Posted by tealady on September 20, 2003, at 23:37:23
In reply to Re: oxygen » tealady, posted by Larry Hoover on September 19, 2003, at 20:22:17
> > IN the next sentence p152, she says "In a study of the relationship between lowered sympathetic nerve activity and obesity, researchers found that we become more sensitive to essential fatty acids when our serotonin levels drop and that makes you not only fat but depressed."
> >
> > http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9769705&dopt=Abstract
> > The MONA LISA hypothesis
> >
> > I wonder what "sensitive to EFA means"...pimples?>
> I don't know what to make of that quoted sentence. Serotonin receptor sensitivity is decreased in omega-3 deficiency states. So is insulin sensitivity. Is she trying to link these two ideas?
>here's a part of the article she was referring to
Seems like some at least don't want a 5HT2C receptor antagonist if you want to lose weight???
.... "A number of neuropeptides and monoamines are involved with modulating of food intake and fat stores. Both serotonin, acting through 5-HT2C receptors, and norepinephrine, acting through beta 2 and/or beta 3 receptors, reduce food intake. A variety of peptides also influence food intake and body fat. Neuropeptide Y, dynorphin, galanin, and melanocyte-stimulating hormone all increase food intake. In contrast, a large number of peptides--including cholecystokinin, corticotrophin-releasing hormone/urocortin, enterostatin, insulin, leptin, alpha-MSH, and TRH--reduce food intake. Chronic administration of neuropeptide Y, acting through Y-5 receptors, can produce chronically increased food intake and obesity.
This syndrome is similar to the VMH syndrome and suggests that NPY must be acting as an inhibitor of a feeding system. The melanocortin receptor system may be particularly important because a mouse that does not express MC4 receptors is massively overweight. These central systems modulate food intake and fat stores by the controlled system. Glucocorticoids from the adrenal gland are important in obesity, since adrenalectomy will reverse or prevent the development of all forms of obesity. The sympathetic nervous system is also important because low sympathetic activity is associated with experimental and clinical obesity. The reciprocal relationship between food intake and sympathetic activity has been a robust relationship, suggesting that beta receptors in the periphery or brain may be involved in feeding control. In one model of dietary obesity resulting when animals eat a high-fat diet, the syndrome is blocked by inhibitory adrenal steroid activity. These animals show a lower level of sympathetic activity and a low level of brain serotonin. Finally, they show an enhanced sensitivity to essential fatty acids when these are applied to the tongue or given into the gut.In this chapter, the control of energy stores as fat is viewed as a feedback system. Leptin is perceived as a key afferent signal and glucocorticoids and the sympathetic nervous system through beta receptors as essential elements of this control system."
Jan
PS anyone know why some SSRI's have 5-HT2C antagonists? ..like why try to block that receptor? Is it's function known..other than to help you lose weight perhaps when stimulated by serotonin?
Just asking as this was a common thing with fluoxetine and lexapro, citalopram..if I got it right
Jan
poster:tealady
thread:261577
URL: http://www.dr-bob.org/babble/alter/20030903/msgs/262078.html