This guest article considers the scholarly studies that find correlations between sleep apnea and depression. This is the second page of this report. Sleep Apnea and Depression, Part 1, begins here.
Correlation studies of OSA and depression
The majority of studies to date report an association between depression and OSA, but methodological considerations render the comparison between investigations difficult. Some of the mixed findings among studies can be explained by differences in sample size, study population, gender distribution, age and AHI cut-off in relation to age, as well as variability in terms of the questionnaires and scales used to assess depressive symptomatology.
Given the heterogeneity of these data and considering the numerous confounding factors, future longitudinal studies of patient populations are required to better understand the relation between both disorders.
Treatment Studies for OSA: reversibility of depressive symptoms?
The gold standard treatment for moderate to severe cases of OSAS is continuous or bilevel positive airway pressure (CPAP/BiPAP) which mechanically maintains the upper airways space open during sleep via the administration of ambient air with a certain pressure. The minimum necessary pressure level has to be titrated individually for each patient .
Other treatments, especially for mild cases of OSA, include weight loss, dental devices (which advance the tongue or mandible to increase posterior airway space) or upper airway surgery (e.g. combined tonsillectomy/ adenoidectomy, nasal reconstruction, and uvulopalatopharyngoplasty). Different upper airway surgical procedures can be used for particular cases with craniofacial abnormalities .
Treatment for OSA May Have Little Affect on Depression
Overall, CPAP treatment studies for OSA and its effect on depressive symptoms have yielded controversial findings.
Among the negative studies on CPAP therapy and its effect on depression, Borak et al. did not observe any improvement in emotional status after 3 and 12 months of CPAP therapy in 20 patients with severe OSA, similar to Munoz et al. who also did not show improvement of BDI scores in 80 subjects with severe OSA after 12 months of CPAP. Using subtherapeutic CPAP as the placebo control, Yu et al. and Henke et al. found no difference in improvement on depression scores between the treatment and the control group, over a short treatment duration (1–3 weeks). However, whereas Borak, Munoz and Henke do not find any effect of CPAP therapy on mood, Yu observed a positive effect on mood of both CPAP therapy and the subtherapeutic CPAP control group.
Intriguingly, there are no systematic differences with regards to the sample size, the initial severity of OSA or the duration of CPAP therapy which might explain the differences between studies observing an improvement after CPAP therapy and those who did not. Several issues have to be considered: First, it is difficult to design a good control (“placebo”) condition for CPAP treatment. “Sham-CPAP” which uses insufficient positive airway pressure as a placebo condition (1 – 2 cm H20), is now used more frequently. Two of the negative studies employed this method for their control group, which raises the possibility that the previously observed positive effects of CPAP on mood may have been a placebo effect.
Second, compliance to CPAP treatment is problematic, because patients have to wear a nasal or even an oranasal device during the entire night. The compliance may even be particularly decreased in depressed patients.
Indeed, Edinger et al. reported a positive correlation between lower depression scores on the MMPI prior to treatment and CPAP compliance at 6 months of treatment in 28 patients. However, Lewis et al. did not find any association between baseline depression scores and subsequent CPAP use for the first month of treatment.
The most important factor to explain the differences among these studies may be the variability in the severity of initial depressive symptoms.
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