Posted by shar on December 6, 2000, at 14:47:09
In reply to Drug-Induced Weight Gain - Some Mechanisms, posted by SLS on December 6, 2000, at 8:52:59
SLS,
I commend you on your courage to post so soon after that sense of humor fiasco... JKJKJKJK. 8-) ((SLS))I actually appreciate you reposting this info, because it is hard for me to remember some of the more technical info I see here.
This might not have anything to do with your treatise, but when I kept pressing my doctor on how a drug that is supposedly circulating in my brain and affecting receptors in my brain would cause constipation (not in my brain) and similar non-brain side effects, she finally said we have receptors all over our body.
So, if that is true, and the action of the AD isn't even mostly limited to our brains, but goes all over our bodies to receptors all over our bodies, who knows what is really happening? All of our systems could be affected.
I often wondered if she was exaggerating, just wanted to shut me up, or if that could really be happening. If so, it seems we haven't even begun to figure out the AD's "how do I affect thee" ?
Shar
> I thought I would repost my short treatise on drug-induced weight gain. Someone had asked about it this week, so I figured I would cease another opportunity to see my name appear on the board.
>
> Oops. Was that a joke? :-)
>
>
> - Scott
>
>
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> 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.
>
> 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.
>
>
> ---------------------------------------------------------
>
>
> 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?
>
>
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>
> 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.
>
>
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>
> 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 higher 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).
>
>
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> 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.
>
>
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poster:shar
thread:50044
URL: http://www.dr-bob.org/babble/20001130/msgs/50068.html