In this article we will succinctly explore the interesting webwork that exists among sleep apnea, TMDs, Ehlers-Danlos syndrome, and POTS, beginning with sleep apnea.
Sleep apnea is a condition in which airflow repeatedly ceases or is markedly reduced during sleep (resulting in intermittent hypoxia and sleep fragmentation) [1]. Mechanical occlusion of the upper airway characterizes obstructive sleep apnea, while central sleep apnea involves faulty respiratory signaling from the brain. The term ‘complex sleep apnea’ is typically used to describe the emergence of central sleep apnea following the initiation of CPAP therapy (these occurrences usually resolve on their own with time) [2]. With a pause in breathing comes a buildup of carbon dioxide in the blood which triggers the brain to wake the individual so that oxygen levels can be restored [3]. These recurring interruptions rob the apnea sufferer of restorative sleep because there is not a normal progression through the sleep cycle. With obstructive sleep apnea, some degree of soft tissue collapsing or narrowing, usually within the oropharynx, obstructs the airway (nasal congestion or a deviated septum can block things as well) [4] [5]. This narrowing comes from a reduction in the activity of upper airway dilator muscles which is more pronounced in those with OSA [6]. Significant diminishing of upper airway dilator muscle activity can lead to pharyngeal collapse [7]. So problems in pharyngeal anatomy, pharyngeal dilator muscle activation, and ventilatory control can all contribute to the experiencing of apneas (these can include damage to or dysfunction in upper airway dilator motoneurons) [8] [9]. Lung volume, upper airway surface tension, and rostral fluid shift can all play a part too [10]. In central sleep apnea, there is a lack of neurological drive to breathe during sleep, which results in repetitive periods of poor and aberrant ventilation and gas exchange [11]. But there can be overlap between central and obstructive sleep apnea, which can make the elucidation of individual etiologies more complicated [12]. Diagnosis of sleep apnea can be based on a physical exam and the results of a sleep study (the individual’s medical history may also be consulted) [13]. Polysomnography is the gold standard for evaluating sleep [14]. Some surgical options for the treatment of sleep apnea include the removal of tissues in the throat (using a scalpel, laser, or radiofrequency radiation) to open the airway, repositioning of the jawbones (maxillomandibular advancement), and hypoglossal nerve stimulation to move the tongue forward [15]. Non-surgical options involve the use of an airway pressure device (APAP, CPAP, or BiPAP) or oral appliance, as well as exercises from orofacial myofunctional therapy to restore proper oral rest posture [16]. Oral pressure therapy and nasal EPAP are newer modalities that have demonstrated some efficacy [17] [18]. A continuous positive airway pressure (CPAP) device is the most commonly prescribed, yet side effects such as dry mouth and tooth movement can arise in some users [19]. Oral appliance therapy has been shown to be safe and effective in general, though oral appliances can vary greatly and undesirable tooth position and occlusion changes are possible with extended use [20]. Tongue-stabilizing devices are simpler and can be quite effective while carrying less potential for side effects [21]. Combining modalities is also an option and doing so may give better success [22]. In the neuropsychological domain, depression and anxiety are commonly seen with obstructive sleep apnea, as well as executive dysfunction and impaired vigilance (translates to difficulty with concentration, planning, organizing, time management, regulating emotions, sustaining motivation, and remaining alert) [23]. Obstructive sleep apnea has been linked to insulin resistance and hyperlipidemia (both of which can contribute to non-alcoholic fatty liver disease), and hypoxia is considered an aggravating factor for non-alcoholic fatty liver disease (NAFLD) [24] [25]. The increase in lipogenesis and inhibition of fatty acid oxidation by hypoxia play into the development of NAFLD [26]. And hypoxia seems to decrease adiponectin and increase leptin concentrations (adiponectin is a hormone that heightens insulin sensitivity and fatty acid oxidation while leptin signals satiety) [27] [28]. Insulin resistance and glucose intolerance are probably the main factors linking OSA with PCOS, but high testosterone and low progesterone can have notable influences too [29] [30]. There is some evidence that impaired leptin signaling in the brain may contribute to respiratory depression or hypoventilation in humans [31]. And it seems to at least be possible for proinflammatory cytokines released from adipose tissue to directly or indirectly impact respiratory control [32]. Thus it is wise to view OSA as more of a systemic condition rather than a simple local one [33]. Levels of nitric oxide have been found to be decreased in OSA patients but they normalize with CPAP therapy [34]. OSA patients present with a heightened production of superoxide by neutrophils and increased lipid peroxidation, and cyclical episodes of hypoxia-reoxygenation may deplete ATP and boost the making of free radicals [35]. In remediation, airway pressure devices can ameliorate oxidative stress, improve sleep, lower blood pressure, and reduce plasma renin and angiotensin 2 [36] [37]. Hypothyroidism and sleep apnea (both obstructive and central) have clinical presentations that overlap and it has been suggested that upper airway obstruction, neuropathy, and respiratory center depression are the variables that relate the two conditions to each other [38]. In fact, thyroid hormone replacement therapy has been shown to “diminish or completely eliminate apneic episodes and arterial oxygen desaturation, as well as to effect many improvements in sleep patterns and overall sleep efficiency,” per Kittle and Chaudhary and corroborated by Jha et al. [39] [40]. Moving on to POTS, postural orthostatic tachycardia syndrome is a form of autonomic dysregulation highlighted by excessive tachycardia upon standing with a kind of intolerance to the upright position (orthostasis) [41]. Typical symptoms consist of lightheadedness, fatigue, headache, weakness, palpitations, exercise intolerance, and presyncope or syncope [42]. And most individuals with POTS report sleep disturbances or non-restorative sleep and daytime sleepiness [43]. Technically, POTS is classified as a group of disorders that present as a common clinical picture, with primary POTS being considered idiopathic and secondary POTS occurring in tandem with another disease state [44]. The pathophysiology of POTS can consist of excessive sympathetic drive, volume dysregulation, impaired sympathetic vasoconstriction, and deconditioning [45]. Neuropathic POTS is the predominant form, and its onset usually abruptly follows viral illness, vaccination, pregnancy, sepsis, concussion, surgery, or traumatic stress [46]. Neuropathic POTS has been tied to partial autonomic neuropathy or damage to autonomic nerves [47]. POTS is mostly seen in women, and women with POTS have a much higher incidence of such gynecological ailments as uterine fibroids, ovarian cysts, endometriosis, and galactorrhea [48]. The greater prevalence of POTS in females may be partly due to differences in sympathetic nerve discharge characteristics between men and women [49]. At least some with POTS have been found to have a higher prevalence of autoimmune markers and comorbid autoimmune disorders than the general population [50]. In many POTS patients, autoantibodies against alpha 1-adrenergic receptors, angiotensin 2 type 1 receptors, or muscarinic receptors can be detected, and all of these receptors participate in the functionality of the autonomic nervous system [51] [52] [53]. Antibodies against these receptors may explain some of the features of POTS in that they could promote postural tachycardia and lower standing blood pressure, as well as trigger the maturation and degranulation of mast cells [54] [55]. Regular exercise, acupuncture, meditation, and omega-3 fatty acids can all improve vagal tone and thus could be useful in treating POTS [56]. Osteopathy may also be of aid [57]. Tying sleep apnea to POTS, intermittent hypoxia and carbon dioxide retention stimulate sympathetic nervous system activity, which stresses the cardiovascular system [58]. We know there is a strong relationship between OSA and high blood pressure, we know that hypoxia can drive sympathetic activation of the renin-angiotensin-aldosterone system (which could help explain the hyperadrenergic state of many POTS patients), and impairment to the vasodilation response has been seen in humans exposed to prolonged hypoxia [59] [60] [61]. Furthermore, prolonged hypoxia is capable of reducing the mass and respiration of mitochondria [62]. Because of the fragmenting of sleep and the greater hypoxemia during REM sleep, those with sleep apnea achieve less time spent in REM sleep [63]. Changes in heart rate variability (HRV) partly differentiate REM sleep from non-REM sleep, and in persons with POTS we see a pattern different from normal in the HRV changes between REM and non-REM sleep, which points to autonomic imbalance [64]. And manifestations as seemingly unrelated as achiness, eczema, thyroid troubles, sexual dysfunction, nocturia, and brain fog can all be correlated with abnormal sleep [65]. Accordingly, we must place sleep at the axis mundi of our consideration because if the body is not sleeping, it is not healing. Stepping to the next stone, a 2003 study by Gazit et al. suggests that dysautonomia (of which POTS is a type) may occur in roughly 80% of persons with Ehlers-Danlos syndrome [66]. Ehlers-Danlos syndrome is a group of connective tissue disorders characterized by joint hypermobility and can include weakness in the tissues that support organs and blood vessels for problems with collagen are typical with the syndrome [67]. Poor sleep, fatigue, and psychologic distress are common in those with Ehlers-Danlos syndrome (EDS), and adult populations with EDS are more likely to have sleep-disordered breathing or obstructive sleep apnea because of the oral and maxillofacial manifestations of the malady [68]. Exercise therapy can be very beneficial for EDS and supplementation with such nutrients as vitamin C, magnesium, glucosamine, MSM (methylsulfonylmethane), coenzyme Q10, carnitine, and pycnogenol has been proposed to treat the expressions of EDS [69] [70]. Hydrocephalus, CCSVI (chronic cerebrospinal venous insufficiency), and mastocytosis have been labeled potential culprits in the pathogenesis of POTS (especially in Ehlers-Danlos syndrome subjects), which makes sense as problems with the flow or drainage of cerebrospinal fluid and blood in the central nervous system could cause autonomic dysfunction [71] [72]. A faulty capacity to drain cerebrospinal fluid or a weak blood-brain barrier (which can be seen in Ehlers-Danlos) could make the brain more susceptible to the sudden onset of POTS symptoms after trauma to or viral infection of the brain (which is frequently seen) [73]. Now let’s look at the final node in our web: TMDs. Temporomandibular disorders (TMDs) frequently stem from abnormal muscular tension around the temporomandibular joint or anatomical derangements affecting the joint [74]. Hypermobility and arthritis can have a role too [75]. TMDs can certainly have a multifactorial etiology, with dental occlusion often being a misunderstood piece of the puzzle [76]. Multiple criteria can be referenced for the diagnosis of a TMD, which is often done clinically but can be aided by medical imaging [77]. Temporomandibular disorders are more common in POTS patients [78]. Manual therapy and therapeutic exercise can be used effectively for treating TMDs [79]. Acupuncture and low-level laser therapy may also be helpful, and while there are surgical options for the treatment of TMDs, they are usually not recommended [80] [81] [82]. On average, the modern human has smaller jawbones and a smaller airway than those of our predecessors, and this is a result of our conventional diet and means of feeding infants [83]. So it stands to reason that a firm relationship exists between TMDs and obstructive sleep apnea because TMD-related orofacial issues can compromise airway patency [84]. Oral appliances can be successfully employed for TMDs (including sleep bruxism or teeth grinding) and OSA, but there is potential for these devices to exacerbate or even promote the development of TMDs [85] [86]. However, sometimes the pain or discomfort that can come with the initiation of oral appliance therapy subsides on its own [87]. Long-term use tends to bring about a higher risk of dental changes and issues with the temporomandibular complex [88]. Extensive literature indicates that TMDs are around one and a half to two times more prevalent in women than in men [89]. And TMDs have been associated with multiple comorbidities, as Hoffmann et al. have uncovered: “The most frequent comorbid conditions included fibromyalgia, chronic fatigue syndrome, irritable bowel syndrome, rheumatoid arthritis, chronic headache, depression, and sleep disturbances. Commonly associated comorbidities will surely provide clues about pathophysiology. For example, a relevant finding was the high prevalence of allergies that preceded the TMJD diagnosis suggesting an autoimmune etiology for a subset of TMJD patients” [90]. So temporomandibular disorders (including sleep bruxism), sleep-disordered breathing, and POTS can all be connected to each other [91] [92]. The pathway to correcting one or more of these hardships can vary and therefore must be individualized. But we understand the webwork, and with natural medicine we can put the necessary pieces together and place the person in the best position to heal. The body is capable of amazing turnarounds when we remove its restraints, and when we permit the life force to flow freely, we can be gifted with a displaying of true medicine. References:
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AuthorDenton Coleman is an Exercise Physiologist and Medical Researcher. Archives
October 2023
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