![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 14 of 14. This is the beginning of the thread.
Posted by Sherry on November 15, 2000, at 17:30:15
Hi All,
Does anyone have any theory's as to why many antidepressants cause so many of us to gain weight? Would it have anything to do with insulin levels? I would love to hear some feedback.
Thanks,
Sherry
Posted by R.Anne on November 15, 2000, at 22:17:28
In reply to Any one have a theory?, posted by Sherry on November 15, 2000, at 17:30:15
Offhand I don't have all the different names of brain parts and chemicals and neurotransmitters but it seems to me that some of the antidepressants are also stimulating the "hunger" centers of the brain. But also people who may not have been eating during depression may want to eat again when they are feeling better. Perhaps both of those ideas combined plus more I can't think of right now. The benzodiazapines make me hungriest it seems. I find that the lower doses of medicines, for me, help in not overeating, too. One more thing, a lot of us who take antidepressants may have had eating disorders or weight maintainance problems in the first place-I know I do-but the medicines increase that so I try to keep busy and far from the food! Doesn't always work, though. I just try again, that's all.
> Hi All,
>
> Does anyone have any theory's as to why many antidepressants cause so many of us to gain weight? Would it have anything to do with insulin levels? I would love to hear some feedback.
>
> Thanks,
>
> Sherry
Posted by SLS on November 16, 2000, at 0:54:43
In reply to Any one have a theory?, posted by Sherry on November 15, 2000, at 17:30:15
> Hi All,
>
> Does anyone have any theory's as to why many antidepressants cause so many of us to gain weight? Would it have anything to do with insulin levels? I would love to hear some feedback.
>
> Thanks,
>
> Sherry
Dear Sherry,Thanks for the homework assignment.
>:-/
In answer to your question, one of the mechanisms by which certain drugs produce weight-gain does involves insulin. Smart girl. :-)
---------------------------------------------------------I don't have the energy to proof-read this, and it's past my bedtime. Suffer.
---------------------------------------------------------
* SSRI-induced weight-gain is poorly understood. Weight-gain produced by SSRIs is considered to be a paradoxical reaction. That this paradoxical reaction is so frequently seen on Psycho-Babble may be an indicator of a bias towards an array of serotonergic (5-HT) dysregulations that is overrepresented in a population biased towards treatment-resistance and "poop-out".Serotonergic systemic and synaptic relationships are very complex and, in my way of thinking, vulnerable to a broader set of potential dysregulations.
In addition, despite their claimed selectivity, SSRIs still interact with various other important systems. The term "selective" was originally chosen to describe the tendency of these drugs to interact more exclusively relative to the three major monoamine neurotransmitters recognized as being important at the time (dopamine, norepinephrine, and serotonin). It is a misconception to think of SSRIs as being selective with respect to all other neurotransmitters and neuromodulatory systems.
In other words, most of you Babblers are just plain f_cked-up.
The SSRIs is obviously the class of drug in the greatest demand for an understanding as to why they cause weight-gain. I apologize for not being able to more precisely report the mechanisms underlying this "unappetizing" side-effect.
- Scott
---------------------------------------------------------
---------------------------------------------------------SOME MECHANISMS OF PSYCHOTROPIC-INDUCED WEIGHT-GAIN:
I. Increased secretion of prolactin by the pituitary gland.
Medications:1. The older typical neuroleptic antipsychotics: Haldol, Thorazine, Loxitane, Navane, Mellaril, etc.
2. Sulpiride and amisulpride
3. Paxil (paroxetine)
Mechanisms:1. The body thinks it's pregnant. It wants to store as much fat as possible for postnatal care. Got milk?
----------------------------------------------------------------
II. Blockade of histamine H1 receptors (H1 antagonists):
Medications:1. The newer atypical antipsychotics: Clozaril, Zyprexa, Risperdal. Clozaril and Zyprexa are the highest.
2. Tricyclics
3. Remeron
4. Many other psychotropics
Mechanisms:1. Increased hunger and food intake.
2. Carbohydrate craving.
3. Lowered basal metabolism rate (BMR). The rate of energy burned through thermogenesis (heat production) is decreased in brown adipose tissue (BAT) and as well as white adipose tissue (WAT). Psychotropic medications prevent the H1-induced increase in the expression of energy-releasing uncoupling proteins (UCP) located in the inner mitochondria of these tissues.
4. Decreased insulin sensitivity in muscle and heart. More glucose winds up being metabolized and stored as fat.
----------------------------------------------------------------
III. Chronic NE-beta receptor stimulation.
Medications:1. Tricyclics
2. Ludiomil
3. Remeron
4. Effexor
Mechanisms:1. Decreased expression of uncoupling proteins (UCP) in skeletal muscle and heart muscle, resulting in lower energy efficiency; energy is burned more slowly. (NE-beta receptor downregulation?)
2. Reduced plasma levels of insulin and free fatty acids (FFA). This produces a reduced uptake of glucose (energy) by skeletal muscle and heart muscle. The extra energy is stored in adipose tissue (fat).
----------------------------------------------------------------
IV. Changed glucose / insulin dynamics. Influences how much energy is stored.
Medications:1. Hydrazine MAOIs: Nardil and Marplan
2. Newer atypical neuroleptic antipsychotics: Clozaril, Risperdal, Zyprexa, Seroquel, and Zeldox. (I don't know to what extent each of these drugs affect glucose/insulin dynamics, but some are known to exacerbate diabetes).
Mechanisms:1. Decreased insulin sensitivity in muscle. Reduces the rate of glucose uptake by muscles. This extra glucose is stored as fat.
2. Inhibition of gluconeogenesis resulting in a decrease in the liberation of energy from protein reserves.
-----------------------------------------------------------------
Posted by SLS on November 16, 2000, at 6:52:23
In reply to Re: Any one have a theory?, posted by SLS on November 16, 2000, at 0:54:43
Proofreading #1
Corrected passage:"resulting in DECREASED energy efficiency; energy is burned more slowly."
=================================================================
> Hi All,
>
> Does anyone have any theory's as to why many antidepressants
cause so many of us to gain weight? Would it have anything to do
with insulin levels? I would love to hear some feedback.
>
> Thanks,
>
> Sherry
Dear Sherry,Thanks for the homework assignment.
>:-/
In answer to your question, one of the mechanisms by which certain
drugs produce weight-gain does involves insulin. Smart girl. :-)
---------------------------------------------------------I don't have the energy to proof-read this, and it's past my
bedtime. Suffer.---------------------------------------------------------
* SSRI-induced weight-gain is poorly understood. Weight-gain
produced by SSRIs is considered to be a paradoxical reaction. That
this paradoxical reaction is so frequently seen on Psycho-Babble
may be an indicator of a bias towards an array of serotonergic
(5-HT) dysregulations that is overrepresented in a population
biased towards treatment-resistance and "poop-out".Serotonergic systemic and synaptic relationships are very complex
and, in my way of thinking, vulnerable to a broader set of
potential dysregulations.In addition, despite their claimed selectivity, SSRIs still
interact with various other important systems. The term
"selective" was originally chosen to describe the tendency of
these drugs to interact more exclusively relative to the three
major monoamine neurotransmitters recognized as being important at
the time (dopamine, norepinephrine, and serotonin). It is a
misconception to think of SSRIs as being selective with respect to
all other neurotransmitters and neuromodulatory systems.In other words, most of you Babblers are just plain f_cked-up.
The SSRIs is obviously the class of drug in the greatest demand
for an understanding as to why they cause weight-gain. I apologize
for not being able to more precisely report the mechanisms
underlying this "unappetizing" side-effect.
- Scott
---------------------------------------------------------
---------------------------------------------------------SOME MECHANISMS OF PSYCHOTROPIC-INDUCED WEIGHT-GAIN:
I. Increased secretion of prolactin by the pituitary gland.
Medications:1. The older typical neuroleptic antipsychotics: Haldol,
Thorazine, Loxitane, Navane, Mellaril, etc.2. Sulpiride and amisulpride
3. Paxil (paroxetine)
Mechanisms:1. The body thinks it's pregnant. It wants to store as much
fat as possible for postnatal care. Got milk?
----------------------------------------------------------------
II. Blockade of histamine H1 receptors (H1 antagonists):
Medications:1. The newer atypical antipsychotics: Clozaril, Zyprexa,
Risperdal. Clozaril and Zyprexa are the highest.2. Tricyclics
3. Remeron
4. Many other psychotropics
Mechanisms:1. Increased hunger and food intake.
2. Carbohydrate craving.
3. Lowered basal metabolism rate (BMR). The rate of energy
burned through thermogenesis (heat production) is decreased in
brown adipose tissue (BAT) and as well as white adipose tissue
(WAT). Psychotropic medications prevent the H1-induced
increase in the expression of energy-releasing uncoupling
proteins (UCP) located in the inner mitochondria of these
tissues.4. Decreased insulin sensitivity in muscle and heart. More
glucose winds up being metabolized and stored as fat.
----------------------------------------------------------------
III. Chronic NE-beta receptor stimulation.
Medications:1. Tricyclics
2. Ludiomil
3. Remeron
4. Effexor
Mechanisms:1. Decreased expression of uncoupling proteins (UCP) in
skeletal muscle and heart muscle, resulting in decreased
energy efficiency; energy is burned more slowly. (NE-beta
receptor downregulation?)2. Reduced plasma levels of insulin and free fatty acids
(FFA). This produces a reduced uptake of glucose (energy) by
skeletal muscle and heart muscle. The extra energy is stored
in adipose tissue (fat).
----------------------------------------------------------------
IV. Changed glucose / insulin dynamics. Influences how much energy
is stored.
Medications:1. Hydrazine MAOIs: Nardil and Marplan
2. Newer atypical neuroleptic antipsychotics: Clozaril,
Risperdal, Zyprexa, Seroquel, and Zeldox. (I don't know to
what extent each of these drugs affect glucose/insulin
dynamics, but some are known to exacerbate diabetes).
Mechanisms:1. Decreased insulin sensitivity in muscle. Reduces the rate
of glucose uptake by muscles. This extra glucose is stored as
fat.2. Inhibition of gluconeogenesis resulting in a decrease in
the liberation of energy from protein reserves.
-----------------------------------------------------------------
Posted by MarkinBoston on November 16, 2000, at 15:15:47
In reply to Any one have a theory?, posted by Sherry on November 15, 2000, at 17:30:15
Worse yet, weight gain is a upward spiral, generally called syndrome-X where fat increase, estrogen increase, and insulin insensitivity all reinforce each other to the point you are at risk for type2 diabetes, hypertension, heart attack etc. - men and women.
Posted by Noa on November 16, 2000, at 16:01:56
In reply to No, but it should not be ignored., posted by MarkinBoston on November 16, 2000, at 15:15:47
That's what I have--insulin resistance. It is apparently a vicious cycle---insulin resistance leads to weight gain leads to more resistance, etc. Also, then, insulin resistance leads to hormone changes leads to more depression, menstrual irregularities, acne, infertility, etc. I have to start taking glucophage to break the cycle, although I know that increasing exercise has also been known to help a lot. But I guess my endo is worried about the diabetes developing.
Posted by SLS on November 16, 2000, at 18:18:02
In reply to Re: Any one have a theory? - Oops #1, posted by SLS on November 16, 2000, at 6:52:23
Proofreading #2
Can you believe it? Duh.The original passage was correct. (I really wanted an excuse to see my name appear three times along this thread).
Corrected uncorrected passage:"resulting in INCREASED energy efficiency; energy is burned more slowly."
=================================================================
> Hi All,
>
> Does anyone have any theory's as to why many antidepressants
cause so many of us to gain weight? Would it have anything to do
with insulin levels? I would love to hear some feedback.
>
> Thanks,
>
> SherryDear Sherry,
Thanks for the homework assignment.
>:-/
In answer to your question, one of the mechanisms by which certain
drugs produce weight-gain does involves insulin. Smart girl. :-)
---------------------------------------------------------I don't have the energy to proof-read this, and it's past my
bedtime. Suffer.---------------------------------------------------------
* SSRI-induced weight-gain is poorly understood. Weight-gain
produced by SSRIs is considered to be a paradoxical reaction. That
this paradoxical reaction is so frequently seen on Psycho-Babble
may be an indicator of a bias towards an array of serotonergic
(5-HT) dysregulations that is overrepresented in a population
biased towards treatment-resistance and "poop-out".Serotonergic systemic and synaptic relationships are very complex
and, in my way of thinking, vulnerable to a broader set of
potential dysregulations.In addition, despite their claimed selectivity, SSRIs still
interact with various other important systems. The term
"selective" was originally chosen to describe the tendency of
these drugs to interact more exclusively relative to the three
major monoamine neurotransmitters recognized as being important at
the time (dopamine, norepinephrine, and serotonin). It is a
misconception to think of SSRIs as being selective with respect to
all other neurotransmitters and neuromodulatory systems.In other words, most of you Babblers are just plain f_cked-up.
The SSRIs is obviously the class of drug in the greatest demand
for an understanding as to why they cause weight-gain. I apologize
for not being able to more precisely report the mechanisms
underlying this "unappetizing" side-effect.
- Scott
---------------------------------------------------------
---------------------------------------------------------
SOME MECHANISMS OF PSYCHOTROPIC-INDUCED WEIGHT-GAIN:
I. Increased secretion of prolactin by the pituitary gland.
Medications:1. The older typical neuroleptic antipsychotics: Haldol,
Thorazine, Loxitane, Navane, Mellaril, etc.2. Sulpiride and amisulpride
3. Paxil (paroxetine)
Mechanisms:1. The body thinks it's pregnant. It wants to store as much
fat as possible for postnatal care. Got milk?
----------------------------------------------------------------
II. Blockade of histamine H1 receptors (H1 antagonists):
Medications:1. The newer atypical antipsychotics: Clozaril, Zyprexa,
Risperdal. Clozaril and Zyprexa are the highest.2. Tricyclics
3. Remeron
4. Many other psychotropics
Mechanisms:1. Increased hunger and food intake.
2. Carbohydrate craving.
3. Lowered basal metabolism rate (BMR). The rate of energy
burned through thermogenesis (heat production) is decreased in
brown adipose tissue (BAT) and as well as white adipose tissue
(WAT). Psychotropic medications prevent the H1-induced
increase in the expression of energy-releasing uncoupling
proteins (UCP) located in the inner mitochondria of these
tissues.4. Decreased insulin sensitivity in muscle and heart. More
glucose winds up being metabolized and stored as fat.
----------------------------------------------------------------
III. Chronic NE-beta receptor stimulation.
Medications:1. Tricyclics
2. Ludiomil
3. Remeron
4. Effexor
Mechanisms:1. Decreased expression of uncoupling proteins (UCP) in
skeletal muscle and heart muscle, resulting in increased
energy efficiency; energy is burned more slowly. (NE-beta
receptor downregulation?)2. Reduced plasma levels of insulin and free fatty acids
(FFA). This produces a reduced uptake of glucose (energy) by
skeletal muscle and heart muscle. The extra energy is stored
in adipose tissue (fat).
----------------------------------------------------------------
IV. Changed glucose / insulin dynamics. Influences how much energy
is stored.
Medications:1. Hydrazine MAOIs: Nardil and Marplan
2. Newer atypical neuroleptic antipsychotics: Clozaril,
Risperdal, Zyprexa, Seroquel, and Zeldox. (I don't know to
what extent each of these drugs affect glucose/insulin
dynamics, but some are known to exacerbate diabetes).
Mechanisms:1. Decreased insulin sensitivity in muscle. Reduces the rate
of glucose uptake by muscles. This extra glucose is stored as
fat.2. Inhibition of gluconeogenesis resulting in a decrease in
the liberation of energy from protein reserves.
-------------------------------------------------------------------------------------------------------------------------------------------------
Posted by SLS on November 17, 2000, at 22:49:23
In reply to Re: No, but it should not be ignored., posted by Noa on November 16, 2000, at 16:01:56
Hi.
> That's what I have--insulin resistance. It is apparently a vicious cycle---insulin resistance leads to weight gain leads to more resistance, etc. Also, then, insulin resistance leads to hormone changes leads to more depression, menstrual irregularities, acne, infertility, etc. I have to start taking glucophage to break the cycle, although I know that increasing exercise has also been known to help a lot. But I guess my endo is worried about the diabetes developing.Diabetes is also a disease displaying a positive-feedback loop. High concentrations of blood glucose kills the insulin-producing cells of the pancrease known as the beta Islets of Langerhans.
fewer islets - > less insulin - > higher blood-sugar - > fewer islets - > less insulin - > higher blood-sugar - > fewer islets...
The higher and more chronic the elevation of blood glucose, the faster the insulin-producing cells of the pancrease die. I do not believe that these cells divide. There is but a limited number of beta-cells that you will depend on for the rest of your life. Therefore, controlling glucose can be a matter of life and death. I lost a cousin to diabetes, but not before she lost both legs.
Just thought I would mention it.
------------------------------------------------
I hope I got at least a C on my homework assignment.The research took me 3-4 hours. I don't mean to be facetious, but I don't remember coming across a single abstract on Medline devoted to reviewing *all* the diverse mechanisms that account for the weight-gain associated with the major classes of psychotropics. I am often amazed at how little attention is often paid to the most obvious and relevant of issues and phenomena.
It was somehow a let-down to see my 4 hours of research reduced to a few sentences. I tried to make the post as organized and concise as possible, as I thought it would be more informative and understandable that way. (Who am I trying to convince, anyway)?
The real reason for this post is to pose a question for others to follow-up on. It occurred to me that there might be an association between the atypical paradoxical weight gain produced by the SSRIs and treatment-resistance and/or specific symptomatic presentations. I can't help to consider the population of Psycho-Babblers to be skewed in the direction of treatment-resistance. In addition, atypical depression may be overrepresented. Perhaps SSRI-induced weight gain is a marker of treatment-resistance and possibly a criterion to use when choosing therapies.
Any thoughts?
- Scott
Posted by Noa on November 18, 2000, at 13:18:52
In reply to Re: No, but it should not be ignored., posted by SLS on November 17, 2000, at 22:49:23
Interesting, Scott. I have to think about this one.
I do think that people who stick around here for more than one or two med questions might be more prone to treatment resistant depression. A hunch, for what it's worth.
Maybe the research can be something you write up for publication somewhere--it is a hot topic. something for the popular press, maybe? How about salon.com for example?
Posted by Sherry on November 19, 2000, at 16:10:16
In reply to Re: No, but it should not be ignored., posted by SLS on November 17, 2000, at 22:49:23
Hi Scott,
Thank you for completing the homework assignment so throughly. You get an A+ from me.
Diabetes runs in my family, and I definitely fall into the treatment resistant category. In fact, I can not take most of the antidepressants because they disable my cognitive abilities even worse than the depression. I too, am going to give the glucophage a trial, and I can only hope and pray that it improves my capabilities. I have a very hard time following the intellect on this site sometimes, eventhough it is within my abilities. Very, very frustrating.
Here's an excerpt from a book describing insulin resistance:
Today, each of the stages in the progression of Insulin Resistance Syndrome has been described and studied, and though you might not be a scientist, if you are addicted to [carbs], chances are you have experienced some of these stages firsthand. The cells in your brain and the rest of the nervous system appear to be the first to become insulin resistant. In order to protect you from a flood of insulin, your body simply closes these cells down (that is, it makes them resistant to insulin). Unfortunately, when the doors to the cells in your brain and nervous system close to insulin, they also close to the blood sugar that insulin ushers in and that would normally nourish them. The First Stage of Insulin Resistance Syndrome [IRS] In this first stage of [IRS], you may find that within two hours after eating high-[carb] foods, you feel light-headed, irritable, or unable to concentrate. In addition to craving high-[carb] foods, you may gain weight easily as an increased quantity of the food energy (transformed into blood sugar ) is channeled through the liver, turned into blood fat, then stored in your fat cells. The Second Stage of Insulin Resistance Syndrome [IRS] If hyperinsulinemia continues, a second stage of [IRS] may occur, and the postmeal cravings, tiredness, light-headedness, irritability, or inability to concentrate that you felt before may become more noticeable. Your muscles, liver, and other organs will likewise begin to block insulin's entry and, in doing so, will also close off their ability to get nourishment from blood sugar. As muscles experience a decrease in blood sugar fueling, you may experience a decrease in your desire or willingness to be active or to exercise. You might feel less inclined to do very much except what is absolutely necessary. If you do feel motivated to be active or find you must be active, you may lose your desire to continue activity or find that you tire easily. In this second stage of [IRS], weight gain is almost inevitable, as food energy (in the form of blood sugar transformed into blood fat) is channeled increasingly into the fat cells for storage. In addition to weight problems, in particular abdominal obesity, the second stage of [IRS] can herald a wide variety of noticeable heart disease risk factors, including an increase in risk-related blood fats, increases in blood pressure levels, and more. During both the first and second stages, insulin is able to continue to usher some blood sugar into the cells of many organs, but if no corrective action is taken, these cells will grow more and more insulin resistant, closing the doors (or sites) through which blood sugar had previously entered. The liver, sensitive to these high levels or insulin and blood sugar in the bloodstream, transforms the excess blood sugar into blood fat so that it can be removed from the blood, and the blood sugar (now in the form of fat) is stored in the fat cells. In the first two stages of [IRS], then, as insulin resistance grows, insulin has transformed your body into a fat-making machine. As the cells of many organs throughout your body become insulin resistant, your fat cells become the preferred storage site for blood sugar. The Third Stage of Insulin Resistance Syndrome [IRS] In the third stage of [IRS], brain-related low blood sugar swings can become severe, and your muscles may literally be starving for nourishment. At this stage you may experience extreme mood swings, irritability, inability to concentrate, tiredness, muscle shakes, depression, headaches, and foggy thinking. You may gain weight more easily than you ever thought possible and find that cravings for starches, snack foods, junk foods, and sweets has become uncontrollable. Much of the weight you gain may be deposited as abdominal or tummy fat. Most likely, you find that you prefer frequent snacks rather than typical mealtimes, and when you do snack or eat a meal, you may continue to eat even though you are uncomfortable and/or no longer enjoy the food. The Fourth Stage of Insulin Resistance Syndrome [IRS] Chances are, as you enter the fourth stage of [IRS], you will no longer be able to ignore or deny the physical changes that have sprung for your body's insulin imbalance. At this stage even your fat cells can become insulin resistant and close down to insulin and to the blood sugar/blood fat it brings along with it. Many of the symptoms you experienced at earlier stages in the progression reach a peak in the fourth stage, with the significant exception of low blood sugar and weight gain. Two of the signs of [IRS], rising blood sugar levels and weight gain, reverse in the fourth stage. At this final level, even fat cells closedown. Now insulin, blood sugar, and blood fat are caught with no place to go. They cannot leave the bloodstream and remain blocked there. So in this final stage, rather than channeling the energy into fat cells, leading to weight gain, your body may no longer be able to channel energy into your fat cells, and your weight may suddenly drop a bit (though usually not to normal levels). In the same way, the low blood sugar swings that you might have experienced when blood sugar and blood fat are being channeled into your fat cells in the third stage will disappear and be replaced by high levels of blood sugar. At this point, as blood sugar is trapped in your bloodstream, unable to enter the organs or to be converted and then stored as fat in your fat cells, you may be said to have adult-onset diabetes."-------------
I can actually feel food work on my mind. Every doctor I have been to, I told them when I eat that my ears begin ringing, my vision blurs, and my mind goes blank. I had to do the research myself and demand the tests. Then and only then, did I get a referral to an Endo. I guess you could say that I'm just a little disappointed in the medical camp.
Enough already of my babbling. At least in my case, the answer to you're question is, yes. *Every* AD I have tried has caused weight gain and I'm definitely treatment resistant. In fact, every AD I have tried has made many of my symptoms worse. But, I have a really screwed up system.Have a great Thanksgiving.
Sherry
>
> > That's what I have--insulin resistance. It is apparently a vicious cycle---insulin resistance leads to weight gain leads to more resistance, etc. Also, then, insulin resistance leads to hormone changes leads to more depression, menstrual irregularities, acne, infertility, etc. I have to start taking glucophage to break the cycle, although I know that increasing exercise has also been known to help a lot. But I guess my endo is worried about the diabetes developing.
>
> Diabetes is also a disease displaying a positive-feedback loop. High concentrations of blood glucose kills the insulin-producing cells of the pancrease known as the beta Islets of Langerhans.
>
> fewer islets - > less insulin - > higher blood-sugar - > fewer islets - > less insulin - > higher blood-sugar - > fewer islets...
>
> The higher and more chronic the elevation of blood glucose, the faster the insulin-producing cells of the pancrease die. I do not believe that these cells divide. There is but a limited number of beta-cells that you will depend on for the rest of your life. Therefore, controlling glucose can be a matter of life and death. I lost a cousin to diabetes, but not before she lost both legs.
>
> Just thought I would mention it.
>
>
> ------------------------------------------------
>
>
> I hope I got at least a C on my homework assignment.
>
> The research took me 3-4 hours. I don't mean to be facetious, but I don't remember coming across a single abstract on Medline devoted to reviewing *all* the diverse mechanisms that account for the weight-gain associated with the major classes of psychotropics. I am often amazed at how little attention is often paid to the most obvious and relevant of issues and phenomena.
>
> It was somehow a let-down to see my 4 hours of research reduced to a few sentences. I tried to make the post as organized and concise as possible, as I thought it would be more informative and understandable that way. (Who am I trying to convince, anyway)?
>
>
>
> The real reason for this post is to pose a question for others to follow-up on. It occurred to me that there might be an association between the atypical paradoxical weight gain produced by the SSRIs and treatment-resistance and/or specific symptomatic presentations. I can't help to consider the population of Psycho-Babblers to be skewed in the direction of treatment-resistance. In addition, atypical depression may be overrepresented. Perhaps SSRI-induced weight gain is a marker of treatment-resistance and possibly a criterion to use when choosing therapies.
>
> Any thoughts?
>
>
> - Scott
Posted by fitgrl on November 22, 2000, at 12:21:42
In reply to Re: Any one have a theory?, posted by SLS on November 16, 2000, at 0:54:43
Hi,
I just wanted to respond to the "hunger" thing with these drugs. I WAS taking paxil (been off of it a week and feel like crap) anyway, Just in this week being off the drug I can't believe the difference in my hunger and even the taste of foods. I don't crave breads and mostly sweets like I did. It feels so good to be able to have that one cookie. before, I went crazy and felt as if I couldn't stop eating. All that has gone away now. I don't have that constant hunger. And it IS a constant hunger.
Paxil has been really great for me. I was on it 2 years, but i have reached a point in my life that I am ready to try this thing on my own. Wish me luck. :o)))
Posted by R.Anne on November 22, 2000, at 19:33:23
In reply to Any one have a theory?, posted by Sherry on November 15, 2000, at 17:30:15
Dear Scott,
I was going to ignore something but I want you to know that I did not appreciate your statement in here that I have marked with three asterisks. I don't like to be referred to that way.r.anne* SSRI-induced weight-gain is poorly understood. Weight-gain produced by SSRIs is considered to be a paradoxical
reaction. That this paradoxical reaction is so frequently seen on Psycho-Babble may be an indicator of a bias
towards an array of serotonergic (5-HT) dysregulations that is overrepresented in a population biased towards
treatment-resistance and "poop-out".Serotonergic systemic and synaptic relationships are very complex and, in my way of thinking, vulnerable to a
broader set of potential dysregulations.In addition, despite their claimed selectivity, SSRIs still interact with various other important systems. The term
"selective" was originally chosen to describe the tendency of these drugs to interact more exclusively relative to the
three major monoamine neurotransmitters recognized as being important at the time (dopamine, norepinephrine, and
serotonin). It is a misconception to think of SSRIs as being selective with respect to all other neurotransmitters and
neuromodulatory systems.*** In other words, most of you Babblers are just plain f_cked-up.
The SSRIs is obviously the class of drug in the greatest demand for an understanding as to why they cause
weight-gain. I apologize for not being able to more precisely report the mechanisms underlying this "unappetizing"
side-effect.
Posted by SLS on November 23, 2000, at 6:43:04
In reply to Re: Any one have a theory? SLS: SCOTT, posted by R.Anne on November 22, 2000, at 19:33:23
I apologize.
- Scott
Posted by R.Anne on November 24, 2000, at 1:55:07
In reply to Re: Any one have a theory? SLS: SCOTT » R.Anne, posted by SLS on November 23, 2000, at 6:43:04
> I apologize.
>
>
> - Scott*****
Thank you very much Scott! Love to you. r.anne
This is the end of the thread.
Psycho-Babble Medication | Extras | FAQ
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.org
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