I wonder if anybody has seen or heard on any published results from a
study of a drug intended to increase the metabolism and hence lead to
weight loss. I heard about three years ago that trials would be complete
in about three years, but nothing since then.
Sorry to be so vague, it was a magazine article on the radio and I didn’t
take details of the experiment nor the drug involved. The idea interested
me, however. I seem to have a very slight memory that it was going on
in the UK, possibly Oxford or Cambridge.
I am aware that it is not close to April the 1st.
Peter Brooks
In article <6350…@otter.hpl.hp.com> p…@otter.hpl.hp.com (Peter Brooks) writes:
>I wonder if anybody has seen or heard on any published results from a
>study of a drug intended to increase the metabolism and hence lead to
>weight loss. I heard about three years ago that trials would be complete
>in about three years, but nothing since then.
Well, I know there have been some studies on a set of beta-adrenergic
agonists which appear to be relatively selective for receptors on
adipose tissue. I’m not sure how well they actually work. There
have also been some human studies of the combination of ephedrine and
aspirin, which, at least in animals, increases the metabolic rate
synergistically.
–
Steve Dyer
d…@ursa-major.spdcc.com aka {ima,harvard,rayssd,linus,m2c}!spdcc!dyer
d…@arktouros.mit.edu, d…@hstbme.mit.edu
A number of drugs have demonstrated a modest, reversible,
weight reduction effect via increased metabolism.
Caffiene, Bennies, Ephedrine, Theopylline, Fluotexine,
(no spelling flames please) you name it. The weight
comes back when the drug is withdrawn. One must kill
fat cells to achieve lasting fat loss.
In article <1…@omen.UUCP> c…@omen.UUCP (Chuck Forsberg WA7KGX) writes:
>A number of drugs have demonstrated a modest, reversible,
>weight reduction effect via increased metabolism.
>Caffiene, Bennies, Ephedrine, Theopylline, Fluotexine,
>(no spelling flames please) you name it. The weight
>comes back when the drug is withdrawn. One must kill
>fat cells to achieve lasting fat loss.
Fluoxetine almost certainly exerts its effects on body weight by encouraging
satiety, and not via an increased metabolism. Much the same is true even for
typical sympathomimetic "anorectic" drugs–the effect on reducing appetite is
much more prominent than any effect on metabolism. Caffeine and theophylline
certainly have no primary clinical utility as weight loss aids.
Some clinicians believe that drugs like these, if they are to be
given at all, shouldn’t be stopped.
—
Steve Dyer
d…@ursa-major.spdcc.com aka {ima,harvard,rayssd,linus,m2c}!spdcc!dyer
d…@arktouros.mit.edu, d…@hstbme.mit.edu
I didn’t notice a definition for "increased metabolism" on this thread —
are we talking about brown fat thermogenesis, or about lean tissue mass
burning fat or about something else?
My admitedly non-standard view on many anorectic drugs is that depression
of appetite (or increase of satiety) is just another damaging side effect
and that thermogenesis increase (I should be a lot more general here, call
it fat matabolism modification) is the beneficial component. I would
expect that Any medication that resulted in reduced food intake would
set the stage for a bounce-back upon withdrawal. This is consistent
with the quote from Steve below (tho I don’t pretend he supports my
entire contention):
> Some clinicians believe that drugs like these, if they are to be
> given at all, shouldn’t be stopped.
And Chuck, specifically, I was unaware that the ephedrine + aspirin
combinations had the typical post-drug bounce-back. If it’s not in
your Adiposity 101, could you mention where this came from? Again,
I think that reduced eating for whatever reason sets the stage for a
bounce-back, over and above the bounce-back that the drug might
trigger on its own.
—
Bob Yazz — y…@lccsd.sd.locus.com
Payphone ripoff? Californians call Pac Bell at 800/352-2201, M-F, 8-5.
From elsewhere try the FCC’s enforcement division at 202/632-7553.
The most well-known "drug" that stimulates metabolism is thyroid hormone
or thyroxine. Thyroxine is produced by the thyroid gland and circulates
throughout the body to set an overall metabolic "thermostat."
People with hyperthyroidism from Graves Disease and other disorders
literally can burn away body stores of fat and muscle (usually, not always
– Barabara Bush had Graves disease but yet she tended to gain weight…go
figure). Also, hyperthyroid people have their appetites tremendously
increased…people have been known to eat entire cakes everyday and still
experience weight loss and wasting. The problem with thyroxine is that in
the doses needed to rev up your metabolism for signficant weight loss, it
tends to be toxic to a lot of organs…e.g. your heart.
In article <24…@dice.la.locus.com> y…@locus.com (Bob Yazz) writes:
-And Chuck, specifically, I was unaware that the ephedrine + aspirin
-combinations had the typical post-drug bounce-back. If it’s not in
-your Adiposity 101, could you mention where this came from? Again,
-I think that reduced eating for whatever reason sets the stage for a
-bounce-back, over and above the bounce-back that the drug might
-trigger on its own.
The problem here is: bounce-back to what? This is not Jennie Craig’s
favorite research topic.
In short, weight loss by energy shortfall causes certain
individuals to reduce metabolism and/or grow more fat cells.
The operative word here is *certain*. In general, these are the
same individuals that that are genetically susceptible to
obesity in the first place. (This explains why not everyone who
goes on a religious fast turns into a blimp.) Lower blood
pressure and resting pulse rate after dieting may reflect
metabolic slowdown more than general improvement in health.
Exercise, Growth Hormone, DHEA, etc. without energy deprivation
cause reversible weight loss, but there is no reported
pattern of net weight gain after the treatment is withdrawn.