• Talk of, or preoccupation with, suicide or death; threatening suicide; writing about death or suicide
• Signs of serious depression, including desperation; feelings of hopelessness; feeling no sense of purpose; loss of interest in things one used to care about; trouble sleeping
• Withdrawal from family and friends
• Reckless behavior, increased risk-taking, irritability
• Making statements about life not being worth living, hating life, that the “world would be better off without me,” and similar feelings
• Increased alcohol or drug use
• Feelings of rage or uncontrolled anger
• Seeking access to firearms, pills, or other methods to commit suicide
• Changing wills, preoccupation with putting one’s affairs in order
• Dramatic changes in personality

While recovery from mood disorders such as anxiety and depression can be lifesaving, weight gain often can be an unwanted side effect of treatment for many people. In this Health Alert, Johns Hopkins provides nine practical strategies to head off unwanted weight gain.

Psychiatric medications including antidepressants, mood stabilizers, and antipsychotics may increase weight by stimulating the appetite or slowing the body’s metabolism, and that gain can range from minimal (a few pounds) to significant (up to 50 pounds).

Such rapid weight gain may increase the risk of many health conditions associated with being overweight, such as high blood pressure, diabetes, heart disease, arthritis, and some types of cancer. Despite the fact that many psychiatric medications have weight gain as a side effect, that does not mean it’s a fait accompli. Be aware of the potential for weight gain and follow these strategies to head off extra pounds:

• *Weight Loss Strategy 1: Weigh yourself weekly and keep a diary of your weight so you can notice small increases quickly and take steps to counter further gains. Also keep a food diary for an accurate gauge of how much you’re really eating on a daily basis.

• *Weight Loss Strategy 2: Avoid or limit high-calorie, high-fat foods.

• Weight Loss Strategy 3: Eat smaller portions — and smaller meals and snacks overall.

• Weight Loss Strategy 4: Don’t keep large quantities of junk foods in your home. If you need to snack, choose healthy foods such as fresh fruit or vegetables or unbuttered popcorn.

• Weight Loss Strategy 5: Eat slowly. Many people eat too quickly — the brain needs about 20 minutes to recognize that the stomach is full , so if you eat too fast, you’ll be apt to consume more calories than you need to satisfy your hunger.

• Weight Loss Strategy 6: Don’t skip meals. Going for long periods of time without food only serves to make you hungrier in the long term and more likely to overeat once you do eat.

• Weight Loss Strategy 7: Exercise every day to counteract any extra calories you’re consuming and give a boost to your metabolism. Try resistance training and aerobic exercise. To build muscle, lift weights or use resistance machines three times a week.

• Weight Loss Strategy 8: Drink frequently. Hunger is one of the symptoms of dehydration, so quench your thirst with calorie-free beverages such as water, seltzer, diet soda, and decaffeinated coffee and tea.

• Weight Loss Strategy 9: If all else fails, talk to your healthcare provider about switching to a medication that is less likely to cause weight gain or adding another one that might help avoid weight gain. Don’t stop taking your medication without discussing it with your doctor, as your depression or anxiety may return or you may experience withdrawal side effects.

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The brains of individuals with major depressive disorder appear to react more strongly when anticipating pain and also display altered functioning of the neural network that modifies pain sensitivity, according to a report in the November issue of Archives of General Psychiatry.

“Chronic pain and depression are common and often overlapping syndromes,” the authors write as background information in the article. Recurring or chronic pain occurs in more than 75 percent of patients with depression, and between 30 percent and 60 percent of patients with chronic pain report symptoms of depression “Understanding the neurobiological basis of this relationship is important because the presence of comorbid pain contributes significantly to poorer outcomes and increased cost of treatment in major depressive disorder.“

Irina A. Strigo, PhD, of the University of California San Diego, La Jolla, and colleagues studied 15 young adults with major depressive disorder (average age 24.5) who were not taking medication and 15 individuals who were the same age (average 24.3 years) and had the same education level but did not have depression. Patients with depression completed a questionnaire that evaluated their tendencies to magnify, ruminate over or feel helpless in the face of pain.

All participants underwent functional magnetic resonance imaging (fMRI) while their arms were exposed to a thermal device heated to painful levels (an average of 46.4 degrees to 46.9 degrees Celsius, or about 115 degrees to 116 degrees Fahrenheit) and also to non-painful temperatures. Visual cues (a green shape for non-painful warmth and a red shape for painful warmth) were presented before the heat was applied.

Compared with the controls, patients with depression showed increased activation in certain areas of their brain – including the right amygdala – during the anticipation of painful stimuli. They also displayed increased activation in the right amygdala and decreased activation in other areas, including those responsible for pain modulation (adjusting sensitivity to pain), during the painful experience.

To examine whether the activation of the amygdala was associated with passive coping styles, the researchers compared the percentage change in the activations of the amygdala with the helplessness, rumination and ramification reported by the participants with depression. “Significant positive correlations were observed in the major depressive disorder group between greater helplessness scores and greater activity in the right amygdala during the anticipation of pain,” the authors write.

“The anticipatory brain response may indicate hypervigilance to impending threat, which may lead to increased helplessness and maladaptative modulation during the experience of heat pain,” the authors write. “This mechanism could in part explain the high comorbidity of pain and depression when these conditions become chronic.“

“Future studies that directly examine whether maladaptive response to pain in major depressive disorder is due to emotional allodynia [a pain response to a non-painful stimulus], maladaptive control responses, lack of resilience and/or ineffectual recruitment of positive energy resources will further our understanding of pain-depression comorbidity,” they conclude.

The study was supported by Barrow Neurological Foundation, grants from the National Institute of Mental Health, the National Association for Research in Schizophrenia and Depression and the University of California San Diego Center of Excellence for Stress and Mental Health.

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Strigo IA, Simmons AN, Matthews SC, et al. Association of Major Depressive Disorder With Altered Functional Brain Response During Anticipation and Processing of Heat Pain. Arch Gen Psychiatry. 2008;65(11):1275-1284.   [Abstract]

Comparative Benefits and Harms of Second-Generation Antidepressants: Background Paper for the American College of Physicians

Gartlehner G, Gaynes BN, Hansen RA, Thieda P, DeVeaugh-Geiss A, Krebs EE, Moore CG, Morgan L, Lohr KN.

Background: Second-generation antidepressants dominate the management of major depressive disorder, dysthymia, and subsyndromal depression. Evidence on the comparative benefits and harms is still accruing.

Purpose: To compare the benefits and harms of second-generation antidepressants (bupropion, citalopram, duloxetine, escitalopram, fluoxetine, fluvoxamine, mirtazapine, nefazodone, paroxetine, sertraline, trazodone, and venlafaxine) for the treatment of depressive disorders in adults.

Data Sources: MEDLINE, EMBASE, PsychLit, Cochrane Central Register of Controlled Trials, and International Pharmaceutical Abstracts from 1980 to April 2007, limited to English-language articles. Reference lists of pertinent review articles were manually searched and the Center for Drug Evaluation and Research database was explored to identify unpublished research.

Study Selection: Abstracts and full-text articles were independently reviewed by 2 persons. Six previous good- or fair-quality systematic reviews or meta-analyses were included, as were 155 good- or fair-quality double-blind, placebo-controlled, or head-to-head randomized, controlled trials of at least 6 weeks’ duration. For harms, 35 observational studies with at least 100 participants and follow-up of at least 12 weeks were also included.

Data Extraction: Using a standard protocol, investigators abstracted data on study design and quality-related details, funding, settings, patients, and outcomes.

Data Synthesis: If data were sufficient, meta-analyses of head-to-head trials were conducted to determine the relative benefit of response to treatment and the weighted mean differences on specific depression rating scales. If sufficient evidence was not available, adjusted indirect comparisons were conducted by using meta-regressions and network meta-analyses. Second-generation antidepressants did not substantially differ in efficacy or effectiveness for the treatment of major depressive disorder on the basis of 203 studies; however, the incidence of specific adverse events and the onset of action differed. The evidence is insufficient to draw conclusions about the comparative efficacy, effectiveness, or harms of these agents for the treatment of dysthymia and subsyndromal depression.

Limitation: Adjusted indirect comparisons have methodological limitations and cannot conclusively rule out differences in efficacy.

Conclusion: Current evidence does not warrant the choice of one second-generation antidepressant over another on the basis of differences in efficacy and effectiveness. Other differences with respect to onset of action and adverse events may be relevant for the choice of a medication.

Source + Full text… © 2008 American College of Physicians

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