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


Welcome to the EliteFitness.com Bodybuilding Site! Please join this discussion about More on Set Point theories, compulsive eating, SSRIs, etc... within the Women's Fitness (Female Bodybuilding and Training) category.

Excerpt: I found this to be an entertaining discussion on some of these concepts. More anecdotal than scientific, but i think it encompasses a lot of good stuff. I have a strong feeling that a lot of the cravings induced by BB type diets are from similar chemical imbalances and that maybe dieting BBs should be considered to be suffering from a self-induced compulsive eating disorder! Compulsive Eating From

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  1. #1
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    More on Set Point theories, compulsive eating, SSRIs, etc...

    I found this to be an entertaining discussion on some of these concepts. More anecdotal than scientific, but i think it encompasses a lot of good stuff. I have a strong feeling that a lot of the cravings induced by BB type diets are from similar chemical imbalances and that maybe dieting BBs should be considered to be suffering from a self-induced compulsive eating disorder!

    Compulsive Eating

    From http://www.t0.or.at/~ascharf/links/k.../comp.eat.html

    In 1995 the DSM-IV was published. This is the Diagnostic Services Manual 4th edition and is the basis for billing for psychiatric services as well as setting criteria for psychiatric diagnosing. In this edition all but 3 conditions were changed to reflect the view that all mental illness (or conditions) are based in the anatomy, physiology and biochemistry of the brain.

    I have an evolving concept of the "Set-Point Thermostat". I believe that this is a structure or gland in the brain which sends out neurotransmitters (chemical messengers to other parts of the brain) to increase or decrease our eating behavior. A paper, about Leptin, has been published by the Rockefeller University Medical Center giving indirect evidence that this thermostat exists and is genetically programmed. The exact site and structure of the "Set-Point Thermostat" has not been proven but many of us believe that it is the hypothalamus.

    We have many examples of this kind of feedback controls in the human body. The thyroid gland is controlled by the hypothalamus by a constant supply of TSH (Thyroid Stimulating Hormone) sent out by the hypothalamus (the master gland in the brain). When not enough thyroid hormone in the blood is detected, the hypothalamus increases the TSH and the thyroid gland releases more thyroid. When there is too much, such as when people take unnecessary thyroid during dieting, the supply of TSH is turned down so the level of thyroid in the blood remains at the "proper" level. "Proper" can sometimes be too high or too low and this causes hyper-thyroidism or hypo-thyroidism.

    Another feedback loop is from the hypothalamus in the brain and the ovary. This controls the menstrual cycle by sending out several controlling hormones and stimulating or shuting off estrogen and progestrogen hormones and setting the timing for the release of the egg.

    Like those two examples we now have had revealed the possible basis for a feedback loop involving the "Set-Point Thermostat" and our body fat cells. This is the recently discovered hormone Leptin. This was used to knock off 30% of a mouse's total body weight in 2 weeks. You can get lots of information from my web site at http://www.loop.com/~bkrentzman/. The original Rockefeller Press Release is linked from there.

    In my theory the Leptin produced from the fat cells causes a Leptin level in our blood. When there is "enough" the appetite stimulation slows down and we crave less. When this "Set-Point Thermostat" does not detect "enough" Leptin, it sends out neurotransmitters demanding we eat more. This could be how people keep their weight steady at, any level, without trying.

    I believe that it is the chemically resetting of the "Set-Point Thermostat" which produces the good results from the phentermine/fenfluramine medicines. Most of the cravings and strong urges to eat are relaxed. It's like getting a monkey off your back.

    Thin people do not understand how we overweight FEEL, when we are compelled to eat, whether hungry or not. I ask them to hold their breath for 2 minutes and tell them "That is about how we feel". If I push away from the table I will feel something like that "forever". That is what they are asking us to do for the rest of our lives. Talk about cruel and unusual punishment.

    Do people lose "All" their excess weight on the phentermine/fenfluramine medicines? Some do and some don't. Like everything else people differ from each other and live in different enviornments and families and socioeconomic situations. We also start out with different bodies. No two people will react the same and any one person will react differently at different ages.

    How safe is the phentermine/fenfluramine course of therapy? There are pesky side effects to these medicines, like there are to all other medicines, even aspirin. By working closely with your doctor you can usually make adjustments to the doses of the medicines to work around any unpleasant side effects. Only rarely does someone, who is truly motivated, have to discontinue the medicines.

    How long do I have to take these medicines? Since this is a chemical way of reseting the "Set-Point Thermostat", if the medicines are stopped without finding a way to make this change permanent, 95% of us will regain all the weight we lost. I plan to stay on these medicines until a better way is discovered. Many of the big drug companies are throwing big money into research since they have finally noticed the $30,000,000,000.00 market out there, mostly being serviced by modern day snake-oil salesmen.

    More written below, between the reflected lines:
    ------------------------------------------------------------------------

    >>>ONE cookie, ONE Candy bar. ONE bowl of cereal will not make much of an effect

    >[Deleted] writes:

    >>[Deleted], my good buddy, I have to disagree with you on this one!

    >>Some of us, me included, are compulsive eaters - we have a disease as bad or worse than alcoholism - one bite of a cookie or one bite of a "Snickers" is as lethal for me as "Miller's Time" is to a drunk. One spoonful of "Heavenly Hash" could set me off on a three-day ice cream binge!

    >This is an interesting thread. I'd like to know other's opinions. Having once been a compulsive over-eater and now no longer one, I tend to agree with [Deleted]. FOR ME (see, I can do it) the change took place when my view of food changed from good food/ bad food to food. [Deleted] accused me of simply changing the terms from good/bad to healthy/fat-laden but that is not quite true. I should perhaps change healthy to "nutrient laden" and then what I would be doing is describing the content of the food without labelling to "good" or "bad". Because we do need SOME fat in our diets as well as nutrients, fat-laden foods are not "bad" foods. (But I digress; sorry, this is one of my pet peeves).
    -+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+
    [BZK]-- I agree. There are no BAD foods. There is only a BAD DIET. Many of my patients come to me saying they have been "bad". I refuse to accept this self judgement. So long as we are not harming others I do not believe any of our acts are bad. Not even our decisions about food.

    [BZK]-- Researchers have now identified at least 13 neurotransmitters in the brain which create a complex control system for eating. 2 of those are controling fat intake, 2 for carbohydrate intake levels and 2 for protein intake. The composition of the foods we eat are strongly influenced by this set of controling hormones. One of the others called cystokinin, created in the bowel wall when we eat and carried to the brain sites by the blood stream, helps influence when we cease eating. Serotonin, another brain chemical, is known to be involved with both depression and satiety (the feeling of contentment after eating). Prozac, Paxil and other Serotonin Reuptake Inhibitors are very close to Pondimin (fenfluramine) in action and a combination of these drugs may cause side effects from too much serotonin. Great caution must be taken when using combinations of these drugs. I have only been able to hint at how complex is the human beings control system governing eating behavior. Much more is already known and I am sure much more is still to come out of the research labs.
    ------------------------------------------------------------------------
    >I think that the difference between alcohol and food is that alcohol has an addictive substance to it which the acloholic's body chemistry reacts to. I don't THINK food is the same, though recent medical research may be proving me wrong. One common thread among alcoholics is that they do not know when they have had enough to drink. One common thread among the obese seems to be that they, too, do not know when they have had enough to eat.

    >>From my experience, I tend to think of compulisve over-eating as something >mentally controllable through changing one's relationship to food and through becoming more aware of the physical impact certain foods have on my body (increased body awareness, I suppose). One cookie does not make me feel ill. A dozen cookies do. This has always been the case, but before I got more in tune with my body, I either never drew the connection or chose to ignore it, going for the instant gratification.
    -+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+
    [BZK]-- I do not believe that there are any simple answers to the overeating problem. Wishing ourselves thin (i.e. "eating as something mentally controllable through changing one's relationship to food") just does not work. If it did I would have been thin somewhere in the 20 years of therapy, and dozens of diets and fasts I put myself through. Also the hypnosis treatments I went through would have worked. Hypnosis NEVER works on obesity. It is great to stop smoking, but not to control overeating.
    ------------------------------------------------------------------------
    >Rambling on (sorry these thoughts aren't better organize), I was also deep in depression while a compulsive over-eater. When I pulled out of the depression I pulled out of the compulsive eating habit. And there is lots of medical evidence that chemical changes take place in the body during depression. I wonder if the chemical changes that happened when I came out of the depression might not have enabled me to feel full where before I was unable to.
    -+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+
    [BZK]-- Since lower levels of serotonin in the brain is known to be related to depression, and raising the serotonin levels is known to relieve both depression and urges to eat, then yes, there is lots of evidence that chemical changes could have enabled you to resist where before you were helpless and driven to eat.
    ------------------------------------------------------------------------
    >Anyway, I've rambled long enough. But I'd like other people's opinions of compulsive eating. Is it a mental crutch or the ramifications of a chemical imbalance?
    -+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+-+
    [BZK]-- Since phentermine/fenfluramine has been shown to reduce binge eating in 18 of 19 people who were in a recent trial, I think there is good proof that it is chemical.

  2. #2
    Elite Bodybuilder SteelWeaver's Avatar
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    OMG there's so much, it's so huge, this is a HUGE topic! So many factors: genetic, social, chemical, psychological ...

    I take it this was written before phen/fen proved to be dangerous.

    Are these chemical imbalances really similar, though? Between lean/shredded hypocaloric BB dieters and obese, possibly diabetic, hypercaloric compulsive eaters? Does that mean that the compulsive over-eaters are getting the same "starving" signals that BB dieters get?

    And would the persistence of these signals even after a hypercaloric state has been reinstated explain cravings experienced then?

  3. #3
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    Yes, this was written before Phen-Fen was withdrawn, and before they realized that obese HUMANS mostly suffer from excess leptin (in the form of leptin resistance). But the physiology of the cravings are pretty similar IMHO. In the lean case there is an absolute lack of leptin/serotonin etc....whereas the obese person may have plenty of these hormones floating around, but the message can't get through=relative deficiency symptoms. It now appears that drugs that affect uptake and recycling of neurotransmitters (such as Phen-fen) may work in obese humans by increasing their sensitivity to these hormones through changes in neurotransmitter levels, receptors, reuptake transporters and possibly even uptake into the brain. Kinda like giving metformin to a type 2 diabetic to make them more sensitive to their own insulin, or giving them more insulin to increase the strength of the signal. Using the diabetic analogy, this is why I think that ketogenic diets work well for many obese people. It's kinda like decreasing your sugar intake instead of increasing your insulin levels. Over time, low carb diets will reduce chronic serotonergic signals, thus sensitizing the brain to 'normal' neurotransmitter levels. They will also often resensitize insulin receptors to the insulin signal, and leptin receptors to the leptin signal. Because low carb diets are also dopaminergic, many people like the wired, more alert feeling they get on these diets. But again, I suspect this is because they are suffering from relative serotonergic excess/dopamine deficiency and the desensitization that goes with chronically high carb high insulin diets.

    Persistance of these "OMG I'm starving" signals is likely to continue in normal females until they have regained enough bodyfat to be reproductively viable. In other words, we're stuffed when it comes to staying chronically lean without some pretty strong pharmaceutical intervention. For me, it took about a year for my diet induced cravings to completely disappear after my last competition

  4. #4
    Elite Bodybuilder FitFossil's Avatar
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    Originally posted by MS
    ...Because low carb diets are also dopaminergic, many people like the wired, more alert feeling they get on these diets. But again, I suspect this is because they are suffering from relative serotonergic excess/dopamine deficiency and the desensitization that goes with chronically high carb high insulin diets. ...
    MS,

    Can you tell me more about this, specifically how it relates to levels of brain neurotransmitters? For me, I find low carb diets impossible. They don't make me alert, they make me completely dopey, slow and stupid.

    I'm already pretty certain I have a serotonin definciency (OCD, depression, eating disorder) and SSRI's work well for me. Does my reaction to low carbs say anything about my other neurotransmitters? The SSRI's have reduced my carb cravings/appetite considerably. Unfortunately they exacerbate my excessive daytime sleepiness, which a sleep study points to possible mild narcolepsy, though I'd need a different sleep study to confirm this.

    I recently started taking Monafidal (Provigil), and this definitely helps, but I'm worried about long term usage. I believe it affects dopamine, so does that mean I'm deficient in that too? Is there anything I can do from a dietary standpoint to help this? I've read about Tyrosine, would that help? Thanks!

  5. #5
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    FitFossil, this is a huge topic as I'm sure you can appreciate. Let me just say that at all ages, women in general respond better (from an anti-depression AND weight loss point of view) with SSRIs or carb-based diets, and men respond better to non-SSRIs and lowered carb diets (That last point is purely observational on my part). Men and women are not even close to the same when it comes to neurochemistry of dieting or depression.

    In other words your statement "For me, I find low carb
    diets impossible. They don't make me alert, they make me completely dopey, slow and stupid. " is more common for women than men.

    It also fits with the known biological differences in terms of leptin setpoint theories, serotonergic fluctuations throughout a women's cycle, the dopaminergic activity of androgens etc.... As a gross generalization, men will prefer a dopaminergic rush (cocaine, amphets, ECA, ketosis, MAOIs, Bupropion, testosterone etc...) and women will prefer a serotonergic rush, or an anti-dopaminergic substance (SSRIs, chocolate, non-ketogenic diets, estrogenic compounds, sedatives etc...) more often. Of course there are always exceptions to these rules, and the exceptions prolly do reflect distinct and individual neurochemical imbalances.

    Men are used to having more cholinergic stimulation. Their threshold for what feels 'good' is higher than a normal women's. Most antidepressants will have a long term impact on all major neurotransmitters, but a more distinct short term impact on specific neurotransmitters. It's the short term effects that seem to help with dieting, and the long term effects that assist with depression.

  6. #6
    Amateur Bodybuilder PowerPrincess's Avatar
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    Originally posted by FitFossil



    I'm already pretty certain I have a serotonin definciency (OCD, depression, eating disorder) and SSRI's work well for me. Does my reaction to low carbs say anything about my other neurotransmitters? The SSRI's have reduced my carb cravings/appetite considerably.
    What exactly are SSRI's??? How do you get them and do you need to be tested for this type of serotonin definiciency or insulin resistence - what tests should you ask the doc for???

  7. #7
    Elite Bodybuilder FitFossil's Avatar
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    Originally posted by PowerPrincess

    What exactly are SSRI's??? How do you get them and do you need to be tested for this type of serotonin definiciency or insulin resistence - what tests should you ask the doc for???
    SSRI's are selective serotonin reuptake inhibitors, a class of anti-depressants. They are prescribed by my doctor for OCD (obsessive-compusive disorder) and depression. I do NOT take them as a weight loss aid, that's just been a nice side effect.

    Since SSRIs allow serotonin to circulate in the brain longer, I guess I'm less inclined to binge on carbs. Carbs cause the brain to produce serotonin, so carb-binging can be self-medicating for those with serotonin definciency.

    For many people, SSRI's make them gain weight. They also have other unpleasant side-effects, so it's really not anything anyone would want to take unless they had a psychiatric need.

  8. #8
    Elite Bodybuilder FitFossil's Avatar
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    MS - thanks for answering my questions!

  9. #9
    Elite Bodybuilder SteelWeaver's Avatar
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    Originally posted by MS

    Persistance of these "OMG I'm starving" signals is likely to continue in normal females until they have regained enough bodyfat to be reproductively viable. In other words, we're stuffed when it comes to staying chronically lean without some pretty strong pharmaceutical intervention. For me, it took about a year for my diet induced cravings to completely disappear after my last competition
    A YEAR!! Oh, NO!

    So I wasn't imagining things when, despite being stuffed to the gills on chick peas, oatmeal, even yummy nutty bread and cafe lattes, I STILL wanted sugar, sugar, chocolates, cookies. And peanuts.

    I wish there were some way to let my body know I'm not interested in babies, so it can dump all the baby-prep stuff.

    "I'm not exactly sure how I feel about using SSRI's for competition dieting. I think that is the point being discussed, but I may be off. "

    Yes, this is part of it - MS also mentioned it on another thread a few days ago. But I think she used the word "acute" as opposed to chronic use.

    Somehow I think I prefer having regular high-carb refeeds to deal with the cravings.

  10. #10
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    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.

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