Sunday, October 11, 2009

OSA, Sleep Deprivation, and Alcohol

Once a person has one sleep problem, they are less able to cope with another one. For example, persons with obstructive sleep apnea are less able to cope with the demands of shift work.

A. Vakulin and colleagues pubished "Effects of Alcohol and Sleep Restriction on Simulated Driving Performance in Untreated Patients With Obstructive Sleep Apnea" in this months issue of Annals of Internal Medicine. This study compared patients with untreated OSA and matched controls on a driving simulator. The study found that "Patients with OSA are more vulnerable than healthy persons to the effects of alcohol consumption and sleep restriction on various driving performance variables. "


TSC said...

"Michael Rack, MD said...
I am not aware of any doctor trying go prevent slow wave sleep in infants. Please provide a link."

You wrote this a while back. The reason the SIDS Back to Sleep Campaign works is because infants who sleep on their backs get less Slow Wave Sleep (SWS). SWS begins at about 2-3 months of age and that's also when there is a spike in infants dying of SIDS. Thus, they realized that if you prevent SWS you can prevent SIDS. But, limiting SWS has very negative raminfications since that's when temporary memories stored in the Hippocampus are transferred to the Neocortex for permanent storage (see Gais, etc.). Read Dr. Rafael Pelayo, et al's, letter to the editor in Pediatrics from 2006 and Dr. John Kattwinkels, et al's reply and it's clear to see that the prevention of SWS via back sleep is the key driver in preventing SIDS. The fact that severe deprivation of SWS can cause autism like symptoms and that the SIDS Back to Sleep Campaign correlates with the general timeline of the Autism epidemic is generally considered a coincidence. I think it is not.

My comments on this website summarize my theory and will give you many citations on why the reason the Back to Sleep Campaign was implemented to decrease the SWS in infants:

Good articles I have summarized:

All the Best!


doctorstevenpark said...

Interesting fact about SWS developing around 2-3 months. I'm assuming this is also when muscle relaxation occurs. There's another variable that occurs around 3-4 months: loss of the epiglottis/palate lockup. As the infant transitions from an obligate nose breather to a mixed nose/mouth breather, the larynx descends and the epiglottis separates away from the soft palate, creating a space called the oropharynx. The infant has to relearn how to breathe and swallow.

xyz said...

"Interesting fact about SWS developing around 2-3 months. I'm assuming this is also when muscle relaxation occurs. There's another variable that occurs around 3-4 months: loss of the epiglottis/palate lockup. As the infant transitions from an obligate nose breather to a mixed nose/mouth breather, the larynx descends and the epiglottis separates away from the soft palate, creating a space called the oropharynx. The infant has to relearn how to breathe and swallow."

I Know. That's the whole point I'm making. I don't have to do the paint by numbers thing and explain every last detail. The muscle relaxation which increases apnea then has the effect of causing a dimunition in SWS which theoretically reduces the rate of SIDS. I've actually seen Dr. Park reply to some of my comments but he apparently doesn't get the Big Picture. It's pretty obvious to me.

Steven Y. Park, M.D. said...


I was merely pointing out an anatomic process (laryngeal descent in infants) that supports your theory. Your reply was a little out of context in relation to the main post. I do understand the implications of what you're suggesting. It makes total sense. But is there something we can do about it?

xyz said...

Hi Dr. Park, Thanks for your response.

What can we do?

(1) For the last several years I've been writing to hundreds of researchers been rejected by about 25 journals trying to publish my various papers. I've now published a book on which includes all my articles, theories, and attempts to get published. You can download it here for $5 or buy a hardcopy for $36. It's called "How the SIDS Back to Sleep Campaign Caused the Autism Epidemic" by T. McCabe:

(2) You can also sign my petition here:

(3) We can prove or disprove that the SIDS Back to Sleep campaign has caused the worldwide Autism Epidemic by getting hold of the ALSPAC dataset. That's a population cohort of 15,000 children born between 1990-1991 in Avon, UK that has sleep position data (back, side, stomach, other), Autism data, and developmental delay data. If I had that data for 2-3 hours I could use SAS to determine whether or not the SIDS Back to Sleep campaign caused the autism epidemic or not. If you know of anyway I could get hold of that data (perhaps via and IRB???) please let me know.

Regarding my theories:
Infants die of SIDS during Deep Sleep. You and I both know that Deep Sleep (Slow Wave Sleep) is the most restorative form of sleep and is (theoretically) when memory traces are transferred from the hippocampus to the neocortex. The inhibition of memory transfer in infants is my main concern.

All the Best and thanks for commenting!

T. McCabe

Steven Y. Park, M.D. said...

Thanks for the clarification. I'll definitely take a look at your book.

xyz said...

Dr. Park, FYI, I don't have WORD at home at the moment so I couldn't edit the book properly. Therefore, below is basically a summary of how the book is written.

The most important pages to read are 96-119, 48, 54.

Anyways, my most recent (and well-written) paper I tried to get published in May 2009:

P. 96-119
See Table of Contents on page 96

Interesting reviews of my 2nd Original Paper by eminent sleep researchers (written Oct. 2007):
P. 48 by Buszaki
P. 54 by Luis Carcoba

2nd Original Paper I tried to publish in October, 2007:
P. 1-46

1st Original Paper (very short) I submitted for publication in Pediatrics on Sept. 11, 2007:
P. 68-79

Rejection Letter for 1st Original Paper from Journal of Pediatrics:
P. 47

1st Original Paer
Rejection Letters by Journals:
P. 58-67

Interesting reviews by various sleep researchers/pediatricians:

P. 127-157

In addition, the book contains various other papers I tried to get published in 2008-2009.

BTW, Steffen Gais (an expert on SWS) also reviewed my theory and thought it was interesting but I forgot to put it in the book. In addition, some random pediatricians agreed with me and were very enthusiastic but I left them out purposely as I didn't want anything perceived as cheerleading to be in the book.

All the Best!

T. McCabe

Steven Y. Park, M.D. said...

Thanks for pointing out the important sections. I downloaded your book and look forward to reading it.

Michael Rack, MD said...

TSC, XYZ, Dr. Park, thanks for your comments

xyz said...

BTW, for anyone interested here is my finalized theory in a nutshell*.

I propose that the supine sleep position increases the risk of the autism variant pervasive developmental disorder – not otherwise specified (PDD-NOS) in six ways:
(1) interferes with SWA during SWS and increases arousals during REM sleep leading to
impaired memory consolidation, procedural learning, and declarative learning;
(2)increased arousals (Footnote A) lead to a sleep deprived state in which the right inferior frontal
gyrus is used as a secondary buffer (hippocampus is the primary memory buffer) (Footnote B) thus
impairing the proper functioning of the mirror neuron system;
(3) increased arousals are caused by intermittent hypoxia episodes and initiate long term facilitation (LTF) which yields increased genioglossus muscle activity (Footnote C) which in turn is the underlying cause of ongoing gastrointestinal problems and sleep disorders associated with autism and accounts for the higher ratio of males to females;
(4) increased arousals (Footnote D) due to supine sleep during REM sleep contribute to the social and emotional problems;
(5) impaired synaptic downscaling (neural pruning) leads to regression of language skills;
(6) increased minicolumnar abnormalities (Footnote E) and increased white matter (Footnote F) are the result of impaired synaptic downscaling (neural pruning). In addition, I propose that other methods to decrease arousal thresholds such as infants sleeping with pacifiers will also increase autism rates.

A.Skadberg B, Markestad T. Behaviour and physiological responses during prone and supine sleep in early infancy. Arch Dis Child. 1997;76:320-324(April)
B. Yoo SS, Gujar N, Hu P, Jolesz FA, Walker MP. The Human Emotional Brain without sleep - a
prefrontal amygdala disconnect. Curr. Biol., 17, Issue 20 R877-R878, 23 October 2007
C. Harris DP, Balasubramanian A, Badr MS, Mateika JH. Long-term facilitation of ventilation and
genioglossus muscle activity is evident in the presence of elevated levels of carbon dioxide in awake humans. Am J Physiol Regul Integr Comp Physiol. 2006. 291, R1111-R1119.
D. Skadberg BT, Markestad T. Consequences of Getting the Head Covered During Sleep in Infancy.
Pediatrics 1997;100;e6
E. Casanova MF, van Kooten IA, Switala AE, Ven Engeland H, Heinsen H, Steinbusch HW, Hof
PR, Trippe J, Stone J, Schmitz C. Minicolumnar abnormalities in autism. Acta Neuropathol. 2006
Sep; 112(3); 287-303.
F. Mostofsky SH, Burgess MP, Larson JCG. Increased motor cortex white matter volume predicts
motor impairment in autism. Brain (2007), 130, 2117-2122

*Conclusion is on pages 117-118 of my book "How the Back to Sleep Campaign Caused the Autism Epidemic"
**Footnotes A-F are Footnotes 117-122 in my book "How the Back to Sleep Campaign Caused the Autism Epidemic" on
page 123.

doctorstevenpark said...


I went through your entire book PDF, and although it's a bit technical, I got the gist of it. What you're proposing has huge implications. I can see why the mainstream medical community is resistant to even re-evaluating this issue.

You may want to contact Dr. Brain Palmer at and also take a look at his work. He has a PDF slideshow on the anatomic basis of SIDS ( His work and many others' work had a profound influence in how I view sleep-breathing disorders and the human upper airway.

At around 4-6 months, due to the separation of the soft palate away from the epiglottis, the tongue (which was normally completely in the oral cavity), now can rotate back into the oropharynx. This makes the tongue much more susceptible to relaxation in REM sleep and diminishing SWS in general. The two of you complement each other very well.

If you take a look at my book, Sleep, Interrupted, you'll see that I've extended similar concepts that you present and extrapolated it to the entire human lifespan. You could even apply these same principle to Alzheimer's (there are a lot of supporting studies).

Thanks for sharing this information with me. I'll sign your petition recommending that the experts take another objective look at the data.

I'm going to write about this in my blog at


xyz said...

Thank you Dr. Park. I briefly looked at that PDF and I plan on looking at it more closely this weekend. For anyone interested in looking at how "successful" the SIDS Back to Sleep campaign has been I suggest they look at this simple spreadhseet from Boston University which reports the sleep position of U.S. infants from 1992-2009. I know correlation does not imply causation but simply consider the trend:

Thanks again Dr. Park. I think that PDF might fill in one of the weak parts of my theory.


xyz said...

Not that it proves anything but:
on Page 150 of my book I quote Susan Syron:
"Since the implementation of the "Back to Sleep" campaign, therapists are seeing
increasing numbers of kindergarten-aged children who are unable to hold a
Susan Syron, Pediatric Physical Therapist

...and here's a story on autism which many news organizations are covering:
Children with autism may have lower quality handwriting and trouble forming letters compared to children without autism, according to a study published in the November 10, 2009, print issue of Neurology, the medical journal of the American Academy of Neurology.

I'm not surprised.

scheuer79 said...

I don't doubt this at all. I know that when I have had a few drinks, for sure I am more likely to have difficulty driving than my wife,and as you guessed, my rdi is way higher than hers. I wonder about my driving sometimes when I have not been drinking compared to my wifes when she has had one or two, she would probably argue that my driving is still worse than hers.

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