Anxiety is also more frequent in those with diabetes. Some of the symptoms of anxiety, such as sweating, tremor, palpitations, nausea and headache, may be confused with hypoglycemia by both patients and doctors (Box 25.2). Fear of hypoglycemia is a major problem and may be severe enough to meet the criteria for phobia. Fear of needles can also cause significant anxiety in diabetes. Anxiety may exacerbate hyperglycemia or cause hypoglycemia in diabetes through the effects of stress hormones, such as catecholamines and cortisol, and by the disruption of self-care behaviors.
Some studies have found that children diagnosed under the age of 5 or 6 years are most at risk of cognitive dysfunction with defects in visuospatial ability (copying, solving jigsaws), which by adolescence can progress to impaired learning and memory, verbal ability and school achievement (Figure 25.2). Links have been made with number of episodes of severe hypoglycemia because the developing brain might be more vulnerable to insult. However, not all studies support this and there is increasing evidence that chronic hyperglycemia might be a greater problem. Other factors such as school attendance (which might be affected in those having recurrent hypoglycemia) and home problems (including psychosocial) have to be taken into account and were often neglected in earlier studies.
In adults with type 1 diabetes and older adults with type 2 diabetes, chronic hyperglycemia is associated with defects in psychomotor tasks, attention, learning and memory (Table 25.3). The reasons are probably multiple: microvascular damage to central nervous system neurons, macrovascular (cerebrovascular) disease, amyloid deposits as in Alzheimer’s (ApoE4 deficiency), insulin resistance and possibly hypoglycemia may all play a role. There are no data conclusively linking hypoglycemia alone to cognitive dysfunction in adults with diabetes. A meta-analysis has shown an increased risk of both vascular and Alzheimer’s dementia in adults with type 2 diabetes for reasons which are not clear. Prospective studies are under way to explore this relationship.
Treatment of depression begins with general measures such as sympathetic discussion, advice about improving glycemic control and attention to specific causes of anxiety, such as fear of blindness, infertility, impotence, amputation, etc. (Box 25.3). Sleep disorders are common and may be helped by taking regular exercise and avoiding daytime naps, large meals, tobacco, alcohol and caffeine-containing drinks in the evening.
Meta-analysis of psychological interventions (including cognitive behavioral therapy, counselling, family systems therapy and psychoanalysis) shows a significant impact on glycemic control and psychological distress for children and adolescent patients with type 1 and adults with type 2 but not adults with type 1 diabetes (HbA1c reductions 0.48%, 0.76% and 0.22% respectively). A more recent randomised controlled trial of a combination of cognitive behavioral therapy and motivational enhancement versus motivational enhancement alone or usual care showed a reduction in HbA1c for the combination treatment of 0.46% at 12 months but no effect of either intervention on quality of life or psychological distress.
Moderate or severe depression usually requires antidepressant medication (Box 25.4). NICE guidance for type 1 diabetes does not specify a particular therapy, but most reviews recommend selective serotonin reuptake inhibitors (e.g. fluoxetine, sertraline) because they have the advantages of low cardiotoxicity, greater safety in overdose, less sedation, lack of weight gain and lack of anticholinergic side effects. Tricyclic antidepressants can raise blood glucose levels, cause sedation and weight gain, and have some cardiotoxicity and anticholinergic side effects (e.g. dry mouth, blurred vision, hesitancy or urinary retention). Some tricyclics, such as imipramine, nortriptyline and lofepramine, have weaker sedative properties and are useful in withdrawn or apathetic patients; tricyclic drugs with sedative action (e.g. amitriptyline) are more suitable for agitated or anxious patients. Monoamine oxidase inhibitors are currently little used.
It is difficult to estimate precise prevalence, but there is general agreement that eating disorder may complicate up to 5% of (mainly female) adolescent type 1 diabetes which is probably at least twice the rate seen in the non-diabetic population. There is also a high prevalence of abnormal eating behaviors in type 2 diabetes. Eating disorder is associated with poorer long-term outcome in terms of complications, probably because of its link to omission of insulin, erratic glycemia and recurrent DKA. The management is extremely difficult and requires multidisciplinary team work from the mental health and diabetes teams. Early recognition and referral are recommended by NICE.
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Rudy Bilous MD, FRCP, Professor of Clinical Medicine, Newcastle University, Honorary Consultant Endocrinologist, South Tees Foundation Trust, Middlesbrough, UK Richard Donnelly MD, PHD, FRCP, FRACP, Head, School of Graduate Entry Medicine and Health, University of Nottingham, Honorary Consultant Physician, Derby Hospitals NHS Foundation Trust, Derby, UK
A John Wiley & Sons, Ltd., Publication This edition first published 2010, © 2010 by Rudy Bilous and Richard Donnelly. Previous editions: 1992, 1999, 2004
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