Psychiatric Criteria for WLS Psych Evaluation

Feb 27, 2009

  MAYO CLINIC PROCEEDINGS

www.mayoclinicproceedings.com/content/81/10_Suppl/S11.full

Assessment and Preparation of Patients for Bariatric Surgery

  1. Maria L. Collazo-Clavell, MD,
  2. Matthew M. Clark, PhD,
  3. Donald E. McAlpine, MD and
  4. Michael D. Jensen, MD

+Author Affiliations

  1. From the Division of Endocrinology, Diabetes, Metabolism, and Nutrition (M.L.C.-C., M.D.J.) and Department of Psychiatry and Psychology (M.M.C., D.E.M.), Mayo Clinic College of Medicine, Rochester, Minn
  1. Address correspondence to Maria L. Collazo-Clavell, MD, Division of Endocrinology, Diabetes, Metabolism, and Nutrition, Mayo Clinic College of Medicine, 200 First St SW, Rochester, MN 55905 (e-mail: [email protected])
  Next Section

Abstract

The number of bariatric surgical procedures performed in the United States has increased steadily during the past decade. Currently accepted criteria for consideration of bariatric surgery include a body mass index (calculated as weight in kilograms divided by the square of height in meters) of 40 kg/m2 or greater (or >35 kg/m2 with obesity-related comorbidities), documented or high probability of failure of nonsurgical weight loss treatments, and assurance that the patient is well informed, motivated, and compliant. Appropriate patient selection is important in achieving optimal outcomes after bariatric surgery. In this article, we review our approach to the medical and psychological assessment of patients who want to undergo bariatric surgery. The medical evaluation is designed to identify and optimally treat medical comorbidities that may affect perioperative risks and long-term outcomes. The psychiatric and psychological assessment identifies factors that may influence long-term success in maintaining weight loss and prepares the patient for the lifestyle changes needed both before and after surgery.

BMI = body mass index; CAD = coronary artery disease; OSA = obstructive sleep apnea; RYGB = Roux-en-Y gastric bypass

The number of bariatric surgical procedures performed in the United States has increased steadily during the past decade.1,2 Several factors have contributed to this trend, including the continued increase in the prevalence of extreme (class III) obesity, the limited effectiveness of medical therapies in this patient population, and a growing body of literature supporting the positive effects of weight loss after bariatric surgery on weight-related comorbidities.3-5 As a result, patients, physicians, and third-party payers have become more receptive to this intervention.

The main incentive for considering bariatric surgery should be to improve health. This can be achieved only when the potential benefits of the surgery outweigh the risks for the individual patient. Bariatric surgery is neither completely safe nor unfailingly effective. Some patients will experience major complications or will have a poor weight-loss outcome. Discussion of both potential positive and negative outcomes is an important aspect of the assessment of patients considering bariatric surgery. Appropriate patient selection is important in achieving beneficial outcomes.6-8 The currently published criteria for consideration of bariatric surgery do not adequately address the intricacies of the assessment and preparation of these patients for surgery.9 All domains of functioning should be evaluated: physical health, activity level, nutritional intake, and psychiatric status. Health care professionals evaluating patients who want to undergo bariatric surgery should work closely with their colleagues, preferably in integrated, multidisciplinary treatment teams composed of nutritionists and medical, surgical, and psychiatric specialists. Expert consultants (cardiologists, pulmonologists, gastroenterologists) should be involved in the evaluation of the patient when clinically indicated.5

Previous SectionNext Section

RECOMMENDED CRITERIA FOR BARIATRIC SURGERY

In 1991, the National Institutes of Health Consensus Development Conference Panel9 outlined criteria for patients considering bariatric surgery (Table 1). A weight criterion was established using body mass index (BMI) (calculated as weight in kilograms divided by the square of height in meters). In addition, patients should have a documented or high probability of failure of nonsurgical weight-loss treatments and be well informed, motivated, and compliant.6-11 Various additional requirements are often imposed by third-party payers before authorizing coverage. Both the patient and the clinician should be well informed regarding the criteria that need to be fulfilled before planning bariatric surgery.

Previous SectionNext Section

MEDICAL ASSESSMENT OF THE PATIENT CONSIDERING BARIATRIC SURGERY

Ideally, the medical assessment of the patient considering bariatric surgery should be completed by a multidisciplinary team representing the fields of nutrition, psychiatry, medicine, and surgery.5 The assessment should have 3 main goals: (1) determine that the patient meets the recommended criteria for bariatric surgery, (2) identify issues that increase the patient's operative risk and intervene to reduce risk when possible, and (3) identify and modify, if possible, the factors that may reduce the probability of long-term successful weight loss and put the patient at risk for long-term complications.

View this table: TABLE 1.

Criteria for Consideration of Bariatric Surgery10

Creating a welcoming and patient-friendly environment is essential for obese patients. This includes handicap parking access, armless chairs in the patient waiting area, scales capable of weighing obese patients in a private setting, and examination offices that accommodate patients with special needs (eg, doors and furniture wide enough for patients, space for wheelchairs, low-height hydraulic tables, oversized gowns, and large blood pressure cuffs).

A comprehensive nutritional and weight history should be obtained, including weight trends (lowest, highest, actively gaining), current dietary habits, and current physical activity and/or exercise habits. Previous weight-loss efforts, especially those under medical supervision, should be reviewed. Factors such as the amount of weight loss achieved, the duration of weight-loss maintenance, those contributing to weight regain, and perceived obstacles to successful weight management (stress, time constraints, motivation, medical comorbidities, etc) should be documented.5,10 A detailed nutritional history may provide insight into the efficacy of specific bariatric procedures in achieving desired weight-loss outcomes. Several investigators have reported improved weight-loss outcomes with Roux-en-Y gastric bypass (RYGB) compared to gastroplasty in individuals with high intakes of sugar and sugar-containing foods.12,13 Education regarding expected dietary habits after surgery represents a key component of informed consent.

Identification of weight-related comorbidities and medical comorbidities that may increase surgical risk or potentially worsen after surgery (Table 2) is important. Although secondary causes of obesity are rare, they should be pursued when clinically suspected. Screening for hypothyroidism is recommended. Individuals at high risk for hypothyroidism include older women, those with a family history of thyroid disease, and patients with clinical findings suggestive of a

View this table: TABLE 2.

Factors That May Increase Surgical Risk or Worsen Postoperatively14,15

thyroid disorder.16 Cushing syndrome is a rare condition, and screening should be initiated if there is strong clinical suspicion of this disorder. Numerous medications promote weight gain, and alternative treatments should be considered. The social history should document current smoking, alcohol or substance abuse, and stability of the patient's social environment.7,8,17 A family history of obesity or weight-related comorbidities should be noted, although a strong family history in the absence of a personal history of weight-related comorbidities will not fulfill the medical criteria for surgery.

Previous SectionNext Section

PHYSICAL EXAMINATION AND ROUTINE LABORATORY TESTING

At physical examination, pulse rate, blood pressure, height, weight, and BMI should be recorded. Measurement of waist circumference provides additional information regarding health risk; a circumference greater than 102 cm in men and 88 cm in women is associated with higher risk of metabolic complications.10 However, measurement of waist circumference is a cumbersome and less useful tool in patients whose BMI values are greater than 40 kg/m2. Physical findings suggestive of weight-related metabolic or cardiopulmonary disorders should be noted, as well as signs of secondary causes of obesity such as Cushing syndrome.

Recommended laboratory tests are outlined in Table 3. These tests may reveal potential secondary causes of obesity, metabolic complications of obesity, and/or unrecognized nutritional deficiencies that may worsen after surgery. Additional testing should be guided by the clinical situation and the surgical procedure being contemplated.7,8,17 Preoperative laboratory testing is outlined in the article by McGlinch et al18 elsewhere in this supplement.

Previous SectionNext Section

PSYCHIATRIC AND PSYCHOLOGICAL ASSESSMENT OF THE PATIENT CONSIDERING BARIATRIC SURGERY

Currently, no evidenced-based models or consensus guidelines are available to identify patients whose psychological profile and motivation make them appropriate candidates for bariatric surgery.19,20 Many individuals considering weight-loss surgery have a psychiatric disorder or are experiencing psychological difficulties. Fifty percent or more of patients referred for bariatric surgery are reported to have a psychiatric Axis I disorder, an Axis II personality disorder, or doubtful motivation for surgery.21-26 Approximately half are taking psychotropic medications when they present for evaluation.27 Common diagnoses include somatization, social phobia, obsessive-compulsive disorder, substance abuse/dependence, binge-eating disorder, night eating syndrome, posttraumatic stress disorder, generalized anxiety disorder, and depression.28 In the United States, 15% to 30% of patients with psychosocial difficulties are referred for additional treatment, and 0% to 10% are not recommended for surgery.19,27,29,30

Although consensus for a standardized protocol for the psychiatric and psychological evaluation of bariatric surgical candidates is lacking, many centers use a structured interview. Examples include the Boston interview for gastric bypass,31 the structured clinical interview with the Weight and Lifestyle Inventory from the University of Pennsylvania,32 and guidelines from Montefiore Medical Center/Albert Einstein College of Medicine.33 Because many bariatric centers use a number of mental health professionals to conduct their assessments, a structured clinical interview allows the treatment team to identify key psychosocial areas that may need further evaluation. Psychological testing is often part of this assessment, and many clinicians use the Beck Depression Inventory or the Minnesota Multiphasic Personality Inventory.30 Key areas to identify include current depressive symptoms, personality disorders, trauma history, substance abuse, or purging.

In general, the influence of psychological factors on long-term outcome in bariatric surgical patients is not well understood.31 A 2005 review of the published literature examining the psychological evaluation of bariatric candidates confirmed that the presence of binge-eating disorder, a personality disorder, or an untreated Axis I disorder, particularly a depressive disorder, warrants additional attention.34 These factors were found to be highly prevalent in presurgical patients and have been proposed to contribute to poor long-term outcome. In a review of 29 studies that assessed possible psychosocial predictors of weight loss, serious psychiatric disorders that required inpatient hospitalization and personality disorders were found to predict suboptimal weight loss after surgery.22 Further research is needed to provide a better understanding of how an untreated psychiatric condition such as major depression can impact weight loss and other outcomes of bariatric surgery.

Some bariatric surgical candidates are denied surgery on the basis of their psychiatric status, and others have surgery postponed until their psychological difficulties have improved.33 A survey of 81 bariatric surgery programs found that the most commonly ranked potential psychosocial contraindications for surgery were current illicit drug abuse, active uncontrolled symptoms of schizophrenia, severe mental retardation (IQ <50), heavy alcohol use, and lack of knowledge about surgery.30 Although empirical evidence does not demonstrate how problematic psychosocial issues will influence outcome, in our clinical practice, bariatric surgery is postponed until the following criteria are

View this table: TABLE 3.

Recommended Laboratory Evaluation of Candidates for Bariatric Surgery

fulfilled: no psychiatric hospitalization for 12 months, professional treatment and demonstrated 12 months of abstinence for patients with substance abuse, and treatment by a licensed mental health professional for patients with ongoing psychological issues (personality disorders, trauma survivorship difficulties, low-grade depression). In addition, the mental health professional should support the patient's desire to have surgery and agree to provide postoperative follow-up care.

Another area that should be assessed is the perception of positive aspects of being overweight. Being overweight prevents some individuals from addressing painful issues. In our clinical experience, surgery and major weight loss can produce sudden onset of symptoms of posttraumatic stress disorder in some survivors of sexual abuse or trauma. Even after these patients have successfully managed horrific memories for many years, substantial weight loss seems to trigger frequent flashbacks, daily intrusive memories, and nightmares. A history of childhood trauma is distressingly common in those considering bariatric surgery. In a sample of 340 consecutive patients studied by Grilo et al,35 32% reported being sexually abused. These same investigators also examined the effect of childhood sexual abuse on 1-year outcome. Although no difference in weight loss was noted at 1-year follow-up, the sexual abuse survivors had higher levels of depression on the Beck Depression Inventory compared with those who had not been abused.36 We believe that a history of trauma is insufficient for excluding an individual from bariatric surgery. However, patients with a history of trauma, those who have experienced psychiatric difficulties when they lost weight in the past, and individuals who perceive being overweight as protective warrant special attention. After preoperative assessment, these patients should initiate mental health care to address these issues. Although a history of sexual abuse has reportedly been related to poor weight-loss outcome after a low-energy diet program,37 weight-loss outcomes after bariatric surgery have not differed significantly between sexual abuse survivors and those with no history of abuse.38,39

A history of psychological difficulties or the presence of a psychiatric disorder that is well managed is not a contraindication to bariatric surgery. Clark et al40 reported that a history of treatment for mental illness or substance abuse was predictive of acceptable weight-loss outcomes at 2-year follow-up in patients who had undergone bariatric surgery.

Previous SectionNext Section

ASSESSING PREOPERATIVE RISK

Mortality rates after bariatric surgery have been commonly reported at less than 1%.41 Recently, higher mortality rates were reported among Medicare recipients.42 The highest mortality rates were seen in older patients (due to age and comorbidities) and patients whose operations were performed by less experienced surgeons. The article by McGlinch et al18 elsewhere in this supplement reviews perioperative risks and management in detail. Thus, this article briefly discusses preoperative risk assessment.

When appropriately evaluated, patients with known coronary artery disease (CAD) can safely undergo bariatric procedures without increased morbidity or mortality.43 The risks of perioperative complications are increased in men, in patients older than 45 years, and in those with high blood pressure, diabetes mellitus, BMI greater than 50 kg/m2, obstructive sleep apnea (OSA), asthma, and risk factors for pulmonary embolus and cirrhosis.14,44,45 Portenier et al46 have proposed a simple scoring system that uses 5 patient characteristics—age, hypertension, BMI, sex, and pulmonary embolus risk—to predict perioperative mortality risk. The Obesity Surgery Mortality Risk Score was developed after the authors retrospectively reviewed more than 2000 medical records of patients who had undergone bariatric surgery at Virginia Commonwealth University between 1995 and 2004. Scores define a patient's 90-day mortality risk as low (<1%), medium (<2%), or high (>5%). Although this scoring system has not been validated in prospective studies, it promises to be a useful tool for the assessment of patients contemplating bariatric surgery. Thus, preoperative and perioperative assessment and care should focus on modifiable risk factors that may increase mortality risk (eg, optimizing glycemic control, asthma management).47,48

Although the impact of unrecognized or inadequately treated OSA on perioperative risk remains controversial,49,50 we routinely screen our patients for OSA. Overnight oximetry can be a useful screening tool but is not highly sensitive. Proceeding directly to overnight polysomnography is appropriate when clinical suspicion for this disorder is high.47 Patients in whom clinically important OSA is identified are advised to initiate recommended therapy with continuous or bilevel positive airway pressure before surgery, and therapy is continued throughout the perioperative period.

Symptomatic gallbladder disease can occur after substantial weight loss, particularly in patients with preexisting gallbladder abnormalities. As a result, imaging of the gallbladder is frequently performed in preparing for surgery. Prophylactic cholecystectomy may be recommended during open procedures for RYGB and biliopancreatic diversion. However, this practice has not been vigorously studied.15,51 Alternatively, therapy with ursodiol has been shown to decrease the incidence of symptomatic gallbladder disease.11,52

The most common cause of abnormal liver function in bariatric surgical candidates is nonalcoholic fatty liver disease, which can progress to cirrhosis. When liver function studies show elevated levels, imaging of the liver with either ultrasonography or computed tomography is recommended.53 Liver biopsy remains the gold standard for determining the extent of disease. Steatosis frequently improves with weight loss, but the presence of inflammation and fibrosis suggests more advanced disease with less predictable outcomes.54 Although several investigators have noted favorable changes in liver histology after bariatric surgery,55-57 a careful examination of these and other reports44 reveals incomplete histologic data to allow definitive conclusions. Determining the extent of liver disease is recommended to assess perioperative risks and postoperative outcomes. In many centers, cirrhotic liver disease with portal hypertension is considered a contraindication to bariatric surgery due to the risk of deterioration in liver function.

Preexisting gastrointestinal symptoms are often evaluated to identify undiagnosed pathology that may affect surgical outcome. Preoperative screening for Helicobacter pylori in patients with dyspepsia who are considering bariatric surgery has been proposed but not universally practiced.58 When identified, H pylori is treated empirically with currently accepted medical regimens.

The literature is sparse regarding the impact of bariatric surgery on many common medical conditions and the effect of these conditions on surgical outcomes. Information regarding the effect of bariatric surgery on inflammatory bowel disease, renal stone disease, and autoimmune disorders is restricted to case reports. Although these conditions do not represent absolute contraindications to bariatric surgery, appropriate treatment and monitoring are essential.

Previous SectionNext Section

MEDICAL CONTRAINDICATIONS TO BARIATRIC SURGERY

Few preexisting medical conditions represent absolute contraindications to bariatric surgery. Notable exceptions in our practice include the presence of mental/cognitive impairment that limits the individual's ability to understand the proposed therapy and advanced liver disease with portal hypertension. Occasionally, we do not recommend surgery because of unacceptable operative risks due to multiple preexisting medical comorbidities such as unstable CAD, uncontrolled severe OSA, or an uncontrolled psychiatric disorder. However, in most situations, preoperative management of medical comorbidities will reduce operative risks to acceptable levels. Age is not an absolute contraindication to bariatric surgery,10 although the combination of older age and preexisting medical conditions may be associated with unacceptable risks. The presence or history of cancer is considered a contraindication when the prognosis for 5-year survival is poor.

Previous SectionNext Section

PATIENT PREPARATION: MAXIMIZING SUCCESS

A successful weight-loss outcome after bariatric surgery has been defined as a loss of at least 50% of excess weight.9 Variations in how weight-loss outcomes are reported make comparisons of studies difficult. Reported rates of weight loss associated with currently offered bariatric procedures are discussed in the article by Kendrick and Dakin59 elsewhere in this supplement. However, success should not be measured solely in pounds lost but also in health benefits. Reviewing with the patient anticipated weight-loss outcomes, potential health benefits, and surgical risks associated with the planned procedure is important to avoid unrealistic expectations.

Failure to maintain weight loss at 10 years after bariatric surgery has been reported in 10% to 25% of patients who undergo this intervention.4,11 Factors contributing to weight regain are complex, vary with the surgical procedure performed, and are not fully understood. Evidence consistent with our clinical experience suggests that nonadherence to dietary and activity recommendations contributes to poor long-term outcome.60

To assess motivation and predict adherence to postsurgical recommendations, some programs mandate that the patient achieve some weight loss before surgery. Two published studies have examined presurgical weight loss and its association with short-term outcome (1 year). One study reported no effect,61 whereas the other reported that presurgical weight loss was related to greater postoperative weight loss.62 Several multidisciplinary programs have focused on a more comprehensive approach, namely, the benefits of behavioral therapy in medically supervised weight-loss programs designed to improve weight-loss outcomes.63-66 To our knowledge, no published randomized controlled trial has examined the potential benefits of receiving behavioral therapy before bariatric surgery in regard to weight-loss outcomes. Nonetheless, on the basis of our clinical experience, we recommend and often require that patients receive behavioral therapy for lifestyle changes (eating, exercise, social support, and stress management) from a licensed mental health professional before surgery. The goal of behavioral therapy is to provide guidance and support as individuals pursue lifestyle changes before and after bariatric surgery. Their efforts at behavioral change will aid in fulfilling our preoperative requirements of no weight gain and adherence to lifestyle changes in diet and physical activity.

Little data are available in the medical literature regarding the physical activity requirements imposed by various bariatric programs, the physical activity habits of those considering bariatric surgery, and how to help obese, sedentary individuals increase their activity level. In preparation for surgery, we encourage our patients to initiate physical activities that they are able to perform comfortably with their physical limitations. The American College of Cardiology and American Heart Association practice guidelines recommend screening for CAD in individuals with multiple risk factors before initiation of an exercise program.67 The challenge often lies in which functional cardiac assessment study to pursue in view of the weight limitations imposed by the available technologies and the patient's limitations for exercise. Ultimately, the study performed will depend on which one is deemed most appropriate at each institution.

Some individuals may be able to perform only 5 to 10 minutes of aerobic activity daily. For those with serious joint limitations, water exercises are recommended; unfortunately, facilities at which such exercises can be performed are not always available to our patients. We often refer patients to physical therapists or sports medicine specialists for advice on safe activity programs. The expectation is that after surgery individuals will be able to gradually increase both the duration and the intensity of their activity program. Individuals who have undergone bariatric surgery tend to be more active than medically treated controls.4

Noncompliance to preoperative recommendations often identifies an unmotivated patient who may be a poor surgical candidate because of potential nonadherence to recommended long-term follow-up, vitamin and mineral supplementation, and lifestyle changes required for successful weight maintenance. In these patients, surgery is often postponed or not performed.

Psychotropic medications can seriously affect weight. One third of bariatric surgical candidates are taking psychotropic medications preoperatively,29 typically antidepressants. In addition, the presurgery assessment may identify mood or anxiety disorders that require initiation of psychotropic agents. Selection or modification of psychotropic regimens that favor weight loss is a useful intervention whether or not bariatric surgery is pursued.

Antidepressants considered most likely to promote weight gain include amitriptyline, mirtazapine, and imipramine. Those least likely to promote weight gain include bupropion and nefazodone. The selective serotonin reuptake inhibitors (fluoxetine, sertraline, citalopram, fluvoxamine, escitalopram, paroxetine) cause a modest initial weight loss typically followed by weight regain and in some patients a small net gain. Antidepressants with relatively neutral effects on weight include duloxetine, venlafaxine, nortriptyline, desipramine, tranylcypromine, and phenelzine.68-72

Presurgical assessment also provides an opportunity to consider the possible ramifications of surgery on psychotropic vehicle and dosage. Despite bariatric surgery's increasing popularity, no data exist to guide psychotropic dosing in patients with altered gastrointestinal environments or in those who experience massive postoperative weight loss. One novel in vitro study examined the dissolution of 22 psychotropic agents in a simulated gastrointestinal environment of control and post-RYGB states.73 Twelve agents dissolved differently in the postoperative environment than in the control state; 10 dissolved much less than expected. The effect of bariatric surgery on in vivo absorption of commonly used psychotropics has not been studied. Synthesis of the available information yields the following clinical considerations.

  • Consider using immediate-release psychotropics.

    • Time-release medications are designed to dissolve gradually within the full intestinal tract and thus may be expected to have different pharmacokinetics after RYGB.

  • Consider monitoring of psychotropic serum levels before and after surgery.

    • Some psychotropics, such as tricyclic antidepressants, have a narrow therapeutic index. A preoperative blood level obtained while the patient feels well emotionally may provide a target goal for the patient who has a postoperative relapse.

  • Anticipate effects of postoperative weight loss on dosage.

    • Many physiologic factors influence drug absorption, such as gastric emptying time and the integrity and surface area of the epithelium. The gut has an impressive ability to compensate for loss of function, and absorption after surgery may eventually normalize. However, marked weight loss may then complicate the clinical picture.

  • Obese persons have an increased proportion of adipose tissue, as well as increased total body water, lean body mass, and visceral organ mass and higher glomerular filtration rate.

    • Awareness of the volume of distribution and the importance of renal clearance is necessary.74 Increased monitoring of lithium levels is warranted during the postoperative period.

Previous SectionNext Section

SUMMARY

The number of individuals seeking bariatric surgery for the treatment of extreme obesity is increasing. The medical evaluation has several goals: assuring that the patient meets currently accepted criteria for consideration of bariatric surgery, identifying and optimally treating medical conditions that may affect perioperative risks, and educating and preparing patients in the hope of maximizing long-term successful weight loss and improving health. Clearly outlining characteristics of the “ideal” patient for bariatric surgery is challenging because of active investigation and evolution of the procedures being offered, their associated risks, and long-term outcomes. Most of the information in the current literature is based on retrospective studies and expert opinion. Future investigations should be designed to clarify the important aspects of the bariatric surgical evaluation to achieve optimal outcomes.

Previous SectionNext Section

Footnotes

Previous Section  

REFERENCES

    1. Steinbrook R
    . Surgery for severe obesity. N Engl J Med. 2004;350:1075-1079. FREE Full Text
    1. Santry HP,
    2. Gillen DL,
    3. Lauderdale DS
    . Trends in bariatric surgical procedures. JAMA. 2005;294:1909-1917. Abstract/FREE Full Text
    1. Manson JE,
    2. Skerrett PJ,
    3. Greenland P,
    4. VanItallie TB
    . The escalating pandemics of obesity and sedentary lifestyle: a call to action for clinicians. Arch Intern Med. 2004;164:249-258. Abstract/FREE Full Text
    1. Sjorstrom L,
    2. Lindroos AK,
    3. Peltonen M,
    4. et al.,
    5. Swedish Obese Subjects Study Scientific Group
    . Lifestyle, diabetes, and cardiovascular risk factors 10 years after bariatric surgery. N Engl J Med. 2004;351:2683-2693. Abstract/FREE Full Text
    1. Buchwald H,
    2. Consensus Conference Panel
    . Bariatric surgery for morbid obesity: health implications for patients, health professionals, and third-party payers. J Am Coll Surg. 2005;200:593-604. CrossRefMedline
    1. Cowan GS, Jr,
    2. Hiler ML,
    3. Buffington C
    . Criteria for selection of patients for bariatric surgery. Eur J Gastroenterol Hepatol. 1999;11:69-75. Medline
    1. Collazo-Clavell ML
    . Safe and effective management of the obese patient. Mayo Clin Proc. 1999;74:1255-1259. Abstract
    1. Kim JJ,
    2. Tarnoff ME,
    3. Shikora SA
    . Surgical treatment for extreme obesity: evolution of a rapidly growing field. Nutr Clin Pract. 2003;18:109-123. FREE Full Text
    1. Consensus Development Conference Panel
    . NIH conference: gastrointestinal surgery for severe obesity. Ann Intern Med. 1991;115:956-961. Medline
    1. National Institutes of Health
    . Clinical guidelines on the identification, evaluation, and treatment of overweight and obesity in adults: the evidence report [published correction appears in Obes Res. 1998;6:464]. Obes Res. 1998;6(suppl):51S-209S. Medline
    1. Balsiger BM,
    2. Luque de Leon E,
    3. Sarr MG
    . Surgical treatment of obesity: who is an appropriate candidate? Mayo Clin Proc. 1997;72:551-557. Abstract
    1. Sugerman HJ,
    2. Starkey JV,
    3. Birkenhauer R
    . A randomized prospective trial of gastric bypass versus vertical banded gastroplasty for morbid obesity and their effects on sweets versus non-sweets eaters. Ann Surg. 1987;205:613-624. Medline
    1. Burge JC,
    2. Schaumberg JZ,
    3. Choban 0 comments

Plastic Surgeons blog about psychiatric issues post WLS

Feb 27, 2009

0 comments

Psychiatric Disorders in Gastric Bypass Candidates

Feb 27, 2009

Psychiatry News March 16, 2007
Volume 42, Number 6, page 20
© 2007 American Psychiatric Association
   
 

Clinical & Research News

Psychiatric Disorders Prevalent in Gastric Bypass Candidates

Joan Arehart-Treichel

There is reason to think, from a study of obese individuals seeking gastric bypass surgery, that substance abuse and overeating may activate a common reward circuitry in the brain.

As Americans grow heavier, their demand for gastric bypass surgery is growing as well (Psychiatric News, September 16, 2005). And the increasing demand for such surgery is attracting interest in the psychiatric realm.

Last year, for example, Duke University psychiatrists and internists reported on the case of a man who became acutely psychotic a few weeks after undergoing gastric bypass surgery. The psychosis was presumably due to rapid weight loss because he recovered completely without the need for antipsychotic medications. Psychotic manifestations after gastric bypass surgery have been reported by some other medical-specialty groups as well.


Figure 1
Now the prevalence of psychiatric disorders among obese individuals who seek gastric bypass surgery has been studied by researchers at the University of Pittsburgh's Western Psychiatric Institute and Clinic. The investigators reported their results in the February American Journal of Psychiatry. Psychiatric illnesses—especially anxiety disorders—appear to be widespread among such gastric surgery candidates.

Melissa Kalarchian, Ph.D., an assistant professor of psychiatry and psychology at the Western Psychiatric Institute and Clinic, and her colleagues evaluated 288 obese individuals seeking gastric bypass surgery for both lifetime and current DSM-IV psychiatric diagnoses. Two-thirds of the subjects had had at least one Axis I psychiatric disorder during their lifetimes, and their lifetime prevalence of Axis I disorders tended to be higher than among the general American population (see chart).

Moreover, at the time of preoperative evaluation, more than a third of the subjects were found to have an Axis I psychiatric disorder; most were anxiety disorders. In fact, subjects were more likely to have an anxiety disorder than a mood, substance abuse, or eating disorder. Also at this point, more than a fourth of subjects were found to have an Axis II psychiatric disorder. Most common were cluster C personality disorders characterized by avoidant or obsessive-compulsive behavior.

Further analyses revealed that subjects who had had Axis I disorders at some point in their lives had significantly greater body mass indexes than those who did not have such a history, and that subjects currently with Axis I disorders had significantly greater body mass indexes than those currently without such a disorder.

Kalarchian and her team wrote in their study report that, collectively, these results are "compelling evidence that psychiatric disorders are a major concern for this patient population, not only because they are relatively common, but also because they are associated with severity of obesity...even within a group of extremely overweight individuals."

Why psychiatric illnesses are so common among gastric bypass candidates is not clear, the researchers noted. Nonetheless, they offered several possible explanations. "Psychiatric disorders like major depressive disorder and binge-eating disorder may contribute to the development of severe obesity....However, psychiatric disorders may also be a consequence of severe obesity in a culture that stigmatizes...obesity."

Finally, Kalarchian and her coworkers believe that their results shed some light on the biology of obesity. Specifically, one-third of subjects had a history of substance abuse or dependence, yet only 2 percent had such problems at the time of evaluation.

Thus, "it is intriguing to speculate," they wrote, "that substance and weight problems may...have a shared diathesis, and that substance abuse remits when eating behavior predominates. Drugs and food may activate common reward circuitry in the brain."

The study was funded by the University of Pittsburgh Obesity and Nutrition Research Center and the National Institute of Diabetes, Digestive, and Kidney Diseases.


0 comments

Thyroid issues and mood/behavioral issues

Jan 19, 2009

www.psychiatryweekly.com/aspx/article/ArticleDetail.aspx


The Mood Spectrum and Hypothalamic-Pituitary-Thyroid Axis

Dr. Pfennig is postdoctoral research fellow in the Department of Psychiatry and Psychotherapy at the Charité University Medicine Berlin, Campus Mitte (CCM), in Germany.

Dr. Frye is associate professor of psychiatry in residence, director of the Bipolar Research Program, and associate director of the Mood Disorders Research Program at the David Geffen School of Medicine at the University of California in Los Angeles.

Dr. Köberle is resident in psychiatry in the Department of Psychiatry and Psychotherapy at the Charité University Medicine Berlin, CCM.

Dr. Bauer is professor of psychiatry and head of the Department of Psychiatry and Psychotherapy at the Charité University Medicine Berlin, CCM.

Disclosure: Dr. Frye is a consultant to Abbott, AstraZeneca, Bristol-Myers Squibb, Cephalon, Elan, Eli Lilly, GlaxoSmithKline, Janssen, Johnson & Johnson, Novartis, Ortho-McNeil, Otsuka, Pfizer, and UCB Pharma; is on the speaker’s bureaus of Abbott, AstraZeneca, Bristol-Myers Squibb, Eli Lilly, GlaxoSmithKline, Janssen, Novartis, Ortho-McNeil, and Otsuka; and receives grant support from Abbott, the American Foundation for Suicide Prevention, GlaxoSmithKline, the National Institute of Mental Health, Pfizer, Solvay, and the Stanley Medical Research Institute. Dr. Bauer is on the speaker’s bureaus of AstraZeneca, Eli Lilly, and GlaxoSmithKline; receives grant and/or research support from Deutsche Forschnupgemeinschaft, the Stanley Medical Research Institute, and the Thyroid Research Advisory Council; and is on the advisory board of AstraZeneca, Eli Lilly, GlaxoSmithKline, Novartis, and Wyeth.

Please direct all correspondence to: Mark A. Frye, MD, Psychiatry and Biobehavioral Sciences, Ste 1544, David Geffen School of Medicine, 300 Medical Plaza, Mail Code: 696824, Los Angeles, CA 90095-1361; Tel: 310-794-6587; Fax: 310-794-9915; E-mail: [email protected].

Focus Points

Hyperthyroidism and hypothyroidism are associated with changes in mood and cognitive function.

Thyroid dysfunction is more prevalent in patients with mood disorders than in the general population.

Hypothyroidism is the most frequent disorder of thyroid dysfunction accompanied by depression-like symptoms; subclinical hypothyroidism is prevalent in approximately 15% of depressed patients.

Although most bipolar patients are euthyroid, thyroid measures in the low-normal range or below-normal range seem to be relevant for the pathophysiology of bipolar disorders and may result in a less than optimal outcome.

Thyroid measures in the low-normal or below-normal range seem to be correlated with time to recurrence of affective episodes.

Thyroid hormones are used in the treatment of both depression and bipolar disorders in acceleration and augmentation strategies.

Abstract

Of the endocrine axes linked to the pathophysiology of bipolar disorder, the hypothalamic-pituitary-thyroid (HPT) axis has been extensively studied. Hyperthyroidism and hypothyroidism are associated with changes in mood and cognitive function. Abnormal thyroid indices, for example, are more prevalent in patients with mood disorders than in the general population. Most depressed patients are euthyroid, though subclinical hypothyroidism can be seen in approximately 15% of depressed patients. Furthermore, serum triiodothyronine (T3) levels are inversely correlated with time to recurrence of depressive episodes. Although most manic patients are euthyroid, thyroid measures in the low-normal range or below-normal range appear to be relevant in the pathophysiology of bipolar disorders and may result in suboptimal mood stabilization. Low thyroid function or frank clinical hypothyroidism has been associated with rapid-cycling bipolar disorder. In contrast to the T3/unipolar relapse, illness morbidity in bipolar disorder has more often been correlated with thyroxine (T4) indices. These observations have contributed to the clinical use of thyroid hormones both in acceleration and augmentation strategies. T3 has been mainly utilized in acute depression, while T4 has been used in lithium-maintained bipolar patients or in supraphysiological dosages in acute and maintenance treatment of bipolar depression, rapid cycling, and refractory depressive disorder.

Introduction

Thyroid dysfunction is more prevalent in patients with mood disorders than in the general population. The activity of the thyroid gland is essential for normal brain development and cognitive functioning. In patients with thyroid disease, cognitive, behavioral, and neurovegetative disturbances can all be observed.

The close relationship of thyroid economy and cognitive function has interested clinicians and researchers since the possible association between thyroid functioning and behavior was first described by Parry1 and Graves.2 They related “various nervous affectations” and symptoms of hysteria, restlessness, hyperactivity, and impaired concentration to the diagnosis of hyperthyroidism or thyrotoxicosis.1,2 In 1888, a report of the Clinical Society of London also noted a variety of mental disturbances associated with hypothyroidism.3

The most common psychiatric symptoms related to hypothyroidism are depression and cognitive dysfunction. In severe forms of hypothyroidism (ie, myxedema), psychotic and delusional symptoms may occur, and the syndrome may mimic melancholic depression and dementia.4 In a 1949 case series, Asher5 demonstrated the causative role of hypothyroidism in the psychopathology of these symptoms. Asher’s findings show that thyroid hormone deficiency may lead to depression and psychosis and may be reversed by desiccated thyroid administration.5

As synthetic thyroid hormones became available later in the century, studies of their use alone or preferably in combination with traditional treatment of mood disorders followed. Prange and colleagues,6 for example, found the accelerating effect of thyroid hormone in response to tricyclic antidepressants (TCAs).

More recently, researchers studying the hypothalamic-pituitary-thyroid (HPT) system have suggested that thyroid hormones play an important role in the pathophysiology of mood disorders.7,8 Thyroid hormones may interact with neurotransmitter systems and intracellular mechanisms and are capable of modulating the phenotypic expression of major affective illnesses.7,8 Depressive and bipolar disorders in particular often constitute a mood spectrum; HPT system abnormalities discussed in the following sections therefore pertain to this broad spectrum.

The Hierarchy of the HPT Axis

The thyroid gland produces two hormones, the prohormone thyroxine (T4) and the biologically active triiodothyronine (T3). The predominant T4 is converted to the biologically active T3 by special deiodinases (ie, type-I to type-III deiodinases). The rate of synthesis of the thyroid hormones is regulated by the pituitary thyrotropin-stimulating hormone (TSH), which is stimulated by hypothalamic thyrotropin-releasing hormone (TRH). Thyroid hormones are necessary for the regulation of various metabolic functions and homeostasis. They exert a negative feedback on thyroid hormone release at hypothalamic and pituitary levels (Figure 1).9

Thyroid hormones enter the central nervous system (CNS) mainly in the form of T4,10 which is catalyzed to T3 by specific deiodinases. In the adult brain, the process of deiodination is different from that in peripheral tissue and is associated with a region-specific expression of type-II and type-III isoenzymes in the brain and amygdala.11,12 After the coupling of T3 to nuclear receptors, the transcriptionally active complex binds to thyroid-hormone responsive elements and thus alters gene expression and, accordingly, synthesis of messenger ribonucleic acid and proteins (Figure 2).13 Thyroid hormones affect neuronal processing and integration, glial cell proliferation, myelination, and synthesis of key enzymes required for neurotransmitter synthesis.14,15

Effects of a Disturbed Thyroid System on the Premature and Mature Brain

In the perinatal period, thyroid deficiency results in irreversible brain damage and mental retardation. This syndrome is referred to as cretinism.14 Similar consequences, such as variable degrees of irreversible brain damage, can be associated with clinical hypothyroidism in early childhood, but are generally less severe than cases detected by neonatal screening tests. The neurologic symptoms do not seem to be progressive but are irreversible, despite T4 treatment.16 Delayed growth following childhood hypothyroidism is restored rapidly with treatment.17

The symptoms of thyroid hormone abnormalities in adults primarily manifest as alterations in metabolism. In addition, they also change the synthesis and degradation rates of a variety of other growth factors and hormones.9,18 Nuclear thyroid hormone receptors are widely distributed in the mature brain.19,20

Thyroid Illness and Clinical Symptoms

Thyrotoxicosis is the clinical syndrome of hypermetabolism resulting from increased serum concentrations of T4, T3, or both. Subsequently, the secretion of TSH is suppressed, resulting in decreased serum TSH concentrations. Thus, the term hyperthyroidism refers to an increase in thyroid hormone biosynthesis and secretion by the thyroid gland.8,21 Hyperthyroidism or thyrotoxicosis is accompanied by symptoms including dysphoria, anxiety, restlessness, emotional lability, and impaired concentration. In elderly patients, depressive symptoms, such as apathy, lethargy, pseudodementia, and depressed mood, can also occur.22,23 Approximately 60% of thyrotoxic patients suffer from anxiety disorder and 31% to 69% suffer from depressive disorders.24,25 However, overt psychiatric illness only occurs in approximately 10% of thyrotoxic patients.26,27 Patients developing mania while in a thyrotoxic state typically have a diagnosis of an underlying mood disorder or a positive family history.28-30

Hypothyroidism is the most frequent disorder of thyroid dysfunction.31 In hypothyroid patients, depression-like symptoms frequently occur; they include psychomotor retardation, decreased appetite, fatigue, and lethargy.31 Neurocognitive dysfunction and depression, as well as impaired perception with paranoia and visual hallucinations, may develop.32,33 Severe hypothyroidism mimics melancholic depression and dementia. The neurocognitive deficits reverse rapidly on return to a euthyroid state (Figure 3).34

Thyroid Indices in Mood Disorders

Thyroid function abnormalities are classified following the system devised by Wenzel and colleagues.35 Grade I hypothyroidism is defined as decreased serum T4 level, grade II as an increased serum basal TSH with normal serum T4 level, and grade III as the presence of an isolated exaggeration of the TSH response to TRH stimulation, with normal basal TSH levels.35

Most depressed patients are euthyroid, although subclinical hypothyroidism can be seen in approximately 15% of depressed patients.36,37 Gold and colleagues36 reported grade-II or grade-III hypothyroidism in 8% of depressed patients admitted to a psychiatric hospital. Subclinical hypothyroidism may be a risk factor for depression in women.38

The time to recurrence of depressive episodes was found to be inversely correlated with serum T3 but not T4 levels in patients with unipolar depression.39 Studying the HPT axis, investigators have found abnormal TSH response to TRH stimulation in depressed patients.38,40-42 The peak response was blunted in 25% to 30% of patients43 and exaggerated in 10%.44 Elevated levels of cerebrospinal fluid (CSF) TSH have also been reported in depressed patients.45

Although most bipolar patients are euthyroid, thyroid measures in the low-normal or below-normal range seem to be relevant for the pathophysiology of bipolar disorders and may result in a less than optimal outcome. Frye and colleagues46 reported an association of low levels of T4, within the normal range, with greater mood instability and depression severity during prophylactic lithium treatment in bipolar patients. Cole and colleagues47 found poorer treatment response in bipolar patients with lower free T4 index values and higher TSH values within the normal range.

The idea that thyroid hormones act as modulators in affective illnesses is further strengthened by studies of the relationship between thyroid function and the clinical course of rapid-cycling bipolar disorder, which affects 10% to 15% of all bipolar patients. Treatment-resistant rapid cycling is much more common in women than men.48 Studies7,49-51 have found associations of low thyroid function or clinical hypothyroidism with rapid cycling. The incidence of grade-II hypothyroidism is 25% higher in rapid cyclers than in depressed patients in general (2% to 5%) or depressed patients taking lithium (9%).7,52

In a study by Gyulai and colleagues,53 bipolar patients received 4 weeks of treatment with lithium carbonate followed by stimulation with TRH. Rapid-cycling patients showed a higher increase of TSH after stimulation with TRH than healthy controls, although at baseline (without lithium treatment) no differences in response to the stimulation had been found.

It can be argued that latent hypofunction of the HPT system is present in rapid-cycling bipolar patients and manifests following antithyroid stress (eg, as induced by lithium treatment). This could explain the reversion of the rapid-cycling pattern and the reduction in number of episodes in refractory bipolar disorder following high dosage T4 treatment additive to established pharmacotherapy.54-56

Antithyroid antibodies are present in autoimmune thyroiditis, a major cause of hypothyroidism, and are useful to identify subclinical hypothyroid states. Anticolloid antibodies mainly react with thyroglobulin; anticytoplasmic antibodies react with components in the microsomal fraction of the thyrocytes (antimicrosomal antibodies) and are specific for the enzyme thyroid peroxidase.57,58 TSH receptor antibodies influence the function and growth of the gland.59

Studies are inconsistent as to whether thyroid antibodies are elevated in bipolar patients, with reported rates ranging from 0% to 43%, and as to whether lithium exposure is associated with the occurrence of thyroid antibodies.60-63 Kupka and colleagues64 found a higher prevalence of thyroid peroxidase antibodies in bipolar patients than in the general population or in nonbipolar psychiatric patients. A positive antibody status was associated with an increased risk for lithium-induced hypothyroidism but not with current or former lithium treatment.64

Approximately 30% to 40% of patients insufficiently respond to antidepressant treatment. This could be due in part to altered thyroid hormone availability in the CNS. Sullivan and colleagues65 reported lower CSF transthyretin (ie, thyroid hormone-binding globulin) levels in depressed patients than in healthy controls despite normal peripheral blood thyroid hormone measures. Reduced levels of central transthyretin—responsible for the uptake of T4 across the blood-brain barrier and its distribution throughout the brain—could attenuate trafficking of thyroid hormones within the blood-brain barrier despite functioning thyroid hormone feedback to the hypothalamus and anterior pituitary.65

Effects of Pharmacologic and Nonpharmacologic Treatment on the HPT System

Antidepressant treatment with TCAs, tetracyclic antidepressants, selective serotonin reuptake inhibitors (SSRIs), carbamazepine, and lithium is followed by a decrease in peripheral T4 serum concentrations which is correlated with clinical effectiveness.42,66,67 A decrease in T4 could also be observed following nonpharmacologic treatment, such as sleep deprivation, light therapy,68 electroconvulsive therapy, and psychotherapy.69 After establishing the antidepressant effect of rapid transcranial magnetic stimulation (rTMS) on prefrontal cortex regions, George and colleagues70 found an increase in TSH when applying rTMS over the prefrontal but not the occipital or cerebellar cortex.

A variety of brain imaging techniques offer the chance to evaluate the relationship between the brain, thyroid hormones, and behavior in healthy subjects and patients with mood disorders. Using positron emission tomography, Marangell and colleagues71 demonstrated that serum TSH was inversely related to both global and regional cerebral blood flow and glucose metabolism, with prefrontal areas showing maximal negative correlations in patients with bipolar and unipolar depression. Treating bipolar patients with supraphysiological dosages of T4, Bauer and colleagues34 found significant cerebral metabolic effects in frontal, limbic, and subcortical regions accompanying mood improvement.

Thyroid Hormone Mechanisms of Action

To date, the mechanisms of thyroid hormone effects on the brain are not fully known. Besides influencing brain metabolism, they seem to modulate gene expression and affect intracellular signaling pathways and neurotransmitter systems, including the noradrenergic, serotonergic,72 and g-aminobutyric acid (GABA) systems. Downstream of receptors, thyroid hormones appear to exert important influences on the activity and synthesis of G-proteins in the adult brain. Lack of this hormone leads to an impairment in adenylate cyclase and phosphoinositide-based signaling pathways.72

Treatment Strategies

The close association between the HPT system and mood disorders has led to different approaches for the therapeutic use of thyroid hormones (ie, T3 and levothyroxine [L-T4]) in affective disorders.

T3 is mainly applied in the treatment of acute depression. One strategy is acceleration, which is speeding up the response to antidepressants. A recent meta-analysis,73 which included studies where T3 was initiated within 5 days after starting TCAs, found T3 to be significantly more effective than placebo in accelerating response to the antidepressant.73 Women especially benefited from a primary combination of an antidepressant with T3.74,75 The treatment was generally well-tolerated. Another approach is the augmentation strategy in refractory depression. In a meta-analysis, Aronson and colleagues76 evaluated the effect of T3 augmentation. They found that subjects were twice as likely to respond under T3 augmentation compared to placebo.76 No data are available so far for long-term T3 treatment of affective disorders.

L-T4 has been investigated in augmentation approaches for treatment-resistant depression. An open-label trial by Bauer and colleagues77 found promising results in unipolar and bipolar patients given L-T4 as add-on therapy to antidepressants or mood-stabilizers; side effects were surprisingly mild in this trial.77 In a recent case series78 observing unipolar and bipolar subjects with refractory depression, investigators again found a high remission rate.78 Successful treatment with supraphysiological doses of L-T4 has also been reported in several case reports of rapid-cycling bipolar disorder.79,80 An open-label study81 in prophylaxis-resistant non–rapid-cycling subjects did show significantly decreased relapse rates and fewer hospitalizations. Only mild side effects were reported.81

Whether the promising data of the use of T3 and T4 in acceleration and augmentation strategies extend to their use in combination with SSRIs is still to be studied since almost all data relate to the combination with TCAs.82-84

Thyroid hormone treatment alone in affective disorders has only rarely been studied. Wilson and colleagues85 compared T3 alone with imipramine alone in depressed patients in a double-blind study. At a dose of 50 µg/day, T3 alone was as effective as imipramine. However, the study had to be terminated because of signs of mild thyrotoxicity when T3 doses reached 62.5 µg/day.85 In patients with primary major depressive disorder without apparent thyroid dysfunction, 50–100 µg/day of T4 alone for 2 weeks showed only modest average effects, although some patients improved markedly.86

Treatment approaches using TRH showed promising antidepressant effects by intrathecal infusion87 and longer-term intravenous or subcutaneous injection.88 Prange and colleagues89 found that when TSH was administered intramuscularly in addition to TCAs the response rate was twice that of placebo; however, this approach has not been pursued by others and thus the findings have not been replicated.

Conclusion

Since the 19th century, observations of behavioral and mood changes in patients suffering from thyroid disorders have stimulated research to understand the relationship between thyroid function, behavior, and mood.

Both excess and inadequate thyroid hormones can induce disturbances of behavior that mimic depression, mania, and dementia. The neurocognitive impairments accompanying these dysfunctions are generally reversible following return to euthyroid status.

Thyroid hormones appear to be capable of modulating the phenotypic expression of major affective illness. Research aims to answer the question of whether changes in the functioning of the HPT system play a role in the pathophysiology of mood disorders. Furthermore, stress asserts inhibiting effects on the HPT axis. Pharmacologic, as well as nonpharmacologic, antidepressant treatment influences thyroid hormone levels in relation to treatment response. Beginning in the early 20th century, thyroid hormones were studied as a treatment option in depression and bipolar disorders. Data so far show good response rates in augmentation strategies in severely ill patients (ie, those with rapid-cycling bipolar disorder and refractory depression) with surprisingly mild side effects.

The mechanisms of thyroid hormone effects on the brain are still not fully known. Besides influencing brain metabolism, they seem to modulate gene expression and affect intracellular signalling pathways and neurotransmitter systems, including catecholamine, serotonin, and GABA systems.72

As clinicians gain more profound knowledge about the interactions of thyroid hormones, behavior, and mood, they advance their understanding of the pathophysiology and treatment options for bipolar disorder and depression. Additional research with rigorous scientific designs is still needed to confirm the efficacy, safety, and feasibility of thyroid hormone therapy in severely ill patients. PP

References

1. Parry CH. Collections From the Unpublished Writings of the Late C.H. Parry. Vol 2. London, UK: Underwoods; 1825.

2. Graves RJ. Newly observed affection of the thyroid gland in females. Lond Med Surg J. 1835;7:516-517.

3. Clinical Society of London. Report on myxedema. Trans Clin Soc Lond. 1888;(suppl):18-21.

4. Treadway CR, Prange AJ Jr, Doehne EF, Edens CJ, Whybrow PC. Myxedema psychosis: clinical and biochemical changes during recovery. J Psychiatr Res. 1967;5(4):289-296.

5. Asher R. Mysoedematous madness. Br Med J. 1949;22:555-562.

6. Prange AJ Jr, Wilson IC, Rabon AM, Lipton MA. Enhancement of imipramine antidepressant activity by thyroid hormone. Am J Psychiatry. 1969;126(4):457-469.

7. Bauer MS, Whybrow PC, Winokur A. Rapid cycling bipolar affective disorder. I. Association with grade I hypothyroidism. Arch Gen Psychiatry. 1990;47(5):427-432.

8. Bauer M, Whybrow PC. Thyroid hormone, neural tissue and mood modulation. World J Biol Psychiatry. 2001;2(2):59-69.

9. Larsen PR. The thyroid gland. In:  Williams RH, Foster DW, Kronenberg HM, Larsen PR, Wilson JD, eds. Williams Textbook of Endocrinology. 9th ed. Philadelphia, PA: Saunders; 1998:389-515.

10. Leonhard JL, Kohrle J. Intracellular pathways of iodothyronine metabolism. In: Braverman LE, Utiger RD, eds. Werner & Ingbar’s The Thyroid: A Fundamental and Clinical Text. 8th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2000:136-171.

11. St Germain DL, Galton VA. The deiodinase family of selenoproteins. Thyroid. 1997;7(4):655-668.

12. Kohrle J. Thyroid hormone metabolism and action in the brain and pituitary. Acta Med Austriaca. 2000;27(1):1-7.

13. Brent GA. The molecular basis of thyroid hormone action. N Engl J Med. 1994;331(13):847-853.

14. Porterfield SP, Hendrich CE. The role of thyroid hormones in prenatal and neonatal neurological development—current perspectives. Endocr Rev. 1993;14(1):94-106.

15. Bernal J, Nunez J. Thyroid hormones and brain development. Eur J Endocrinol. 1995;133(4):390-398.

16. Arii J, Tanabe Y, Makino M, Sato H, Kohno Y. Children with irreversible brain damage associated with hypothyroidism and multiple intracranial calcifications. J Child Neurol. 2002;17(4):309-313.

17. Dussault JH, Ruel J. Thyroid hormones and brain development. Annu Rev Physiol. 1987;49:321-434.

18. Smallridge RC. Metabolic, physiologic, and clinical indexes of thyroid function. In: Braverman LE, Utiger RD, eds. Werner & Ingbar’s The Thyroid: A Fundamental and Clinical Text. 8th ed. Philadelphia , PA: Lippincott Williams & Wilkins; 2000:393-401.

19. Schwartz HL, Oppenheimer JH. Nuclear triiodothyronine receptor sites in brain: probable identity with hepatic receptors and regional distribution. Endocrinology. 1978;103(1):267-273.

20. Ruel J, Faure R, Dussault JH. Regional distribution of nuclear T3 receptors in rat brain and evidence for preferential localization in neurons. J Endocrinol Invest. 1985;8(4):343-348.

21. Braverman LE, Utiger RD. Introduction to thyrotoxicosis. In: Braverman LE, Utiger RD, eds. Werner & Ingbar’s The Thyroid: A Fundamental and Clinical Text. 8th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2000:515-517.

22. Taylor JW. Depression in thyrotoxicosis. Am J Psychiatry. 1975;132(5):552-553.

23. Peake RL. Recurrent apathetic hyperthyroidism. Arch Intern Med. 1981;141(2):258-260.

24. Kathol RG, Delahunt JW. The relationship of anxiety and depression to symptoms of hyperthyroidism using operational criteria. Gen Hosp Psychiatry. 1986;8(1):23-28.

25. Trzepacz PT, McCue M, Klein I, Levey GS, Greenhouse J. A psychiatric and neuropsychological study of patients with untreated Graves’ disease. Gen Hosp Psychiatry. 1988;10(1):49-55.

26. Lidz T, Whitehorn JC. Psychiatric problems in a thyroid clinic. JAMA. 1949;139:698-701.

27. Bursten B. Psychoses associated with thyrotoxicosis. Arch Gen Psychiatry. 1961;4:267-273.

28. Checkley SA. Thyrotoxicosis and the course of manic-depressive illness. Br J Psychiatry. 1978;133:219-223.

29. Hasan MK, Mooney RP. Mania and thyrotoxicosis. J Fam Pract. 1981;13(1):113,117-118.

30. Reus VI, Gold P, Post R. Lithium-induced thyrotoxicosis. Am J Psychiatry. 1979;136(5):724-725.

31. Braverman LE, Utiger RD. Introduction to hypothyroidism. In: Braverman LE, Utiger RD, eds. Werner & Ingbar’s The Thyroid: A Fundamental and Clinical Text. 8th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2000:719-720.

32. Whybrow PC, Prange AJ Jr, Treadway CR. Mental changes accompanying thyroid gland dysfunction. A reappraisal using objective psychological measurement. Arch Gen Psychiatry. 1969;20(1):48-63.

33. Whybrow PC, Bauer M. Behavioral and psychiatric aspects of hypothyroidism. In: Braverman LE, Utiger RD, eds. Werner & Ingbar’s The Thyroid: A Fundamental and Clinical Text. 8th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2000:837-842.

34. Bauer M, London ED, Silverman DH, Rasgon N, Kirchheiner J, Whybrow PC. Thyroid, brain and mood modulation in affective disorder: insights from molecular research and functional brain imaging. Pharmacopsychiatry. 2003;36(suppl 3):S215-S221.

35. Wenzel KW, Meinhold H, Raffenberg M, Adlkofer F, Schleusener H. Classification of hypothyroidism in evaluating patients after radioiodine therapy by serum cholesterol, T3-uptake. Total T4, FT4-index, total T3, basal TSH and TRH-test. Eur J Clin Invest. 1974;4(2):141-148.

36. Gold MS, Pottash AL, Extein I. Hypothyroidism and depression. Evidence from complete thyroid function evaluation. JAMA. 1981;245(19):1919-1922.

37. Haggerty JJ Jr, Prange AJ Jr. Borderline hypothyroidism and depression. Annu Rev Med. 1995;46:37-46.

38. Haggerty JJ Jr, Stern RA, Mason GA, Beckwith J, Morey CE, Prange AJ Jr. Subclinical hypothyroidism: a modifiable risk factor for depression? Am J Psychiatry. 1993;150(3):508-510.

39. Joffe RT, Marriott M. Thyroid hormone levels and recurrence of major depression. Am J Psychiatry. 2000;157(10):1689-1691.

40. Loosen PT, Prange AJ Jr. Serum thyrotropin response to thyrotropin-releasing hormone in psychiatric patients: a review. Am J Psychiatry. 1982;139(4):405-416.

41. Bauer MS, Whybrow PC. Thyroid hormones and the central nervous system in affective illness: interactions that may have clinical significance. Integr Psychiatry. 1988;6:75-100.

42. Baumgartner A, Graf KJ, Kurten I, Meinhold H. The hypothalamic-pituitary-thyroid axis in psychiatric patients and healthy subjects: Parts 1-4. Psychiatry Res. 1988;24(3):271-332.

43. Loosen PT. The TRH-induced TSH response in psychiatric patients: a possible neuroendocrine marker. Psychoneuroendocrinology. 1985;10(3):237-260.

44. Mason GA, Garbutt JC, Prange AJ. Thyrotropin-releasing hormone. In: Bloom, FE, Kupfer DJ, eds. Psychopharmacology: The Fourth Generation of Progress. New York, NY: Raven Press; 1995:493-503.

45. Banki CM, Bissette G, Arato M, Nemeroff CB. Elevation of immunoreactive CSF TRH in depressed patients. Am J Psychiatry. 1988;145(12):1526-1531.

46. Frye MA, Denicoff KD, Bryan AL, et al. Association between lower serum free T4 and greater mood instability and depression in lithium-maintained bipolar patients. Am J Psychiatry. 1999;156(12):1909-1914.

47. Cole DP, Thase ME, Mallinger AG, et al. Slower treatment response in bipolar depression predicted by lower pretreatment thyroid function. Am J Psychiatry. 2002;159(1):116-121.

48. Whybrow PC. Sex differences in thyroid axis function: relevance to affective disorder and its treatment. Depression. 1995;3:33-42.

49. Bartalena L, Pellegrini L, Meschi M, et al. Evaluation of thyroid function in patients with rapid-cycling and non-rapid-cycling bipolar disorder. Psychiatry Res. 1990;34(1):13-17.

50. Kusalic M. Grade II and grade III hypothyroidism in rapid-cycling bipolar patients. Neuropsychobiology. 1992;25(4):177-181.

51. Oomen HA, Schipperijn AJ, Drexhage HA. The prevalence of affective disorder and in particular of a rapid cycling of bipolar disorder in patients with abnormal thyroid function tests. Clin Endocrinol (Oxf). 1996;45(2):215-223.

52. Cowdry RW, Wehr TA, Zis AP, Goodwin FK. Thyroid abnormalities associated with rapid-cycling bipolar illness. Arch Gen Psychiatry. 1983;40(4):414-420.

53. Gyulai L, Bauer M, Bauer MS, Garcia-Espana F, Cnaan A, Whybrow PC. Thyroid hypofunction in patients with rapid-cycling bipolar disorder after lithium challenge. Biol Psychiatry. 2003;53(10):899-905.

54. Bauer MS, Whybrow PC. Rapid cycling bipolar affective disorder. II. Treatment of refractory rapid cycling with high-dose levothyroxine: a preliminary study. Arch Gen Psychiatry. 1990;47(5):435-440.

55. Baumgartner A, Bauer M, Hellweg R. Treatment of intractable non-rapid cycling bipolar affective disorder with high-dose thyroxine: an open clinical trial. Neuropsychopharmacology. 1994;10(3):183-189.

56. Bauer M, Berghofer A, Bschor T, et al. Supraphysiological doses of L-thyroxine in the maintenance treatment of prophylaxis-resistant affective disorders. Neuropsychopharmacology. 2002;27(4):620-628.

57. Mariotti S, Chiovato L, Vitti P, et al. Recent advances in the understanding of humoral and cellular mechanisms implicated in thyroid autoimmune disorders. Clin Immunol Immunopathol. 1989;50(1 pt 2):S73-S84.

58. Vitti P, Mariotti S, Marcocci C, et al. Thyroid autoimmunity and thyroid autonomy. Acta Med Austriaca. 1990;17(suppl 1):90-92.

59. Gupta MK. Thyrotropin receptor antibodies: advances and importance of detection techniques in thyroid diseases. Clin Biochem. 1992;25(3):193-199.

60. Haggerty JJ Jr, Silva SG, Marquardt M, et al. Prevalence of antithyroid antibodies in mood disorders. Depress Anxiety. 1997;5(2):91-96.

61. Haggerty JJ Jr, Evans DL, Golden RN, Pedersen CA, Simon JS, Nemeroff CB. The presence of antithyroid antibodies in patients with affective and nonaffective psychiatric disorders. Biol Psychiatry. 1990;27(1):51-60.

62. Leroy MC, Villeneuve A, Lajeunesse C. Lithium, thyroid function and antithyroid antibodies. Prog Neuropsychopharmacol Biol Psychiatry. 1988;12(4):483-490.

63. Lazarus JH, John R, Bennie EH, Chalmers RJ, Crockett G. Lithium therapy and thyroid function: a long-term study. Psychol Med. 1981;11(1):85-92.

64. Kupka RW, Nolen WA, Post RM, et al. High rate of autoimmune thyroiditis in bipolar disorder: lack of association with lithium exposure. Biol Psychiatry. 2002;51(4):305-311.

65. Sullivan GM, Hatterer JA, Herbert J, et al. Low levels of transthyretin in the CSF of depressed patients. Am J Psychiatry. 1999;156(5):710-715.

66. Baumgartner A. Thyroxine and the treatment of affective disorders: an overview of the results of basic and clinical research. Int J Neuropsychopharmacol. 2003;3:149-165.

67. Bauer M, Whybrow PC. Thyroid hormone and brain behavior. In: Pfaff DW, Arnold AP, Etgen AM, Fahrbach SE, Rubin RT, eds. Hormones, Brain and Behavior. San Diego, CA: Academic Press; 2002:239-264.

68. Baumgartner A, Volz HP, Campos-Barros A, Stieglitz RD, Mansmann U, Mackert A. Serum concentrations of thyroid hormones in patients with nonseasonal affective disorders during treatment with bright and dim light. Biol Psychiatry. 1996;40(9):899-907.

69. Joffe R, Segal Z, Singer W. Change in thyroid hormone levels following response to cognitive therapy for major depression. Am J Psychiatry. 1996;153(3):411-413.

70. George MS, Wassermann EM, Williams WA, et al. Changes in mood and hormone levels after rapid-rate transcranial magnetic stimulation (rTMS) of the prefrontal cortex. J Neuropsychiatry Clin Neurosci. 1996;8(2):172-180.

71. Marangell LB, Ketter TA, George MS, et al. Inverse relationship of peripheral thyrotropin-stimulating hormone levels to brain activity in mood disorders. Am J Psychiatry. 1997;154(2):224-230.

72. Bauer M, Heinz A, Whybrow PC. Thyroid hormones, serotonin and mood: of synergy and significance in the adult brain. Mol Psychiatry. 2002;7(2):140-156.

73. Altshuler LL, Bauer M, Frye MA, et al. Does thyroid supplementation accelerate tricyclic antidepressant response? A review and meta-analysis of the literature. Am J Psychiatry. 2001;158(10):1617-1622.

74. Coppen A, Whybrow PC, Noguera R, Maggs R, Prange AJ Jr. The comparative antidepressant value of L-tryptophan and imipramine with and without attempted potentiation by liothyronine. Arch Gen Psychiatry. 1972;26(3):234-241.

75. Wheatley D. Potentiation of amitriptyline by thyroid hormone. Arch Gen Psychiatry. 1972;26(3):229-233.

76. Aronson R, Offman HJ, Joffe RT, Naylor CD. Triiodothyronine augmentation in the treatment of refractory depression. A meta-analysis. Arch Gen Psychiatry. 1996;53(9):842-848.

77. Bauer M, Hellweg R, Graf KJ, Baumgartner A. Treatment of refractory depression with high-dose thyroxine. Neuropsychopharmacology. 1998;18(6):444-455.

78. Pfeiffer H, Scherer J, Albus M. L-thyroxin-hochdosierung bei therapieresistenter depression: fallauswertung und katamnese als qualitätskontrolle. Nervenarzt. 2004;75(3):242-248.

79. Hurowitz GI, Liebowitz MR. Antidepressant-induced rapid cycling: six case reports. J Clin Psychopharmacol. 1993;13(1):52-56.

80. Afflelou S, Auriacombe M, Cazenave M, Chartres JP, Tignol J. Administration of high dose levothyroxine in treatment of rapid cycling bipolar disorders. Review of the literature and initial therapeutic application apropos of 6 cases [in German]. Encephale. 1997;23(3):209-217.

81. Bauer M, Priebe S, Berghofer A, Bschor T, Kiesslinger U, Whybrow PC. Subjective response to and tolerability of long-term supraphysiological doses of levothyroxine in refractory mood disorders. J Affect Disord. 2001;64(1):35-42.

82. Jackson IM. Does thyroid hormone have a role as adjunctive therapy in depression? Thyroid. 1996;6(1):63-67.

83. Joffe RT, Sokolov ST. Thyroid hormone treatment of primary unipolar depression: a review. Int J Neuropsychopharmacol. 2000;3(2):143-147.

84. Agid O, Lerer B. Algorithm-based treatment of major depression in an outpatient clinic: clinical correlates of response to a specific serotonin reuptake inhibitor and to triiodothyronine augmentation. Int J Neuropsychopharmacol. 2003;6(1):41-49.

85. Wilson IC, Prange AJ Jr, Lara P. L-triiodthyronine alone and with imipramine in the treatment of depressed women. In: Prange AJ Jr, ed. The Thyroid Axis, Drugs, and Behavior. New York, NY: Raven Press; 1974:49-62.

86. Okuno Y, Nakayasu N. Thyroid function and therapeutic efficacy of thyroxine in depression. Jpn J Psychiatry Neurol. 1988;42(4):763-770.

87. Marangell LB, George MS, Callahan AM, et al. Effects of intrathecal thyrotropin-releasing hormone (protirelin) in refractory depressed patients. Arch Gen Psychiatry. 1997;54(3):214-222.

88. Callahan AM, Frye MA, Marangell LB, et al. Comparative antidepressant effects of intravenous and intrathecal thyrotropin-releasing hormone: confounding effects of tolerance and implications for therapeutics. Biol Psychiatry. 1997;41(3):264-272.

89.  Prange AJ Jr, Wilson IC, Knox A, McClane TK, Lipton MA. Enhancement of imipramine by thyroid stimulating hormone: clinical and theoretical implications. Am J Psychiatry. 1970;127(2):191-199.


1 comment

Important DS info links

Jan 09, 2009

Needed labs from Babycatcher

Vitalady's suggested vits
from Majormom

DS Math from Diana and Flagyl info from Leann



How to search OH: (copied from Levitown_Loser's blog)

How to Search This Site (Or any site)

1) Go to http://www.google.com and click the "Advanced Search" link
2) Enter the words or phrases for which you are searching, e.g., chewable vitamin
3) Decide which OH forum or forums you want to search. Go to the forum(s) and copy the URLs.
 For example: 
 (Duodenal Switch Forum)  http://www.obesityhelp.com/forums/DS/
 (LapBand Forum) http://www.obesityhelp.com/forums/lapband/
 (RNY Forum)  http://www.obesityhelp.com/forums/rny/
 (Ontario Forum) http://www.obesityhelp.com/forums/ON/
4) Enter the URL(s) in the field labelled, "Search within site or domain".  Separate URLs by a comma.
5) Click the "Advanced Search" button.  You will only see results from the OH forum(s) you specify.

Tips: 
To search the entire OH site (every forum), just enter http://www.obesityhelp.com as the URL

Want to see ALL posts by a person (as opposed to only the Latests posts within the current forum)?
Search for their username and their location (found below their avatar).  If you just specify their username, you will get their posts as well as all posts ABOUT them. (Some people are talked about more than they actually post!)


0 comments

Treatment of Eating Disorders

Jan 07, 2009


Publication Logo Complex CBT Effective in Treatment of Severe Eating Disorders
Pauline Anderson

Medscape Medical News 2008. © 2008 Medscape

To earn CME related to this news article, click here.

December 23, 2008 — A complex form of enhanced cognitive behavioral therapy (CBT-E) that targets perfectionism and low self-esteem as well as extreme dieting, binge eating, or purging appears to be a valid treatment option for patients with particularly severe eating disorders.

A study by investigators at Oxford University, in the United Kingdom, found that this complex form of CBT-E is effective for some eating-disorder patients, although it also found that most patients derive more benefit from the standard form of CBT-E.

"Now, for the first time, we have a single treatment that can be effective at treating the majority of cases [of eating disorders] without the need for patients to be admitted to the hospital," principal investigator Christopher G. Fairburn, MD, said in a statement.

These study results add important information to the current knowledge surrounding eating-disorder treatments, said Susan Ringwood, CEO of BEAT, the United Kingdom's only national charity supporting people affected by an eating disorder.

"We encourage people seeking treatment to make sure that any therapy they are offered has a sound evidence base, and this study adds to that evidence base," she told Medscape Psychiatry. "It will give hope and encouragement to people affected by eating disorders and their families to know that treatment can work and that recovery is possible."

The study is published online December 15 in the American Journal of Psychiatry.

Anorexia Not Included

The study included patients with bulimia nervosa or an eating disorder not otherwise specified, which includes binge-eating disorder. The latter is the most common eating disorder, followed by bulimia and then anorexia nervosa, which was not included in the current study.

Among other things, the study compared patients receiving 1 of 2 forms of CBT-E — CBT-Ef, which focuses exclusively on eating-disorder psychopathology, and CBT-Eb, a broader, more complex form that also addresses problems such as mood intolerance, perfectionism, low self-esteem, and interpersonal difficulties.

Patients in the study had to have a body-mass index (BMI) higher than 17.5 and be older than 18 years. A total of 154 patients were recruited between March 2002 and July 2005 — 93 from Oxford and 61 from Leicester.

Study subjects were randomized to 1 of 4 groups:

  • Immediate CBT-Ef (53).
  • Immediate CBT-Eb (50).
  • An 8-week waiting-list control group whose members eventually received CBT-Ef.
  • An 8-week waiting-list control group whose members eventually received CBT-Eb.

The groups were balanced by sex, eating-disorder diagnosis, BMI, and need to remain on psychotropic drugs.

Therapies Identical for 4 Weeks

Both forms of CBT-E comprised a 90-minute preparatory session followed by weekly 50-minute sessions and then a review session. The therapies were identical for the first 4 weeks, both concentrating on the eating disorder itself — for example, dealing with excessive concern with shape and weight, extreme dieting, binge eating, and purging.

For the rest of the study, the CBT-Ef continued to focus on these features while the CBT-Eb began to also address perfectionism, low self-esteem, and the other complex features of eating disorders.

Of the original 154, 5 did not attend their initial assessment. Of the 149 subjects remaining, 92 (61.7%) had a diagnosis of an eating disorder not otherwise specified (7 had binge-eating disorder) and 57 (38.3%) had a diagnosis of bulimia.

Patients were assessed before treatment, after 8 weeks of treatment, and at the end of treatment. Those in the control group were assessed at the end of the waiting-list period preceding treatment. After treatment, patients were reassessed 20, 40, and 60 weeks later.

Trained therapists assessed patients using the 16th edition of the Eating Disorder Examination Interview (EDE) and its self-report version (EDE-Q). Treatment outcomes included changes in severity of eating-disorder features and having a global EDE score less than 1 standard deviation (SD) above the community mean (1.74).

Of the 149 patients who started the study, 33 (22.1%) did not complete treatment or were withdrawn because of lack of response.

Substantial Change

The study authors found that patients in the waiting-list group experienced little change in symptoms. However, they noted substantial and very similar changes in those in the 2 CBT-E groups.

At the end of 20 weeks, more than half of the overall sample had a level of eating-disorder features less than 1 SD above the community mean of 1.74 — 52.7% of those with bulimia and 53.3% of those with an eating disorder not specified.

At the 60-week follow-up, these percentages were 61.4% for those with bulimia and 45.7% for those with an eating disorder not specified. As well, the mean changes in global EDE at the 60-week follow-up were similar in the CBT-Ef and CBT-Eb groups: 1.36 (SD = 1.42) and 1.33 (SD = 1.30), respectively.

At the end of treatment, 38.5% of patients with bulimia reported no episodes of binge eating or purging over the previous 28 days. At 60-week follow-up, the proportion was 45.6%.

Compliance with follow-up was high, with 95.1% of the assessments being successfully completed.

Focused Form Should Be Default

The only notable difference between the 2 forms of CBT-E was that the broader version appeared to be more effective than the focused form in patients with substantial additional psychopathology, whereas the opposite seemed to be the case for the remaining patients. The authors, however, stress the need to verify this finding.

"In the meantime, it would seem reasonable to use the present findings to guide clinical practice," they write. "Thus, the simpler focused form of the treatment, CBT-Ef, should perhaps be viewed as the default form, as it is easier to learn and implement, with the more complex form, CBT-Eb, reserved for patients with marked additional psychopathology."

Knowing that therapies have been proven effective for most eating disorders is a relief for families struggling with such issues, said Ms. Ringwood. "We know that anorexia nervosa is the rarest eating disorder, making up only 10% of all cases, so potentially this treatment (enhanced CBT) may benefit many of the remaining 90%."

The investigators are close to revealing results of research using CBT in patients with anorexia. Ms. Ringwood said she's encouraged by this news.

If CBT succeeds in improving outcomes and reduces the rate of hospitalization, then it could translate into significant healthcare savings, noted Ms. Ringwood. "We know that the sooner someone gets the specialist treatment they need, the more likely they are to recover and avoid the long-term consequences of an eating disorder."

She added that in-patient treatment is often lengthy and costly, "not only for healthcare services, but also in terms of the impact it makes in the life of the person affected and their loved ones."

However, there are currently not enough therapists in the United Kingdom qualified to offer CBT to everyone who might benefit from it, she said. "The UK government has recently committed significant extra funding for CBT training, and we look forward to this additional capacity becoming available."

Dr. Fairburn reports receiving royalties from Guilford Press.

Am J Psychiatry. Published online December 15, 2008. Abstract

 



0 comments

Obesity and Depression

Jan 03, 2009





Science News

www.sciencedaily.com/releases/2008/06/080602152913.htm Obesity And Depression May Be Linked

ScienceDaily (June 6, 2008) — A major review reveals that research indicates people who are obese may be more likely to become depressed, and people who are depressed may be more likely to become obese.


To understand the potential links between obesity and depression, researchers led by Sarah M. Markowitz, M.S., examined the correlational data that suggest a connection between the conditions and found evidence for causal pathways from obesity to depression and depression to obesity.

People who are obese may be more likely to become depressed because they experience themselves as in poor health and are dissatisfied with their appearance. This occurrence was particularly prevalent among women and those of high socio-economic status.

People who are depressed may be more likely to become obese because of physiological changes in their hormone and immune systems that occur in depression. Also, they have more difficulty taking good care of themselves because of symptoms and consequences of depression, such as difficulty adhering to fitness regiments, overeating, and having negative thoughts.

Treatments such as exercise and stress reduction can help to manage both obesity and depression at the same time. Potentially, dieting, which can worsen mood, and antidepressants, which can cause weight gain, should be minimized.

"The treatment of depression and obesity should be integrated," the authors conclude. "This way, healthcare providers are working together to treat both conditions, rather than each in isolation."

This study is published in the March 2008 issue of Clinical Psychology: Science and Practice. 


0 comments

Mental Health Resources

Dec 31, 2008

Support and information about Mental Illness including medications
www.nami.org/

Referrals for Counseling:

Social Work
www.helpstartshere.org/

Psychologist
locator.apa.org/

Psychoanalyst
www.apsa.org/MEMBERDIRECTORYbrFINDANANALYST/tabid/62/Default.aspx


I will be adding updated information and resources. Feel free to PM me with any questions you may have.

Be well


0 comments

Random Links

Nov 29, 2008

0 comments

Tired but better

Aug 17, 2008

I slept all day today and didnt really eat much. I have been feeling better. I am able to drink and eat without getting sick.
I had a yougurt tonight and will see how that goes down. so far so good.

with the funny taste in my mouth I can  not tolerate any diet drinks/foods (splenda) i am hoping that this taste will go away.

time for bed

About Me
Cherry Hill Area, NJ
Location
28.4
BMI
DS
Surgery
07/21/2008
Surgery Date
Jul 31, 2008
Member Since

Friends 35

Latest Blog 12
Tired but better

×