Origin of 10 seconds
Question:
On 2 May 1999 03:11:32 GMT, lyntek…@aol.com (Lyntekcom) wrote: >Joe, we are a group of scientists including a group of computer scientists and >health professionals developing new methods of evaluationg this disease outside >the mainstream of scientific thought in Sleep medicine. We believe that >dynamic relationships of biologic systems define diseased physiologic processes >like OSA. …….. (omitted) >Recovery times could be analysed in relation to the force and >the cummulative nature of multiple closely spaced consecutive punches >determined. In this way one could analyse a real probability of biologic >injury.
Sounds very reasonable and very interesting. Have you been able to develop any predictive capability? This is after all, the true test of any modeling. I have some questions about this. What is the output of the modeling that one would compare to a patient for example? You mention recovery times; what exactly does that mean and are there other outputs from the modeling that can be used to test for predictive capability? Is the modeling merely quantitative, that is something I can input into a back-propagation neural network approach for example or is there a more sophisticated theoretical basis behind the modeling? Finally, what is the consequence of the better modeling? Would it lead to better methods of treatment or are we only considering better diagnostic capability? >All compared back to the basic counted number for a correlation. >And, not surprisingly, the correlation is weak as discovered by Wright et. al. >in the Landmark Article in the British Med. Journal.
I’m a little confused about what you are trying to say about the work of Wright. (I’ve reproduced the abstract below for those interested in this discussion). Are you agreeing with the central conclusion that "The relevance of sleep apnoea to public health has been exaggerated"? or are you saying that the overreliance on the RDI has led to this conclusion. I haven’t read the paper yet, but its my understanding that they just reviewed the literature; they didn’t actually do any research themselves. Hoffstein did the same thing a couple years before. The major complaint seems to be that most studies didn’t have adequate controls and didn’t take into account all the variables (for example, not accounting properly for obesity when trying to understand the relationship between OSA and hypertension.) Terry Young actually did her own research, taking into account many of the variables and did NOT show weak correlations but rather some fairly strong correlations. I think the Wright and Co. did not review Young’s work, but I could be wrong. *************************************************************************** ** BMJ 1997 Mar 22;314(7084):851-60 Health effects of obstructive sleep apnoea and the effectiveness of continuous positive airways pressure: a systematic review of the research evidence. Wright J, Johns R, Watt I, Melville A, Sheldon T Bradford Royal Infirmary, West Yorkshire. j.wri…@leeds.ac.uk OBJECTIVE: To examine the research evidence for the health consequences of obstructive sleep apnoea and the effectiveness of continuous positive airways pressure. DESIGN: A systematic review of published research, studies being identified by searching Medline (1966-96), Embase (1974-96), and CINAHL (Cumulative Index to Nursing and Allied Health Literature) (1982-95); scanning citations; and consulting experts. Studies in all languages were considered which either investigated the association between obstructive sleep apnoea in adults and key health outcomes or evaluated the effectiveness of treatment of obstructive sleep apnoea with continuous positive airways pressure in adults. MAIN OUTCOME MEASURES: Mortality, systematic hypertension, cardiac arrhythmias, ischaemic heart disease, left ventricular hypertrophy, pulmonary hypertension, stroke, vehicle accidents, measures of daytime sleepiness, and quality of life. RESULTS: 54 epidemiological studies examined the association between sleep apnoea and health related outcomes. Most were poorly designed and only weak or contradictory evidence was found of an association with cardiac arrhythmias, ischaemic heart disease, cardiac failure, systemic or pulmonary hypertension, and stroke. Evidence of a link with sleepiness and road traffic accidents was stronger but inconclusive. Only one small randomised controlled trial evaluated continuous positive airways pressure. Five non-randomised controlled trials and 38 uncontrolled trials were identified. Small changes in objectively measured daytime sleepiness were consistently found, but improvements in morbidity, mortality, and quality of life indicators were not adequately assessed. CONCLUSIONS: The relevance of sleep apnoea to public health has been exaggerated. The effectiveness of continuous positive airways pressure in improving health outcomes has been poorly evaluated. There is enough evidence suggesting benefit in reducing daytime sleepiness in some patients to warrant large randomised placebo controlled trials of continuous positive airways pressure versus an effective weight reduction programme and other interventions.
Response:
Lyntekcom, I’m enjoying your posts–I agree that current methods of apnea diagnostics leave much to be desired (and I’d dare say treatment options are in the same category). All diagnostic research and development seems to be focused on the machinery of technology (such as labor-saving computer scoring vs. paper scoring, or developing CPAP diagnostics capabilities for monitoring apnea). These are fine, but I think you’re saying that we should be questioning the basic assumptions that underlie such scoring, and I agree. If the foundation is flawed, the conclusions and implications will also be flawed. It’s worth examining these issues far more than has been done to date. Now that you’ve touched on the problem (or at least part of it), let me ask about your own thoughts on solutions and conclusions. 1. If RDI is a flawed measurement, what would you say are the most important measurements that should be looked at in terms of health risk? From earlier posts, I gather you’d say that the time between apneas should be measured, and more weight given to apneas in a cluster where little recovery time is involved. In addition, I think you’d say more weight should be given to the length of apneas. How dangerous are desaturations in your view, and how should they be measured? What about arousals? How dangerous are they in and of themselves, and are the standard EEG classifications of sleep staging adequate? 2. Do you feel that the dangers of obstructive sleep apnea are overall understated, overstated, or simply mis-stated? Thanks. Tim W. Lyntekcom wrote in message
<19990501231132.13129.00002…@ng-ch1.aol.com>… – Hide quoted text — Show quoted text ->Joe, we are a group of scientists including a group of computer scientists and >health professionals developing new methods of evaluationg this disease outside >the mainstream of scientific thought in Sleep medicine>
Response:
> If RDI is a flawed measurement, what would you say are the most important >measurements that should be looked at in terms of health risk?
We are not sure but the points I made earlier are representative of the issues having potential importance .>How dangerous are desaturations in your view, and how >should they be measured?
We think they should be considered as a function of time as a series of interelated events rather than simply counted. >What about arousals? How dangerous are they in >and of themselves
Arousals cause daytime sleepiness. Beyond that they either induce physiologic stress or are a signal of its presence. >are the standard EEG classifications of sleep staging >adequate?
Not sure, we have not studied their origin, but they are more qualitative, more descriptive, in nature and therefore more reasonably arbitrary as long as alternative ways of measuring sleep stages are vigilently sought. >2. Do you feel that the dangers of obstructive sleep apnea are overall >understated, overstated, or simply mis-stated?
Mistated– Based on an arbitrary measure of the disease state. Sleep apnea is very dangerous and until better methods are available, I strongly reccommend that standard treatment guidelines should be followed. Thankyou for your thoughtful post.
Response:
Sorry Joe Ive been out of town >… is there a more sophisticated theoretical basis behind >the modeling?
Yes, We are looking at the physiologic parameters (e.g. airflow or oxygen saturation) in the time domain as objects for comparison. Very quantitative. This is quite suitable for neural net approach but the OO method may make that superfluous. >Finally, what is the consequence of the better modeling?
Better determinates of the true state of disease and therfore better determinates of optimal mitigation of the disease state. >I’m a little confused about what you are trying to say about the work >of Wright.
Your correct Wright is not a true meta-analysis of data more like a qualitive meta-analysis of the methods and findings of the prior research relating to OSA. His findings were the basis for the reassesment of the RDI including a review of its origin. Regards
Response:
28. Rechtschaffen, A., and A. Kales. 1968. A manual of standardized terminology: techniques and scoring system for sleep stages of human subjects. Brain Info Service/Brain Research Institute, UCLA, Los Angeles. NIH Publication No. 204. — ———————————————————————— Kevin C Welch There are questions we could never get over capu.net/~kwelch/ if we were not delivered from them by the operation of nature. (Kafka, 54)
Response:
Joe, we are a group of scientists including a group of computer scientists and health professionals developing new methods of evaluationg this disease outside the mainstream of scientific thought in Sleep medicine. We believe that dynamic relationships of biologic systems define diseased physiologic processes like OSA. In its most simplified form, the behavior of a dynamical biologic system exposed to repetetive, sequential, traumatic events (like apneas) might be illustrated by the "1-2 punch". When considered as individuals each punch is insufficient to knock the boxer out. If for example, I said the boxer is struck with X force and then Y force, you will need to know the relationship between X and Y to determine if the boxer is likely to be knocked out. In a series of punches over 10 minutes, for example, this gets more complex and requires computer analysis. To compare, suppose boxers used the simple RDI method. They would not care about the magnitude of the punches or the relationship between punches, they would only care about the number of punches. Indeed, they would also count a push or bite as equal to a punch and just add them right in. Now tell me, how, doing that, you could determine who would win (inflict the greatest damage).— Jonny, who in a 1 hr. fight hit, bit or pushed Jack 30 times, or Jack, who pushed, hit, or bit Jonny 10 times. In the 1990s there is a different way to analyse the boxing fight or other dynamic biologic systems using a microprocessor. Suppose that both the force of each punch and the relationship of each punch to every other punch could be stored on a relational data base (using an Object Oriented method of computer programming). Recovery times could be analysed in relation to the force and the cummulative nature of multiple closely spaced consecutive punches determined. In this way one could analyse a real probability of biologic injury. Unfortunately, we, developing this technolgy for OSA have to deal with "Sleep Science", these scientists as a pack, are counters. Yes 12345 kind of stuff! As if caught in a 60s time warp which started when the studies were hand scored page by page so you simply counted how many time something occurred. So we looked into the origin of this gold standard diagnostic counting method to which we are forced to compare our methods and were stunned by what we found. It was artificial, man-made, a guess!!!! Not just the numbers, the entire gold standard method of OSA diagnosis–out of thin air. This was a relavation. Two decades of research in the late 20th century all using criteria that were originally simply guessed?…., it could not be true. But there it was. How, as a scientist, do you accept the study the true dynamic and complex nature of a biologic system wherein you are required to compare your results to a 20 year old guess (wherein the guess is assumed to be correct). You feel like a scientist in the 15th century. The guess is more than the ubiquitous 10s rule. It was also guessed that counting and averaging apneas was the best way of characterizing them. And that different event types could be added to the count. This simple adding and dividing rule was never in 2 decades seriously questioned. If facteach new (and very different) things (like RERAs and hypopneas) were just "added in to the cummulative average" as they were discovered and the threshold duration for each was always guessed as 10 seconds. You might say, "ok its a guess, but so what, what would have been the difference if 20 seconds or 25 seconds were chosen". But that is the point, what would have been different? All the research and thousands of computer programs use the 10s rule, and they add them and average them and this is compared in hundreds of studies to the frequency clinical sleepiness, hypertension, heart atttacks, strokes (as in the study of Young et. al you mentioned). All compared back to the basic counted number for a correlation. And, not surprisingly, the correlation is weak as discovered by Wright et. al. in the Landmark Article in the British Med. Journal. This is why a group of sleep clinitians can see remarkable clincal response to their therapy and be unable to prove it. They have the wrong measure of the disease state. They guessed it in the 60s and the guess was discovered to be wrong in the 90s. Time to "WAKE UP". Take these points to a sleep Dr. and he or she is likely to be unmoved. Like claiming the world is round. "So what if its not flat, what would be different?" and "prove to me that your spherical calculations have good correlations with the earths flat surface" and "I use my clinical judgement along with the RDI so it dosen’t matter if the RDI is not a good index" Hello!
