Curbing nocturnal binges in sleep-related eating disorder
Sleep-related eating disorder (SRED) can be associated with disrupted sleep, weight gain, and major chronic morbidity. In SRED—involuntary eating while asleep, with partial or complete amnesia—the normal suppression of eating during the sleep period is disinhibited. The disorder can be idiopathic, associated with medication use, or linked to other sleep disorders such as somnambulism (sleepwalking), restless legs syndrome (RLS), periodic limb movement disorder (PLMD), or obstructive sleep apnea (OSA).
SRED is more common in women than men; it usually begins in the third decade of life but can begin in childhood or middle age.
About one-half of SRED patients also have a psychiatric illness, usually a mood disorder. Unremitting SRED may lead to psychopathology, as the onset of sleep-related eating usually precedes the onset of a psychiatric disorder by years.
SRED often is unrecognized, but it can be effectively identified and treated. This article examines how to:
* distinguish SRED from nocturnal eating syndrome (NES) and other disorders
* identify precipitating causes
* select effective pharmacologic therapy.
Ms. G, age 39, has a body mass index (BMI) >35 kg/m2 and is pursuing bariatric surgery to treat obesity. She is frustrated with dieting and describes a decade of unconscious nocturnal eating, including peanut butter and uncooked spaghetti.
This behavior began after her divorce 10 years ago. Initially she had partial recall of the nocturnal binges, but now describes full amnesia. Treatment for a depressive episode did not control her nocturnal eating.
Michael J. Howell, MD
Minnesota Regional Sleep Disorders Center, Hennepin County Medical Center, Assistant professor, department of neurology
Carlos Schenck, MD
Minnesota Regional Sleep Disorders Center, Hennepin County Medical Center, Associate professor, department of psychiatry
Scott J. Crow, MD
Director, Clinical Populations/Assessment Core, Minnesota Obesity Center, Professor, department of psychiatry
University of Minnesota, Minneapolis
Sleeping and eating: Closely linked activities
Because hormones that regulate appetite, food intake, and body weight also play a role in sleep regulation, patients with eating disorders often have associated sleep disorders. For example, obesity is related to obstructive sleep apnea (OSA)—weight gain is a risk factor for OSA, and weight loss often is an effective treatment. Moreover, patients with Anorexia Nervosa frequently demonstrate sleep initiation and maintenance insomnia.
Conversely, epidemiologic studies have demonstrated that sleep duration is inversely correlated with body mass index. In particular, individuals with shorter sleep times are more likely to be overweight. The nature of this association is unclear; however, hormones that normally regulate appetite are disrupted in patients with sleep deprivation. For instance, leptin is an appetite suppressant that is normally released from adipocytes during sleep, so sleep deprivation may promote hunger by restricting its secretion.
Differences between expressive and supportive psychotherapy
- Recurrent episodes of involuntary eating and drinking during the main sleep period
- One or more of the following must be present with these recurrent episodes:
1. Consumption of peculiar, inedible, or toxic substances
2. Insomnia related to repeated episodes of eating, with a complaint of nonrestorative sleep, daytime fatigue, or somnolence
3. Sleep-related injury
4. Dangerous behavior while preparing food
5. Morning anorexia
6. Adverse health consequences from recurrent binge eating
- The disturbance is not better explained by another sleep, medical, or neuropsychiatric disorder
Source:International classification of sleep disorders: diagnostic and coding manual, 2nd ed. Westchester, IL: American Academy of Sleep Medicine; 2005:174-5.
Pharmacotherapy
SRED is treatable and a reversible cause of obesity. The choice of medication depends on:
* which form of SRED the patient exhibits (drug-induced or idiopathic)
* whether the patient has treatable comorbid conditions.
Temazepam. Switch patients whose SRED is triggered by zolpidem or another hypnotic to a different agent. We have had excellent success with temazepam, 15 to 30 mg at bedtime.
Topiramate. For idiopathic SRED or the sleepwalking variant of SRED, trials from 2 academic institutions suggest that off-label use of topiramate, 25 to 150 mg at bedtime, may be the treatment of choice.
Start topiramate at 25 mg, and increase in 25-mg increments every 5 to 7 days until the night eating episodes are eliminated. Paresthesias, visual symptoms, and (rarely) renal calculus are reported side effects.
Other medications. Other agents that have shown at least some benefit in patients with SRED include dopaminergic agonists, opiates, and clonazepam. Patients with SRED and a history of chemical dependency may respond to combined levodopa, trazodone, and bupropion (dopaminergic/noradrenergic antidepressant) therapy at bedtime. Also focus treatment on any coexisting sleep disorder, such as RLS or OSA.
Drug brand names
Bupropion • Wellbutrin
Clonazepam • Klonopin
Levodopa/carbidopa • Sinemet
Lithium • Eskalith, Lithobid
Olanzapine • Zyprexa
Risperidone • Risperdal
Temazepam • Restoril
Topiramate • Topamax
Trazodone • Desyrel
Triazolam • Halcion
Zolpidem • Ambien
References
1. Flemons WW. Obstructive sleep apnea. N Engl J Med 2002;347:498–504.
2. Levy AB, Dixon KN, Schmidt H. Sleep architecture in Anorexia Nervosa and bulimia. Biol Psychiatry 1988;23:99–101.
3. Gangwisch JE, Malaspina D, Boden-Albala B, Heymsfield SB. Inadequate sleep as a risk factor for obesity: analyses of the NHANES I. Sleep 2005;28:1289–96.
4. Mullington JM, Chan JL, Van Dongen HP, et al. Sleep loss reduces the diurnal rhythm amplitude of leptin in healthy men. J Neuroendocrinol 2003;15:851–4.
5. International classification of sleep disorders: diagnostic and coding manual, 2nd ed. Westchester, IL: American Academy of Sleep Medicine; 2005.
6. Rogers NL, Dinges DF, Allison KC, et al. Assessment of sleep in women with night eating syndrome. Sleep 2006;29:814–19.
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