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ED In women, the incidence, prevalence, etiology, and treatment options are much less clear Studies of sexual dysfunction in diabetic women, although still lagging behind studies in men, have improved methodologically over the past 20 years and have provided strong evidence for the presence of sexual problems in women Psychosocial factors may be more strongly related to sexual dysfunction in women than in men, but this conclusion remains tentative and may be, in part, linked to the lack of a consistent etiologic factor in women Future studies should include longitudinal designs, larger sample sizes, and control groups; studies in women should incorporate factors such as diabetes type, menopausal status, and obesity/body image concerns Given that sexual functioning is an important part of life, sexual dysfunction is integral to the challenge of improving quality of life in individuals with diabetes.



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(This formulation of the foundational etiology of psychoanalysis supersedes the one I gave at the suggestion of Carl Hempel and Morris Eagle [in Gr nbaum, 1984, p. 181, last paragraph]. The revised formulation here is faithful to Breuer and Freud s reference to accompanying affect [p. 6] apropos of the traumatic events whose repression occasioned the symptoms.) Clearly, this etiologic hypothesis E permits the valid deduction of the therapeutic finding reported by Breuer and Freud as codified in their therapeutic hypothesis T: The cathartic lifting of the repressions of traumatic memories of events that occasion symptoms engendered the disappearance of the symptoms. And, as they told us explicitly (1893, p. 6), this therapeutic finding is their evidence for their cardinal etiologic hypothesis E. But I maintain that this inductive argument is vitiated by what I like to call the fallacy of crude hypothetico-deductive (H-D) pseudo-confirmation. Thus, note that the remedial action of aspirin consumption for tension headaches does not lend H-D support to the outlandish etiologic hypothesis that a hematolytic aspirin deficiency is a causal sine qua non for having tension headaches, although such remedial action is validly deducible from that bizarre hypothesis. Twenty-five years ago, Wesley Salmon called attention to the fallacy of inductive causal inference from mere valid H-D deducibility by giving an example in which a deductively valid pseudo-explanation of a man s avoiding pregnancy can readily give rise to an H-D pseudo-confirmation of the addle-brained attribution of his nonpregnancy to his consumption of birth control pills. Salmon (1971, p. 34) states the fatuous pseudo-explanation:





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Hypoglycemia With the recognition that tight glycemic control can reduce the risk of complications associated with diabetes (DCCT, 1993; UKPDS, 1998), intensi ed treatment regimens (eg, multiple daily insulin injections, subcutaneous insulin pumps) have been increasingly important in diabetes management One well-documented side effect of such tight glycemic control is hypoglycemia (Cryer, 1994) Hypoglycemia (BG levels 70 mg/dl) has been estimated to occur three times more often in patients on intensive insulin regimens (DCCT, 1993) and is more common in patients with a history of hypoglycemia and lower BG levels (Gonder-Frederick, Clarke, & Cox, 1997) Hypoglycemia is designated as either mild or severe depending on whether the person is able to treat his or her BG, loses consciousness, and/or experiences seizures However, mild hypoglycemia is associated with serious physical, emotional, and social consequences (Gonder-Frederick, Clarke, et al, 1997).

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Consequences of Hypoglycemia Hypoglycemia, if undetected and thus untreated, can progress to loss of consciousness, coma, and death Severe hypoglycemia is the fourth leading cause of mortality in type 1 diabetes (Gonder-Frederick, Cox, & Clarke, 1996) Hypoglycemia is also associated with a variety of physical symptoms as well as behavioral, emotional, and social consequences that may affect patients quality of life The symptoms of hypoglycemia stem from the autonomic nervous system s release of counter-regulatory hormones (such as epinephrine) to raise BG levels and from neuroglycopenia (when the brain is not receiving suf cient glucose for normal.

Ironically, despite major advances in behavioral neuroscience, evolutionary ecology, personality research, and clinical science in the past two decades (see Millon, 2003), personality-in-politics inquiry appears to have stagnated, with little cross-pollination from these adjacent disciplines. At this juncture, all of the dominant trends in political personality assessment date back to the establishment of organized political psychology in

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