PTSD, Sleep Apnea and GERD: A Hypothesis
Wanted to share some thoughts I had today about the difficult problem of treating sleep apnea in people who are hypervigilant and therefore sleep too lightly to use CPAP. A group which includes me (as you will know if you have read any of my books on the subject)
Recent studies have shown that Post Traumatic Stress ( PTSD) is strongly associated with sleep apnea. For instance, servicemen and women returning from combat will often have a constellation of problems including PTSD/sleep apnea/migraine headaches. In order to treat any one of these three problems, all must be addressed. Many of these soldiers are young, have normal body weight and have no family history of sleep apnea (or migraines or mental illness). Compare this to the average sleep apnea sufferer in the civilian world who tends to be older, heavier and to have a strong family history of sleep apnea. These PTSD/sleep apnea patients tend to sleep more lightly, and they often cannot tolerate CPAP (which wakes them up).
Recently, dronabinol, the marijuana derivative that is used for intractable nausea and vomiting due to chemotherapy has been shown to decrease the severity of sleep apnea by one half in people with sleep apnea who are intolerant of CPAP. How does a medication whose primary effect is on the stomach and GI tract improve sleep apnea?
Let’s go back a moment to early infancy. There is something called the laryngeal chemoreflex that is very active in the new born up until about 6 months of age. When gastric acid creeps up the throat and gets near the airway---bam!—the airway squeezes shut, the baby stops breathing for a few seconds, the heart rate goes down, the baby swallows—and then the apneic spell is over. These spells happen an average of one to two times an hour in the sleeping infant. Usually no harm is done. The baby does not even wake up.
This type of reflex is important in the infant who spends most of his time lying on his back including immediately after meals. Aspiration pneumonia is dangerous. Eventually, the child outgrows the laryngeal chemoreflex---
But what if the chemical changes associated with PTSD bring the laryngeal chemoreflex back? A patient suffering from post-traumatic stress lies down to sleep. A little bit of stomach acid regurgitates into the esophagus—not enough to actually threaten the airway with aspiration. But if the same mechanism that makes that woman a bundle of nerves who jumps at every slammed door and car backfire during the day is working overtime at night too, then maybe the mere hint of stomach acid near the airway is enough to shut down breathing activity altogether. And, in an adult, such apneic spells are more likely to disturb the sleep, taking one from deep to light sleep or even causing the sleeper to wake to a feeling of panic or smothering.
The next part will get a little technical, so feel free to skip if biochemistry and neuroanatomy are not your hobbies. There is a portion of the vagus nerve called the nodose ganglion which, when 5HT receptors are stimulated causes reflex apnea. Researchers injected that ganglion with cannabinoids---and respiration improved, the apnea stopped. PTSD has been linked to disruption of normal neuroendocrine hormones including 5HT and serotonin.
If this hypothesis is correct, then perhaps we should be applying the lessons learned by pediatric sleep experts to the sleep apnea of young adults with PTSD. Gastroesophageal reflux disease is understood to be a factor in infantile sleep apnea. Perhaps it is a factor in certain forms of adult sleep apnea. This in turn raises the possibility that control of GERD might do more to help PTSD patients get a good night sleep than CPAP. It is also possible that we will see real progress in sleep apnea therapy, either through medications or treatments that affect the vagus nerve or even biofeedback to down grade the laryngeal chemoreflex.
Below are two particularly well written abstracts followed by a list of other references.
Obstructive sleep apnea (OSA) affects one in five adult males and is associated with significant comorbidity, cognitive impairment, excessive daytime sleepiness, and reduced quality of life. For over 25 years, the primary treatment has been continuous positive airway pressure, which introduces a column of air that serves as a pneumatic splint for the upper airway, preventing the airway collapse that is the physiologic definition of this syndrome. However, issues with patient tolerance and unacceptable levels of treatment adherence motivated the exploration of other potential treatments. With greater understanding of the physiologic mechanisms associated with OSA, novel interventions have emerged in the last 5 years. The purpose of this article is to describe new treatments for OSA and associated complex sleep apnea. New approaches to complex sleep apnea have included adaptive servoventilation. There is increased literature on the contribution of behavioral interventions to improve adherence with continuous positive airway pressure that have proven quite effective. New non-surgical treatments include oral pressure devices, improved mandibular advancement devices, nasal expiratory positive airway pressure, and newer approaches to positional therapy. Recent innovations in surgical interventions have included laser-assisted uvulopalatoplasty, radiofrequency ablation, palatal implants, and electrical stimulation of the upper airway muscles. No drugs have been approved to treat OSA, but potential drug therapies have centered on increasing ventilatory drive, altering the arousal threshold, modifying loop gain (a dimensionless value quantifying the stability of the ventilatory control system), or preventing airway collapse by affecting the surface tension. An emerging approach is the application of cannabinoids to increase upper airway tone.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4242689/
The classic fight-or-flight response to perceived threat is a reflexive nervous phenomenon that has obvious survival advantages in evolutionary terms. However, the systems that organize the constellation of reflexive survival behaviors following exposure to perceived threat can under some circumstances become dysregulated in the process. Chronic dysregulation of these systems can lead to functional impairment in certain individuals who become “psychologically traumatized” and suffer from post-traumatic stress disorder (PTSD), A body of data accumulated over several decades has demonstrated neurobiological abnormalities in PTSD patients. Some of these findings offer insight into the pathophysiology of PTSD as well as the biological vulnerability of certain populations to develop PTSD, Several pathological features found in PTSD patients overlap with features found in patients with traumatic brain injury paralleling the shared signs and symptoms of these clinical syndromes.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3182008/
Some additional references:
https://academic.oup.com/sleep/article/41/1/zsx184/4600041
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5448577/
https://www.sciencedirect.com/science/article/pii/S1569904813003273
https://www.biomed.cas.cz/physiolres/pdf/62/62_227.pdf
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3629370/
= new reply since forum marked as read
because of the shape of the stomach.. 
I had severe gastritis as a young adult
Sleep apnea for the last 20 years
and was recently diagnosed with PTSD
Your effort couldn't be more timely. 
Seriously bad sleep. People wonder why I live on coffee. 
