“Anyone who is willing to sleep while wearing a CPAP is being terribly misled.” Ray Peat PhD
According to Western Medicine, Sleep Apnea is a medical sleep disorder that is characterized by pauses in breathing while asleep. Sleep apnea is commonly undiagnosed and can lead to heart issues, insomnia, high blood pressure, moodiness, slow-reflexes and weight gain.
The common recommendations to resolve sleep apnea include weight loss, quitting drinking and smoking, avoiding caffeine, avoiding sleeping pills and sedatives and altering your sleep position. Worse case scenario a continuous positive airway pressure (CPAP) is recommended. These recommendations have proved to be effective in managing the problem yet not so convincing in their ability to “fix” the problem.
In our clinical practice what we have witnessed are the most severe cases resolve by using nutrition to boost cellular respiration, an effective approach in managing hypothyroidism. Interestingly enough, thereis a high incidence of sleepapnea in patients with untreated hypothyroidism.
The thyroid gland lies in the front of the neck below the Adam’s apple and is usually larger in women. Thyroid hormone regulates metabolism by teams up with other hormones and processes to insure the body produces the energy it needs. It is the only gland to store its own hormones (100 day supply) and over 80% is converted peripherally and only about 10% in the thyroid.
Metabolism depends on fuel intake, the quality and the quantity of food eaten. The enzymes work as part of the energy production team, the adrenal hormones control storage and transport and a host of hormones including insulin handle the main fuel glucose. Thyroid hormone is the regulators of these processes. When thyroid hormone is inadequate energy production by the body will be inadequate.
The thyroid, by way of its production of thyroid hormones (T4 and T3), activates over 100 cellular enzymes responsible for a number of functions in every cell of the body. Every metabolic process is affected by thyroid hormone. The production of thyroid hormone is regulated by a feedback mechanism involving the hypothalamus and pituitary gland. As a monitoring station, the hypothalamus releases thyrotrophic releasing hormone (TRH) in response to levels of T4 in the blood. TRH then stimulates the pituitary to release thyroid stimulating hormone (TSH), which then signals the thyroid to produce and release hormones.
Once the signal comes through the thalamus to the hypothalamus that thyroid hormones are adequate, the following takes place: hypothalamus shuts down the production of TRH, the pituitary shuts down production of TSH and the thyroid stops releasing thyroid hormones.
Two things can cause the pituitary to secrete excessive amounts of gonadotropins:
- A deficiency of the steroids
- Damage to the steroid-sensing nerves that regulate the pituitary
- Most endocrine glands such as the anterior pituitary excrete their hormones out in spurts, so the actual blood level depends upon when the last spurt occurred. Circadian rhythms, dependent upon the time of day, are involved in hormone control. This is true for the output of TSH, suggesting that thyroid output also has a daily rhythm. TSH is higher at night, secondary to the liver doing most of its repairs and utilizing more thyroid hormone.
According to Julia Ross MD, “One of the main causes of sleep apnea is serotonin deficiency. Studies using AA tryptophan and 5HTP have shown them to be helpful. Why? To begin, serotonin directly affects the lungs. Second, lots of O2 is required for serotonin production, so if physical obstructions block O2 flow, serotonin production is diminished. Third, if a preexisting low-serotonin condition caused characteristic afternoon and evening carb craving, increased weight could easily result, contributing to obstructed breathing.”
Unfortunately, theorizing a relationship solely between serotonin and tryptophan can be dangerous as there is no consideration of the other hormones and enzyme factors at play within this relationship. Maintaining a functional level of serotonin is a tricky game in modern day society as serotonin plays a leading role in chronic inflammatory cycles associated with hypothyroidism.
Hypometabolic/hypothyroid conditions exacerbate the rate in which tryptophan is being converted to serotonin by as much as 60%! According to Ray Peat PhD, this elevated conversion of tryptophan to serotonin increases estrogen and estrogen promotes serotonin, and there begins the vicious cycle. Serotonin in excess:
· Lowers CO2 levels further down regulating the thyroid
· Increases cortisol production, decreases T3 and increases rT3 (inactive thyroid hormone).
· GI Leakiness- Increases in the absorption of endotoxin in the small intestine
· Promotes a state of hibernation not the appropriate REM sleep necessary for adequate cellular recovery.
These processes of inflammation inhibit mitochondrial respiration by restraining carbon dioxide (CO2) production, reducing O2 to the tissues and increasing lactic acid production.
Additionally, in a hypometabolic state there is an adaptive increase in the sympathetic nervous system, which produces more adrenaline (up to 40x the normal rate). The adrenaline helps to sustain blood sugar and body temperature by causing vasoconstriction to the skin (cold hands and feet), but can also lead to disrupted sleep and an accelerated heart beat.
“Hypothyroidism can also worsen depression, cognitive function, arthritis, muscular aches, memory, respiratory problems, and sleep apnea.” Kenneth Ain MD
Three key aspects of CO2 production are oxygen, T3 and sucrose. In an efficient state our cells produce CO2 through optimal cellular respiration: the mitochondrial use of O2 to produce CO2 and energy (ATP). If our cells are not receiving optimal O2, they are being pushed toward anaerobic glycolysis, a very inefficient energy system. Low levels of O2 will interrupt cellular respiration and shift cells energy production away from CO2 and towards producing lactic acid.
Lactic acid is a huge metabolic burden to the metabolism. It is not only inflammatory and moves your cells away from energy production but it also causes the liver to use up stored glycogen. The body depends on this stored energy for times of stress. Stress of any kind will increase the cells need for glucose, signaling adrenaline. Because no glycogen is available for conversion the adrenaline encourages the release of fatty acids to be converted into useable energy. This can be sustained for a short period of time however these conditions are very common and equally as chronic.
The effects of adrenaline on respiration have been studied and sited since way back showing adrenaline causes apnea partly by increasing the cerebral blood flow and washing out CO2 and partly by a direct action on the nerve cells of the respiratory center.
Acta Neurobiol Exp (Wars). 2007;67(2):197-206. Role of hypercapnia in brain oxygenation in sleep-disordered breathing. Brzecka A. Adaptive mechanisms may diminish the detrimental effects of recurrent nocturnal hypoxia in obstructive sleep apnea (OSA). The potential role of elevated carbon dioxide (CO2) in improving brain oxygenation in the patients with severe OSA syndrome is discussed. CO2 increases oxygen uptake by its influence on the regulation of alveolar ventilation and ventilation-perfusion matching, facilitates oxygen delivery to the tissues by changing the affinity of oxygen to hemoglobin, and increases cerebral blood flow by effects on arterial blood pressure and on cerebral vessels. Recent clinical studies show improved brain oxygenation when hypoxia is combined with hypercapnia. Anti-inflammatory and protective against organ injury properties of CO2 may also have therapeutic importance. These biological effects of hypercapnia may improve brain oxygenation under hypoxic conditions. This may be especially important in patients with severe OSA syndrome.
Respiration or breathing is the exchange of gases between the organism and their environment. When something interferes with the normal productive use of O2 (as seen above with estrogen, lactic acid and serotonin), there is an increase in the destructive forms of oxidation, such a lipid peroxidation with PUFA’s. Excessive inflammatory processes induced by rapid and chronic oxidation leads to “tissue suffocation” or hyperventilation.
The definition of hyperventilation states that you are breathing more than your body requires. There is so much CO2 lost in the breath that our tissue and cell respiration is impaired and/or lost, creating this “tissue suffocation.”
“Hypothyroid people do not make enough carbon dioxide (CO2) or progesterone, and so they are in a chronic state of hyperventilation-hypocapnia (Ray Peat PhD).
Eliminating sleep apnea requires a decrease in the factors inhibiting optimal cellular respiration (estrogen, serotonin, adrenaline, low thyroid hormones, vitamin and mineral deficiencies, etc. Doing so will reduce hyperventilation and allow for an increased retention of CO2.
Using the right combination of digestible carbohydrates proteins and fats along with the appropriate supplementation (if needed) is very effective in restoring efficient energy production in the body. Normalizing cellular respiration and eliminating the negative effects of adrenaline on respiration leads to more restful sleep and the debilitating effects of sleep apnea.References:
1. Ain, Kenneth MD. The Complete Thyroid Book. 2012
2. Brzecka A. Role of hypercapnia in brain oxygenation in sleep-disordered breathing. Acta Neurobiol Exp (Wars). 2007;67:197-206.
3. Chiang AA. Obstructive sleep apnea and chronic intermittent hypoxia: a review. Chin J Physiol. 2006;49:234-243.
4. Ekstedt M, Akerstedt T, Soderstrom M. (2004). Microarousals during sleep are associated with increased levels of lipids, cortisol, and blood pressure. Psychosom Med. 2004;66:925-931.
5. Lee, Lita PhD. Thyroid and Enzyme Nutrition. 2011
6. Hirshkowitz M. The clinical consequences of obstructive sleep apnea and associated excessive sleepiness. J Fam Pract. 2008;57(suppl 8):S9-S16.
7. Peat, Ray PhD. Protective CO2 and Aging.
8. Rubin, Joshua and Jeanne. The Metabolic Blueprint: CO2 Made Simple. 2012
9. Rubin, Joshua and Jeanne. The Metabolic Blueprint: Understanding Oxidative Metabolism. 2012
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