• Ei tuloksia

5. DISCUSSION

5.6. Conclusions and practical implications

The present study found that being a carrier of a LQTS-linked mutation is not associated with the risk of depressive symptoms. In LQTS mutation carrier men, depressive symptoms and their three dimensions (i.e., affective, cognitive, and somatic) may increase the risk of arrhythmic events independently of age, the use of β-blockers and antidepressants, social support, and education level.

These increased risks appear not to exist in women, although arrhythmic events can be more common in women with LQTS than men. Moreover, women in overall were shown to experience higher levels of depressive symptoms and more frequently than men screen positive for depressive disorder. This female preponderance could result from the fact that women may simply be more willing than men to reveal distress and health problems (Barsky, Peekna, & Borus, 2001).

These findings can be especially beneficial to the Finnish health care system, given that the prevalence of LQTS in Finland has been reported to be the highest in the world (Marjamaa et al., 2009; Schwartz et al., 2009). The results suggest that prevention and treatment of depressive symptoms might be an important component of the health care of men with a LQTS-causing mutation. If depressive symptoms are proven to trigger arrhythmias in men with LQTS, future studies, in particular clinical trials, will need to examine whether routine screening for depressive symptoms in LQTS mutation carriers and the management of those patients who exhibit depressive symptoms would be safe and efficient in preventing cardiac events. Considering benefits of genetic counseling for coping with distress and depressive symptoms in individuals with hypertrophic cardiomyopathy (i.e., a genetic disease predisposing to sudden cardiac death; Ingles, Lind, Phongsavan, & Semsarian, 2008), this form of psychotherapy (Austin, Semaka, & Hadjipavlou, 2014) could be of value in LQTS mutation carriers and their family members. This, however, needs to be first verified in clinical trials. Moreover, as women in our sample scored higher on depressive

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symptoms compared with men, further research is required to investigate whether LQTS mutation carrier women and female relatives without a familial LQTS mutation are more depressed than women in the general population.

The results of the present study also suggest that elevated glucose levels are unlikely to be a mechanism underlying the association in the direction of T2D leading to depressive symptoms. It seems possible, however, that this association might be due to low concentrations of glucose or that increased glucose levels might protect against depressive symptoms. These conclusions, however, need to be treated cautiously, considering the methodological limitations of the Mendelian randomization approach, and replicated in future studies. Furthermore, our findings provide evidence that depressive symptoms can be a risk factor for elevated glucose levels, and thus, for the development of T2D in women but not in men, and that this association may not be mediated by changes in body fat, inflammation, alcohol consumption, or tobacco or cigarette smoking.

The above findings are relevant to current public health concerns given the steadily increasing rates of T2D worldwide. Health care providers should be aware that women with depressive symptoms may be at risk of increased glucose concentrations, and thus may have an increased risk for T2D development. We recommend that future research, especially clinical trials, should examine whether the initiation of routine screening for depressive symptoms in women at the beginning of the fourth decade of life could be beneficial for prevention of abnormal blood glucose.

Studies that examine the effects of screening for glucose abnormalities in women already at the end of the fourth decade of life could also be of value.

Our results do not preclude the possibility that the relationship going from T2D to depressive symptoms can result from distress associated with the diagnosis of T2D, management of this disease, and its complications (Tabak et al., 2014). Given this, if following the recommendation of the American Association of Clinical Endocrinologists (Handelsman et al., 2015) and the Canadian

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Diabetes Association (Robinson, Luthra, & Vallis, 2013), all individuals diagnosed with T2D should continue to be screened for depressive symptoms.

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