Insomnia and Hypertension: Connecting the Zzzots

Abstract

THE STUDY OF VGONTZAS ET AL ON INSOMNIA AND HYPERTENSION ASSERTS THAT THE COMPLAINT OF INSOMNIA COUPLED WITH OBJECTIVELY DETERMINED short sleep duration (<5 or 5-6 h) increased risk for hypertension by 350% to 500% compared to individuals without insomnia who slept longer than 6 hours per night.1 The pathophysiology of insomnia and its related effects on the HPA axis as well as the hyperarousal described in Bonnet's accompanying commentary2 are offered as likely pathways through which insomnia and hypertension might be linked. This outstanding work provides critically important information to the scientific literature in support of the emerging perspective that: the patho-physiologicalcomponent of insomnia must be appreciated; healthcare providers must evaluate insomnia with greater precision; and, this complex medical and psychological condition must be treated more aggressively. To this excellent work, however, Occam's razor might shave away some of the authors' elaborations. Specifically, three crucial elements seem to be missing from their protocol or discussion, which upon further reflection might steer the interpretation of findings towards a more parsimonious theory. First, the protocol used only thermocouple technology and a thoracic strain gauge, did not score flow limitation events, and therefore likely underestimated the severity of obstructive sleep apnea in the population tested. (As a reminder, AASM current nosology supplants the term UARS with the term OSA. If a patient has UARS, then per new nosology the patient has OSA.3) In our clinical and research experience, we have consistently shown that whenever a proportion of insomnia patients test positive for OSA, there are always an equal or greater number of UARS cases present in the same sample when efficacious respiratory sensor technology is used.4 In the Vgontzas et al's group with the highest hypertension rates (sleeping 6 h). In our experience, at least another 20% would have been diagnosed with OSA or UARS in the group with highest hypertension rates had pressure transducer technology been used. Second, in 1996 Guilleminault et al developed strong anecdotal evidence that UARS without any pertinent comorbid factors, including apneas, hypopneas, hypoxemia, or obesity, was linked to hypertension. Indeed, aggressive treatment of this very bland form of UARS resulted in a return to normal blood pressure in every patient who faithfully used positive airway pressure therapy.5 Third, virtually every point discussed in the article on the potential impact of insomnia on various physiological parameters has already been investigated in OSA patients, and many links have been discovered6. Specifically, well-documented OSA interactions with the HPA axis, the metabolic syndrome, and hypertension indicate it would not be unreasonable to speculate that insomnia and sleep disordered breathing are merely opposite sides of the same coin, which might explain more about the relationships between sleep disturbances and hypertension than currently appreciated6. Then again, it would be tempting to dismiss such a relationship because the authors controlled for OSA in their analyses. Perhaps, but it cannot go without saying that current OSA metrics have a long history of yielding weak or equivocal associations with a large number of sleep symptoms as well as other mental and physical health complaints. In sum, we suspect that “complex insomnia”4—the condition of comorbid insomnia and SDB—was significantly and markedly higher in Vgontzas et al's sample of patients with hypertension compared to those without hypertension. Although it does not necessarily follow that a link between complex insomnia and hypertension would obtain, the association would be stronger, thus pointing to the need for further research. Regrettably, this speculation cannot be retroactively tested due to the absence of the necessary technology that would have measured all sleep breathing events instead of only apneas and some hypopneas. For future insomnia research, we recommend the use of more advanced respiratory technology so that those patients with complex insomnia can be accurately contrasted with those patients with classic insomnia.