Intervall-Hypoxie-Hyperoxie-Therapie (IHHT)

[maguli]

Neu für mich ist jetzt die Kombniation aus "zuwenig" und "zuviel" Sauerstoff, also die Intervall-Hypoxie-Hyperoxie-Therapie (IHHT) oder auch  nur  Intervall-Hypoxie-Therapie (IHT), natürlich mit dem natürlichen Wirkstoff Höhenluft http://www.ipam.eu/fileadmin/Zelltraining_IPAM.pdf.
(Geschäftsidee: O₂-Mineralwasser jetzt auch mit Höhenluft, also besonders wenig O₂ LOL)
Also eine Kombination der "positiven Wirkungen der Sauerstofftherapien" mit den positiven Wirkungen eines aus der Sportmedizin bekannten Aufenthalts in großen Höhen zur Anreicherung roter Blutkörperchen (aber erst bei einem Aufenthalt von mind. einer Woche in Höhen über 2000m).
Ich seh grad, der Wiki-Artikel is gerage am Entstehen:  http://www.psiram.com/ge/index.php?title=CellGym Und das soll jetzt auch noch, natürlich "positive" Auswirkungen auch auf die Mitochondrien  haben
Mist, den Workshop im März hab ich auch verpasst ( http://www.interbiologica.de/kongress-2012/workshops/intervall-hypoxie-hyperoxie-therapie-ihht/)

[Dr. Ici Wenn]

Und das soll jetzt auch noch, natürlich "positive" Auswirkungen auch auf die Mitochondrien  haben

LOL!

Mist, den Workshop im März hab ich auch verpasst

Ganz böse. Wo kriegst Du jetzt die Fortbildungspunkte her?

[maguli]

Ich hab schon Ersatz gefunden: über 100 FB-Punkte in (-Achtung: bitte festhalten!-) MITOCHONDRIEN-MEDIZIN !
http://www.mito-medizin.de/app/download/5784552965/Flyer+zum+Studienmodul+Klinische+MitochondrienMedizin+und+Umweltmedizin.pdf
(wohl bemerkt: Ärztekammer-anerkannt und an einer deutschen Uni)
Für schlappe 2100 Euros. Der Kurs muss es wohl wert sein. Kann man sich alles Hundertfach von Patienten/Kunden wiederholen, locker! (IRONIE!)

PS: Ich hab mir den CV des Mitgründers der CellGym-(IHHT)-Firma Bernd Löffler http://www.cellgym.de/unternehmen/dr-bernd-michael-loeffler.html angeschaut. Für mich echt beeindruckend seine Forschungstätigkeiten, MPI und so,  die ja eigentlich gar nix Pseudowissenschaftliches beinhaltet. Wie kann man so in die Pseudomedizin abrutschen? Wahrscheinlich, weil man da fast unendlich Kohle abgreifen kann? (Obwohl, als Berater der Pharma-Industrie dürfte er, so fleißig wie er zu sein scheint, auch nicht wenig bekommen haben.)
Oder welch andere Gründe lassen einen zum "Pseudo" werden?

[Conina]

Ich glaube, Pseudomedizin lohnt sich finanziell nur für die Seminaranbieter und für die ganz dicken Fische.

[Dr. Ici Wenn]

Wie kann man so in die Pseudomedizin abrutschen?

Darüber wird hier auch seit Jahren spekuliert ...

Guck mal in Deine PN (Private Nachrichten)

[Conina]

Was haben wir 2009 noch gewettert:
http://blog.psiram.com/?p=285

Da gab´s 16 Punkte für Orgonheilkunde.

Der aktuelle Stil im Blog gefällt mir besser.

[HealthySide]

Wenn man auf PubMed mal recherchiert, dann gibt es aber eine ganze Reihe von wissenschaftlichen Studien, die positive Effekte bei IHT gefunden haben, auch zu IHHT finden sich positive Studien.

[Binky]

Wir freuen uns iimer wieder über Links, die solche Behauptungen untermauern.

[HealthySide]

Ich dachte, bei den eindeutig negativen Aussagen wäre schon recherchiert worden. Ist das nicht der Fall gewesen? Ich spreche allerdings ausschließlich von IHT (oder IHHT) selber, nicht von den Geräten bzw. Anbietern, die da wohl teilweise für nicht wenig Geld Geräte anbieten. Die Studien dazu scheinen aber mehrheitlich sehr jung zu sein. Andererseits wird Höhentraining ja von vielen Sportlern seit mehr als 50 Jahren als "legales Doping" genutzt, auch wenn die Wirkung nicht so extrem zu sein scheint wie bei EPO. Ich denke, was viele Hersteller heute machen ist, eine bekannte Methode aufzuhübschen und dann zu verkaufen. Andererseits, nicht jeder kann regelmäßig ins Höhentraining fahren ;-).

Ein paar Veröffentlichungen zum Thema Hypoxie, wenn Sie mal selber z.B. bei medline o.ä. nach hypoxia+therapy suchen, finden sie mehrere hundert Treffer.

Exp Physiol. 2012 May 4.
Mitochondrial Energy Metabolism Plays a Critical Role in the Cardioprotection Afforded by Intermittent Hypobaric Hypoxia.
Wang ZH, Cai XL, Wu L, Zhuo Y, Liu JL, Zhou ZN, Liu JK, Yang HT.
Abstract
Intermittent hypobaric hypoxia (IHH) is an effective protective strategy against myocardial ischemia/reperfusion (I/R) injury, but the precise mechanisms are far from clear. To understand the overall effects of IHH on the myocardial proteins during I/R, we analyzed functional performance and protein expression profile in isolated hearts from normoxic and IHH (5000 m, 4 h/d, 4 w) adapted rats following I/R (30 min/45 min) injury. IHH significantly improved the post-ischemic recovery of left ventricular function compared with the recovery in time-matched normoxic control. Two-dimensional electrophoresis with matrix-assisted laser desorption/ionization and time-of-flight mass spectrometric analysis was then used to assess protein alterations in left ventricles (LV) from normoxic and IHH groups with or without I/R. Expressions of sixteen proteins changed by over 5-fold; nine of these proteins are involved in energy metabolism. Immunoblot and real-time PCR analysis confirmed the IHH-increased expressions of ATP synthase subunit beta, mitochondrial aldehyde dehydrogenase, and heat shock protein 27 in LVs. Furthermore, IHH significantly attenuated the reduction of myocardial ATP content and mitochondrial ATP synthase activity, membrane potential as well as respiratory control ratios due to I/R. In addition, inhibition of mitochondrial ATP synthase by oligomycin (1 μmol/L) abolished the IHH-induced improvements in three parameters: post-ischemic recovery of LV function, mitochondrial membrane potential, and respiratory control ratios. These results suggest that improvement in mitochondrial energy metabolism makes an important contribution to the IHH-afforded cardioprotection against post-ischemic myocardial dysfunction.


Sleep Breath. 2012 Apr 18.
Lipid peroxidation and paraoxonase activity in nocturnal cyclic and sustained intermittent hypoxia.
Okur HK, Pelin Z, Yuksel M, Yosunkaya S.
Abstract
PURPOSE:
Obstructive sleep apnea (OSA) and chronic obstructive pulmonary disease (COPD) have been known to be associated with atherosclerosis and hypoxia which was suggested to have an important role in this process by the way of increased oxidative stress. In the present study, we aimed to evaluate the effects of nocturnal hypoxia pattern (intermittent versus sustained) on serum lipid peroxidation and paraoxonase (PON) activity.
METHODS:
Blood collections were performed in 44 OSA, 11 non-apneic, nocturnal desaturated COPD, and 14 simple snorer patients after full-night polysomnographic recordings. Nocturnal sleep and respiratory parameters, oxygen desaturation indexes, serum malondialdehyde (MDA) levels by measuring with the help of the formation of thiobarbituric acid reactive substances (TBARS), and PON activity were assessed in all subjects.
RESULTS:
OSA and COPD patients showed nocturnal hypoxemia, with a minimum oxygen saturation (SaO(2)) in ranges of 53-92 % and 50-87 %, respectively. The mean levels of TBARS was 15.7 ± 3.6 nmol and 15.3 ± 3.4 nmol malondialdehyde (MDA)/ml in OSA and COPD patients, respectively, while the mean level of the control group was 4.1 ± 1.2 nmol MDA/ml. The mean PON activity was found to be 124.2 ± 35.5 U/l in OSA patients and 124.6 ± 28.4 U/l in COPD patients. The mean PON activity of the control group was 269.0 ± 135.8 U/l. The increase in TBARS levels and the decrease in PON1 levels were statistically significant in both OSA and COPD patients according to controls (p < 0.001 for TBARS as well as PON1).
CONCLUSION:
The results of this study revealed that both OSA and non-apneic, nocturnal desaturated COPD patients showed increased levels of lipid peroxidation and decreased PON activity despite the differences in nocturnal hypoxia pattern.



Indian J Med Res. 2012 Feb;135:211-6.
Effect of intermittent hypobaric hypoxia on efficacy & clearance of drugs.
Vij AG, Kishore K, Dey J.
Abstract
BACKGROUND &#38; OBJECTIVES:
People travelling to high altitude for occupational, recreational or religious purposes are mostly healthy and fit but sometimes they use drugs for common ailments like influenza, acute mountain sickness or chronic disease like diabetes. Limitation of oxygen at high altitude may compromise metabolism of drugs. Hence, we undertook this study to assess the effect of hypobaric hypoxia on some commonly used drugs in rats and rabbits.
METHODS:
Effect of intermittent hypobaric hypoxia on phenotypic expression of anesthetic drugs pentabarbitone, thiopentone and zoxazolamine (sleeping time) was assessed in rats exposed to 282.4 mm Hg equivalent to 25000 feet in a decompression chamber. Plasma clearance of some commonly used drugs was investigated in rabbits exposed to 429 mm Hg equivalent to 15000 feet. Pharmacokinetic parameters were computed by plotting drug concentration versus time curve on semi log scale.
RESULTS:
A significant delay in regaining rightening reflex was observed in rats exposed to intermittent hypobaric hypoxia in response to zoxazolamine, pentobarbitone and thiopentone sodium. Pharmacokinetics of acetyl salicylic acid, gentamicin, phenobarbitone and acetazolamide showed increase in plasma half life (t 1/2), decrease in elimination rate constant (k el) and hence prolonged residence of these drugs in hypoxic animals.
INTERPRETATION &#38; CONCLUSIONS:
This experimental study showed that hypoxia altered therapeutic effectiveness and clearance of several drugs, in rats and rabbits exposed to intermittent hypobaric hypoxia. s0 uch studies need to be done in human volunteers to see the effect of hypoxia on pharmacokinetics of some common drugs.


J Neurosci. 2012 Mar 14;32(11):3591-600.
Repetitive intermittent hypoxia induces respiratory and somatic motor recovery after chronic cervical spinal injury.
Lovett-Barr MR, Satriotomo I, Muir GD, Wilkerson JE, Hoffman MS, Vinit S, Mitchell GS.
Abstract
Spinal injury disrupts connections between the brain and spinal cord, causing life-long paralysis. Most spinal injuries are incomplete, leaving spared neural pathways to motor neurons that initiate and coordinate movement. One therapeutic strategy to induce functional motor recovery is to harness plasticity in these spared neural pathways. Chronic intermittent hypoxia (CIH) (72 episodes per night, 7 nights) increases synaptic strength in crossed spinal synaptic pathways to phrenic motoneurons below a C2 spinal hemisection. However, CIH also causes morbidity (e.g., high blood pressure, hippocampal apoptosis), rendering it unsuitable as a therapeutic approach to chronic spinal injury. Less severe protocols of repetitive acute intermittent hypoxia may elicit plasticity without associated morbidity. Here we demonstrate that daily acute intermittent hypoxia (dAIH; 10 episodes per day, 7 d) induces motor plasticity in respiratory and nonrespiratory motor behaviors without evidence for associated morbidity. dAIH induces plasticity in spared, spinal pathways to respiratory and nonrespiratory motor neurons, improving respiratory and nonrespiratory (forelimb) motor function in rats with chronic cervical injuries. Functional improvements were persistent and were mirrored by neurochemical changes in proteins that contribute to respiratory motor plasticity after intermittent hypoxia (BDNF and TrkB) within both respiratory and nonrespiratory motor nuclei. Collectively, these studies demonstrate that repetitive acute intermittent hypoxia may be an effective and non-invasive means of improving function in multiple motor systems after chronic spinal injury.


Respir Physiol Neurobiol. 2012 Apr 30;181(2):132-42. Epub 2012 Mar 2.
Short intermittent hypoxic exposures augment ventilation but do not alter regional cerebral and muscle oxygenation during hypoxic exercise.
Debevec T, Mekjavic IB.
Abstract
This study investigated the effects of four exposures to normobaric hypoxia (SIH group; [Formula: see text] N=10) or placebo-control normoxia (Control group; [Formula: see text] N=9) on cardio-respiratory responses to hypoxic exercise. Before and after the exposures all subjects performed a constant power test (CP) to exhaustion in hypoxia [Formula: see text] at a work load corresponding to 75% of previously determined normoxic [Formula: see text] . Arterial oxygen saturation [Formula: see text] and minute ventilation (V˙(E)) were measured continuously. NIRS was used to monitor regional changes in oxygenated, de-oxygenated and total hemoglobin concentrations of the frontal cortex, vastus lateralis and serratus anterior. Although neither group improved CP time, the SIH group exhibited increases in both V˙(E) (+15%; P<0.05) and [Formula: see text] (+4%; P<0.05) after intermittent hypoxia.


J Appl Physiol. 2012 May;112(10):1706-14. Epub 2012 Mar 8.
Intermittent hypoxia conditioning protects mitochondrial cytochrome c oxidase of rat cerebellum from ethanol withdrawal stress.
Ju X, Mallet RT, Downey HF, Metzger DB, Jung ME.
Abstract
Intermittent hypoxia (IH) conditioning minimizes neurocognitive impairment and stabilizes brain mitochondrial integrity during ethanol withdrawal (EW) in rats, but the mitoprotective mechanism is unclear. We investigated whether IH conditioning protects a key mitochondrial enzyme, cytochrome c oxidase (COX), from EW stress by inhibiting mitochondrially directed apoptotic pathways involving cytochrome c, Bax, or phosphor-P38 (pP38). Male rats completed two cycles of a 4-wk ethanol diet (6.5%) and 3 wk of EW. An IH program consisting of 5-10 bouts of 5-8 min of mild hypoxia (9.5-10% inspired O(2)) and 4 min of reoxygenation for 20 consecutive days began 3 days before the first EW period. For some animals, vitamin E replaced IH conditioning to test the contributions of antioxidant mechanisms to IH's mitoprotection. During the second EW, cerebellar-related motor function was evaluated by measuring latency of fall from a rotating rod (Rotarod test). After the second EW, COX activity in cerebellar mitochondria was measured by spectrophotometry, and COX, cytochrome c, Bax, and pP38 content were analyzed by immunoblot. Mitochondrial protein oxidation was detected by measuring carbonyl contents and by immunochemistry. Earlier IH conditioning prevented motor impairment, COX inactivation, depletion of COX subunit 4, protein carbonylation, and P38 phosphorylation during EW. IH did not prevent cytochrome c depletion during EW, and Bax content was unaffected by EW ± IH. Vitamin E treatment recapitulated IH protection of COX, and P38 inhibition attenuated protein oxidation during EW. Thus IH protects COX and improves cerebellar function during EW by limiting P38-dependent oxidative damage.

J Appl Physiol. 2008 Aug;105(2):510-7. Epub 2008 May 22.
Intermittent hypoxia conditioning prevents behavioral deficit and brain oxidative stress in ethanol-withdrawn rats.
Jung ME, Simpkins JW, Wilson AM, Downey HF, Mallet RT.
Abstract
Intermittent hypoxia (IH) has been found to protect brain from ischemic injury. We investigated whether IH mitigates brain oxidative stress and behavioral deficits in rats subjected to ethanol intoxication and abrupt ethanol withdrawal (EW). The effects of IH on overt EW behavioral signs, superoxide generation, protein oxidation, and mitochondrial permeability transition pore (PTP) opening were examined. Male rats consumed dextrin or 6.5% (wt/vol) ethanol for 35 days. During the last 20 days, rats were treated with repetitive (5-8 per day), brief (5-10 min) cycles of hypoxia (9.5-10% inspired O2) separated by 4-min normoxia exposures. Cerebellum, cortex, and hippocampus were biopsied on day 35 of the diet or at 24 h of EW. Superoxide and protein carbonyl contents in tissue homogenates and absorbance decline at 540 nm in mitochondrial suspensions served as indicators of oxidative stress, protein oxidation, and PTP opening, respectively. Although IH altered neither ethanol consumption nor blood ethanol concentration, it sharply lowered the severity of EW signs including tremor, tail rigidity, and startle response. Compared with dextrin and ethanol per se, in the three brain regions, EW increased superoxide and protein carbonyl contents and accelerated PTP opening in a manner ameliorated by IH. Administration of antioxidant N-acetylcysteine throughout the IH program abrogated the reductions in EW signs and superoxide content, implicating IH-induced ROS as mediators of the salutary adaptations. We conclude that IH conditioning during chronic ethanol consumption attenuates oxidative damage to the brain and mitigates behavioral abnormalities during subsequent EW. IH-induced ROS may evoke this powerful protection.

[HealthySide]

Es gibt auch ältere Studien zu der Theamatik:

High Alt Med Biol. 2003 Fall;4(3):291-304.
Intermittent hypoxia improves endurance performance and submaximal exercise efficiency.
Katayama K, Matsuo H, Ishida K, Mori S, Miyamura M.
AbstractThe purpose of the present study was to elucidate the influence of intermittent hypobaric hypoxia at rest on endurance performance and cardiorespiratory and hematological adaptations in trained endurance athletes. Twelve trained male endurance runners were assigned to either a hypoxic group (n = 6) or a control group (n = 6). The subjects in the hypoxic group were exposed to a simulated altitude of 4500 m for 90 min, three times a week for 3 weeks. The measurements of 3000 m running time, running time to exhaustion, and cardiorespiratory parameters during maximal exercise test and resting hematological status were performed before (Pre) and after 3 weeks of intermittent hypoxic exposure (Post). These measurements were repeated after the cessation of intermittent hypoxia for 3 weeks (Re). In the control group, the same parameters were determined at Pre, Post, and Re for the subjects not exposed to intermittent hypoxia. The athletes in both groups continued their normal training together at sea level throughout the experiment. In the hypoxic group, the 3000 m running time and running time to exhaustion during maximal exercise test improved. Neither cardiorespiratory parameters to maximal exercise nor resting hematological parameters were changed in either group at Post, whereas oxygen uptake (.V(O2)) during submaximal exercise decreased significantly in the hypoxic group. After cessation of intermittent hypoxia for 3 weeks, the improved 3000 m running time and running time to exhaustion tended to decline, and the decreased .V(O2) during submaximal exercise returned to Pre level. These results suggest that intermittent hypoxia at rest could improve endurance performance and submaximal exercise efficiency at sea level in trained endurance athletes, but these improvements are not maintained after the cessation of intermittent hypoxia for 3 weeks.


Eur J Appl Physiol. 2002 Jun;87(2):187-91. Epub 2002 Mar 28.
Enhanced chemosensitivity after intermittent hypoxic exposure does not affect exercise ventilation at sea level.
Katayama K, Sato Y, Shima N, Qiu JC, Ishida K, Mori S, Miyamura M.
Abstract
The purpose of the present study was to test the hypothesis that the ventilatory response to exercise at sea level may increase after intermittent hypoxic exposure for 1 week, accompanied by an increase in hypoxic or hypercapnic ventilatory chemosensitivity. One group of eight subjects (hypoxic group) were decompressed in a chamber to 432 torr (where 1 torr=1.0 mmHg, simulating an altitude of 4,500 m) over a period of 30 min and maintained at that pressure for 1 h daily for 7 days. Oxygen uptake and pulmonary ventilation (V(E)) were determined at 40%, 70%, and 100% of maximal oxygen uptake at sea level before (Pre) and after (Post) 1 week of daily exposures to hypoxia. The hypoxic ventilatory response (HVR) was determined using the isocapnic progressive hypoxic method as an index of ventilatory chemosensitivity to hypoxia, and the hypercapnic ventilatory response (HCVRSB) was measured by means of the single-breath carbon dioxide method as an index of peripheral ventilatory chemosensitivity to hypercapnia. The same parameters were measured in another group of six subjects (control group). In the hypoxic group, resting HVR increased significantly ( P<0.05) after intermittent hypoxia and HCVRSB increased at Post, but the change was not statistically significant ( P=0.07). In contrast, no changes in HVR and HCVRSB were found in the control group. There were no changes in either V(E) or the ventilatory equivalent for oxygen during maximal and submaximal exercise at sea level throughout the experimental period in either group. These results suggest that the changes in resting hypoxic and peripheral hypercapnic chemosensitivities following short-term intermittent hypoxia have little effect on exercise ventilation at sea level.


J Appl Physiol. 2007 Sep;103(3):828-34.
The effects of nightly normobaric hypoxia and high intensity training under intermittent normobaric hypoxia on running economy and hemoglobin mass.
Neya M, Enoki T, Kumai Y, Sugoh T, Kawahara T.
Abstract
We investigated the effects of nightly intermittent exposure to hypoxia and of training during intermittent hypoxia on both erythropoiesis and running economy (RE), which is indicated by the oxygen cost during running at submaximal speeds. Twenty-five college long- and middle- distance runners [maximal oxygen uptake (Vo(2max)) 60.3 +/- 4.7 ml x kg(-1) x min(-1)] were randomly assigned to one of three groups: hypoxic residential group (HypR, 11 h/night at 3,000 m simulated altitude), hypoxic training group (HypT), or control group (Con), for an intervention of 29 nights. All subjects trained in Tokyo (altitude of 60 m) but HypT had additional high-intensity treadmill running for 30 min at 3,000 m simulated altitude on 12 days during the night intervention. Vo(2) was measured at standing rest during four submaximal speeds (12, 14, 16, and 18 km/h) and during a maximal stage to volitional exhaustion on a treadmill. Total hemoglobin mass (THb) was measured by carbon monoxide rebreathing. There were no significant changes in Vo(2max), THb, and the time to exhaustion in all three groups after the intervention. Nevertheless, HypR showed approximately 5% improvement of RE in normoxia (P < 0.01) after the intervention, reflected by reduced Vo(2) at 18 km/h and the decreased regression slope fitted to Vo(2) measured during rest position and the four submaximal speeds (P < 0.05), whereas no significant corresponding changes were found in HypT and Con. We concluded that our dose of intermittent hypoxia (3,000 m for approximately 11 h/night for 29 nights) was insufficient to enhance erythropoiesis or Vo(2max), but improved the RE at race speed of college runners.

[Binky]

Danke, die Links dahin hätten gereicht. 

[HealthySide]

Gibt es auch substanzielle Kritik an Hypoxie-Theraie /-Training? Ich sehe natürlich auch, dass die Studienlage nicht perfekt ist ;-) , aber das, was in dem Thread bislang abgeliefert wurde, bietet nun auch nicht gerade Gegenargumente. Oder bin ich dafür hier falsch? Nur mal draufhauen und gut?

[Binky]

Gibt es auch substanzielle Kritik an Hypoxie-Theraie /-Training? Ich sehe natürlich auch, dass die Studienlage nicht perfekt ist ;-) , aber das, was in dem Thread bislang abgeliefert wurde, bietet nun auch nicht gerade Gegenargumente. Oder bin ich dafür hier falsch? Nur mal draufhauen und gut?

Die Studien sind keine klinischen Wirksamkeitsbelege. Sucht man danach, erscheinen alle möglichen Quacksalberseiten.

[Daggi]

Rattenstudien (ich dachte Esowatch-Kritiker mögen die nicht) sind ja schön und gut, sind aber auf den Menschen nur sehr bedingt übertragbar. Eher dann, wenn es um potentiell schädliche Einflüsse geht. Keine der oben genannten Arbeiten belegt irgendwie, dass man mit der Methode Krebs heilen kann, die Zuckerkrankheit auch noch, nebenbei die Multiple Sklerose, Burn-out, Anti-Aging, Alzheimer, Multiple Sklerose, chronisches Müdigkeitssyndrom, Allergien, Rheuma, Asthma, Borreliose, Übergewicht, Schlafstörungen, Bluthochdruck, Stärkung des Immunsystems, Beschleunigte Heilung von Verletzungen usw.. Habe hier bestimmt noch zig Krankheiten vergessen.

Auf der anderen Seite stehen die Gefahren. Die kann man beispielsweise im Artikel Schlafapnoe-Syndrom bei Wikipedia zum obstruktiven Schlafapnoe-Syndrom (OSAS) nachlesen:

Als Folge eines unbehandelten OSAS treten meistens weitere chronische Gesundheitsstörungen auf, und zwar Herz-Kreislauferkrankungen wie Bluthochdruck, Herzinfarkte sowie Schlaganfälle. Ein plötzlicher Herztod kann bei unbehandeltem OSAS mit erhöhter Wahrscheinlichkeit auftreten. Beschrieben sind auch Depressionen und das gehäufte Auftreten von Stress-Erkrankungen wie Magengeschwür, Tinnitus und Hörsturz. Diabetes mellitus, Typ 2 wird seit Anfang 2002 immer häufiger in Zusammenhang mit dem OSAS gebracht. Es besteht ein linearer Zusammenhang zwischen dem Apnoe-Hypopnoe-Index (AHI) und der Insulin-Resistenz[2]. Der Blutzucker ist also umso höher, je mehr Atempausen pro Stunde Schlaf auftreten. Nach einer eingeleiteten nCPAP-Therapie kann die nächtliche Zuckerneubildung (Gluconeogenese) deutlich vermindert werden und die morgendlichen Blutzucker-Werte sinken. Patienten, deren OSAS durch Behandlung reduziert wurde, berichten von reduzierten Migräneanfällen.

Einer aktuellen Studie zufolge ist das SAS stark mit dem Auftreten von Herzkrankheiten, die einen Herzschrittmacher erforderlich machen, assoziiert.[3]

http://de.wikipedia.org/wiki/Schlafapnoe-Syndrom

[Daggi]

Was ich vergass: Dank für die Artikelsuche, vielleicht ist was für die Wiki-Autoren dabei.

Ein Artikel im Wiki bezieht sich auf die Diskussion hier:

Cellgym:  http://psiram.com/ge/index.php?title=CellGym