's are due simply to their "boosting serotonin."
Could be, tho'. Might be worth a try.
-Brian.
or
P.O. Box 378891
Chicago, IL 60637
312-324-4443
From: Steve Mehalek
To: crsociety@chunks.csn.net
Subject: Re: Dealing w/hunger.
Sender: owner-crsociety@pipeline.csn.net
Precedence: bulk
>Rather than Prozac or some other SSRI's why not boost serotonin by
>taking the nutritional or endogenous precursors? I.E. L-Tryptophan or
While I was back East at UNH last month, I download all the Medline
references to Fluoxetine (Prozac) from 1983 to 1995 Feb. I haven't
finished plowing through all the stuff yet, but I have three
important points.
First, Fluoxetine may have adverse effects on sleep. One of the common side
effects is insomnia. I found the following studies on effects of
sleep in rats and humans (There are probably more, but I haven't had a chance
to read all the citations yets). Note the negative impact on REM:
TI: Short-term effects of fluoxetine and
trifluoromethylphenylpiperazine on electroencephalographic sleep in
the rat.
AU: Pastel-RH; Fernstrom-JD
AD: Department of Psychiatry, University of Pittsburgh, PA.
SO: Brain-Res. 1987 Dec 8; 436(1): 92-102
PY: 1987
LA: ENGLISH
CP: NETHERLANDS
AB: Fluoxetine and trifluoromethylphenylpiperazine (TFMPP) were
studied for their short-term effects on electroencephalographic
sleep in male rats. Following single injection, each drug produced
a sizeable, dose-related suppression of rapid-eye-movement (REM)
sleep that persisted for 4-5 h (fluoxetine, 0.625-5 mg/kg; TFMPP,
0.10-1.25 mg/kg). TFMPP also consistently increased non-REM (NREM)
sleep during the second hour after drug injection, though this
effect was not dose-related (it was seen at all doses tested).
Fluoxetine produced small effects on NREM sleep that varied
non-systematically with dose and time after drug injection. TFMPP,
but not fluoxetine, also increased at all doses the number of delta
waves per minute of NREM sleep in the second hour. A structural
analog of TFMPP that is inactive at serotonin (5-HT) receptors
[4-(m-trifluoromethylphenyl)piperadine; LY97117] was also tested,
and found to be devoid of effects on NREM and REM sleep. Both
fluoxetine (a 5-HT reuptake blocker) and TFMPP (a 5-HT agonist)
enhance transmission across 5-HT synapses, though by different
mechanisms. Because they have the common effect of suppressing REM
sleep, and in a dose-related manner, the data support the notion
that 5-HT neurons in the brain, when active, can suppress REM sleep.
MESH: Animal-; Electroencephalography-; Male-; Rats-; Rats,-Inbred-Strains; Support,-U.S.-Gov't,-P.H.S.
MESH: *Fluoxetin-pharmacology; *Piperazines-pharmacology; *Propylamines-pharmacology; *Sleep-drug-effects; *Sleep,-REM-drug-effects
CN: MH38178; MH00254
RN: 15532-75-9; 54910-89-3
NM: 1-(3-trifluoromethylphenyl)piperazine; Fluoxetin
ISSN: 0006-8993
AN: 88079429
UD: 8804
TI: Studies on the modulation of the sleep-wakefulness continuum in
man by fluoxetine, a 5-HT uptake inhibitor.
AU: Nicholson-AN; Pascoe-PA
AD: Royal Air Force Institute of Aviation Medicine, Farnborough,
Hampshire, U.K.
SO: Neuropharmacology. 1988 Jun; 27(6): 597-602
ISSN: 0028-3908
PY: 1988
LA: ENGLISH
CP: ENGLAND
AB: The effects of an inhibitor of the uptake of 5-hydroxytryptamine
(5-HT) fluoxetine (20, 40 and 60 mg), on nocturnal sleep and on
alertness during the day, were studied in healthy adults.
Fluoxetine reduced the total sleep time and the duration of rapid
eye movement (REM) sleep and increased awake activity and stage 1
(drowsy) sleep during the night. Daytime sleep latencies were
longer after fluoxetine but, paradoxically, the subjects felt more
drowsy and coding ability was impaired. It is considered that the
alerting effect of fluoxetine in man is most likely related to
modulation of 5-HT-mediated transmission, whereas suppression of REM
sleep is a nonspecific effect which arises when the balance of
monoaminergic and cholinergic influences is disturbed. It is
suggested that the serotonergic system has a pervasive influence
throughout the sleep-wakefulness continuum, in contrast with some
other neurotransmitter systems, which may be more concerned with the
subtle manifestations of vigilance.
MESH: Adult-; Attention-drug-effects; Female-; Human-; Male-; Memory-drug-effects
MESH: *Fluoxetine-pharmacology; *Propylamines-pharmacology; *Sleep-drug-effects; *Wakefulness-drug-effects
RN: 54910-89-3
NM: Fluoxetine
AN: 88334798
UD: 8812
Considering the importance that melatonin seems to play in Longevity, I think
that fluoxetine for weight loss should be ruled out right now based on it's
interfere with the normal sleep cycle. I speculate that fluoxetine's effect
on sleep might interfere with night melatonin patterns, which would probably
be bad. Brian seems to think that might actually increase nocturnal melatonin
production. Much more work needs to be done to quantify this issue in my mind.
i.e. a long term study on CR restricted mice + fluoxetine vs CR restricted
only. I would also like to see what effect fluoxetine has on the lifespan
of normally fed rodents.
Second, I wasn't paying much attention to the weight loss aspects of Fluoxetine.
However, I did come accross several references indicating that
Fluoxetine's weight loss properties were only temporary, and in the range
of 5 to 6 months. If didn't bother to clip these references so I can't include
them here. However, I still have the entire 1983 - 1995 medline download for
Fluoxetine. If someone else wants it to look for these citations, I
could mail it in segmented sections.
I did found a an article in Medline 1987 regarding possible adverse
reactions between L-TRYPTOPHAN and FLUOXETINE:
TI: Toxic reaction following the combined administration of fluoxetine and L-tryptophan: five case reports.
AU: Steiner-W; Fontaine-R
SO: Biol-Psychiatry. 1986 Sep; 21(11): 1067-71
PY: 1986
LA: ENGLISH
CP: UNITED-STATES
MESH: Adult-; Arrhythmia-chemically-induced; Case-Report; Drug-Interactions; Female-; Fluoxetin-administration-and-dosage; Human-; Male-; Middle-Age; Movement-Disorders-chemically-induced; Muscle-Cramp-chemically-induced; Nausea-chemically-induced; Tryptophan-administration-and-dosage
MESH: *Fluoxetin-adverse-effects; *Obsessive-Compulsive-Disorder-drug-therapy; *Propylamines-adverse-effects; *Psychomotor-Agitation-chemically-induced; *Tryptophan-adverse-effects
RN: 54910-89-3; 6912-86-3
NM: Fluoxetin; Tryptophan
ISSN: 0006-3223
AN: 86296884
UD: 8612
There was no abstract with this citation. Since the it's Publication Year is
1987. I don't think the toxic reaction can be ascribed to EMS contaminated
L-tryptophan. Just something to look into if you have access to both
L-tryptophan and PROZAC, and were thinking of taking both at the same time.
Sorry about the length of this: Steve
