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Question. I have a diabetic patient in her early 30s who is also exhibiting signs of anxiety and depression. She’s on 100mg Glucophage as well as 100u Humulin Ultralente and 100-150u Humalog (extreme insulin resistance). I am aware that some of her symptoms of anxiety may be related to the gastric side effects of the Glucophage and that her mood problem may be tied to the diabetes itself, but how would you go about ruling out these symptoms as true mental illness?

Answer. That’s a tough question. The bottom line is: if she looks depressed and anxious; sounds depressed and anxious; and acts depressed and anxious, it’s probably best to treat her as if she IS depressed and anxious. But let me back up and give you some background material, drawn from a chapter [in press] written by my colleague, Dr. David Harnett, and edited by Dr. Mantosh Dewan and myself. Depression in patients with diabetes mellitus is common; diagnostically vexing; often malevolent in its course; and frequently associated with poor blood glucose (glycemic) control and diabetic complications. The prevalence of major depression in diabetes-considering both Type I insulin-dependent diabetes mellitus [IDDM] and Type II non-insulin dependent diabetes mellitus [NIDDM] – is about 15 to 20% (Lustman et al, 1997b; Gavard et al, 1993). As with depression in the medically well, depression in diabetic cohorts is characterized by a positive family history of depression and typical depressive symptomatology (Lustman et al, 1992). Some, but not all, studies have found a female predominance of depression in diabetic populations (Lustman et al, 199; Popkin et al, 1988). As in other medical illnesses, diabetics may report apparent “depressive” symptoms such as weight loss, fatigue and hypersomnia that are actually a direct manifestation of diabetes. Indeed, disordered sleep may be characteristic of non-depressed diabetics. (Leedom et al, 1991) One clue to depression in diabetics is the patient’s amplification of somatic symptoms of physical illness, and his difficulty habituating to these aversive symptoms (Katon, 1996). For example, depressed diabetics may report polydypsia that is not correlated with elevated glycosated hemoglobin (gHb or Hb-A1C) values (Lustman et al, 1988b). (gHb reflects glucose control over the previous three months). The clinician’s misinterpretation of such “somatic” complaints may lead to underdiagnosis of depression in these diabetic patients. Mild hyperglycemia with associated polyuria, polyphagia, polydipsia, fatigue, blurred vision, or paresthesia may further confound diagnosis by mimicking hypochondriasis. (Kornstein and Gardner, 1993) Cognition may also be impaired by hyperglycemia, (Reed and Mooradion, 1998) especially in elderly diabetics, (Tun et al, 1990) but can be partially improved by better glycemic control (Meneilly et al, 1993, Testa and Simonson, 1998). Hypoglycemia may present with adrenergic symptoms such as anxiety, diaphoresis, tremor, irritability and palpitations. In the elderly, neuroglycopenic symptoms of hypoglycemia may be more likely, including dizziness, headache, weakness, tiredness, blurred vision, and confusion (Reed and Mooradion, 1998). Another potential variable contributing to depression in such patients is diabetes-related atherosclerotic brain disease causing “vascular depression.” (Alexopoulos et al, 1997). Accumulating research suggests that history of depression, and especially current depression, is associated with poor glycemic control as reflected in elevated gHb (Lustman et al, 1997b, Cohen et al, 1997.) It has even been suggested that major depression increases the risk for NIDDM. (Eaton et al, 1996) Poor glycemic control is clearly associated with diabetic complications. Yet the relationship between depression and diabetic complications is complex. While neuropathy (Leedom et al, 1991) and retinopathy (Cohen et al, 1997) for example, may act as psychosocial precipitants of depression, depression may well contribute to diabetic complications via impaired glycemic control. (Cohen et al, 1997) Depression may impair glycemic control because of lack of adherence to dietary and exercise programs. Obese NIDDM patients were less likely to complete a weight-control program if they had a history of major depression. (Marcus et al, 1992) Alternatively, depression may worsen glycemic control via neuroendocrine mechanisms. Possibilities include hyperglycemia secondary to depression-related hypercortisolemia and complex effects of depression on growth hormone. (Holsboer, 1995). In short: the differential diagnosis is a bear!
What about the treatment of depressed diabetics? SSRIs are certainly worth considering. An open, 10-week study (Goodnick et al, 1997) of depressed NIDDM patients given sertraline 50mg revealed significant improvement on two depression rating scales and dietary compliance. Modest improvement of gHb levels were seen. While SSRIs have advantages over TCAs in depressed diabetics, potential SSRI-related gastrointestinal distress and sexual dysfunction may be hard to discern in a multi-problem medical patient taking many medications. In addition, SSRI-related diarrhea may lead to hypoglycemia in IDDM patients ( Tanya Korkosz, MD, Personal communication 1998). Furthermore, diabetics receiving multiple medications must be monitored for the potential enzyme-inhibiting effects of the SSRIs. For example, the sulfonylurea agent tolbutamide, though now used less frequently, is a substrate for the hepatic cytochrome P450-2C9 isoenzyme, which is inhibited by fluoxetine (Prozac) and fluvoxamine(Luvox).(Harvey and Preskorn, 1996). Sertraline (Zoloft) or citalopram (Celexa) are much less likely to inhibit the cytochromes.
There are few relevant studies of other antidepressants in depressed diabetics. Warnock and Biggs (1997) described a 54-year-old depressed woman with IDDM treated with nefazodone (200-400 mg/day) who showed both a reduced need for insulin and a good antidepressant response. However, nefazodone, a potent P450-3A4 inhibitor, must not be prescribed in diabetics receiving cisapride – a pro-kinetic agent and P450-3A4 substrate sometimes used to alleviate diabetic gastroparesis as well as gastroesophageal reflux – because of potential Q-T prolongation and arrhythmia risk. (Janssen, 1998).
The evidence suggests that depression should be vigorously treated in diabetics. Hopefully, future research will verify that antidepressant treatment will improve not only immediate quality of life, but also the long-term course of diabetes mellitus. The clinician should probably be more willing to consider long-term maintenance treatment. While enthusiasm is warranted for the potential benefits of SSRIs over TCAs in depressed diabetes, such enthusiasm must already be tempered by the increasing realization that SSRIs may cause weight gain, (Sussman and Ginsberg, 1998a, 1998b, Richelson, 1998) especially when taken for many months. Perhaps the proposed benefits of SSRIs on glycemic control are also, to some extent, short-lived. This possibility was anticipated in the study, (O’Kane et al, 1994) mentioned previously, in which fluoxetine lessened weight and gHb of non-depressed obese NIDDM patients at 3 and 6 months, but not 9 and 12 months. Bupropion (Wellbutrin), nefazodone (Serzone) and venlafaxine (Effexor) may be less likely to cause weight gain (Sussman and Ginsberg, 1999).
Finally, I have found the Beck Depression Inventory to be a good guide to the presence of “true” depression, even in medically complicated patients. If your patient has a very high score on the Beck, I’d take that seriously, especially if guilt or self-deprecation are prominent. As for the anxiety component, venlafaxine is now FDA-labelled for generalized anxiety, but has significant GI side effects. If you use it, “start low (18.75 mg/day) and go slow.” Buspirone could also be considered. And, of course, getting a face-to-face consultation evaluation never hurts. Hope this lengthy response helps some!