Dr. Oz's comments about Sleep Apnea

General Discussion on any topic relating to CPAP and/or Sleep Apnea.
annie123
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Post by annie123 » Sun Nov 04, 2007 7:57 am

Dr Oz. was on Oprah again this week. He brought back the guy with sleep apnea (and diabetes and high blood pressure). The guy had lost weight and didn't have high blood pressure or diabetes anymore. His apnea was treated by surgery. (Yet another great message to send.) The surgeon found that part of his obstruction was due to a cancerous tumor.

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Followup on Dr. Oz

Post by kteague » Sun Nov 04, 2007 9:24 am

I saw the guy's "after" story, and the first thought in my mind was "I want to hear some actual numbers from his before and after sleep studies." I can only assume that for Dr. Oz to present him in this manner there has been documentation to confirm that the surgery and weight loss did indeed cure his apnea. Maybe it did, but I think we are such a discriminating audience because of our experiences that skepticism is the knee-jerk response - or maybe I should just speak for me. But for me to convinced of anything, my mind needs facts.

The part of the whole "lose weight and cure your sleep apnea" advice that grieves me is failure to acknowledge the danger in which one lives in the meantime. Even for the percentage of apnea sufferers whose cause and cure really does hinge on their weight, sufficent weight loss for it to not just improve but be gone is a long term effort. What about the here and now? I'm with the camp that believes all apnea should be addressed in conjunction with any weight loss or other treatment effort. It can always be stopped when no longer needed.

The question I still have is "why?" Why can the layman see the logic of this and much of the medical community doesn't? Why does something so seemingly obvious feel like a hidden truth? Maybe I'm missing something.

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Post by Idget » Sun Nov 04, 2007 10:17 am

Losing weight if you are over weight is probably a good idea and may be a cause of sleep apnea for a percentage of people. How much of a percentage I don't know and would be interested in seeing. However, from my own experience, I am on the thin side have always been, have snored since I was at least a teen. I am a 48 year old male, losing weight will have absolutely no effect on my sleep apnea. I still have to see a ENT, but my cause is probably anatomical.

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Post by socknitster » Sun Nov 04, 2007 10:39 am

Personally I believe all apnea is caused by anatomical anomalies. I am sure there must be a percentage of people for whom extra fat can make those anatomical obstructions worse enought to make their apnea far worse. But I just don't buy that weight causes apnea. It just doesn't make sense to me at all. The fat on our necks crushing our windpipes? That just doesn't make sense. I'm a little bit overweight, yes, I'll admit it. But the apnea was there when I was stick thin and people complained that I looked anorexic.

Maybe it is due to the fact that with age two things inevitably happen: we gain weight, an undisputed fact as a part of aging--most people gain a little (and in our culture usually a lot). Second, apnea, if present is going to get worse with age as well due to the relaxation of muscles, stretching of ligaments and the damage that apnea does to the sufferer himself/herself.

People want to blame people for being fat and fat has become a quick and easy scapegoat for apnea. It is so much more complicated than that. I'm glad this guys cancer was caught--but come on! How many people have YOU heard of who's apnea was caused by cancer? This guy had to be one in a million!

The truth is our bodies are being filled with empty calories from processed foods. Our brains are looking for the nutrition and urge us to eat, eat, eat to try to get some nutrition--its like we are starving even though we are full of empty calories. We as a culture have made some bad decisions about what is acceptable food. All this refined flour, sugar etc has completely confused our bodies and made overeating commmon. If we all tried a little harder to include more whole grains and vegetables and lean meats in our diets, the obesity epidemic wouldn't be such an issue. But, I'll be the first to admit that I struggle with this each day--because refined food tastes too damn good.

I once visited an old flour mill and talked to the reinactor there about whole grain flours and he said that they used to have a saying back in the day (and I'll never forget this), "the whiter the bread, the quicker the dead."

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Amazing!!

Post by RipVW » Sun Nov 04, 2007 11:32 am

Yes, I saw this show yesterday (my wife records Oprah, she was watching, I just happened to be in the room). I am forever amazed by the misinformation disseminated by so called "experts." The sad thing here is that there are probably people who saw that show who will not pursue diagnosis and treatment of their apnea symptoms, thinking that "if I just loose a little weight, all will be fine. Dr. Oz said so." Oh, this is too bad--how can he get away with giving such bad advice?

And then there was his "postage stamp method" for diagnosis of ED . . . Hoping I don't get mail from anyone who tried that, then reused their stamps (as he suggested!!).

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Post by mindy » Sun Nov 04, 2007 4:01 pm

socknitster wrote:Personally I believe all apnea is caused by anatomical anomalies. I am sure there must be a percentage of people for whom extra fat can make those anatomical obstructions worse enought to make their apnea far worse. the dead."
I agree with most of that … except I might call it “anatomical variation” rather than “anomalies”. When I first saw the sleep doc, she estimated the size of the back of my throat and said it was on the small side. Combined with my weight, that put me at high risk because the excess fat made my already small passages even smaller. I know others who are very thin and have apnea problems also because of anatomical variation. It’s my understanding that surgery tends to have a higher success rate among those who don’t have apnea because of excess weight.

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Post by floppysleeper » Sun Nov 04, 2007 4:58 pm

So maybe weight loss will help with the OSA........what I would like to know is what does he think we should do in the meantime?? Weight loss does not happen quickly...especially if you are too tired to exercise.

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Post by Guest » Sun Nov 04, 2007 5:52 pm

OZ is not specialist in sleep disorder once he is coomenting about other fields he is out of ordered....he only can see from his own field. He though lossing weight is everthing....but not at all...the secret is "balance of diet, balance of life style, balance of thinking, balance of believes......like the sun-sze art of war said......every doses is different and time changes....is more than science is an ART!

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Post by Slinky » Sun Nov 04, 2007 6:51 pm

Dr Oz?? Like in the Wizard of??

Another bag of hot wind like Dr Phil. Another real winner.

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Post by RosemaryB » Sun Nov 04, 2007 8:49 pm

Slinky wrote:Dr Oz?? Like in the Wizard of??

Another bag of hot wind like Dr Phil. Another real winner.
Dr. Phil doesn't have his doctor's degree in a field related to psychology, it's in some other field. Bag of hot wind is right .
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Post by Guest » Mon Nov 05, 2007 2:48 am

socknitster wrote: Personally I believe all apnea is caused by anatomical anomalies. I am sure there must be a percentage of people for whom extra fat can make those anatomical obstructions worse enought to make their apnea far worse. But I just don't buy that weight causes apnea.
Jen,

I for one will not agree with doctors/researchers/professors simply saying that losing weight will cure your apnea. HOWEVER, there have been several studies showing that weight loss (in overweight/obese) can help to improve or cure OSA in many patients.

Again, this is like saying smoking will always lead to lung cancer. Obviously it doesn't in all smokers. But the risk of developing lung cancer, and other types of cancer increases with smoking. In terms of OSA, there is a greater chance (not a 100% chance) of eliminating or at least reducing OSA severity IF increased adiposity was the predominant cause. Once again, I understand that there are loads of examples which disprove the "rule-of-thumb" e.g. yourself

Whatever the case, I believe that doctors/other professionals should be very careful saying that OSA will go away if you lose weight.

Here is a quick search of the literature showing that weight loss does have its benefits in terms of OSA:

Obes Surg. 2003 Feb;13(1):58-61.Links
Gastric bypass is an effective treatment for obstructive sleep apnea in patients with clinically significant obesity.Rasheid S, Banasiak M, Gallagher SF, Lipska A, Kaba S, Ventimiglia D, Anderson WM, Murr MM.
Department of Surgery, Interdisciplinary Obesity Group, University of South Florida, College of Medicine, Tampa, FL, USA.

BACKGROUND: We have demonstrated that obstructive sleep apnea (OSA) is prevalent in 60% of patients undergoing bariatric surgery. A study was conducted to determine whether weight loss following bariatric surgery ameliorates OSA. METHODS: All 100 consecutive patients with symptoms of OSA were prospectively evaluated by polysomnography before gastric bypass. Preoperative and postoperative scores of Epworth Sleepiness Scale (ESS), Respiratory Disturbance Index (RDI), and other parameters of sleep quality were compared using t-test. RESULTS: Preoperative RDI was 40 +/- 4 (normal 5 events/hour, n = 100). 13 patients had no OSA, 29 had mild OSA, while the remaining 58 patients were treated preoperatively for moderate-severe OSA. At a median of 6 months follow-up, BMI and ESS scores improved (38 +/- 1 vs 54 +/- 1 kg/m2, 6 +/- 1 vs 12 +/- 0.1, P < 0.001, postoperatively vs preoperatively). To date, 11 patients have completed postoperative polysomnography (3-21 months) after losing weight (BMI 40 +/- 2 vs 62 +/- 3 kg/m2, P < 0.001). There was significant improvement in ESS (3 +/- 1 vs 14 +/- 2), minimum O2 saturation (SpO2 86 +/- 2 vs 77 +/- 5), sleep efficiency (85 +/- 2% vs 65 +/- 5%), all P < 0.001, postop vs preop; and RDI (56 +/- 13 vs 23 +/- 7, P = 0.041). Regression analysis demonstrated no correlation between preoperative BMI, ESS score and the severity of OSA; and no correlation between % excess body weight loss and postoperative RDI. CONCLUSION: Weight loss following gastric bypass results in profound improvement in OSA.The severity of apnea cannot be reliably predicted by preoperative BMI and ESS; therefore, patients with symptoms of OSA should undergo polysomnography.

Surgery. 2007 Mar;141(3):354-8. Epub 2006 Dec 8. Links
Objective evidence that bariatric surgery improves obesity-related obstructive sleep apnea.Haines KL, Nelson LG, Gonzalez R, Torrella T, Martin T, Kandil A, Dragotti R, Anderson WM, Gallagher SF, Murr MM.
Department of Surgery, Interdisciplinary Obesity Group, University of South Florida, Health Sciences Center, Tampa, FL 33601, USA.

BACKGROUND: Obstructive sleep apnea (OSA) is associated with obesity. Our aim in this study is to report objective improvement of obesity-related OSA and sleep quality after bariatric surgery. METHODS: Prospective bariatric patients were referred for polysomnography if they scored >or=6 on the Epworth Sleepiness Scale. The severity of OSA was categorized by the respiratory disturbance index (RDI) as follows: absent, 0 to 5; mild, 6 to 20; moderate, 21 to 40; and severe, <40. Patients were referred for repeat polysomnography 6 to 12 months after bariatric surgery or when weight loss exceeded 75 lbs. Means were compared using paired t tests. Chi-square tests and linear regression models were used to assess associations between clinical parameters and RDI; P<.05 was considered statistically significant. RESULTS: Of 349 patients referred for polysomnography, 289 patients had severe (33%), moderate (18%), and mild (32%) OSA; 17% had no OSA. At a median of 11 months (6 to 42 months) after bariatric surgery, mean body mass index (BMI) was 38 +/- 1 kg/m2 (P<.01 vs 56 +/- 1 kg/m2 preoperatively) and the mean RDI decreased to 15 +/- 2 (P<.01 vs 51 +/- 4 preoperatively) in 101 patients who underwent postoperative polysomnography. In addition, minimum oxygen saturation, sleep efficiency, and rapid eye movement latency improved, and the requirement for continuous positive airway pressure was reduced (P<or=.025). Male gender and increasing BMI correlated with increasing RDI (P<.01) by chi-square analysis. In a multivariate linear regression model adjusted for age and gender, preoperative BMI correlated with preoperative RDI (r=0.27; P<.01). CONCLUSIONS: OSA is prevalent in at least 45% of bariatric surgery patients. Preoperative BMI correlates with the severity of OSA. Surgically induced weight loss significantly improves obesity-related OSA and parameters of sleep quality.

Otolaryngol Head Neck Surg. 2001 Oct;125(4):299-302. Links
Bariatric surgery for treatment of sleep apnea syndrome in 15 morbidly obese patients: long-term results.Scheuller M, Weider D.
Department of Otolaryngology, University of California San Francisco, 400 Parnassus Ave., San Francisco, CA 04122-2721, USA. nephi@alum.dartmouth.org

OBJECTIVE: To evaluate the long-term outcomes of bariatric surgery with respect to respiratory disturbance index (RDI) in sleep apnea syndrome (SAS). DESIGN: Case series with long-term follow-up (1 to 12 years). SETTING: Private clinic in an academic tertiary referral center. PATIENTS: Fifteen morbidly obese patients (10 men, 5 women) who were referred for the treatment of severe SAS. INTERVENTION: For all 15 patients who presented with severe SAS, nasal positive airway pressure breathing was either not available or was not tolerated by the patient; therefore, bariatric surgery was performed as a means of treatment for SAS. MAIN OUTCOME MEASURES: RDIs and minimum oxygen saturation were measured both preoperatively and postoperatively (1 to 12 years after surgery). RESULTS: Weight loss ranged from 60 to 220 pounds (27 to 100 kg). RDI decreased by at least 55% in each patient, and all patients with tracheostomies (8 of 15) had their tracheostomy tubes removed. Average RDI preoperatively was 96.9 and average RDI postoperatively was 11.3. Results were similar for all 15 patients in that minimum oxygen saturation increased during sleep from an average preoperative minimum oxygen saturation of 58.7% to an average postoperative minimum oxygen saturation of 85.2%. CONCLUSIONS: Bariatric surgery as a means of treating SAS in the morbidly obese provides effective long-term reduction in RDI. Bariatric surgery also significantly improves minimum oxygen saturation in morbidly obese patients with SAS. Biliopancreatic bypass is more effective in reducing RDI to normal values than vertical banded gastroplasty.


Sleep. 2007 Jun 1;30(6):703-10.Links
Two year reduction in sleep apnea symptoms and associated diabetes incidence after weight loss in severe obesity.Grunstein RR, Stenlöf K, Hedner JA, Peltonen M, Karason K, Sjöström L.
Department of Puhnlmonary and Sleep Medicine, Sahlgrenska University Hospital, Göteborg, Sweden. rrg@med.usyd.edu.au

STUDY OBJECTIVES: To evaluate the effect of bariatric surgery on sleep apnea symptoms and obesity-associated morbidity in patients with severe obesity. DESIGN: Prospective study. SETTING: University hospitals and community centers in Sweden. Intervention: We investigated the influence of weight loss surgery (n=1729) on sleep apnea symptoms and obesity-related morbidity using a conservatively treated group (n=1748) as a control. MEASUREMENTS AND RESULTS: Baseline BMI in surgical group (42.2+/-4.4 kg/m(2)) and control group (40.1+/-4.6 kg/m(2)) changed -9.7+/-5 kg/m(2) and 0+/-3 kg/m(2), respectively, at 2-year follow-up. In the surgery group, there was a marked improvement in all obstructive sleep apnea (OSA) symptoms compared with the control group (P <0.001). Persistence of snoring (21.6 vs 65.5%, adjusted OR 0.14, 95% CI 0.10-0.19) and apnea (27.9 vs 71.3%, adjusted OR 0.16, 95% I 0.10-0.23) were much less in the surgery group compared with controls. Compared with subjects with no observed apnea at follow-up (n=2453), subjects who continued to have or developed observed apnea (n=404) had a higher incidence of diabetes (adjusted OR 2.03, 95% CI 1.19-3.47) and hypertriglyceridemia (adjusted OR 1.86, 95% CI 1.07-3.25) but not hypertension (adjusted OR 1.09, 95% CI 0.65-1.83) or hypercholesterolemia (adjusted OR 0.91, 95% CI 0.53-1.58). CONCLUSION: Bariatric surgery results in a marked improvement in sleep apnea symptoms at 2 years. Despite adjustment for weight change and baseline central obesity, subjects reporting loss of OSA symptoms had a lower 2-year incidence of diabetes and hypertriglyceridemia. Improvement in OSA in patients losing weight may provide health benefits in addition to weight loss alone.


Int J Obes (Lond). 2005 Sep;29(9):1048-54. Links
Polysomnography before and after weight loss in obese patients with severe sleep apnea.Dixon JB, Schachter LM, O'Brien PE.
Centre for Obesity Research and Education, Monash University, Alfred Hospital, Melbourne, Victoria, Australia. john.dixon@med.monash.edu.au

OBJECTIVE: While obstructive sleep apnea (OSA) is strongly related to obesity, few studies have examined polysomnographic (PSG) changes with major weight loss. We examined the effect of weight loss following laparoscopic adjustable gastric banding (LAGB) on the PSG changes in patients with severe OSA. In addition, we studied daytime sleepiness, the metabolic syndrome and quality of life (QOL). METHODS: A prospective study was conducted of 25 severely obese patients (17 men, eight women) with paired diagnostic PSG, biochemical and questionnaire studies, the first prior to LAGB and the second at least 1 y later. Subjects with a baseline apnea-hypopnea index (AHI) >25/h were included. RESULTS: Subject baseline age was 44.7 y, weight 154 kg and body mass index 52.7 kg/m(2). The second PSG study was conducted 17.7+/-10 (range 12-42) months after surgery and mean percentage of excess loss and weight loss were 50.1+/-15% (range 24-80%) and 44.9+/-22 kg (range 18-103 kg), respectively. There was a significant fall in AHI from 61.6+/-34 to 13.4+/-13, improved sleep architecture with increased REM and stage III and IV sleep, daytime sleepiness, as measured by Epworth Sleepiness Scale, of 13+/-7.0 to 3.8+/-3.0, and fewer patients requiring nasal continuous positive airways pressure (CPAP). There were also major improvements in the metabolic syndrome, QOL, body image and fewer symptoms of depression (P<0.05 for all). CONCLUSION: Weight loss provides major improvement or resolution of OSA and CPAP requirements. It also reduces daytime sleepiness, and improves the metabolic syndrome and QOL. LAGB placement should be considered a broadly effective therapy for sleep apnea in the severely obese patient.

socknitster wrote:It just doesn't make sense to me at all. The fat on our necks crushing our windpipes?
The fact is, overweight/obese people tend to have increased fat around their upper airway. This "fat" is contained within a "bony vault." NOTE: There is a lot of work and controversy in regards to whether this bony box is real or not. Nevertheless, due to the surrounding bony structures, any additional fat inside the vault is likely to compress the airway i.e. making it smaller. Richard Schwab has done a lot of work in this area.

Now, another area of research is assessing the tissue pressure surrounding the upper airway. More fat around the airway --> higher tissue pressure --> increased tissue pressure will also compress the airway.

One question I am attempting to answer in my current project is when, in the respiratory cycle, does the airway collapse? Is it ACTIVE collapse i.e. caused by negative pressure generation during inspiration OR PASSIVE COLLAPSE i.e. passively collapses at the end of expiration.

A majority of the main upper airway dialtor muscles are relaxed at the end of expiration. They tend to be activated by negative pressure. Given that there is no bony supportive structures surrounding the upper airway AND the dilator muscles are relaxed at the end of inspiration, the size and shape of the airway will be determined by the forces/pressure acting upon it. Thus, if there is increased tissue pressure, due to larger fat desposits --> the airway is likely to be smaller and more collapsible.

The snapshots I have posted in my "preliminary data" thread indicate that the airway collapses passively i.e. end of inspiration.

Now some other data:

This is an interesting study looking at mass loading upon the airway in anesthetized rabbits:

J Appl Physiol. 1988 Jun;64(6):2294-9. Links
Effects of mass loading on the upper airway.Koenig JS, Thach BT.
Edward Mallinckrodt Department of Pediatrics, Washington University and Children's Hospital, St. Louis, Missouri 63110.

To learn how increased cervical adipose tissue might affect upper airway function, we studied effects of mass loading on upper airway dimensions, stability, and resistance. Eight rabbits were studied (anesthetized and postmortem) using lard-filled bags to simulate cervical fat accumulation. Additionally, a handheld device was used to apply measured loads at localized sites along the airway. Upper airway resistance and closing pressure (a reflection of airway stability) were determined before and after loading. Endoscopy revealed concentric narrowing of the pharynx during loading in anesthetized and postmortem preparations. Upper airway resistance was increased by mass loads, with larger loads having greater effects. Loading caused decreased airway stability as reflected by closing pressures. The area over the thyrohyoid membrane was more vulnerable to mass loading than adjacent areas. Because mass loading of the upper airway causes changes in its configuration and function similar to those seen in obstructive sleep apnea syndrome (OSA), we speculate that such loading may contribute to the pathogenesis of OSA associated with obesity.

The last sentence is important.

And a colleague of mine, Kristina Kairaitis, examined changes in tissue pressure surrounding the airway during respiration in rabbits.

J Appl Physiol. 2003 Oct;95(4):1560-6. Epub 2003 Jun 27. Links
Upper airway extraluminal tissue pressure fluctuations during breathing in rabbits.Kairaitis K, Parikh R, Stavrinou R, Garlick S, Kirkness JP, Wheatley JR, Amis TC.
Dept. of Respiratory Medicine, Westmead Hospital, Hawkesbury Rd., Westmead NSW 2145, Australia. kristinak@westgate.wh.usyd.edu.au

Transmural pressure at any level in the upper airway is dependent on the difference between intraluminal airway and extraluminal tissue pressure (ETP). We hypothesized that ETP would be influenced by topography, head and neck position, resistive loading, and stimulated breathing. Twenty-eight male, New Zealand White, anesthetized, spontaneously breathing rabbits breathed via a face mask with attached pneumotachograph to measure airflow and pressure transducer to monitor mask pressure. Tidal volume was measured via integration of the airflow signal. ETP was measured with a pressure transducer-tipped catheter inserted in the tissues of the lateral (ETPlat, n = 28) and anterior (ETPant, n = 21) pharyngeal wall. Head position was controlled at 30, 50, or 70 degrees, and the effect of addition of an external resistor, brief occlusion, or stimulated breathing was examined. Mean ETPlat was approximately 0.7 cmH2O greater than mean ETPant when adjusted for degree of head and neck flexion (P < 0.05). Mean, maximum, and minimum ETP values increased significantly by 0.7-0.8 cmH2O/20 degrees of head and neck flexion when adjusted for site of measurement (P < 0.0001). The main effect of resistive loading and occlusion was an increase in the change in ETPlat (maximum - minimum ETPlat) and change in ETPant at all head and neck positions (P < 0.05). Mean ETPlat and ETPant increased with increasing tidal volume at head and neck position of 30 degrees (all P < 0.05). In conclusion, ETP was nonhomogeneously distributed around the upper airway and increased with both increasing head and neck flexion and increasing tidal volume. Brief airway occlusion increased the size of respiratory-related ETP fluctuations in upper airway ETP.

While not stated in the abstract, this group found:

"In the majority of rabbits, ETP (extraluminal tissue pressure) decreased in phase with inspiration and increased with expiration."

Tissue pressure was HIGHEST at the end of expiration. This increased pressure would like alter airway structure.

So, increased fat deposits and increased tissue pressure (as evident in obese individuals), along with decreased dilator muscle activity. will likely influence the structure of the upper airway.


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Post by WearyOne » Mon Nov 05, 2007 9:41 am

RosemaryB wrote:
Slinky wrote:Dr Oz?? Like in the Wizard of??

Another bag of hot wind like Dr Phil. Another real winner.
Dr. Phil doesn't have his doctor's degree in a field related to psychology, it's in some other field. Bag of hot wind is right .
Wow, I didn't know that--where have I been?

Split-City---great post!

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Post by Lee Lee » Mon Nov 05, 2007 10:50 am

I lost 47 pounds after starting CPAP.
I had another sleep study, thinking it was all gone.
Not only was it NOT gone, it was worse, and my pressure was higher.
Just one woman's story.


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Post by DreamStalker » Mon Nov 05, 2007 11:11 am

People should approach the benefits of weight loss not just for any specific ailment but rather for good health in general and an improved quality of life. From that perspective, I'm in agreement with the Oz ... but to claim it will eliminate OSA or anything else in particular only sets one up for the potential of a possible disappointment.

I sense some here may get the message that weight loss is not worth working for if it will not eliminate OSA and that is the wrong message IMO.
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Post by dieselgal » Mon Nov 05, 2007 12:14 pm

I watched the show where that slight mention of SA was brought up and even I knew the guy on film probably had SA before he told him. Actually he was very fat around the throat and upper body and sounded hideous when he slept. Even after losing 70 lbs he is still overweight but feels better.
I do know that my own SA is greatly aggravated by my weight so I am sure that many people that are severely overweight would benefit from weight loss and in that part I think he was right,
BUT
I also do know very skinny people that have SA and I think he should not have made a blanket statement which insinuated that all SA is from being overweight. He should have said, you should be tested if you have certain symptoms and to be treated. THEN he should have said and by the way if you are obese you might be able to improve your situation with weight loss.
I know some people do get really miffed when weight is mentioned with SA, but the part that miffs me is making that the only cause and spouting off without giving the full story.

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