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How to Sleep over 300pnds

bluto

Member
Registered
Joined
Aug 9, 2005
Messages
220
How do all the big guys sleep?

The heavier I get the worse my snoring gets and the more times I wake up during the nite. I know I have sleep apnea of some kind but really dont want to strapped to a cpap machine forever.

Do all the big pros use chemical sleep aids, or cpaps or what?
 
You can use a sleep aid to remain sleeping, but if you have sleep apnea you really wont be in the REM sleep and getting the oxygen you need from your sleep.
I use a sleep aid to fall asleep and its make sit easier to use the CPAP.
 
I sleep on my back with a CPAP strapped to my face. I sleep very well. You have 3 choices: 1) Get a sleep study done and get the CPAP or 2) Lose weight or 3) Drop dead at an early age. You make the call. I know 2 people that had CPAPS and didn't use them. One fell asleep at the wheel on his way home from work. He crossed the center line and hit a semi at 55mph. The other died from a heart attack at 42yo.

PB
 
cpaps and bodybuilders

So I take it then that alot of pro bodybuilders/powerlifters/weightlifters/strongmen are using cpaps?
 
I sleep on my back with a CPAP strapped to my face. I sleep very well. You have 3 choices: 1) Get a sleep study done and get the CPAP or 2) Lose weight or 3) Drop dead at an early age. You make the call. I know 2 people that had CPAPS and didn't use them. One fell asleep at the wheel on his way home from work. He crossed the center line and hit a semi at 55mph. The other died from a heart attack at 42yo.

PB

Im trying to loose as much weight as possible because I have a hard time using my CPAP all the time and it really affects me if i don't.
 
So I take it then that alot of pro bodybuilders/powerlifters/weightlifters/strongmen are using cpaps?

I doubt it with bodybuilders, just because the guy is 300 lbs does not mean he has respiratory problems, because they usually do not carry the bodyfat powerlifters do.
 
I doubt it with bodybuilders, just because the guy is 300 lbs does not mean he has respiratory problems, because they usually do not carry the bodyfat powerlifters do.

It does not necessarily have to do with body fat.
 
I hope this is helpful to some of you

OSA-obstructive sleep apnea


MORE ON APPLIANCES



Dental Appliance Therapy in the Treatment of Snoring and 0SA

This is not a comprehensive review of the scientific literature. New information that has emerged since the publication in 1995 of the ASDA Guidelines for the use of dental appliances in the treatment of OSA (12) is presented. This new information comes from studies of how the upper airway changes when the mandible is advanced, and from controlled trials comparing dental appliances to CPAP in the treatment of OSA. Also, a model is presented that explains how dental appliances work in the treatment of snoring and OSA.

OSDB refers to Obstructive Sleep - Disordered Breathing - a term that includes Snoring, OSA, and Upper Airway Resistance Syndrome.



What are Dental Appliances?

A dental appliance is a device that the patient wears in their mouth as they sleep that is intended to prevent vibration and collapse of the upper airway. There are three basic kinds of dental appliances that are used in the treatment of Snoring and OSA:

Devices that pull the tongue forward that are useful in properly selected patients.
Devices that use a flange at the base of the tongue to hold the tongue out of the pharynx which are ineffective and often dangerous.
Devices that advance the mandible and which are the most effective kind.
3 Basic Kinds of Dental Appliances



How Does Advancing the Mandible Improve the Sleeping Airway?

The concept of being able to open the airway by simply pulling the mandible forward to move the base of the tongue out of the back of the throat is an oversimplification. The tongue is part of a complex muscular apparatus that participates in speech, swallowing, and breathing and it cannot be considered in isolation of its anatomic relationships to surrounding structures in the upper airway.

Mandibular Advancement


Recent studies have shown that changes occur in the upper airway at several levels when the mandible is pulled forward. A study by Isono et al (1) used video endoscopy to examine the effects of advancing the mandible on the pharyngeal airway of 13 patients with OSA who were under general anesthesia with total muscle paralysis. They found that advancing the mandible widened the retropalatal airway as well as that at the base of the tongue. They applied negative pressures to the airway and showed that a more negative pressure was required to cause collapse of the airway when the mandible has been advanced. In their discussion, they postulated that one of the mechanisms by which mandibular advancement stabilizes the soft palate and retropalatal airway is through tension transmitted along the palatoglossus muscles to the soft palate.

A study by Schwab et al (2) using MRI on snorers while they were awake showed that advancing the mandible resulted in a greater increase in the lateral than the A-P dimension of the airway. CPAP produces a similar change (3).

Wearing an appliance will also prevent the mouth from falling open during sleep. A study by Meurice et al (4) showed that upper airway collapsibility was increased in normal subjects while awake when their mouths were opened. They postulated that opening the mouth causes narrowing of the upper airway and reduces the efficiency of upper airway dilator muscles.

Therefore, wearing a dental appliance that advances the mandible may stabilize the upper airway by:

pulling the base of the tongue forward,
pulling the soft palate forward and putting the walls of the upper airway under tension,
keeping the mouth from falling open during sleep.
These are primarily passive mechanical effects that can be explained by applying simple physical principles to what is known about the anatomy of the upper airway.

The critical anatomic relationships in terms of improving the sleeping airway with mandibular advancement are as follows:

insertion of the tongue into the mandible anteriorly,
linkage of the soft palate to the tongue by insertion of the palatoglossus muscles into the sides of the tongue,
linkage of the palatopharyngeus muscles to the palatoglossus muscles through the palatine aponeurosis,
linkage of the superior and middle pharyngeal constrictors to the mandible via their insertion on the pterygomandibular raphe, a fibrous band that extends from the inferior hamulus of the pterygoid to the medial surface of the angle of the mandible.
Key Anatomic Relations in Mandibular Advancement

As a result of these linkages, as the mandible is pulled forward the following occurs:

the base of the tongue is pulled forward,
the soft palate is pulled forward by tension developed along the palatoglossus muscles,
as the soft palate comes forward, tension is transmitted along the palatopharyngeus muscles to the back wall of the pharynx,
the pharyngeal constrictors are elevated off of the cervical spine and anterior paraspinous muscles (longus capitis and cervicalis) because of their insertion on the pterygomandibular raphe,
lastly, tension is developed in the side walls of the pharyngeal constrictors by splaying of the arch formed on each side of the oropharynx by the palatoglossus and palatopharyngeus muscles.
It is important to keep the mouth closed. If the mouth is opened, tensile forces that are produced by advancing the mandible are directed partly downwards towards the feet. This increases the longitudinal tension in the pharynx and promotes collapse. However, there are situations in which combining advancement of the mandible with a slight increase in the opening of the jaw will help to further stabilize the soft palate without promoting collapse of other portions of the upper airway.

Effect of Increasing the Vertical Opening with the Mandible Advanced


As the mandible is advanced, the following sequence of events can be seen on endoscopy:

elevation of the base of the tongue which increases the A-P dimension of the hypopharynx,
advancement of the soft palate which increases the A-P dimension of the velopharynx,
forwards and sideways movement of the palatopharyngeus folds which widens and flattens the back of the pharynx,
an increase in the lateral dimension of the upper airway at several levels.
The net result is dilation and splinting of the velopharynx, oropharynx, and hypopharynx.

It is tension that stabilizes the structures in the upper airway. When you are awake, upper airway muscles are activated to produce this tension. A useful analogy to think of is that of tightening the skin on a drum so that it no longer sags. When you are asleep, these muscles become less active and tension is lost. CPAP restores this tension by applying an intraluminal pressure. When the anatomy is favorable, mandibular advancement can be as effective as CPAP in tensing and stabilizing the structures of the upper airway. A recent study by Oshima et al (5) demonstrates that mandibular advancement in properly selected patients with OSA results in a decrease in genioglossal EMG activity during sleep as has been observed in patients with OSA who use CPAP (6).

CPAP applies pressure to the inside of the upper airway that stretches the tissues and prevents their collapse. This pressure also acts as a counter-pressure to the pressure exerted by the tissues surrounding the upper airway. Advancing the mandible decompresses these same tissues. Either way, the net pressure in the tissues surrounding the upper airway is lowered resulting in widening of the upper airway.

Here are the key points:

The tissues of the upper airway are stabilized by putting them under tension.
Lowering the net pressure in the tissues surrounding the upper airway allows the upper airway to expand side to side.
CPAP accomplishes these goals by applying pressure to the inside of the upper airway. When the anatomy is favorable, mandibular advancement with a dental appliance can achieve the same goals.

CPAP vs. Mandibular Advancement


This model also explains why dental appliances that advance the mandible work better than tongue-retaining devices and devices that push the tongue forward by placing a flange at the base of the tongue. Tongue-retaining devices do pull the tongue and soft palate forward (7). Devices using a flange probably push the base of the tongue forward but the presence of the flange may actually increase the narrowing at the level of the soft palate. Neither type of device decompresses the tissues around the upper airway because they do not advance the mandible.



What is the Scientific Evidence that Advancing the Mandible Really Works?

CPAP is the gold standard for the treatment of OSA. There have been three controlled trials comparing dental appliances to CPAP in the treatment of OSA. A different dental appliance was used in each trial. However, all three of these appliances use the principle of advancing the mandible.

The first study, conducted by Clark et al (8), used the AMP or Anterior Mandibular Positioner. This device consisted of two custom fitted acrylic appliances joined by a Herbst attachment on each side which allowed for adjustable protrusion, jaw opening, and limited side to side motion. Twenty-one of 23 patients with OSA (mean apnea-hypopnea index (AHI) before treatment of 33.86 +/- 14.30) completed the crossover study comparing the AMP with CPAP. Although CPAP (mean AHI on CPAP of 11.15 +/- 3.93) was more effective than the AMP (mean AHI with AMP of 19.94 +/- 12.75) in eliminating OSDB in all patients (particularly those with severe OSA). There was no difference between CPAP and AMP in terms of improvement in daytime sleepiness. The patients were then given a choice as to which treatment they wanted to continue to use. At 3 to 10 months after completion of the crossover phase of study, 17 reported using the AMP nightly, 2 reported using the AMP most nights, 1 reported using CPAP, and 1 was not using either treatment.

The second study, conducted by Ferguson et al (9), used a device also referred to as an AMP but which is better known as the Silencer. This appliance uses an elastomeric material and the mandibular advancement is achieved with a special titanium hinge called the Halstrom hinge. This hinge allows stepwise advancement of the mandible and some side-to-side movement. This study also used a crossover design. Twenty-four patients with OSA (mean AHI before treatment of 26.8 +/- 11.9) were recruited to the study. Twenty patients completed all phases of the study. Three patients refused to crossover from the Silencer to CPAP. One patient dropped out of the study. Once again, CPAP (mean AHI on CPAP of 4.2 +/- 2.2) was more effective than the dental appliance (mean AHI with the Silencer of 13.6 +/- 14.5) in eliminating OSDB (particularly for those with the highest AHIs). Seventeen of the patients using the Silencer showed a reduction in their AHI to below 20, fourteen to below 10. All twenty patients showed a reduction of their AHI to below 10 while on CPAP. However, only 1 patient could not tolerate the Silencer whereas 6 patients could not tolerate CPAP. Patient satisfaction was greater with the Silencer than with CPAP. There was no difference between the 2 treatments in terms of improvement in daytime sleepiness.

The third study, conducted by Fleetham and Lowe et al (10), was a two-year randomized controlled trial of a third dental appliance, the Klearway, versus CPAP. The Klearway uses an advancement mechanism that consists of a worm screw in a flat metal plate that is suspended over the tongue by a wire frame. Fifty-nine patients were recruited to the study but only 42 completed the study. Nine patients dropped out because they could not tolerate the Klearway, 8 patients dropped out because they could not tolerate CPAP. For patients completing the CPAP arm of the study, the mean AHI before treatment was 41 +/- 28, and it was 5 +/- 3 while on treatment. For patients completing the Klearway arm of the study, the mean AHI before treatment was 35 +/- 14, and it was 13 +/- 12 while on treatment. There was no difference between the 2 treatments in terms of improvement in daytime sleepiness.

These studies demonstrate that dental appliances that advance the mandible are effective in the treatment of mild to moderately severe OSA. Any appliance that advances the mandible to the same degree can be expected to produce an equivalent reduction in the AHI. The issue then becomes one of comfort and compliance. In that respect, less intrusive appliances, such as the Clark AMP and the Silencer, may be better tolerated than bulkier appliances such as the Klearway (which had the same drop-out rate as CPAP in it’s recent trial). Studies are needed to measure the long-term compliance to these appliances. Of note, in an earlier study, only ~ 50 % of patients treated with the Clark AMP were still using it after 1 year. However, patients who tolerate dental appliances early on may continue to use them for extended periods. A recent study by Loube et al (11) showed that 70% of patients who were initially compliant with dental appliance use were still compliant at 3.4 +/- 0.7 years. However, they did not obtain sleep studies to determine if the appliances were as effective over the long-term as they were initially in this group of patients.



How Dynamic Nasopharyngoscopy Can Help You to Determine if Your Patient Can Use a Dental Appliance for Treatment of Their OSDB

In performing dynamic nasopharyngoscopy, it is best to try and simulate the conditions that exist when the patient is sleeping. The patient is examined while lying on their back with their soft palate and nasal passages anesthetized with topical Lidocaine.

The flexible endoscope is introduced through one of the nasal passages and advanced into the pharyngeal airway. The pharyngeal airway is examined along its entire length extending from the suprapharyngeal recess to the vocal cords. The patient is asked to perform 2 maneuvers during the examination.

In the first maneuver, the patient is asked to try and take a breathe in while keeping their lips sealed and having their nostrils pinched shut. This generates a negative pressure inside the pharynx. Patients with OSDB show one or more of the following responses to this maneuver:

lateral collapse of the velopharynx,
collapse of the soft palate against the back of the pharynx,
concentric collapse of the velopharynx (which invariably indicates Severe OSA),
collapse at the base of the tongue that conceals the epiglottis and the glottis.
In the second maneuver, the patient is asked to slowly advance their mandible to its most forward position. An airway that can be stabilized by mandibular advancement shows the following changes as the patient advances their mandible:

the soft palate moves forward and the velopharynx widens side to side,
the base of the tongue lifts off the epiglottis and the glottis is fully exposed.
Jaw Thrust

The following findings are absolute contraindications to the use of a dental appliance:

the soft palate completely seals off the velopharynx in the awake patient,
the velopharynx is completely or nearly closed off by tissue swelling,
advancing the mandible causes the velopharynx to become more narrow side to side,
the epiglottis and glottis are concealed by the base of the tongue and advancing the mandible does not bring them into view.
Advancing the mandible will not create a satisfactory sleeping airway in patients with these findings.

An example of endoscopic finding in a borderline candidate for dental appliance therapy is that of a partially-occluded velopharynx that shows some dilation as the mandible is advanced. The dilation indicates that some tension is being developed in the tissue by advancing the mandible. In this situation, the results of a sleep study are quite helpful in determining if the patient can safely use a dental appliance for treatment of their OSDB. An appliance can be used if the sleep study shows Primary Snoring, or Mild to Moderately Severe OSA. If it shows Severe OSA, the treatment of choice remains CPAP.

Up to this point, much of what has been said concerns patients with Primary Snoring or OSA. In theory, these concepts should apply equally well to UARS and REM-Specific OSA.

Mandibular Advancement with a Dental Appliance and the Upper Airway



The Potential Impact of Dental Appliance Therapy on the Management of OSDB

The medical community has been slow to accept dental appliance therapy as an effective treatment for OSDB. This is because there has not been an adequate explanation of how these devices work. However, the model presented of how they work makes use of well-established anatomic facts and is based on the same physical principles that underlie CPAP.

Dental appliances should be considered the treatment of choice for Primary Snoring. Most patients with Mild to Moderately Severe OSA can also use them successfully and generally prefer them to CPAP. Dental appliances are very likely to be effective for REM-Specific OSA. The jury is out on the use of dental appliances for the treatment of UARS. However, preliminary data from a study being conducted by Dr. David Rappaport and Dr. Michael Gelb at NYU indicate that dental appliances will be effective in this group of patients.

Dental appliances are not a cure - all for OSDB. However, dental appliances can be used in conjunction with CPAP and surgery to successfully treat a much broader spectrum of OSDB than would otherwise be possible.



References

Isono S, Tanaka A, Sho Y, Konn A, Nishino T: Advancement of the Mandible Improves Velopharyngeal Airway Patency. J Appl Physiol 1995; 79:2132-2138
Schwab RJ, Gupta KB, Duong D, Schmidt-Nowara WW, Pack AI, Gefter WB: Upper Airway Soft Tissue Structural Changes with Dental Appliances in Apneics. Am J Respir Crit Care Med 1996; 153 (part 2 of 2 parts): A719
Schwab RJ, Pack AI, Gupta KB, Metzger LJ, Oh E, Getsy JE, Hoffman EA, Gefter WB: Upper Airway and Soft Tissue Structural Changes Induced by CPAP in Normal Subjects. Am J Respir Crit Care Med 1996; 154:1106-1116
Meurice J, Marc I, Carrier G, Series F: Effects of Mouth Opening on Upper Airway Collapsibility in Normal Sleeping Subjects. Am J Respir Crit Care Med 1996; 153:255-259
Oshima T, Tsai WH, Hadjuk EA, Remmers JE: Mandibular Protrusion Decreases Genioglossal EMG. Am J Crit Care Med 1998; 157(3):A655
Strohl KP, Redline S: Nasal CPAP Therapy, Upper Airway Muscle Activation and Obstructive Sleep Apnea. Am Rev Resp Dis 1986; 134:555-558
Ferguson K, Love LI, Ryan F: Effect of Mandibular and Tongue Protrusion on Upper Airway Size During Wakefulness. Am J Respir Crit Care Med 1997; 155:1748-1754
Clark GT, Blumenfeld I, Yoffe N, Peled E, Lavie P: A Crossover Study Comparing the Efficacy of Continuous Positive Airway Pressure with Anterior Mandibular Positioning Devices on Patients with Obstructive Sleep Apnea. Chest 1996; 109:1477-1483
Ferguson KA, Ono T, Lowe AA, Al-Majed S, Love LI, Fleetham JA: A Short Term Controlled Trial of an Adjustable Oral Appliance for the Treatment of Mild to Moderate Obstructive Sleep Apnea. Thorax 1997; 52:362-368
Fleetham JA, Lowe A, Vasquez JC, Ferguson K, Flemons W, Remmers J: A Long Term Randomized Parallel Multicentre Study of an Oral Appliance vs nCPAP in the Treatment of Obstructive Sleep Apnea. Am J Respir Crit Care Med 1997; 155 (part 2 of 2 parts):A939
Loube DI, Menn SJ, Morgan TD, Berger JS, Erman MK, Mitler MM: Mandibular Repositioning Device: Role in the Treatment of Obstructive Sleep Apnea. Am J Respir Crit Care Med 1997; 155(part 2 of 2 parts):A939
American Sleep Disorders Association Standards of Practice Committee: Practice Parameters for the Treatment of Snoring and Obstructive Sleep Apnea with Oral Appliances. Sleep 1995; 18:511-513


Home Table of Contents Treatments Dental Appliances
 
Neuroendocrine dysfunction in sleep apnea: reversal by continuous positive airways pressure therapy
RR Grunstein, DJ Handelsman, SJ Lawrence, C Blackwell, ID Caterson and CE Sullivan
Sleep Unit, Royal Prince Alfred Hospital, Sydney, Australia.

We studied the effects of sleep apnea on neuroendocrine function in a cross-sectional study of 225 consecutive men undergoing sleep studies and in a longitudinal study of 43 men with severe obstructive sleep apnea before and after 3 months of successful treatment with nasal continuous positive airways pressure to eliminate upper airways obstruction. Blood samples were collected at 0600-0630 h on awakening for measurement of plasma insulin-like growth factor I (IGF-I), total and free testosterone, sex hormone-binding globulin (SHBG), LH, FSH, PRL, T4, T4-binding globulin, and cortisol. The plasma hormone levels were analyzed in relation to the severity of sleep apnea, as indicated by the desaturation index (the hourly rate of episodes of arterial oxygen desaturation greater than 4% of the stable baseline) and the mean minimal oxygen saturation during the desaturation episodes. In the cross-sectional study plasma IGF-I, free and total testosterone, and SHBG levels were significantly lower in relation to the severity of sleep apnea, whereas plasma LH, FSH, PRL, T4, T4-binding globulin, and cortisol were not. The decreases in plasma IGF-I and total and free testosterone were independent of the effects of aging and adiposity by covariance analysis. In the longitudinal study plasma IGF-I, total testosterone, and SHBG, but not free testosterone, significantly increased after 3 months of nasal continuous positive airways pressure treatment. We conclude that sleep apnea causes reversible neuroendocrine dysfunction in men, which is manifested by decreased plasma. IGF-I, testosterone, and SHBG levels. This neuroendocrine dysfunction is related to the severity of the sleep apnea, as indicated by the nadir levels of arterial oxygen desaturation and the rate of desaturation episodes. These hormonal measurements may provide biochemical markers for both the severity of sleep apnea and its response to therapeutic intervention. In addition, sleep apnea may be a previously unrecognized confounder of the neuroendocrine correlates of aging.


Obstructive sleep apnea due to endogenous testosterone production in a woman.

Dexter DD, Dovre EJ.

Department of Neurology, Midelfort Clinic, Eau Claire, Wisconsin 54701, USA.

Obstructive sleep apnea (OSA) is a common condition characterized by snoring, recurrent episodes of cessation of breathing (obstructive apneas), disrupted sleep, and excessive daytime somnolence. Associated serious complications are hypertension, increased risk of heart disease, stroke, and increased susceptibility to industrial and motor vehicle accidents. OSA is considerably more common in men than in women. In postmenopausal women, the incidence of OSA increases. These factors suggest that reproductive hormones have a role in the cause of OSA. Treatment with testosterone has been reported to cause OSA in men, and exogenous androgen administration has been reported to cause OSA in one woman. In a review of the English literature, we found no previous reports of OSA that was induced by endogenous testosterone in women. Herein we describe a nonobese 70-year old woman with clinically significant OSA and a benign testosterone-producing ovarian tumor. After successful removal of the tumor, her OSA resolved, and her testosterone level normalized. This unique case supports the theory of male hormonal (testosterone) influence in the OSA syndrome.
 
I wanted to try a Dental Appliance, but my insurance would not cover it and was $3,000 to make.
 
ARTICLE WITH SOME STUDIES SITED ON TESTOSTERONES ROLE IN SLEEP APNEA. MY SLEEP DOCTOR IS ACTUALLY PISSED THAT I'M ON HRT BECAUSE SHE SAYS THE TEST I'M ON WILL MAKE MY APNEA WORST.



Testosterone and Sleep: Support for Sleep Theory

Copyright ã 1997 by James Michael Howard.



This is new additional support for my sleep theory .

In 1994, it was determined that testosterone makes obstructive sleep apnea worse. This is the finding of the following research from 1994. Following this quotation, however, one can see that it is not a simple effect of testosterone on airway passages.

"Testosterone is thought to play a role in the pathogenesis of obstructive sleep apnea (OSA), but the mechanism is unclear. We present a case in which testosterone administration induced or exacerbated OSA in a 13-year-old male. We demonstrated that exacerbation of OSA by testosterone was associated with an increase in upper airway collapsibility during sleep, and that this improved after cessation of hormone administration. Our data strongly suggest that the mechanism by which testosterone administration may induce or exacerbate OSA is through an influence on neuromuscular control of upper airway patency during sleep." (American Journal of Respiratory and Critical Care Medicine 1994; 149: 530)

This report is supported by some earlier reports. However, some reports suggest that testosterone replacement in hypogonadal men significantly increases "both apneas and hypoapneas" but that this is a "highly variable event with some subjects demonstrating large increases in apneas and hypoapneas when androgen [testosterone] was replaced, whereas others had little change in respiration during sleep." This report also studied airway dimensions and concluded that "Upper airway dimensions, on the other hand, were unaffected by testosterone. These results suggest that testosterone contributes to sleep-disordered breathing through mechanisms independent of anatomic changes in the upper airway." (Journal of Applied Physiology 1986; 61: 618)

Another study of testosterone replacement in hypogonadal men produced some similar results, along with some additional information that allows me to apply my theory of sleep and produce an explanation of the connection of testosterone and sleep apneas.

"Obstructive sleep apnoea developed in one man and markedly worsened in another man in association with testosterone administration. Both of these subjects also exhibited marked decreases in oxygen saturation with the development of cardiac dysrhythmias during sleep and large increases in haematocrit. The remaining three hypogonadal men did not demonstrate significant sleep apnoea either on or off testosterone. The percentage of sleep time spent in REM sleep increased from 14 +/- 3% to 22 +/- 2% when the men were receiving testosterone (P less than 0.01), but the episodes of sleep apnoea tended to occur during non-REM sleep. We conclude that in some hypogonadal men, replacement dosages of testosterone may affect ventilatory drives and induce or worsen obstructive sleep apnoea. The obstructive sleep apnoea syndrome is a potential complication of testosterone therapy." (Clinical Endocrinology 1985; 22: 713)

Testosterone appears to produce apneas due to collapse of the airway and apneas that occur without collapse of the airway. I developed a theory of sleep that may explain this apparent paradox. (For full detail, I invite you to read my theory of sleep on the webpage.) It is my hypothesis that the hormone, dehydroepiandrosterone (DHEA), is necessary for activation of the nervous system. This has allowed me to produce a theory of sudden infant death syndrome (SIDS), based on too little DHEA during sleep to maintain functions of the brainstem. When I was working on my theory of SIDS, it became quite apparent that infants who produce too much testosterone are more prone to SIDS. This has allowed me to explain the connection of testosterone with apneas in men.

My theory suggests that all genes use DHEA to function. Testosterone causes the genes of "testosterone target tissues" to absorb extra DHEA for their functions. For example, this is why men have larger, more powerful muscles than women. So, the increased testosterone of men reduces the availability of DHEA, therefore, I suggest sleep apneas occur more in men because of reduced availability of DHEA for proper nervous stimulation. According to my theory of DHEA function, all tissues compete for DHEA. Therefore, in a man of low DHEA, administering testosterone as in the report above, will cause some tissues to absorb extra DHEA and reduce already low DHEA. This may cause either the nervous stimulation of the airways to decline, resulting in a collapsed airway, or it may reduce the DHEA so low that the brainstem ceases to function momentarily, as in SIDS. This situation would produce the apnea in which the airways do not collapse. Of course, the brainstem malfunction and airway collapse could occur simultaneously. This could explain the variability of effects of administration of testosterone in the quotation, above. Some of the men may be hypogonadal because of a poorly functioning pituitary-adrenal-gonadal axis, caused by low DHEA with low testosterone as a secondary consequence. Some of the men may have simply not produced much testosterone along with ample amounts of DHEA. This second group would represent those individuals in whom testosterone administration had no effect on sleep at all.

I have suggested that testosterone stimulates testosterone target tissues, which absorb extra DHEA. This effect should stimulate some increase in the production of DHEA. In my theory of sleep, I suggest that REM sleep is a time when the low levels of DHEA of night increase slightly to maintain brainstem function. This means that testosterone administration during sleep should increase REM sleep; this in fact is reported in the quotation above. I have suggested that DHEA is necessary for nervous system function, so I would expect apneas, caused by too low DHEA, to occur during non-REM sleep, which is a time of the lowest levels of DHEA, according to my theory of sleep and SIDS. This is reported above: "...but the episodes of sleep apnoea tended to occur during non-REM sleep."

I suggest the reason men exhibit more sleep apneas than women, and why testosterone administration in some individuals induces sleep apneas, is due to abnormally low DHEA during sleep. This low DHEA can manifest itself as lack of nervous support of the muscles of the airway, lack of support of brainstem function, or a combination of both.

Added in Support of Above


Mayo. Clin. Proc. 1998 Mar; 73(3): 246-8 "Obstructive sleep apnea due to endogenous testosterone production in a woman" Dexter DD, Dovre EJ Department of Neurology, Midelfort Clinic, Eau Claire, Wisconsin 54701, USA.

"Obstructive sleep apnea (OSA) is a common condition characterized by snoring, recurrent episodes of cessation of breathing (obstructive apneas), disrupted sleep, and excessive daytime somnolence. Associated serious complications are hypertension, increased risk of heart disease, stroke, and increased susceptibility to industrial and motor vehicle accidents. OSA is considerably more common in men than in women. In postmenopausal women, the incidence of OSA increases. These factors suggest that reproductive hormones have a role in the cause of OSA. Treatment with testosterone has been reported to cause OSA in men, and exogenous androgen administration has been reported to cause OSA in one woman. In a review of the English literature, we found no previous reports of OSA that was induced by endogenous testosterone in women. Herein we describe a nonobese 70-year old woman with clinically significant OSA and a benign testosterone-producing ovarian tumor. After successful removal of the tumor, her OSA resolved, and her testosterone level normalized. This unique case supports the theory of male hormonal (testosterone) influence in the OSA syndrome.
 
I am trying this:

**broken link removed**

This was recommended to be by a friend who has tried a few devices. Im still trying to get use to it.

Any advice what else I could try, I really dont want to be chained to a cpap machine forever if I can avoid it.
 
Last edited:
Bluto, I stopped snoring like a buffalo once I lost weight.

**broken link removed**

This was recommended to be by a friend who has tried a few devices. Im still trying to get use to it.

Any advice what else I could try, I really dont want to be chained to a cpap machine forever if I can avoid it.

I know you aren't going to want to hear this, but, lose weight. I got up to 292 at my heaviest. I had high blood pressure, constant nose bleeds whenever I'd bend over....as in tying my shoes. I'd do leg curls and get a nose bleed. I wasn't as huge as some guys because I am tall like you. However, I noticed I also snored and would wake myself up snoring on occasion. My face was always red.

Things changed for me when my 155-60 lb father had a triple bypass. I figured I could be big and sacrifice my health to some degree or another or be less impressive and healthy. Now I hang around 275-80 during the winter and then lean up in the summer at 262-265.

I am like you....I wouldn't want to be hooked up to some darn machine so I could breath. I don't give a shit about being big if I can't live a normal life.

That being said...you have a great physique! lol.:D
 
Get the sleep study done. Sleeping aids will not help and may actually make you worse. Your brain "needs" to "wake" you when your body needs oxygen. Low saturation levels combined with blood thickened, etc puts a big strain on your heart. One of the best things I've ever done, sorry I did not realize the risk factors sooner. This is much more important than you may ever think. The data coming out is alarming at the connection between sleep apnea and heart problems.

Pekkerwood
 
thx for clarification for the un-informed:confused: -STEELE

CPAP is a mask that you put on at night that covers your nose that has a tube attacked to little black box. this entire devise esentially forces air into and out of your lungs while you sleep.
**broken link removed**
 
I only weigh 245 but I do snore ;-)
I had the dental thingy made just a few weeks ago and it rocks!
After 3 days use I felt much better while getting up in the morning, more refreshed and I dont feel the need for a nap during the day.
Also Im in a better mood all day.

This weekend Im going to sleep next to my girl for the first time in 15 years again :p
(Ok I feel some jokes coming up :rolleyes: )
 
I only weigh 245 but I do snore ;-)
I had the dental thingy made just a few weeks ago and it rocks!
After 3 days use I felt much better while getting up in the morning, more refreshed and I dont feel the need for a nap during the day.
Also Im in a better mood all day.

This weekend Im going to sleep next to my girl for the first time in 15 years again :p
(Ok I feel some jokes coming up :rolleyes: )

Did insurance pick up the cost.
 
How do all the big guys sleep?

The heavier I get the worse my snoring gets and the more times I wake up during the nite. I know I have sleep apnea of some kind but really dont want to strapped to a cpap machine forever.

Do all the big pros use chemical sleep aids, or cpaps or what?

some guys can carry the weight alright while others cant walk 10 steps without losing breathe.
 
some guys can carry the weight alright while others cant walk 10 steps without losing breathe.

True, I am starting to feel luicky and be able to still move around and still be agile. I'm at 340ish and can still run a mile and a half and play some foot ball and B-ball as needed. Not as much as when I was just a tad over 200. No problems sleeping or snoaring or nothing.
 
How do all the big guys sleep?

The heavier I get the worse my snoring gets and the more times I wake up during the nite. I know I have sleep apnea of some kind but really dont want to strapped to a cpap machine forever.

Do all the big pros use chemical sleep aids, or cpaps or what?

Yeh, I have sleep apnea also. The more I weigh the worse it gets. When taking gh like now, the worse it gets. I am supposed to wear my CPAP but I try and the most I can handle it is for an hour or two. I CAN tell a big difference even in an hour with it on. I have a guess that if I wore it I would gain even more muscle mass (the RIM sleep and all).

MIke
 

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