About a week ago I was visiting an addictions treatment center and something that really struck me was the severity of skin issues I saw in many of the residents. Part of that may be due to poor nutrition, part to stress, and part as a result of drug use itself.
In any case, there's a great website I found with information on healthy skin care that I thought would be of interest to some of you reading this blog. I'll post the information as a permanent link, but if you are interested now, the name is http://www.highonhealth.org.
My teaching assistant today comes from Star Wars. He is here with me, because I have lost track of the number of times, when trying to do a serious presentation about neurotransmitters, I have said, "R2D2" when I meant to say "DRD2". I will have to check the Universal Diagnostic and Statistical Manual to see if I meet the criteria for Intergalactical Dyslexia...
What R2D2 and I would like to tell you about his almost-namesake today, the DRD2 receptor, is that this subset of dopamine receptors is sensitive to how we eat. DRD2 is responsible for impulse control. People who have a disturbed DRD2 system are more prone to problems such as shoplifting, gambling, alcohol addiction, nicotine addiction, and binge eating. They also seem to have more intensive carbohydrate cravings.
Scientists recently reported that this receptor is especially sensitive to food restriction. That is, people who restrict their food intake seem to be more sensitive to the reinforcing effects (the effects that make you feel good and want to use) of several addictive substances, including opiates, nicotine, and psychostimulants.
(That is why R2D2 is a little wired today; he was running late and drank his coffee but skipped breakfast to be sure we got this posted.)
This particular study suggests that the same effect can be provoked when restricting food and using dopamine-promoting medications such as pramipexole (Mirapex). For anyone taking medications for Parkinson's disease or restless legs syndrome, this could be important information to discuss with a nutritionist.
One of the enhanced responses with food restriction is locomotion. And that makes me think of people who abuse some of these chemicals. They stimulate themselves, which suppresses their appetite, which enhances their stimulation and increases their physical activity. On an ongoing basis, (and people who abuse drugs tend to not only use them just once) that can create a calorie deficit which reinforces the positive effects of the drug use. And that can reinforce staying addicted.
Even if you're not using illicit drugs, maybe not eating and living on cigarettes and coffee is kind an offbeat, roundabout way to jumpstart the dopamine system into motion. I have had many, many clients who tell me they feel addicted to sugar, and when they simply don't eat it they feel better. Maybe this is one of the reasons for that relationship.
Just a little fun fact on this Friday that will hopefully give you something to think about.
R2D2 and I are now going to eat breakfast.
Collins GT, Calinski DM, Newman AH, Grundt P, Woods JH. Food restriction alters N'-propyl-4,5,6,7-tetrahydrobenzothiazole-2,6-diamine dihydrochloride (pramipexole)-induced yawning, hypothermia, and locomotor activity in rats: evidence for sensitization of dopamine D2 receptor-mediated effects. J Pharmacol Exp Ther. 2008 May;325(2):691-7.
Antipsychotic medications have worked wonders to enhance the lives of many people. However, in recent years, antipsychotics have also been used for an increasing number of off-label uses and in progressively younger populations than they ever were before. Before handing these medications out like they are candy, it's important to evaluate the risks associated with using these medications. A recent study suggested that we should be much more careful about choosing our treatment populations than we have been to date.
Before I get to the meat of the study, I'd like to preface this post with an explanation of the study design. The authors of this study are concerned about safety risks in young children and pregnant women when they are given antipsychotic medications. However, they had to develop a research model that did not place young children and pregnant women at risk in the process of looking into this issue. So...rather than give antipsychotics to these two populations, they chose to administer a battery of antipsychotics to a group of roundworms. Roundworms were chosen because they are an accepted research model for investigating matters related to brain and nervous system development. That is definitely a limitation of the study, as most people I know would not say they have much in common with this guy...but that's one of the tough things about studying medications and their risks...how to investigate those risks without causing more damage.
Anyway...when the roundworms were given three of these medications, clozapine (Clozaril), fluphenazine (Prolixin), and haloperidol (Haldol), there was less development of neurons in general and axons (a specific anatomical feature of a neuron) in neurons devoted to mechanosensory function (that's touching and registering what you're touching). Neurons that were produced also tended to not migrate to the location where they would be expected to migrate, meaning there might have been neurons there, but they were, so to speak, all dressed up with no place to go.
In some neurons, axons grew past their functional anatomical size. And some had abnormal anatomical features.
Other antipsychotics produced similar results, although not to as significant a degree. The drugs mentioned included: risperidone (Risperdal), aripiprazole (Abilify), quetiapine (Seroquel), trifluoperazine (Stelazine) and olanzapine (Zyprexa).
I'm not going to pontificate about the ethical dilemma encountered when treating a pregnant woman with schizophrenia. The choices made in those situations involve complex risk/benefit considerations that are the responsibility of the patient and her physician.
However, I will say that responsible use of these medications in women of childbearing age is imperative. Forty-nine percent of all pregnancies ending in childbirth in 1994 were unintended, and 48% of all women aged 15-44 in 1994 had had at least one unintended pregnancy at some point in their life. It happens, and it happens a lot.
So if you're a physician and you're handing out prescriptions for antipsychotics for off-label uses to women of childbearing age...no matter how much judgment, education, evaluation, etc. you think you're providing, you really are playing with fire.
Donohoe DR, Weeks K, Aamodt EJ, Dwyer DS. Antipsychotic drugs alter neuronal development including ALM neuroblast migration and PLM axonal outgrowth in Caenorhabditis elegans. Int J Dev Neurosci. 2008 May-Jun;26(3-4):371-80.
Friday I participated in a meeting at a chemical dependency treatment center. This is a place where people have been medicating their problems with stimulants and who are learning to use communication, conflict resolution, and coping skills to ride through life's challenges so that life does not defeat them. One of the biggest problems in this population is stimulant use, in the form of methamphetamine.
The message this and other treatment centers are working hard to encourage...is that when you listen to your body, it will tell you if you need to sleep, eat, address a conflict, or participate in a relaxing activity to help ride through situations that cannot be immediately addressed. When you push through feelings and ignore what they're telling you, you can push yourself to a point so low that it becomes tempting to use chemicals to pull out of the situation.
Today, I was reviewing research and ran across an abstract that completely contradicts this point of view. This article discusses the "potential" for treating CFS with neurostimulants, such as bupropion (Wellbutrin), dextroamphetamine (Dexedrine), and methylphenidate (Ritalin, Concerta).
No wonder treatment centers abound. The drug industry is advocating throwing stimulants at problems that very well may best respond to intensive self-care. I'm not trying to say that chronic fatigue is not a genuine problem. I just wonder where the logic is in trying to blast a person out of a fatigued state that may be telling us something very important about the person's overall health, their lifestyle choices, and the way they deal with stress.
It's no wonder our many public service attempts at reducing illicit drug use fall on deaf ears. The message seems to be that if you can figure out a way to present your problem to the doctor in a way that fits with an "official" medical problem, you can legally buy a way out of your problem. If you're less savvy, or don't have access to a doctor who is open to such creative thinking, you can still get the job done. It just might land you in jail at some point down the road.
An addict is an addict, whether legally managed or scoring treatment off the street.
Valdizán Usón JR, Idiazábal Alecha MA. Diagnostic and treatment challenges of chronic fatigue syndrome: role of immediate-release methylphenidate. Expert Rev Neurother. 2008 Jun;8(6):917-27.
Here's an interesting abstract. I post it partly for the important medical information it provides but also to comment on the interesting editorial twist that may affect how readers interpret the information.
The subjects: women with epilepsy and the children they bore. The question: whether epilepsy affects the development of those children. (As quoted by the authors of the study, "We aimed to ascertain the prevalence of cardiac malformation (CM) and its association with antenatal exposure to an antiepileptic drug (AED) in infants of mothers with epilepsy.")
At 3 months of age, 462 babies born to mothers with epilepsy were examined by a cardiologist to see if they had at least one of several heart defects: atrial septal defect, tetrology of Fallot, patent ductus arteriosus, pulmonic stenosis, ventricular septal defect, tricuspid regurgitation, and transposition of great arteries. Possible correlations between the existence of these defects and any of the following were evaluated: mother's epilepsy history, use of antiepileptic medications in the first trimester of pregnancy, mother's age, seizure frequency during pregnancy, and folate supplementation.
There were a few significant relationships. Prematurely born children were more likely to have heart defects. Use of more than one medication was also a significant contributing factor. And there was a trend, though not significant, for children whose mothers who had used valproic acid (Depakote) to have heart defects. No relationships to mother's age, epilepsy history, seizure frequency, or folate usage were noted.
So even though there were only three identified contributing factors, two of which involved antiepileptic medications, the authors were allowed to title their publication in a way that somewhat masked this relationship. It also, for someone skimming research abstracts, could lead to an impression that epilepsy itself, and not the way in which epilepsy is treated, is the problem.
I am a diligent scientist and try to get the facts straight before I put anything on this blog, or in anything I write. But anyone reading this blog knows that all you have to do is turn on the evening news and see how vague headlines become top news stories and "facts" are generated without any meat behind them.
It's simply not fair to generalize to all mothers with epilepsy. There were an awful lot of babies in this study who did not have heart defects, 426 to be exact. That's a lot of unnecessary fear to be putting out there for women with epilepsy. Of course, the take home message is that women of childbearing age may not be the most appropriate candidates for valproic acid, but somehow that got lost in the analysis.
Thomas SV, Ajaykumar B, Sindhu K, Francis E, Namboodiri N, Sivasankaran S, Tharakan JA, Sarma PS. Cardiac malformations are increased in infants of mothers with epilepsy. Pediatr Cardiol. 2008 May;29(3):604-8.
Just a simple straightforward study that validates every mother in history who got out the cod liver oil and told her kids it was good for the brain. Eighty-five fourth graders receiving 400 mg per day of docosahexaenoic acid (DHA) were compared to 90 fourth graders who didn't, with regard to a battery of cognitive tests. There was a positive relationship between blood DHA levels and scores on the Peabody Picture Vocabulary Test, a test of listening comprehension and vocabulary acquisition.
Can't stand the thought of getting fish oil into your kids? Here are some nice options.
1. Coromega makes a pudding-type emulsion that tastes just like a Creamsicle. www.coromega.com.
2. Saturday I tasted tested a new product at a local health food store clearly made with kids in mind--Barlean's Omega Swirl lemon zest flavored fish oil emulsion. You'd never know it was fish, and 2 teaspoons contains 365 mg EACH of DHA and EPA. http://www.barleans.com/omega_swirl.asp
3. For kids who are way too assertive to trust anything that remotely resembles a supplement or a fish...Omega 3 Brain Booster Powder is a tasteless, odorless, water-soluble, heat stable, gluten-free fish oil powder blended into a rice protein base. You can bake with it, cook with it, stir it into your favorite juice. I've done some work for this company and we've tested it on boatloads of kids. They'll take it in anything...the caveat being you don't prompt them to decide they don't like what you're serving by telling them it has fish oil in it. Healthy spaghetti sauce...here we come! You can get 10% off your first online purchase of this particular product by going to www.omega3powder.com. A little note: The owner of the company recently chose to take a major hit on his revenues in order to maintain integrity and customer safety. The rice shortage had reduced his sourcing options for rice protein to imports from China and Denmark. Even though the Chinese option would have allowed him to continue production without disruption, he opted to let his supply run out and run into back order status, and wait for the Danish rice protein. That's one reason why I love working for this man, he'll never make money in a way that compromises the safety of anyone he truly wants to help with his work.
Ryan AS, Nelson EB. Assessing the effect of docosahexaenoic acid on cognitive functions in healthy, preschool children: a randomized, placebo-controlled, double-blind study. Clin Pediatr (Phila). 2008 May;47(4):355-62.
A few years ago I was working with a client with polycystic ovary syndrome. In the course of giving her medical history, she'd also disclosed that she had hyperprolactinemia, a condition in which milk production and let down occurs, even in men, and even in women who are not nursing, if their blood levels of prolactin are too high. She told me that she continued to produce and release milk for four years after delivering her last child, and not a single physician she'd asked about it here in Arizona or over in California seemed to think it was a situation worthy of medical intervention. So she lived with it, until it eventually went away.
As we progressed through our consultation, I explained to her why omega-3 fatty acids are so important--as they are an integral part of the brain's structure and functioning. I then explained to her that breast milk is high in omega-3 fatty acids, and that babies who are nursed are more likely to get these crucial fatty acids than babies on formula.
I looked up from my notepad to see my client red-faced. If steam could have come out of her ears, it would have.
Thinking I'd said something hurtful or offensive, I asked her if something was wrong.
She looked at me and asked, "So you mean to tell me...for four whole years...my brains were leaking out of my boobs and no one seemed to think that was a problem?"
I was the professional in that situation and so it fell on me to keep a completely straight face and answer a serious "yes, yes that's true."
Hyperprolactinemia really is a condition that needs to be taken seriously. As my client correctly deduced, it can drain the body of some of its most essential compounds, which can promote inflammation and potentially disrupt healthy brain function. Some psychiatric medications can increase the risk of hyperprolactinemia. One that has this reputation is risperidone (Risperdal).
A group of Chinese researchers recently tested an herbal remedy for hyperprolactinemia, peony-glycyrrhiza decoction, against a more traditional treatment, a medication called bromocryptine. Their subjects were women whose hyperprolactinemia was a direct result of risperidone use. For the purposes of this study, the women were also experiencing irregular periods (oligomenorrhea) or absence of periods (amenorrhea). Each group was exposed to both the herbal and the pharmaceutical treatment, with one group starting on herbs and switching to medication. The second group received the treatments in the reverse order. Psychotic symptoms, negative side effects, and levels of the hormones prolactin, estradiol, testosterone, and progesterone were all measured at the beginning and end of the study.
Not only did the herbal preparation produce a decrease in prolactin similar to the medication, other hormones were not affected, and psychosis was not worsened. And, more often in the herbal than the pharmaceutical remedy, there were improvements in negative side effects of hyperprolactinemia.
Whether or not you are on a medication, if you're producing breast milk and you are not nursing a baby, it is a medical problem and it does need to be addressed.
And now that you've read this post, you won't need to wait four years until a nutritionist mentions in passing that you should insist that your problem be taken seriously.
Yuan HN, Wang CY, Sze CW, Tong Y, Tan QR, Feng XJ, Liu RM, Zhang JZ, Zhang YB, Zhang ZJ. A randomized, crossover comparison of herbal medicine and bromocriptine against risperidone-induced hyperprolactinemia in patients with schizophrenia. J Clin Psychopharmacol. 2008 Jun;28(3):264-370.
Bowden CR, Voina SJ, Woestenborghs R, Do costerR, Heykants J. Stimulation by risperidone of rat prolactin secretion in vivo and in cultured pituitary cells in vitro. J Pharmacol Exp Ther 1992 Aug;262(2): 699-706.
Kinon BJ, Stauffer VL, McGuire HC, Kaiser CJ, Dickson RA, Kennedy JS. The effects of antipsychotic drug treatment on prolactin concentrations in elderly patients. J Am Med Dir Assoc 2003 Jul-Aug; 4(4): 189-94.
Lee BH, Kim YK. The relationship between prolactin response and clinical efficacy of risperidone in acute psychotic inpatients. Prog Neuropsychopharmacol Biol Psychiatry 2006 Jun;30(4):658-62.
Foley KF, Kast RE. Review of evidence that posttransplantation psychiatric treatment commonly affects prolactin levels and thereby influences graft fate. Gen Hosp Psychiatry 2006 May-Jun;28(3):230-3.
Anderson GM, Scahill L, McCracken JT, McDougle CJ, Aman MG, Tierney E, Arnold LE, Martin A, Katsovich L, Posey DJ, Shah B, Vitiello B. Effects of short- and long-term risperidone treatment on prolactin levels in children with autism. Biol Psychiatry 2007 Feb 15;61(4):545-50.
Staller J. The effect of long-term antipsychotic treatment on prolactin. J Child Adolesc Psychopharmacol 2006 Jun;16(3):317-26.
Madhusoodanan S, Moise D. Risperidone-induced hyperprolactinemia in adolescents: A case series. J Clin Psychiatry 2006 Jul;67(7):1110-3.
Meldersson KI. Prolactin elevation of the antipsychotic risperidone is predominantly related to its 9-hydroxy metabolite. Hum Psychopharmacol 2006 Dec;21(8):529-32.
Kopecek M, Bares M, Horacik J, Mohr P. Low-dose risperidone augmentation of antidepressants or anxiolytics is associated with hyperprolactinemia. Neuro Endocrinol Lett 2006 Dec;27(6):803-6.
Troost PW, Althaus M, Lahuis BE, Buitelaar JK, Minderaa RB, Hoekstra PJ. Neuropsychological effects of risperidone in children with pervasive developmental disorders: a blinded discontinuation study. J Child Adolesc Psychopharmacol 2006 Oct;16(5):561-73.
Eberhard J, Lindstrom E, Holstad M, Levander S. Prolactin level during 5 years of risperidone treatment in patients with psychotic disorders. Acta Psychiatry Scand 2007 Apr;115(4):268-76.
Bushe C, Shaw M. Prevalence of hyperprolactinaemia in a naturalistic cohort of schizophrenia and bipolar outpatients during treatment with typical and atypical antipsychotics. J Psychopharmacol 2007 Sep;21(7):768-73.
Duval F. Guillon MS, Mokrani MC, Crocq MA, Garcia Duarte F. Relationship between prolactin secretion, and plasma risperidone and 9-hydroxyrisperidone concentrations in adolescents with schizophreniform disorder. Psychoneuroendocrinology 2007 Nov 27.
Synek O, Svestka J, Tomanova J, Rodakova I, Cejpkova A. Differences in the effect of second-generation antipsychotics on prolactinaemia: Six weeks open-label trial in female in-patients. Neuro Endocrinol Lett 2007 Dec 6;28(6).
Togo T, Iseki E, Shoji M, Oyama I, Kase A, Uchikado H, Katsuse O, Kosaka K. Prolactin levels in schizophrenic patients receiving perospirone in comparison to risperidone. Neurology 2003 Apr 8;60(7): 1130-5.
Brunelleschi S, Zeppegno P, Risso F, Cattaneo CI, Torre E. Risperidone-associated hyperprolactinemia: evaluation in twenty psychiatry outpatients. Pharmacol Res 2003 Oct;48(4): 405-9.
Volavka J, Czobor P, Cooper TB, Sheitman B, Lindenmayer JP, Citrome L, McEvoy JP, Lieberman JA. Prolactin levels in schizophrenia and schizoaffective disorder patients treated with clozapine, olanzapine, risperidone, or haloperidol. J Clin Psychiatry. 2004 Jan;65(1):57-61.
OK, OK, I succumbed to the blogroll. I wasn't going to contribute to anyone's blog addiction and sore neck and shoulders, but some of my friends and supporters are writing great stuff I don't want you to miss if it should help you! So I've got a few options to get you started.
Only when it's 3 am and you're still sitting in front of your computer, it's your own lack of impulse control and not my reckless lack of editing discretion that your boss needs to hear about when you're caught napping at your desk the next day. :)
Between traveling/speaking 3 times in two cities in 5 days and reviewing the last month's worth of research abstracts, time for writing has been short. I should be back to getting you all some good abstracts starting Monday.
If you've ever dieted, and you have trouble sleeping...there may be a reason. Keep in mind, this study was done on rainbow trout, but there is still a message in it for humans. Three groups of trout were studied with regard to their melatonin (sleep hormone/antioxidant) levels and cortisol (stress hormone) levels. The three groups were defined as fed fish, fish that were fasted for 7 days, and fish that were fasted for 7 days then refed for 5 days.
Melatonin levels were disrupted in fasted fish. If you were human, this would likely mean if you were on a strict fasting/dieting protocol, you were probably having trouble sleeping as well.
Interestingly, nighttime serotonin levels were higher in these fasted fish. Melatonin is made from serotonin, so I would presume that what the body tries to do when you're not eating well is to keep you alert and thinking about getting some food. It does that by hanging on to serotonin and preventing its conversion into melatonin. That's a survival mechanism.
So if you're dieting and you're awake at night with cravings? That's a normal response. Don't obsess about what's wrong with you, don't surf the Internet looking for what to do about your cravings. In this kind of situation, you're thinking about food because you need it. Get some.
As far as cortisol, dieting reduced levels and they stayed low after refeeding. You could argue that this is a benefit of dieting...except for the fact that if you're cutting yourself short on melatonin, you're aging yourself more quickly than you should. There are plenyy of ways to reduce melatonin levels without dieting that don't cut your life short on the back end.
By the way, since I write so much about sleep I thought I should mention...I love naps. The long afternoon kind where my cats curl up with me, and I wake up with a little bit of drool on my pillow. I don't feel guilty at all. I completely buy into the idea of "beauty sleep"--sooooo much cheaper than all those anti-aging potions on the infomercials!
Ceinos RM, Polakof S, Illamola AR, Soengas JL, Míguez JM. Food deprivation and refeeding effects on pineal indoles metabolism and melatonin synthesis in the rainbow trout Oncorhynchus mykiss. Gen Comp Endocrinol. 2008 Apr;156(2):410-7. Epub 2008 Jan 8.
I'm six months into writing this blog, and I took some time to look at the statistics this morning. I am interested to know what interests all of you readers so that I can provide more of that. It was a bit of a shot in the dark at first, guessing what would bring you in to read my thoughts, but I do have a bit more of an idea as time goes on.
The ten most read pages were about: aspartame, topamax and off-label uses, fish oil/anxiety/anger, fibromyalgia, melatonin and REM sleep behavior disorder, topamax and kidney problems, rozerem and sleep apnea, vinpocetine, wheatgrass, olanzapine/stuttering.
The top ten search terms were: fish oil/anxiety, cellular effects of aspartame, acth/paxil, aspartame/depression, rozerem, rozerem/sleep apnea, epa/anxiety, topamax/binge eating, caffeine/antidepressants, olanzapine/stuttering.
So now I know what people found when they looked for it. What I don't know is...what were you looking for that you didn't find? That is something my statistics won't tell me. But if I know what you all wish to see, I can keep that in mind when I get my monthly pile of research from the Nat'l Library of Medicine.
I'm surprised at how many people not only found this blog, but return for more, and I'm delighted at how interactive it's become. I hope to bring more information to you all, and to be challenged to present science in a fun and meaningful way. Your responses and suggestions will definitely guide me toward making this the best possible resource on the 'net when it comes to psych meds.
I don't have to tell you that it's important to keep your blood pressure under control. And if you're intelligent enough to have interest in reading this blog, then you also know that if you're overweight, and your blood pressure is high, it is likely to drop if you take the steps to lose the weight.
Well, some scientists got a little muddled about why it's important to lose weight in the first place. And they developed this medication, sibutramine (Meridia), that is supposed to be a weight loss aid.
The only problem is, sibutramine doesn't help reduce blood pressure. In fact, in enough people so that it routinely shows up in the research literature, sibutramine has been observed to raise blood pressure. I've got twelve references about this in my drug book (listed below for your reference). In addition to raising blood pressure, elevated heart rate, insomnia, and agitation were also reported side effects.
MY blood pressure started to rise as I reviewed these references. Because I couldn't help but wonder if sibutramine would even be allowed on the market if it were a drug for cancer, or ulcers, or arthritis, and it caused hypertension, arrhythmia, and/or agitation? You can bet not.
But there is such a race to see who can create the magic weight loss pill that scientists seem to have forgotten why we even want people to lose weight. I can just see these Dr./patient interactions behind closed doors everywhere..."Well, Mr. Smith, the bad news is you can't sleep, your heart's racing, you're on the verge of a stroke, and you've annoyed the hell out of your family, friends, and coworkers with your new Type A personality. But hey, guess what? (Drum roll..........) You're THIN!!!"
Your blood pressure isn't high because you have a Meridia deficiency. It's high because you have an activity and good food deficiency.
Is it just me, or is this a little bit like a scientific "Who's On First?"
Lechin F, van der Dijs B, Hernandez G, Orozco B, Rodriguez S, Baez S. Neurochemical, neuroautonomic and neuropharmacological acute effects of sibutramine in healthy subjects. Neurotoxicology 2006 Mar;27(2):184-91.
Avenell A, Brown TJ, McGee MA, Campbell MK, Grant AM, Broom J, Jung RT, Smith WC. What interventions should we add to weight reducing diets in adults with obesity? A systematic review of randomized controlled trials of adding drug therapy, exercise, behaviour therapy or combinations of these interventions. J Hum Nutr Diet. 2004 Aug;17(4):293-316.
Rucker D, Padwal R, Li SK, Curioni C, Lau DC. Long term pharmacotherapy for obesity and overweight: updated meta-analysis. BMJ 2007 Dec 8;335(7631):1194-9.
Di Francesco V, Sacco T, Zamboni M, Bissoli L, Zoico E, Mazzali G, Minniti A, Salanitri T, Cancelli F, Bosello O. Weight loss and quality of life improvement in obese subjects treated with sibutramine: a double-blind randomized multicenter study. Ann Nutr Metab 2007;51(1):75-81.
Hanotin C, Thomas F, Jones SP, Leutenegger E, Drouin P. Efficacy and tolerability of sibutramine in obese patients: a dose-ranging study. Int J Obes Relat Metab Disord 1998 Jan;22(1): 32-8.
Dunican KC, Desilets AR, Montalbano JK. Pharmacotherapeutic options for overweight adolescents. Ann Pharmacother 2007 Sep;41(9):1445-55.
Elliott WJ. Drug interactions and drugs that affect blood pressure. J Clin Hypertens (Greenwich). 2006 Oct;8(10):731-7.
Porter JA, Raebel MA, Conner DA, Lanty FA, Vogel EA, Gay EC, Merenich JA. The Long-term Outcomes of Sibutramine Effectiveness on Weight (LOSE Weight) study: evaluating the role of drug therapy within a weight management program in a group-model health maintenance organization. Am J Manag Care. 2004 Jun;10(6):369-76.
Faria AN, Ribeiro Filho FF, Kohlmann NE, Gouvea Ferreira SR, Zanella MT. Effects of sibutramine on abdominal fat mass, insulin resistance and blood pressure in obese hypertensive patients. Diabetes Obes Metab. 2005 May;7(3):246-53.
Perrio MJ, Wilton LC, Shakir SA. The safety profiles of orlistat and sibutramine: results of prescription-event monitoring studies in England. Obesity (Silver Spring). 2007 Nov;15(11):2712-22.
Berube Parent S, Prud’homme D, St. Pierre S, Doucet E, Tremblay A. Obesity treatment with a progressive clinical tri-therapy combining sibutramine and a supervised diet-exercise intervention. Int J Obes Relat Metab Disord 2001 Aug;25(8): 1144-53.
McMahon FG, Fujioka K, Singh BN, Mendel CM, Rowe E, Rolston K, Johnson F, Mooradian AD. Efficacy and safety of sibutramine in obese white and African American patients with hypertension: a 1-year double-blind, placebo-controlled, multicenter trial. Arch Intern Med 2000 Jul 24;160(14): 2185-91.
Weintraub M, Rubio A, Golik A, Byrne L, Scheinbaum ML. Sibutramine in weight control: a dose-ranging, efficacy study. Clin Pharmacol Ther 1991 Sep;50(3): 330-7.
Van Gaal LF, Wauters MA, Peiffer FW, De Leeuw IH. Sibutramine and fat distribution: is there a role for pharmacotherapy in abdominal/visceral fat reduction? Int J Obes Relat Metab Disord 1998 Aug; 22 Suppl 1:S38-40; discussion S41-2.
Hanotin C, Thomas F, Jones SP, Leutenegger E, Drouin P. A comparison of sibutramine and dexfenfluramine in the treatment of obesity. Obes Res 1998 Jul;6(4): 285-91.
Fanghanel G, Cortinas L, Sanchez-Reyes L, Berber A. A clinical trial of the use of sibutramine for the treatment of patients suffering essential obesity. Int J Obes Relat Metab Disord 2000 Feb; 24(2): 144-50.
Bailey DG, Dresser GK. Interactions between grapefruit juice and cardiovascular drugs. Am J Cardiovasc Drugs. 2004;4(5):281-97
Xu J, Chen JD. Peripheral mechanisms of sibutramine involving proximal gastric motility in dogs. Obesity (Silver Spring). 2006 Aug;14(8):1363-70.
Connoley IP, Liu YL, Frost I, Reckless IP, Heal DJ, Stock MJ. Thermogenic effects of sibutramine and its metabolites. Br J Pharmacol 1999 Mar,126(6): 1487-95.
Derosa G, Cicero AF, Murdolo G, Ciccarelli L, Fogari R. Comparison of metabolic effects of orlistat and sibutramine treatment in Type 2 diabetic obese patients. Diabetes Nutr Metab. 2004 Aug;17(4):222-9.
Gokcel A, Karakose H, Ertorer EM, Tanaci N, Tutuncu NB, Guvener N. Effects of sibutramine in obese female subjects with type 2 diabetes and poor blood glucose control. Diabetes Care 2001 Nov; 24(11): 1957-60.
Hauner H, Meier M, Wendland G, Kurscheid T, Lauterbach K, Study Group SA; SAT Study. Weight reduction by sibutramine in obese subjects in primary care medicine: the SAT Study. Exp Clin Endocrinol Diabetes. 2004 Apr;112(4):201-7.
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Founder of the inCYST Institute for Hormone Health, Director of Marketing for Chow Locally. I have a passion for sustainable living initiatives that involve good food, beautiful art, and warm, genuine people. I am blessed that this blog has connected me with people from all around the world and made it feel a whole lot smaller!