Following are excerpts from
i_am_jim's previous post:
i_am_jim wrote:I've seen lists like that before. Forgive me, but it's just this sort of, 'it's the cause and cure of almost everything' that makes sleep apnea have the ring of snake oil.
These bogus claims sound much like your list of ailments associated with sleep apnea, and it’s one of the things that make me leery of the whole area.
In reading posts in apnea discussion groups the majority of the anecdotal reasons people give for the benefits of treatment are things like “I feel better,” “I’m not as stressed out,” “I’m happier and more content,” “My life is better/improved,” etc. These are the kinds of things people say about a wide array of pseudo medicines and quackery.
There are many studies and much evidence regarding SDB and the link to the above listed health issues. Instead of pouring your efforts into questioning the fact that sleep apnea causes many health problems, and instead of asking members of this forum to provide you with the proof, perhaps you should take the time to research the evidence yourself.
May I suggest you start with this from Pulmonary and Critical Care Update:
Cardiovascular Abnormalities in Sleep-Disordered Breathing
Here is an excerpt:
Acute Cardiovascular Changes in Apnea
In patients with SDB, repetitive upper airway obstruction during sleep leads to cyclic decrements in airflow (apneas and hypopneas), which are terminated by cyclic brief arousals that lead to transient resumption of airflow. The apnea-recovery-apnea cycle may occur hundreds of times over the night. Varying levels of cyclic oxygen desaturation are associated with respiratory events, with the oxygen desaturation nadir occurring at the termination of the event. The severity of oxygen desaturation depends upon the length of the respiratory events, the completeness of airway obstruction (apnea vs hypopnea), the frequency of respiratory events, and the oxygen stores in the lung, which, in turn, depend upon body weight, body position, and the presence or absence of respiratory disorders. In addition, other factors that affect oxygen delivery and consumption are likely to be important. Because of the normal motor atonia of REM sleep, individuals are more at risk for the development of apnea during REM sleep than NREM sleep. Oxygen desaturation also tends to be more prominent in REM sleep.
In association with recurrent apneas, there are cyclic changes in blood pressure, heart rate, and central hemodynamics, which may have acute effects (Table 2). Blood pressure is lowest at the start of the apnea, increases gradually during the event, and rises markedly at apnea termination coincident with arousal, the nadir of oxygen saturation, and the release of negative intrathoracic pressure and resumption of airflow. The normal dipping pattern of blood pressure during sleep may disappear and be replaced by a pattern such as the one shown in Figure 1. Heart rate decreases during apnea, particularly just before apnea termination, and accelerates with arousal. Pulmonary artery pressure increases with apnea, with the greatest increments during REM sleep in patients with daytime pulmonary hypertension. Reductions in stroke volume and cardiac output, most marked at apnea termination, have been reported in humans, although more recent animal data suggest that stroke volume declines during apnea and returns to normal at apnea termination. Cerebral autoregulation is insufficient to protect the brain from these hemodynamic changes and cerebral perfusion pressure declines, particularly early in apnea when increased intrathoracic pressure is associated with a fall in systemic blood pressure and a rise in central venous pressure with a concomitant increase in intracerebral pressure. Continuous positive airway pressure (CPAP) therapy of SDB has been shown to improve many of these transient hemodynamic changes.
Table 2—Acute Cardiovascular Changes in Apnea Parameters Altered During Recurrent Apneas
Heart rate
Blood pressure
Central venous pressure
Pulmonary artery pressure
Cardiac output
Stroke volume
Cerebral perfusion pressure
Potential Acute Effects
Arrhythmias
Myocardial ischemia
Cerebral ischemia
Nocturnal pulmonary edema
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Figure 1. A 9-min polysomnographic segment from a patient with SDB. Note the elevations in systemic blood pressure following apnea termination as well as the transient decreases in systolic blood pressure (arrows) when inspiratory efforts were made during the obstructive portion of the mixed apnea. Reprinted with permission from Shepard.
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The acute consequences of SDB during the night may include arrhythmias and conduction disturbances, cardiac and cerebral ischemia, and nocturnal pulmonary edema. Tachy-brady arrhythmia is the most common arrhythmia associated with SDB, but sinus pauses, heart block, and ventricular ectopy have all been described. Owing to an imbalance in oxygen delivery and consumption, acute cardiac and cerebral ischemia may occur in patients with preexisting vascular disease, but this has been less well characterized. Nocturnal pulmonary edema has been described in humans and in animal models of obstructive sleep apnea.
Pathophysiologic Mechanisms of Acute Cardiovascular Changes in Apnea
As detailed in a recent review, the proposed pathophysiologic mechanisms for the acute cardiovascular changes that accompany the apnea-recovery-apnea cycle include (1) negative intrathoracic pressure, (2) hypoxia, and (3) arousals. Negative intrathoracic pressure resulting from upper airway obstruction is associated with increased left ventricular transmural pressure with resultant increased left ventricular afterload and increased venous return to the right heart, leftward shift of the interventricular septum, and resultant decreased preload of the left ventricle. The combination of increased afterload and decreased preload leads to a decrease in stroke volume during apnea and an initial fall in blood pressure. Aortic baroreceptors are activated by the increased transmural intrathoracic aortic pressure, but carotid baroreceptors are inhibited because of the fall in blood pressure related to the decreased cardiac output. Sympathetic nerve activity is initially suppressed because the effect of aortic baroreceptors predominates. As the apnea continues, hypoxia may occur, with or without hypercapnia, and this, in turn, stimulates sympathetic output via peripheral chemoreceptors. Sympathetic activity increases peripheral vascular resistance through a-adrenergic receptors in the peripheral vasculature and increases heart rate and cardiac output through cardiac receptors. Thus, as shown in Figure 2, cyclic changes in blood pressure and heart rate mirror the changes in sympathetic tone. Arousals also contribute to the sympathetic activation at the termination of the apnea.
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As you can plainly see, from just this one article, this is not snake oil, pseudo medicine, or quackery.
You wrote:
i_am_jim wrote:But given all this, and given the fact that I’ve lived with a relatively severe case of the disorder for 50 years, yet none of the dire consequences have come to pass, and given that after using the remedy for a month it isn’t obvious anything other than the immediate and temporal effects of the disorder have been mitigated, I have to wonder how much of the claims are real.
but you also wrote:
i_am_jim wrote:So, I’ve lived with this condition constantly all this time and of the defined side effects, the only major one that could be associated with it is hypertension. But, for many reasons I do not think my hypertension is caused by sleep apnea.
I guess we'll never know what caused your hypertension. But 50 years of sleep apnea is a likely contributing factor based on the proven scientific medical evidence.
