![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 13 of 13. This is the beginning of the thread.
Posted by Quintal on October 3, 2007, at 15:43:00
Well b*gger my socks!!! How did that one slip under my radar? I was just looking through the new edition of the BNF to see if there were any new antidepressants etc, when I spotted the warning about rimonabant causing depression, and I wondered what it was. It turns out to be a cannabinoid receptor antagonist, a CB1 receptor antagonist to be precise. In simple terms, it has the opposite effect of cannabis on appetite, i.e. the munchies. Judging by the list of adverse psychiatric effects, it has the opposite effect of cannabis on the mind as well; depression, anxiety and insomnia are common side effects.
I'm very proud to announce that if I were overweight I could probably march into my GP's surgery and get a script for it - rimonabant has been available in the UK as Acomplia® since 2006, though at £44.00 a pack it's not cheap. Well it's about time we Brits got to sample some interesting new drugs first! It seems unlikely rimonabant will be approved in the US any time soon.
http://en.wikipedia.org/wiki/Rimonabant
http://www.bnf.org/bnf/bnf/54/129838.htmQ
Posted by James_glasgow on October 3, 2007, at 16:01:01
In reply to Rimonabant - New Appetite Suppressant, posted by Quintal on October 3, 2007, at 15:43:00
I was thinking the same as I am also in the UK, but the FDA refused to license the drug as a result of people with no previous mental illness commiting suicide in the trials, the manufacturer Sanfoi-Aventis has decided to pull the product out of the US market completely and the license has been very much tightened up in the UK and the the rest of the EU with a view to withdrawing it. So I would stick with orlistat and maybe one of the new combinations drugs that are being considered for a license for obesity, they are zonisamide/bupropion and naltrexone/bupropion, although both zonisamide and naltrexone can have a detremental effect on mood, I tried zonisamide on its own on the basis of the trials and it made me extremely irritable.
James
Posted by Quintal on October 3, 2007, at 16:28:16
In reply to Re: Rimonabant - New Appetite Suppressant, posted by James_glasgow on October 3, 2007, at 16:01:01
Zonisamide rang a bell, but I had to look it up. So it's another anticonvulsant that reduces appetite, like topiramate. I wouldn't want to take naltrexone either, what with my opioid dependence. Sounds like they're trying to reduce the pleasure people get from binge eating - I've read of it being used to reduce self-injury for that reason too. I don't like the sound of it myself, too much like a restraint on my free spirit.
I once took Orlistat just to see what it did, but I don't think my weight changed much. Caused a terrible crash after I came off it, but there might have been other factors contributing to that. In any case I'm too thin to need any of these drugs, in fact last year I was thinking of asking my GP for pizotifen to help me put on weight after benzo withdrawal. I have been (falsely) accused of being anorexic in the past. If anything I'd benefit from smoking a joint, or even a script for Marinol (but apparently we don't have it in the UK yet). Would nabilone have a similar effect?
Q
Posted by Phillipa on October 3, 2007, at 22:46:19
In reply to Re: Rimonabant - New Appetite Suppressant » James_glasgow, posted by Quintal on October 3, 2007, at 16:28:16
We've had marinol for years used to give to cancer patients so they would have less nausea and haven't nursed in 9 years. Phillipa
Posted by Quintal on October 4, 2007, at 11:52:06
In reply to Re: Rimonabant - New Appetite Suppressant » Quintal, posted by Phillipa on October 3, 2007, at 22:46:19
I was curious because Marinol is approved as an appetite stimulant, while nabilone didn't seem to be at first glance, apparently it is approved to treat weight loss in anorexia and AIDS patients. We do have nabilone in the UK. Apparently it's a synthetic THC analogue, while Marinol is derived from the Cannabis plant. They're both used as anti-emetics when more conventional options have failed.
Q
Posted by Phillipa on October 4, 2007, at 19:33:33
In reply to Re: Rimonabant - New Appetite Suppressant, posted by Quintal on October 4, 2007, at 11:52:06
Short and sweet and a new use too. Phillipa
"Medical" Marijuana - The Facts
Medical marijuana already exists. It's called Marinol.
A pharmaceutical product, Marinol, is widely available through prescription. It comes in the form of a pill and is also being studied by researchers for suitability via other delivery methods, such as an inhaler or patch. The active ingredient of Marinol is synthetic THC, which has been found to relieve the nausea and vomiting associated with chemotherapy for cancer patients and to assist with loss of appetite with AIDS patients.
Unlike smoked marijuana--which contains more than 400 different chemicals, including most of the hazardous chemicals found in tobacco smoke-Marinol has been studied and approved by the medical community and the Food and Drug Administration (FDA), the nation's watchdog over unsafe and harmful food and drug products. Since the passage of the 1906 Pure Food and Drug Act, any drug that is marketed in the United States must undergo rigorous scientific testing. The approval process mandated by this act ensures that claims of safety and therapeutic value are supported by clinical evidence and keeps unsafe, ineffective and dangerous drugs off the market.
There are no FDA-approved medications that are smoked. For one thing, smoking is generally a poor way to deliver medicine. It is difficult to administer safe, regulated dosages of medicines in smoked form. Secondly, the harmful chemicals and carcinogens that are byproducts of smoking create entirely new health problems. There are four times the level of tar in a marijuana cigarette, for example, than in a tobacco cigarette
Morphine, for example, has proven to be a medically valuable drug, but the FDA does not endorse the smoking of opium or heroin. Instead, scientists have extracted active ingredients from opium, which are sold as pharmaceutical products like morphine, codeine, hydrocodone or oxycodone. In a similar vein, the FDA has not approved smoking marijuana for medicinal purposes, but has approved the active ingredient-THC-in the form of scientifically regulated Marinol.
The DEA helped facilitate the research on Marinol. The National Cancer Institute approached the DEA in the early 1980s regarding their study of THC's in relieving nausea and vomiting. As a result, the DEA facilitated the registration and provided regulatory support and guidance for the study.
The DEA recognizes the importance of listening to science. That's why the DEA has registered seven research initiatives to continue researching the effects of smoked marijuana as medicine. For example, under one program established by the State of California, researchers are studying the potential use of marijuana and its ingredients on conditions such as multiple sclerosis and pain. At this time, however, neither the medical community nor the scientific community has found sufficient data to conclude that smoked marijuana is the best approach to dealing with these important medical issues.
The most comprehensive, scientifically rigorous review of studies of smoked marijuana was conducted by the Institute of Medicine, an organization chartered by the National Academy of Sciences. In a report released in 1999, the Institute did not recommend the use of smoked marijuana, but did conclude that active ingredients in marijuana could be isolated and developed into a variety of pharmaceuticals, such as Marinol.
In the meantime, the DEA is working with pain management groups, such as Last Acts, to make sure that those who need access to safe, effective pain medication can get the best medication available.
Posted by Quintal on October 5, 2007, at 19:00:25
In reply to Re: Rimonabant - New Appetite Suppressant » Quintal, posted by Phillipa on October 4, 2007, at 19:33:33
Getting back to the original topic, I was surprised by the amount of research available on rimonabant and the cannabinoid system. There are literally thousands of studies. It's a shame about the adverse psychiatric profile of rimonabant. I wondered if a selective CB1 antagonist that did not cross the blood-brain barrier (like ceterizine etc) would have fewer side effects, and naturally it seems other researchers have had the same idea.
__________________________________________________1: Int J Obes (Lond). 2006 Apr;30 Suppl 1:S30-2.Click here to read Links
The unfolding cannabinoid story on energy homeostasis: central or peripheral site of action?
Horvath TL.Department of Ob/Gyn and Reproductive Sciences, Yale University School of Medicine, New Haven, CT 06510-8016, USA.
Presentations in this symposium addressed effects and modes of action of endocannabinoids in various tissues in relation to metabolic disorders. Endocannabinoids are produced and exert their effect in various brain sites, including the mesolimbic reward circuitry and the hypothalamus. Both of these regions have direct ties to energy metabolism regulation, particularly food intake and energy expenditure. These data clearly suggest that the observed beneficial effects of CB1 (cannabinoid receptor 1) receptor antagonists on obesity may be related to the central endocannabinoid system. On the other hand, data presented on cannabinoid action in the liver and white adipose tissues clearly indicate that CB1-mediated events in affecting metabolic phenotype may occur in peripheral tissues as well. This together with the reported results from human trials on CB1 antagonists showing that the initial anorectic effect of rimonabant is diminished after the first weeks while longer lasting weight loss is achieved do indicate that peripheral action of cannabinoids are very important in body weight regulation. Should this hold true in the long run, antagonizing CB1 receptors with compound not crossing the blood-brain barrier could revolutionize pharmaceutical approaches to obesity by offering a tool that short cuts the central nervous system.
PMID: 16570102 [PubMed - indexed for MEDLINE]
--------------------------------------------------2: Am J Med. 2007 Sep;120(9 Suppl 1):S18-24; discussion S24.Click here to read Links
Understanding metabolic homeostasis and imbalance: what is the role of the endocannabinoid system?
Kunos G.National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland 20817, USA. gkunos@mail.nih.gov
Endogenous endocannabinoids (ECs) (anandamide and 2-arachidonoyl glycerol) are part of the leptin-regulated neural circuitry involved in appetite regulation. One of the sites of the orexigenic action of ECs involves activation of cannabinoid-1 (CB1) receptors in the lateral hypothalamus, from which neurons involved in mediating food reward project into the limbic system. In animal models of obesity, pharmacologic blockade or genetic ablation of CB1 receptors causes a transient reduction in food intake accompanied by sustained weight loss, reduced adiposity, and reversal of hormonal/metabolic changes, such as elevated levels of plasma leptin, insulin, glucose, and triglyceride, and reduced levels of plasma adiponectin (Acrp30). However, the beneficial effects of CB1 blockade on weight and metabolism cannot be explained by appetite suppression alone. Animal studies suggest that CB1 blockade exerts a direct peripheral as well as a central effect on fat metabolism. CB1 receptor blockade with rimonabant has been shown to not only reduce weight and adiposity but also to directly modulate fat metabolism at peripheral sites in skeletal muscle, adipose tissue, and the liver. Preclinical animal studies suggest that CB1 blockade acts on adipocytes to increase Acrp30 expression, on hepatocytes to decrease de novo lipogenesis and increase fatty acid oxidation, and on skeletal muscle to reduce blood glucose and insulin levels. Extrapolating from animal studies to the clinic, CB1 receptor blockade offers a promising strategy not only for reducing weight and abdominal adiposity but also for preventing and reversing its metabolic consequences.
PMID: 17720356 [PubMed - in process]
--------------------------------------------------3: Crit Pathw Cardiol. 2007 Jun;6(2):46-50.Click here to read Links
The endocannabinoid system: a new target for the regulation of energy balance and metabolism.
Després JP.Québec Heart Institute, Québec QC, Canada. jean-pierre.despres@crhl.ulaval.ca
Recent studies have provided evidence that the endocannabinoid (EC) system has very significant effects on energy balance and metabolism through the central control of appetite and by affecting peripheral metabolism. Endocannabinoids are endogenous phospholipid derivatives which bind and activate cannabinoid receptors type 1 and type 2 (CB1 and CB2 receptors). The CB1 receptor, a G-protein coupled receptor, is believed to be responsible for the majority of the central effects of endocannaboids on appetite. Chronic positive energy balance and obesity have been associated with an overactivation of the endocannaboid system which has been suggested to contribute to the development of abdominal obesity and to associated metabolic abnormalities which increase the risk of cardiovascular disease and type 2 diabetes. Animal studies had shown that stimulation of the cannabinoid CB1 receptor with endocannaboids such as anandamide could induce first an increase in food intake leading to body weight gain. Furthermore, an exciting development in this field has been the discovery of CB1 receptors in many peripheral tissues, including key organs involved in carbohydrate and lipid metabolism such as the adipose tissue and liver. Thus, blocking CB1 receptors located in the liver and adipose tissue could have an additional impact on the metabolic risk profile beyond what could be explained by the reduction in food intake and the related body weight loss. Preclinical studies have shown that rimonabant, the first CB1-receptor blocker to be available in clinical practice, could not only induce a reduction in food intake, but could also produce body weight loss beyond what could be explained by its effect on food intake. Thus, the evidence from preclinical studies have suggested that CB1 blockade could represent a relevant approach to reduce food intake, to induce body weight loss, and, most importantly, to "fix" the dysmetabolic state of viscerally obese patients at increased cardiometabolic risk.
PMID: 17667864 [PubMed - indexed for MEDLINE]
--------------------------------------------------4:Nat Neurosci. 2005 May;8(5):585-9.Click here to read Links
Endocannabinoid control of food intake and energy balance.
Di Marzo V, Matias I.Endocannabinoid Research Group, Institute of Biomolecular Chemistry, Consiglio Nazionale delle Ricerche, Via Campi Flegrei 34, 80078, Pozzuoli, Naples, Italy. vdimarzo@icmib.na.cnr.it
Marijuana and its major psychotropic component, Delta(9)-tetrahydrocannabinol, stimulate appetite and increase body weight in wasting syndromes, suggesting that the CB(1) cannabinoid receptor and its endogenous ligands, the endocannabinoids, are involved in controlling energy balance. The endocannabinoid system controls food intake via both central and peripheral mechanisms, and it may also stimulate lipogenesis and fat accumulation. Here we discuss the multifaceted regulation of energy homeostasis by endocannabinoids, together with its applications to the treatment of eating disorders and metabolic syndromes.
PMID: 15856067 [PubMed - indexed for MEDLINE]
__________________________________________________
It seems to me that rimonabant might be producing behavioral patterns that I associate with naturally thin persons, i.e. worry, nervousness, melancholia, introversion, hypersensitivity, agitation etc. Contrast this with the stereotype of the 'jolly fat person' and you can see where there might be a link. Not only in behavioral patterns, but energy metabolism, body shape etc. They seem to be linked, maybe because they are indeed linked in some way via the endocannabionoid system.I eat mostly soft, fatty, palatable foods but never gain much weight (unless on medication). This is the first piece of evidence to shed light on this phenomena. I know of a few overweight people who never seem to change much despite doing more physical exercise than me, and eating a low-calorie, low-fat diet. Thinness seems to imply pain and un-ease (if not dis-ease) to me, and these cannabinoid receptor antagonists seems to be producing a sense of mental un-ease. It makes sense. No such thing as a free lunch they say... I think it's largely a myth that thin people feel better. And in order to be thin, naturally obese people may have to 'pay the price' in mental un-ease - as naturally thin people do, at least if they use rimonabant. I note that dietary restriction also tends to produce much the same effect in naturally large people.
__________________________________________________
1: Int J Obes Relat Metab Disord. 2004 Apr;28(4):640-8.Click here to read Links
CB1 cannabinoid receptor knockout in mice leads to leanness, resistance to diet-induced obesity and enhanced leptin sensitivity.
Ravinet Trillou C, Delgorge C, Menet C, Arnone M, Soubrié P.Central Nervous System Research, Sanofi-Synthélabo, Toulouse Cedex, France. christine.ravinet-trillou@sanofi-synthelabo.com
OBJECTIVE: There is growing evidence for an implication of the CB1 receptor subtype of the endocannabinoid system in the regulation of eating and fat deposition. To further define the physiological role of these receptors in the control of energy balance, we characterized the phenotype of CB1 receptor knockout (CB1(-/-)) mice maintained on an obesity-prone regimen or on a standard chow. DESIGN: CB1(-/-) male mice were compared to wild-type animals (CB1(+/+) male mice) in two feeding paradigms: (1) with a standard laboratory regimen (3.5 kcal/g, 14.5% of energy as fat) and (2) on a free-choice paradigm consisting of offering both the standard laboratory chow and a high-fat diet (HFD) (4.9 kcal/g, 49% of energy as fat). RESULTS: When maintained on the standard diet, CB1(-/-) mice are lean. At the age of 20 weeks, their body weight and adiposity are, respectively, 24 and 60% lower than that of CB1(+/+) mice. They are slightly hypophagic, but when expressed as percent of body weight, their relative energy intake is similar to that of the wild-type animals. Furthermore, inactivation of CB1 receptors reduces plasma insulin and leptin levels, and enhances the response to intracerebroventricular leptin injection. The free-choice paradigm shows that the preference for a high-fat highly palatable chow is slightly delayed in onset but maintained in CB1(-/-) mice. However, loading CB1(-/-) mice with this obesity-prone diet does not result in development of obesity. Knockout mice do not display hyperphagia or reduction of their relative energy intake in contrast to CB1(+/+) mice, and their feeding efficiency remains low. These data suggest an improved energetic metabolism with the high-fat regimen. Furthermore, the insulin resistance normally occurring in HFD-fed mice is not present in CB1(-/-) mice. CONCLUSION: These results provide evidence that the stimulation of CB1 receptors is a key component in the development of diet-induced obesity, and that these receptors and their endogenous ligands are implicated not only in feeding control but also in peripheral metabolic regulations. The lack of effect of SR141716, a selective CB1 receptor antagonist, in CB1(-/-) mice further supports this hypothesis, as this compound was previously shown to display potent anti-obesity properties in diet-induced obese C57BL/6 mice.
PMID: 14770190 [PubMed - indexed for MEDLINE]
--------------------------------------------------2 FASEB J. 2005 Sep;19(11):1567-9. Epub 2005 Jul 11.Click here to read Links
The CB1 receptor antagonist rimonabant reverses the diet-induced obesity phenotype through the regulation of lipolysis and energy balance.
Jbilo O, Ravinet-Trillou C, Arnone M, Buisson I, Bribes E, Péleraux A, Pénarier G, Soubrié P, Le Fur G, Galiègue S, Casellas P.Oncology Research Department, Sanofi-Synthelabo Recherche, Montpellier, France.
We investigated the molecular events involved in the long-lasting reduction of adipose mass by the selective CB1 antagonist, SR141716. Its effects were assessed at the transcriptional level both in white (WAT) and brown (BAT) adipose tissues in a diet-induced obesity model in mice. Our data clearly indicated that SR141716 reversed the phenotype of obese adipocytes at both macroscopic and genomic levels. First, oral treatment with SR141716 at 10 mg/kg/d for 40 days induced a robust reduction of obesity, as shown by the 50% decrease in adipose mass together with a major restoration of white adipocyte morphology similar to lean animals. Second, we found that the major alterations in gene expression levels induced by obesity in WAT and BAT were mostly reversed in SR141716-treated obese mice. Importantly, the transcriptional patterns of treated obese mice were similar to those obtained in the CB1 receptor knockout mice fed a high-fat regimen and which are resistant to obesity, supporting a CB1 receptor-mediated process. Functional analysis of these modulations indicated that the reduction of adipose mass by the molecule resulted from an enhanced lipolysis through the induction of enzymes of the beta-oxidation and TCA cycle, increased energy expenditure, mainly through futile cycling (calcium and substrate), and a tight regulation of glucose homeostasis. These changes accompanied a significant cellular remodeling and contributed to a reduction of the obesity-related inflammatory status. In addition to a transient reduction of food consumption, increases of both fatty acid oxidation and energy expenditure induced by the molecule summate leading to a sustained weight loss. Altogether, these data strongly indicate that the endocannabinoid system has a major role in the regulation of energy metabolism.
PMID: 16009704 [PubMed - indexed for MEDLINE]
__________________________________________________Q
Posted by James_glasgow on October 6, 2007, at 4:29:54
In reply to Re: Rimonabant - New Appetite Suppressant, posted by Quintal on October 5, 2007, at 19:00:25
Hi Qunital
"It seems to me that rimonabant might be producing behavioral patterns that I associate with naturally thin persons, i.e. worry, nervousness, melancholia, introversion, hypersensitivity, agitation etc. Contrast this with the stereotype of the 'jolly fat person' and you can see where there might be a link. Not only in behavioral patterns, but energy metabolism, body shape etc. They seem to be linked, maybe because they are indeed linked in some way via the endocannabionoid system."
That is a good point and ceraintly rings a bell with me, pre-SSRI's and thin and post-SSRI's and not so thin (and a few years of taking Mellaril on and off), it is just a shame in the UK no Doctor I have ever come across is willing to see that good mental health and being overweight are not mutally inclusive.
James
Posted by Quintal on October 6, 2007, at 9:06:59
In reply to Re: Rimonabant - New Appetite Suppressant, posted by James_glasgow on October 6, 2007, at 4:29:54
Hi James,
It seems more of a catch 22 to me. Rather one of nature's traps than an oversight on the part of psychiatrists. At least that's what the evidence I've seen so far seems to suggest. There are always exceptions of course. Do you think your current weight is the will of your psychiatrist, or failure thereof on his/her part?
Q
Posted by James_glasgow on October 6, 2007, at 13:43:35
In reply to Re: Rimonabant - New Appetite Suppressant » James_glasgow, posted by Quintal on October 6, 2007, at 9:06:59
Hi Quintal
I have noticed that bar a very few medicines that are prescribed for mental health or neurological problem, they generally increase my BMI to just under 30 over time. This is I beleive through a combination of increase in appetite, and probably a metabolic change as even on a hypocalorific diet it can be very diffcult to lose the weight while still taking the drugs, and as you said the manner in which you act as if you are relatively restless naturally and are placed on something that stops this then you obvious stop buring up the energy.
My experience of psychiatry in the UK is one of "its not the drugs, you just are greedy", "it is the drugs but we cant do anything about it", "it is the drugs, we will change it to another (often of the same class) and see what happens" (even after many goes they dont seem to learn that doing this does not work), and a few others I cannot recall at present. Increase energy expenditure through exercise also has little effect at this point.
I would like them do to what is done at Harvard snd weight everyone before and while they are on psychotropic medication and where necessary use adjuvants to the drugs proactively, not let the probelm occur, then try and deal with it, or pretend it is not happening, "you look fine to me".
I recently read a piece of peer reveiwed literature about psychiatry, science, and body mass, and how as it is difficult to objectively measure much in psychiatry and many Psychiatrist were ignoring the fact, while claiming their profession to be evidence based science, that the one thing that can be done empirically and results in indisputable fact is to meause someones weight change, and look at a correlation between it and the drug or drugs the patient is taking. There is a great relutance from where I sit for them to do this, at I beleive anything beyond a 7% change in mass is considered clinically significant which would result in them need to act.
I beleive you are also in the UK and this where I have developed this view, I dont know if you have tried but if you ask an NHS Psychiatrist to try bupropion (at least in my experience) to help with SSRI induced fatigue, lack of sex drive and weight gain you get a blank look or worse. However, look around this board and you will see it is common practice in the US. This also goes for topiramate and just about anything you can think of that would assist side effects, modafanil, orlistat, amantadine with the exception being the use of procyclidine.
Maybe I have become rather cynical over the years as a result of my experience. I recently saw an Orthopaedic Surgeon and walked out of the Hospital asking myself if I had been in a Private Hospital only to realise I had been comparing it to psychiatry.
James
Posted by Quintal on October 7, 2007, at 18:51:19
In reply to Re: Rimonabant - New Appetite Suppressant, posted by James_glasgow on October 6, 2007, at 13:43:35
Hi James,
I understand where you're coming from. I gained a lot of weight on a combo of SSRI and clonazepam, at my heaviest I weighed about 14 stone, but I have a small frame.
>My experience of psychiatry in the UK is one of "its not the drugs, you just are greedy",
We both know they tend to increase appetite and alter metabolism. It's really frustrating to be on the receiving end of this, but I do think you're likely to hear this from some psychiatrists in the US too, especially if they're poorly trained and on a budget.
>"it is the drugs but we cant do anything about it",
I think this could be true, up to a point.
>"it is the drugs, we will change it to another (often of the same class) and see what happens" (even after many goes they dont seem to learn that doing this does not work)
Yeah, that's frustrating too. I have to say that this seems to be true of psychiatry worldwide. There are many people here from all corners of the globe that have been through the book, and nothing seems to work very well. I think we're really very lucky to have this safety net. It was only after being deprived of it that I learned its true value. I guess this could be part and parcel of psychiatry still being in its infancy.
>However, look around this board and you will see it is common practice in the US. This also goes for topiramate and just about anything you can think of that would assist side effects, modafanil, orlistat, amantadine with the exception being the use of procyclidine.
Yes, and I think that's likely because the private sector is a buyer's market. The Americans who are dependent on public welfare of some sort, a bit like our NHS, tend to be more limited in their options. In both countries the patient can buy private healthcare if they can afford it, and private healthcare practitioners can afford to indulge their patients. Public healthcare practitioners have to be more practical and realistic wherever they are in the world. I can see how 'additional extras' like bupropion might seem extravagant to the doctor on a tight budget, when weight can allegedly be reduced by diet and exercise alone. I can see why a doctor might feel pressured into telling you >"its not the drugs, you just are greedy"< even if I don't agree with it. It gets you out the door with minimal expense. It's a whole different ballgame if you profit from the consultation and the prescription. Different priorities. I wish it weren't as cold and clinical as that, and I know there are exceptions, but still that's how the world works, for better or worse. I've been on the receiving end of it myself, and I empathize with others who are in the same position.
I notice that many people in the US have trouble getting MAOIs because 'they're too old and dangerous', all the usual tricks that we have to put up with. And the great fear of prescribing pain meds in the US - contrast that with the Great British benzo inquisition. Every medical system has its own little quirks. Still they do lumber on, somewhat blindly it seems at times, but at least we have the advantage of being able to apply a little steering in our own cases.
This is why I was so shocked that rimonabant was marketed first in the UK, big market share an appetite suppressant would have and all. Now it seems rimonabant may not be entirely fit for human consumption. Oh well...
Q
Posted by Phillipa on October 7, 2007, at 20:26:00
In reply to Re: Rimonabant - New Appetite Suppressant » James_glasgow, posted by Quintal on October 7, 2007, at 18:51:19
Seems my medicaire and co-pay pay the docs sometimes more than private insurance. And the docs just write prescriptions you pay the pharmacists for the meds. That is where the cost comes in unless it is a generic med. Phillipa ps how come benzos and the luvox don't cause wt gain in me? But the more I excercise the bigger I get and now lack of hormones don't help.
Posted by James_glasgow on October 8, 2007, at 0:32:48
In reply to Re: Rimonabant - New Appetite Suppressant » James_glasgow, posted by Quintal on October 7, 2007, at 18:51:19
Hi QunintaI
Thank you for your understanding, I also see your points, I maybe being rather one sided seeing "the grass as greener on the otherside". It was finally tranylcypromine that brought my weight down I was just off for 14 too and it feel to 10 in 3-4 months which I must admit did shock some people, but I have been on mainly paroxetine for nearly 10 years. I even managed to convince my GP to let me try it after previous trying phenelzine and being able to show I was not going to end up having an "accident" by mixing it with the wrong medicines or foods.
Take care.
James
This is the end of the thread.
Psycho-Babble Medication | Extras | FAQ
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.org
Script revised: February 4, 2008
URL: http://www.dr-bob.org/cgi-bin/pb/mget.pl
Copyright 2006-17 Robert Hsiung.
Owned and operated by Dr. Bob LLC and not the University of Chicago.