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More on Set Point theories, compulsive eating, SSRIs, etc...

Starfish, I am not trying to push SSRIs here, just trying to inform people of some cutting edge applications of these types of drugs that your doctor won't even know about. FYI here are a handful (of many) research articles that show that acute and sometime chronic treatment with prozac (but not necessarily other SSRIs) can lead to weight loss, and some other stuff that shows that the weight gain that people anecdotally associate with anti depressants is likely due to their recovery rather than the drugs. These articles don't even touch on Prozac potential ability to modify or even replace the action of leptin in the brain of people dieting.....

My experience is that most competition female bodybuilders are gonna suffer weight gain rebound post extreme dieting no matter what. When there are people taking T3, DNP, clen etc... in desperation to shed that last bit of fat, I hardly think SSRI use is THAT bad of an idea, especially if you continue it for a while post competition to slow down the rebound. And many people may do best if they stay on drugs like Prozac for lief (in terms of depression prevention, PMS etc...).

Anyway, here's some more food for thought:




: Ann Clin Psychiatry 2001 Mar;13(1):31-41

Use of antidepressants in treatment of comorbid diabetes mellitus and
depression as well as in diabetic neuropathy.

After a brief review of epidemiology, the focus is on biochemistry of diabetes. Animal and human
studies are reviewed in terms of the impact of alterations in catecholamines and serotonin
(5-hydroxytryptamine, 5HT) on glucose utilization. Then, the implications of these experimental
results for the choice of antidepressant in comorbid diabetes mellitus and depression as well as in
diabetic neuropathy are discussed. Results of clinical investigations are then reviewed in terms of
the above hypotheses. An Index Medicus Search for the past 10 years was supplemented by
references from previous related reviews of the topic as well as by pending results, where
available, not previously published. The range of prevalence of depression in diabetic patients has
been 8-27%, depending on study criteria and procedures. An increase of catecholamines
appears to increase glucose while both reducing insulin release and reducing sensitivity to insulin
that is available. In contrast, increases in serotonergic function by increased precursor, increased
release, or blocked metabolism and blocked reuptake in contrast seem to increase sensitivity to
insulin and reduce plasma glucose. THERE HAVE BEEN SIX STUDIES OF FLUOXETINE, A SELECTIVE SEROTONIN REUPTAKE INHIBITOR (SSRI), AT A DOSE OF 60 MG/DAY PURSUED UP TO 12 MONTHS THAT HAVE
DEMONSTRATED THAT MEDICATION'S USEFULNESS IN DIABETIC PATIENTS, WITH REDUCTIONS IN WEIGHT (TO 9.3 KG), in FPG (to 45 mg%), and in HbA1c (to 2.5%). In studies in comorbid diabetes mellitus and
depression, nortriptyline, a norepinephrine reuptake inhibitor that produces increased synaptic
catechols, has led to worsening of indices of glucose control. However, fluoxetine and sertraline,
both selective serotonin reuptake inhibitors, in the same patient group, have produced results
consistent with reductions in glucose levels. In diabetic neuropathy, perhaps due to the fact that
catecholamines and serotonin may both be implicated in pain pathways, dual-action
antidepressants appear more effective at lower doses than do specific serotonergic agents. The
tricyclic antidepressants (TCA) (66.7%) have had success in double-blind studies, particularly
imipramine, with a 81% response rate. Yet, there are positive reports concerning the SSRIs
(paroxetine, citalopram, sertraline), as well as nefazodone, that focus on serotonin selectivity.
CONCLUSIONS: In comorbid diabetes mellitus and depression, most evidence supports the
use of fluoxetine in control of glucose handling. Other characteristics in terms dosing, drug
interactions, cognition, and sleep make sertraline an attractive alternative agent. In diabetic
neuropathy without depression, the best choices among non-TCAs may include sertraline,
citalopram, and perhaps, venlafaxine, since the TCAs appear to increase cravings and increase
FBG levels.


Effects of nefazodone on body weight: a pooled analysis of selective
serotonin reuptake inhibitor- and imipramine-controlled trials.


BACKGROUND: Evidence suggests that the newer antidepressant drugs may differ with respect
to their effects on body weight, especially during long-term treatment. However, the published
data about treatment-emergent weight change with the newer antidepressants are limited. MOST
REPORTS OF UNEXPECTED SELECTIVE SEROTONIN REUPTAKE INHIBITOR (SSRI)-ASSOCIATED WEIGHT GAIN ARE ANECDOTAL OR FROM SMALL CONTROLLED TRIALS. To determine if differences exist among the newer antidepressants, the authors retrospectively analyzed data from clinical trials comparing
nefazodone with SSRIs and with imipramine. ………………... Acute phases of the trials lasted either 6 or 8 weeks, and long-term phases varied in duration from 16 to 46 weeks. ……………………. RESULTS: Using 7% or greater weight change as the measure of clinical significance, 4.3% of SSRI-treated patients had lost weight at any point in the acute phase versus 1.7% of those treated with nefazodone (p = .017)………………….. At any point in the acute phase, significantly
more imipramine-treated patients than nefazodone-treated patients had a 7% or greater increase
in body weight (4.9% vs. 0.9%; p = .027), and for the long-term phase the comparison yielded
24.5% versus 9.5%. The difference during the long-term phase was statistically significant in
women (p = .017), but not in men (p = .078) . CONCLUSION: SSRIs caused more weight loss during short-term treatment but more weight gain during long-term treatment. These results lend support to the observation that some antidepressants have a greater expected risk of weight gain than others during long-term therapy.

Pharmacology of paradoxic weight gain with selective serotonin
reuptake inhibitors.

It has been suggested that weight gain associated with tricyclic antidepressants (TCA) reflect
actions on dopamine (DA) and histamine receptors. However, a definitive cause is purely
assumptive given the nonselective pharmacology of these agents. The selective serotonin reuptake
inhibitors (SSRIs), as well as agents like dexfenfluramine (DFF), have EMPHASIZED THE PIVOTAL ROLE
OF SEROTONIN (5HT) IN REDUCING CARBOHYDRATE (CHO) INTAKE, and have provided a more selective
tool with which to study appetite regulation. It would be expected that all SSRIs should exert a
similar anorectic action. However, recent reports provide evidence to the contrary. Despite their
claimed selectivity, SSRIs still interact, either directly or indirectly, with various critical
neurotransmitter systems. In addition, although THE ANORECTIC ACTION OF FLUOXETINE (FLX) IS WELL
RECOGNIZED, LONG-TERM FOLLOW-UP STUDIES IN DEPRESSED PATIENTS AND IN OBESE NONDEPRESSED
PATIENTS REVEAL THAT ITS WEIGHT-REDUCING EFFECTS ARE TRANSIENT, ………………………………..

n depression remitted with antidepressants: pharmacological
or recovery effect?


BACKGROUND: Depression remission is often associated with weight gain. It is not clear if
weight gain is caused by a pharmacological effect of antidepressants, or if instead it is an effect of
recovery from depression. The aim of this study was to try to clarify this point. METHODS: One
hundred consecutive unipolar/bipolar remitted depressed private practice outpatients (DSM-IV
diagnoses with structured interview) were interviewed with structured questions about weight
changes occurring during depression and remission. Comparisons were made between remitted
weight gainers and remitted nonweight gainers. RESULTS: Seventy-two percent of patients
showed weight gain when they remitted from depression, in comparison with their weight when
they were depressed. No significant differences were found in age, gender, diagnoses, duration of
remission, use of tricyclics, tricyclic-SSRI combination, benzodiazepines, neuroleptics, and mood
stabilizers in remitted weight gainers versus nonweight gainers. SSRIs were significantly more
used in remitted nonweight gainers. Significantly more weight loss and less weight gain when
depressed were found in remitted weight gainers versus nonweight gainers. CONCLUSIONS:
THESE FINDINGS SUGGEST THAT WEIGHT GAIN IN REMITTED DEPRESSED PATIENTS MAY NOT NECESSARILY BE A
PHARMACOLOGICAL EFFECT OF ANTIDEPRESSANTS, BUT MAY RATHER BE AN EFFECT, AT LEAST IN PART, OF
RECOVERY FROM DEPRESSION.

Fluoxetine versus sertraline and paroxetine in major depressive disorder:
changes in weight with long-term treatment.

BACKGROUND: The effects of extended selective serotonin reuptake inhibitor (SSRI)
treatment on weight are not well characterized. Also unknown is whether different agents have
differential effects. To examine these questions, we assessed weight changes in patients randomly
assigned to long-term treatment with fluoxetine, sertraline, or paroxetine. METHOD: Patients (N
= 284) with major depressive disorder (DSM-IV) were randomly assigned to double-blind
treatment with fluoxetine (N = 92), sertraline, (N = 96), or paroxetine (N = 96) for a total of 26
to 32 weeks. The mean percent change in weight was compared for each group, as was the
number of patients who had > or = 7% weight increase from baseline. RESULTS: Patients
(fluoxetine, N = 44; sertraline, N = 48; paroxetine, N = 47) who completed the trial were
included in these analyses. Paroxetine-treated patients experienced a significant weight increase,
FLUOXETINE-TREATED PATIENTS HAD A MODEST WEIGHT DECREASE, and patients treated
with sertraline had a modest but nonsignificant weight increase. The number of patients whose
weight increased > 7% from baseline was significantly greater for paroxetine-treated compared
with either fluoxetine-treated or sertraline-treated patients. CONCLUSION: Risk of weight gain
during extended SSRI treatment differs depending on which SSRI is used.

Changes in weight during a 1-year trial of fluoxetine.

OBJECTIVE: FLUOXETINE HAS BEEN ASSOCIATED WITH WEIGHT LOSS DURING ACUTE TREATMENT, but no
controlled studies of weight change during long-term treatment with fluoxetine or other selective
serotonin reuptake inhibitors have been reported. Weights were assessed for patients whose
depressive symptoms had disappeared with acute fluoxetine treatment. Patients were then
randomly assigned to continuation treatment with fluoxetine or placebo…………………... CONCLUSIONS:ACUTE THERAPY with fluoxetine is associated with modest weight loss. After remission of depressive symptoms, weight gain for patients taking
fluoxetine for longer periods is not different from that for patients taking placebo and is most
likely related to recovery from depression.
 
MS said:
My experience is that most competition female bodybuilders are gonna suffer weight gain rebound post extreme dieting no matter what. When there are people taking T3, DNP, clen etc... in desperation to shed that last bit of fat, I hardly think SSRI use is THAT bad of an idea, especially if you continue it for a while post competition to slow down the rebound.



I'm sorry but if someone is that "desperate to shed bodyfat" maybe the should reevaluate some things. That is just my opinion, but to each their own.

I still would not use an SSRI for short term goals. I can tell you all about SSRI withdrawal after only two months and it was not fun. Cold sweats, nightmares, electric shocks throughout my body, dizzy, terrible flu like symptoms,etc.
 
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Withdrawal Reactions from SSRI's

Withdrawal when Stopping Serotonin Boosters

The withdrawal reactions from SSRI's which may be seen within 8-hours, often includes:
a spontaneously experience of a "flu-like" syndrome, feeling "crummy", tired, achy, etc. In addition to the flu-like symptoms, visual phenomena (e.g., "moustaches on men and women but only smudges on the upper lips of babies") are not rare.
anxiety
dizziness
fatigue
headache
insomnia
nausea
restlessness
tremors
visual hallucinations/illusions
ringing in ears and throbbing in head
"electrical shock" like phenomena/electrical surges
tinnitus and a vertiginous-like experience
depressive (suicidal) thoughts

A patient said:
"I took Effexor only for a month. I was very surprised at the intensity of the withdrawal. The worst withdrawal effect for me was a sense of my nerves jangling when I moved my eyes and continuous indigestion, sort of a migraine-like feeling without the headache. The withdrawal took almost six weeks to get through, but I am now drug-free with tolerable levels of neck and back pain".

A doctor said:
"I was tapering a patient off an SSRI a few weeks ago and he had what I considered a severe withdrawal reaction with nausea and vomiting and flu-like symptoms although he was already started on fluoxetine. A slower tapering worked better".

A doctor said:
"I have been treating a teenaged boy who presented with some symptoms of depression and also psychological problems, especially difficulty with authority figures that goes way beyond the usual adolescent stuff. I decided to try him on sertraline, and the dose was gradually increased to 150 mg, with modest benefit. He decided abruptly to stop taking the medication and didn't tell me or his parents. Three days later he got in a disagreement with a security guard at his high school. The patient didn't remove his cap upon entering the school, as is required by the school to limit gang-associated clothing, and the guard knocked the cap off his head. The patient reacted by knocking the guard's eyeglasses off, breaking them. The guard pressed charges, and the patient now has an assault charge pending. The patient has no history of any aggressive behavior and admits that he "overreacted". After this incident, he resumed the medication until a month or so later, when he again stopped taking it and this time he told me and his parents. The patient and his parents noticed a marked irritability and a tendency to overreact and generally to be too emotional beginning 2 or 3 days after stopping the sertraline. The patient then began to wonder if his previous episode was in any way related to going "cold turkey". His lawyers as well as his family would like to use this in his defense".

A doctor said:
"I have had several patients -- all children and adolescents -- who have developed extreme irritability, often very unlike their usual personality, beginning a few days after abruptly discontinuing a short-acting serotonergic antidepressant. I'm aware of reports of withdrawal symptoms from paroxetine and sertraline, but I've not seen anything about exclusively behavioral symptoms in the absence of physical sxs".

A doctor said:
"I see all sorts of strange complaints from stopping SSRIs too soon. These include mood disturbance, psychotic features such as illusions or frank hallucinations, extreme agitation, and severe malaise".

A doctor said:
"Irritability and "over-reacting" don't suprise me in the least, and I find the story as you present it quite consistent with SSRI sudden-withdrawal syndrome. Having learned the hard way how terrible the effects of suddenly stopping SSRIs and venlafaxine (Effexor) can be I now routinely urge all my patients to come off these drugs gradually. I have seen the worst reactions from paroxetine (Paxil), but I have seen them in all the SSRIs. I have seen the withdrawal syndrome at low doses, like Paxil 20 mg and even Zoloft 50 mg".

A doctor said:
"I too have had experience with sertraline withdrawal. The two patients that come to mind complained of general dysphoria, derealization, and somatic sensations that led to a panic attack in one of them".
 
OK Starfish, I can see you have had some very bad experiences with SSRIs. But we seem to be on different channels here. First of all, I'm talking about Prozac, which has such a long half-life compared to other SSRIs, so the withdrawal sypmtoms are much more gradual. This is considered one of biggest benefits of using Prozac over other SSRIs. Secondly, I'm not talking about getting 'hooked' on the stuff. This takes a minimum of 6-8 weeks of continuous use which is how long it takes for it to make semi-permanent changes in transcription of receptors and neurotransmitters (all sorts of neurotransmitters, not just serotonin) and even changes in neuronal connections. This is in stark contrast to using it for 10 days each month where the only major change is in reuptake of serotonin in the synapse. It just gives you a serotonin boost at a time in a woman's cycle when she needs it most (especailly on a diet when tryptophan avaialibilty or uptake may be limiting so recycling the serotonin you already have is economical). This is not long enough to get hooked on it or develop withdrawal symptoms. Aside from that, there is a strong feeling (which I obviously share) that the extreme hormonal fluctuations that so many woman now experience each month are neither natural nor healthy. But that's a different topic. Suffice it to say that I believe that foods, drugs or exercise that can reduce these symptoms (or the hormonal fluctuations) are a good thing for women that suffer them.

" I'm sorry but if someone is that "desperate to shed bodyfat" maybe the should reevaluate some things. That is just my opinion, but to each their own. "

I won't disagree with that, but if that weren't the case then bodybuilding would die an instant death. Women do not just casually diet down to 6-8% bodyfat. Maybe it would be a good thing if that sport DID die out, but for now drugs of all sorts (I include stuff like caffeine, ephedrine etc... in the class of drugs) are an integral part of bodybuilding. They all have withdrawal problems. As I said earlier, I provide this info as just that...info so that women can make the most informed choices possible about what they put in their bodies. All drugs have benefits and side effects and each person should be given enough info to decide if the benefits outweigh the side effects, but side effects are an individual thing which cannot always be predicted until you actually try it. After all, carbohydrates are also serotonin boosters, and you should see the withdrwal symptoms some people go through when they try to stop those!!!!

Personally I agree with SteelWeaver. I would rather incorporate regular high carb refeeds to keep my serotonin levels in a healthy range. And I just give in to my sweet craving for ~1.5 days each month. 1 1/2 days is not going to make or break your physique, and it's much less traumatic than trying to fight the cravings and feeling guilty if you fail.
 
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