*This is an article from the Winter 2022 issue of Contentment Magazine.

By Lewis Coleman, MD, FAIS

“Alcohol is the anesthesia by which we endure the operation of life.”George Bernard Shaw

Emotions are powerful and painful. We seek solace from them in the form of alcohol, tranquilizers, vacations, psychotherapy, religion, and counseling. It’s common knowledge, backed by abundant evidence, that emotional pain is not only unpleasant, but also harmful to health. Nevertheless, exactly how and why emotions are harmful has remained a stubborn mystery. This essay will review the surprising similarities of sleep and anesthesia from the perspective of stress theory to illustrate the nature of emotional stress and explain how and why it causes disease and devastates health.


Sleep, that knits up the ravell’d sleave of care Shakespeare, Macbeth

Sleep is essential for life, and it is vaguely assumed to conserve energy, relieve stress, and optimize brain function, but its purpose has never been clear. Stress theory confers a fresh explanation that is consistent with known science: sleep enables the “fight or flight” mechanism that enhances survival by pre-emptively detecting dangerous environmental circumstances, inducing fear and anxiety that facilitates flight from the danger, and optimizing fighting ability when flight fails to avoid life-threatening confrontations in the wild.1,2

The Fight or Flight Mechanism

The ”fight or flight” mechanism consists of four sub-mechanisms that work together:

  1. Consciousness interprets nervous sensory information as sight, sound, smell, taste, and touch. It interprets nociception as pain.
  2. The memory mechanism records and retains an audiovisual record of all waking moments throughout life, and works closely with consciousness to produce a cohesive perception of the surrounding environment.
  3. The dreaming mechanism automatically reviews accumulating memories during sleep to identify dangerous environmental circumstances.
  4. The emotional mechanism induces fear and anxiety that activates sympathetic nervous system hyperactivity to facilitate fight or flight when consciousness detects dangerous environmental circumstances previously identified by the dreaming mechanism.

The fight or flight mechanism explains clinical psychology. Though its survival role in humans is minimal, it affects human emotion, pathophysiology, and behavior in countless ways. It explains PTSD (post-traumatic stress disorder), the “Stockholm Syndrome,” voodoo death,3 drug addiction, alcoholism, the lingering effects of childhood abuse, criminal behavior, and the “social behavior” of both humans and animals that causes them to instinctively form hierarchies, tribes, and governments.4 It explains how emotion induces harmful sympathetic nervous activity that elevates blood pressure and pulse rate, releases stress hormones, and promotes harmful stress mechanism hyperactivity that causes disease.

Though the fight or flight mechanism enhances survival, it is innately harmful. It causes stress mechanism hyperactivity that consumes and wastes body resources, and produces harmful excesses and defective versions of its products. It diverts blood flow to some organs at the expense of others. It induces sympathetic nervous system hyperactivity, which releases von Willebrand hormone that consumes fibrinogen to generate insoluble fibrin that increases blood coagulability, and exaggerates microvascular flow resistance.2,5,6 This minimizes blood loss in the event of injury, and diverts blood flow and oxygen to the heart and brain. Sympathetic activity also releases HPA “stress hormones” such as glucagon, cortisol, and epinephrine that elevate cellular metabolism and convert glycogen to glucose to increase blood glucose levels.

Extreme sympathetic hyperactivity can precipitate heart attacks, strokes, and sudden death. Prolonged, subacute sympathetic hyperactivity accelerates amyloidosis, atherosclerosis, capillary senescence, and systemic inflammation, which causes heart disease, cancer, chronic illnesses, and premature death. My favorite example is the earthquake studies of Kario et al. that demonstrated how uninjured people near the epicenter of the earthquake suffered higher rates of sudden death than those far away. Uninjured survivors exhibited elevations in blood coagulability, von Willebrand Factor, and factor VIII activity for months.7-15

Nociception and Sympathetic Nervous Activity

Nociception is nervous activity generated by tissue disruption sensors called “nociceptors” that are located in organs and peripheral tissues. Peripheral sensory nerves conduct nociception to specialized nociception pathways in the spinal cord. The spinal cord conducts nociception simultaneously to the brain AND to sympathetic nervous ganglia in the chest and abdomen.

The sympathetic ganglia convert nociception into sympathetic nervous activity, and they directly innervate internal organs including the brain, heart, lungs, adrenal glands, and the GI tract. The sympathetic nervous activity increases blood coagulability and controls the capillary gate2,5 to govern blood flow. 2, 14 The adrenal glands release HPA hormones including glucagon, which elevates blood glucose, and epinephrine, which closes the capillary gate in peripheral tissues that are not directly innervated by sympathetic ganglia.

Corticofugal Control of Nociception

The cerebral cortex generates consciousness, which interprets nociception as pain. Consciousness regulates nociception in accord with emotion via descending (“corticofugal”) inhibitory nervous pathways from the cerebral cortex to spinal cord nociception pathways.16 Thus, consciousness regulates both sympathetic nervous activity and the perception of pain. This facilitates fight or flight despite injury in life-threatening situations. The classical example is a soldier who suffers a severe wound during fearsome combat but remains unaware of the pain while he continues to fight. When the combat subsides, he suddenly becomes aware of the excruciating pain caused by his injury.

Anesthesia extinguishes consciousness, which eliminates its inhibition of nociception. This has the unfortunate effect of exaggerating harmful sympathetic nervous hyperactivity induced by surgical nociception unless anesthesia is supplemented with analgesia.

Analgesia beneficially inhibits nociception. This prevents pain, but has no effect on consciousness, so the fight or flight mechanism can still be activated by other senses.

Nociception and Respiratory Drive

Specialized nociceptors called “respiratory chemoreceptors” enable respiratory drive, which stimulates breathing. There are three sources of respiratory drive:

  1. Primary respiratory drive dominates breathing in the presence of consciousness. Carbon dioxide reacts weakly with water to form a harmless acid called carbonic acid. This causes blood to be mildly acidic. Blood pH rapidly equilibrates with cerebrospinal fluid, and primary respiratory pH chemoreceptors located in the brain ventricles thus stimulate breathing in accord with CO2 levels within the body. However, both sleep and anesthesia extinguish consciousness and paralyze primary respiratory drive.
  2. Secondary respiratory drive sustains breathing in the absence of consciousness, during either sleep or general anesthesia. Its chemoreceptors are strongly sensitive to hypercarbia, and weakly sensitive to hypoxia. They are less sensitive than the primary chemoreceptors, so carbon dioxide levels are harmlessly elevated during normal sleep. The resulting hypercarbia has little effect on hemoglobin saturation in arterial blood. Instead, it lowers microvascular flow resistance, enhances cardiac efficiency, speeds the transport of oxygenated blood from the lungs to organs and tissues, and enhances the release of oxygen from blood into tissues. Mild hypercarbia during sleep thus optimizes oxygen transport and delivery. In contrast, hyperventilation depletes CO2 tissue reserves, which paralyzes secondary respiratory drive chemoreceptors. This creates a dangerous condition similar to “Ondine’s curse” in Greek Mythology. The Gods cursed Ondine so that she would stop breathing and die if she ever fell asleep.
  3. Nociception directly stimulates breathing despite general anesthesia. During anesthesia, this can cause hyperventilation that depletes CO2 body reserves and paralyzes secondary respiratory drive. Supplementation of general anesthesia with narcotic analgesia inhibits surgical nociception, prevents hyperventilation and CO2 depletion during surgery, and protects postoperative respiratory drive.


Our brains possess a memory mechanism that records and retains vivid audiovisual records of all waking moments throughout life, including infancy. These memories are normally suppressed, so that most people are unaware of them. This startling phenomenon was accidentally discovered by Dr. Wilder Penfield, a neurosurgeon who stimulated the brains of awake patients with weak electrical currents while attempting to find better ways to treat epilepsy.17 More recently, a woman named Jill Price sought the help of memory experts at UC Irvine because her consciousness was flooded with vivid childhood memories that disrupted her ability to function.18 They gave her condition a name: “Hyperthymestic syndrome.”19 Since then, several similar patients have been identified. For example, the actress Marilu Henner of “Taxi” fame recalls her acting scripts effortlessly.


The dreaming mechanism provides the key to understanding how the fight or flight mechanism works. There are three “stages” of sleep. Dreaming occurs during the third stage, which is called “deep sleep” or “REM” (rapid eye movement) sleep.20 During dreaming, brain activity approaches awake levels and the body experiences temporary paralysis of voluntary muscles, with the exception of eye and breathing muscles. This prevents violent movements related to the dreaming process. The dreaming mechanism reviews memories during REM sleep to identify dangerous environmental circumstances. Sometimes there is inadequate paralysis of the skeletal muscles, which causes “Rapid Eye Movement (REM) Sleep Behavior Disorder” while people are acting out their dreams. This can manifest as small twitches and leg movements, sleepwalking, or even violent attacks on sleeping companions.21

Obstructive Sleep Apnea

Sleep Apnea Oxygen Mask Equipment And CPAP Machine

In patients with abnormal airway anatomy, pharyngeal muscle relaxation during REM sleep can cause soft tissues to collapse into the airway and obstruct air flow. This is called “obstructive sleep apnea (OSA).” This becomes extremely dangerous when patients with abnormal airway anatomy are hyperventilated during anesthesia, because this depletes CO2 body reserves, and paralyzes secondary respiratory drive during general anesthesia.22,23 Such a patient may regain consciousness, which restores primary respiratory drive after anesthesia, but the combination of abnormal anatomy and inadequate respiratory drive is a prescription for disaster, especially is sent home in the care of medically ignorant  friends and family.22,24-30


The emotional mechanism works closely with consciousness to pre-emptively perceive dangerous environmental circumstances previously identified by the dreaming mechanism, whereupon it induces fear and anxiety, which activates sympathetic nervous activity that increases blood coagulability, diverts blood flow to heart and brain, and releases HPA “stress” hormones. This enhances survival by causing animals to flee from dangerous circumstances, and simultaneously enhancing survival in the event of life-threatening encounters.

Anesthesia and the Fight or Flight Mechanism

Today it is forgotten that before the discovery of anesthesia, surgery was not only excruciatingly painful, but also was plagued by a “surgical stress syndrome (SSS)” that worsened inexorably during the two days following successful surgery, and often culminated in agonizing death. It consists of symptoms distant from the time and site of surgery, including fever, tachycardia, hypertension, exaggerated pain, delirium, dementia, and organ failure. This syndrome was so fearsome that most physicians avoided surgery.

Anesthesia was considered miraculous because it prevented the perception of surgical pain and mitigated the life-threatening effects of the SSS enough to enable most patients to survive life-saving surgery, but the SSS persists despite anesthesia in the form of acute renal failure, atelectasis, pneumonia, bowel ileus, heart attacks, strokes, delirium, and dementia. Its distant effects include increased cancer, heart disease, and chronic illnesses.

Anesthesia inhibits the SSS by paralyzing the fight or flight mechanism. It eliminates the ability of consciousness to perceive pain and danger, generate fear, and exaggerate harmful sympathetic nervous activity. However, anesthesia alone cannot abolish surgical stress. It doesn’t inhibit spinal cord nociception pathways that activate harmful sympathetic nervous activity independent of brain activity. Worse yet, it paralyzes the descending cortical pathways that inhibit spinal cord nociception. This has the unfortunate effect of exaggerating spinal cord nociception pathway activity induced by surgery that elevates harmful sympathetic nervous system activity. This jeopardizes organ safety, and induces hyperventilation that depletes CO2 body reserves, undermines respiratory drive, and threatens unexpected postoperative respiratory arrest.

The depletion of CO2 tissue reserves deserves special attention, because CO2 is so widely misunderstood. CO2 is persistently vilified in the mass media as a supposed cause of “global warming” and as a “toxic waste gas” that must be “rid from the body.” This represents scientific and cultural insanity, because nothing could be further from the truth. CO2 is benign, beneficial, and essential for life. It is as essential as oxygen, because it enables all aspects of the mechanism of oxygen transport and delivery that captures oxygen from the atmosphere and delivers it to cells deep within the animal body. Those who wish to know more can begin with my published review of CO2 pathophysiology called “Four Forgotten Giants of Anesthesia History that can be downloaded from the Internet free of charge.31

CO2 depletion undermines primary respiratory drive, and paralyzes secondary respiratory drive altogether, causing a deceptive and dangerous condition called the “hyperventilation-hypoventilation syndrome.”32 CO2 depleted patients emerging from surgery appear to breathe normally after they regain consciousness, which restores primary respiratory drive that resists CO2 depletion. However, the CO2 depletion inhibits the release of oxygen from blood into tissues and organs. The resulting hypoxia causes postoperative heart attacks, strokes, atelectasis, bowel ileus, nausea, vomiting, and pneumonia.

Even scarier, if patients fall asleep in this dangerous condition, they may suffer sudden, unexpected respiratory arrest because sleep extinguishes primary respiratory drive, and secondary respiratory drive remains paralyzed by CO2 depletion.33,34 This problem caused considerable consternation during the early days of modern anesthesia, and became the first recognized anesthetic safety issue.23 Amazingly, this problem persists to the present, even though its cause has been understood for more than 100 years, and continues to kill countless patients. The problem is commonly attributed to narcotics, which beneficially prevent harmful surgical nociception.33-36


Like anesthesia, analgesia is stress control. Analgesics inhibit stressful surgical nociception, which prevents pain, but they don’t otherwise affect brain activity, so they don’t eliminate the fight or flight mechanism.

There are three types of analgesics:

  1. Narcotics inhibit spinal cord nociception pathways. These are virtually devoid of toxicity but they cause respiratory depression that is readily counteracted by beneficial hypercarbia. They are devoid of toxicity, and they offer the most practical, predictable, safe, and reliable means to prevent harmful surgical nociception.
  2. NSAIDs (Non-Steroidal Anti-Inflammatory Drugs) inhibit nociceptors. These are inherently toxic and often lethal, especially when used for prolonged periods at high doses to control pain.
  3. Local analgesics such as lidocaine inhibit nociception by blocking nociceptors, peripheral nerves, and spinal cord nociception pathways. Compared to narcotics, they are toxic and unpredictable.

Optimizing Anesthetic Management

Stress theory postulates three synergistic pathways that activate the stress mechanism:2

  1. Cognitive pathway, which encompasses the mechanism of fight or flight. Anesthesia controls this pathway.
  2. Nociception pathway, which consists of nociceptors that generate nociception, and the peripheral nerves and spinal cord pathways that conduct nociception to the brain and sympathetic ganglia. Analgesics control this pathway.37
  3. Tissue disruption pathway, which consists of blood-borne enzyme factors VII, VIII, IX and X that are isolated from tissue factor in extravascular tissues by the vascular endothelium. This pathway is activated by surgical tissue disruption that exposes tissue factor to the blood enzymes. At present there is no treatment available to control this pathway.

Surgery activates all three of these pathways, causing stress mechanism hyperactivity that manifests as the surgical stress syndrome (SSS). It is presently impossible to eliminate the SSS altogether, because there is no available treatment to control the tissue disruption pathway. However, synergistic combinations of anesthesia, analgesia, and hypercarbia can produce a beneficial state that mimics normal sleep, minimizes the SSS, and optimizes safety and outcome better than either anesthesia or analgesia alone. The anesthesia abolishes consciousness and paralyzes the dangerous fight or flight mechanism. The narcotic analgesia inhibits surgical nociception. The hypercarbia mitigates microvascular flow resistance, optimizes organ perfusion, and releases oxygen from arterial blood to elevate tissue oxygenation. My book provides a detailed explanation of this technique.6

Unfortunately, anesthesia practice is presently dominated by a set of counterproductive beliefs and assumptions that undermine safety and outcome and have cost the lives and longevity of countless patients. These superficially reasonable dogmas include the following:

  1. Blood pressure is the “driving force” of blood flow, tissue perfusion, and tissue oxygenation.38 If this be so, then why does blood pressure vary from point to point throughout the arterial tree?39 Why is atherosclerosis absent in distal arterioles, and why does it appear first in the bifurcations and greater curvatures of large proximal arteries such as the aorta and carotids? Conventional theory cannot explain this.
  2. Low blood pressure implies impending disaster, while high blood pressure indicates healthy “cardiac reserve.” On the contrary, high blood pressure is invariably associated with low cardiac output, poor tissue perfusion, limited exercise tolerance, and tachycardia. In contrast, trained athletes exhibit abnormally low blood pressure at rest and normal blood pressure during exercise. Synergistic combinations of anesthesia and analgesia beneficially lower blood pressure by reducing microvascular flow resistance and optimizing tissue and organ perfusion, but excessive levels of toxic inhalation agents lower blood pressure by inhibiting cardiac contractility.
  3. “Vasopressor” drugs enhance cardiac output, tissue perfusion, and tissue oxygenation by elevating blood pressure. These drugs are routinely used to treat hypotension, but they have never demonstrated any ability to improve cardiac output, tissue perfusion, tissue oxygenation, or outcome. Instead, they elevate blood pressure by closing the capillary gate and increasing microvascular flow resistance, which undermines tissue perfusion and oxygenation.
  4. The heart is the “Charles Atlas” of the body that drastically increases its contractile force to increase its output ten-fold during intense exercise.38 This was the imaginary notion of Walter B. Cannon, a WWI Harvard researcher. In reality, cardiac contractility is so weak that it can barely propel blood to the top of the head, which explains why vertebrate heads are located only a short distance above the heart. The secret of exercise tolerance is the non-Newtonian nature of mammalian blood, which eliminates turbulent flow resistance and optimizes cardiac efficiency.2,6
  5. Anesthetic inhalation agents have analgesic properties. This is founded on the observation that inhalation agents eliminate the ability of consciousness to perceive nociception as pain before they abolish the ability to speak. True analgesics inhibit nociception and prevent harmful sympathetic nervous hyperactivity, but inhalation agents possess no such ability.
  6. Carbon dioxide is “toxic waste, like urine, that must be rid from the body.” This is a quote from Dr. Ralph Waters, the founder of the MD Anesthesiology profession, who sought successfully to tarnish the reputation of the nurse-anesthetists who dominated anesthesia service after WWI.31 Unfortunately, his destructive influence persists in anesthesia practice, and has permeated medicine in general.

Because of these flawed beliefs and assumptions, anesthetists are trained to hyperventilate their patients, which dangerously depletes CO2 tissue reserves, and avoid beneficial narcotics that prevent harmful nociception.40-45 They use paralyzing agents to promote surgical convenience by preventing muscle tension and untoward movements caused by “spinal cord windup” during surgery. As a result, uncontrolled sympathetic hyperactivity exaggerates the morbidity and mortality of the SSS.46 Anesthesiology residents are taught to employ mechanical hyperventilation to eliminate carbon dioxide. This deceptively exaggerates pulse oximeter readings but simultaneously inhibits tissue and organ perfusion and oxygenation.47 It also undermines respiratory drive and causes unexpected postoperative respiratory arrest.32-34 Those interested may learn how these dogmas became entrenched in anesthesia practice by reading either my paper entitled “Four Forgotten Giants of Anesthesia History”31 or my book entitled “Fifty Years Lost in Medical Advance.”6


The fight or flight mechanism is the “Ghost in the Machine” hypothesized by Arthur Koestler.48 It provides a unified theory of psychology that explains the purpose of sleep, emotion, memory, and their relationships to physiology and disease. In animals it explains ethology. However, much work remains to be done to clarify the operations of these mysterious mechanisms.

The fight or flight mechanism is a sub-component of the mammalian stress mechanism. It exemplifies the extended implications of stress theory which characterize all powerful theories. It is undoubtedly shared in similar form by the stress mechanisms of other vertebrate classes. The discovery of the mammalian stress mechanism explains how stress theory works, and thereby enables the “unified theory of medicine” that Hans Selye anticipated. It explains the nature of disease, and provides revolutionary, reliable treatments and guided research that promises a new era of human existence that is free from disease and premature death. It further implies a “unified theory of biology” that explains embryology, ethology, evolution, taxonomy, the Cambrian Explosion, dinosaurs, and the nature and origin of life. It also resolves the disparities of Darwin, Lamarck, Baldwin, and Saltation, and paves the path to altering evolution at will, with results that reside in the realm of science fiction.6


  1. Fight or Flight Response. <http://en.wikipedia.org/wiki/Fight-or-flight_response>.
  2. Coleman, L. S. A Stress Repair Mechanism that Maintains Vertebrate Structure during Stress. Cardiovasc Hematol Disord Drug Targets, doi:BSP/CHDDT/E-Pub/00015 [pii] (2010).
  3. Cannon, W. B. Voodoo death. Psychosom Med 19, 182-190 (1957).
  4. Coleman, L. S. Take a Walk on the Wild Side, <http://voluntaryist.com/letters/007.html#.X6bD4C9h1Bw> (1995).
  5. Coleman, L. S. A capillary hemostasis mechanism regulated by sympathetic tone and activity via factor VIII or von Willebrand’s factor may function as a “capillary gate” and may explain angiodysplasia, angioneurotic edema, and variations in systemic vascular resistance. Med Hypotheses (2005).
  6. Coleman, L. S. 50 Years Lost in Medical Advance: The Discovery of Hans Selye’s Stress Mechanism. (The American Institute of Stress Press, 2021).
  7. Kario, K. & Matsuo, T. Increased incidence of cardiovascular attacks in the epicenter just after the Hanshin-Awaji earthquake. Thromb Haemost 74, 1207 (1995).
  8. Kario, K. et al. Earthquake-induced cardiovascular disease and related risk factors in focusing on the Great Hanshin-Awaji Earthquake. J Epidemiol 8, 131-139 (1998).
  9. Kario, K. et al. Factor VII hyperactivity and endothelial cell damage are found in elderly hypertensives only when concomitant with microalbuminuria. Arterioscler Thromb Vasc Biol 16, 455-461 (1996).
  10. Kario, K., Matsuo, T., Kobayashi, H., Yamamoto, K. & Shimada, K. Earthquake-induced potentiation of acute risk factors in hypertensive elderly patients: possible triggering of cardiovascular events after a major earthquake. J Am Coll Cardiol 29, 926-933 (1997).
  11. Kario, K., McEwen, B. S. & Pickering, T. G. Disasters and the heart: a review of the effects of earthquake-induced stress on cardiovascular disease. Hypertens Res 26, 355-367 (2003).
  12. Matsuo, T. & Kario, K. [Some aspects of newly developed instruments for blood coagulation tests]. Rinsho Byori 43, 1209-1213 (1995).
  13. Matsuo, T., Kobayashi, H., Kario, K., Suzuki, S. & Matsuo, M. [Role of biochemical and fibrinolytic parameters on cardiac events associated with Hanshin-Awaji earthquake-induced stress]. Rinsho Byori 46, 593-598 (1998).
  14. Matsuo, T., Suzuki, S., Kario, K. & Kobayashi, H. [Acute myocardial infarction in the 1995 Hanshin-Awaji Earthquake]. Rinsho Byori Suppl 104, 133-141 (1997).
  15. Matsuo, T., Suzuki, S., Kodama, K. & Kario, K. Hemostatic activation and cardiac events after the 1995 Hanshin-Awaji earthquake. Int J Hematol 67, 123-129 (1998).
  16. Melzack, R. & Wall, P. D. Pain mechanisms: a new theory. Science 150, 971-979 (1965).
  17. Penfield, W. Gordon Wilson Lecture, The Mechanism of Memory. Trans Am Clin Climatol Assoc 62, 165-169 (1950).
  18. Price, J. The Woman Who Can’t Forget: The Extraordinary Story of Living with the Most Remarkable Memory Known to Science–A Memoir. (Free Press, a division of Simon and Schuster, 2008).
  19. Hyperthymestic Syndrome. <http://en.wikipedia.org/wiki/Hyperthymesia>.
  20. Suni, e. Stages of Sleep, <https://www.sleepfoundation.org/stages-of-sleep> (2022).
  21. Ingravallo, F. et al. Sleep-related violence and sexual behavior in sleep: a systematic review of medical-legal case reports. J Clin Sleep Med 10, 927-935, doi:10.5664/jcsm.3976 (2014).
  22. Gross, J. B. et al. Practice guidelines for the perioperative management of patients with obstructive sleep apnea: a report by the American Society of Anesthesiologists Task Force on Perioperative Management of patients with obstructive sleep apnea. Anesthesiology 104, 1081-1093; quiz 1117-1088 (2006).
  23. Henderson, Y. Resuscitation with Carbon Dioxide. Science 83, 399-402, doi:10.1126/science.83.2157.399 (1936).
  24. Deflandre, E. & Lacroix, S. OSA and adverse perioperative outcomes: we should distinguish them. Reg Anesth Pain Med 44, 754, doi:10.1136/rapm-2019-100484 (2019).
  25. 25 Kronemyer, B. in Anesthesiology News    (McMahon, New York, NY, October 12, 2016).
  26. Savini, S. et al. Assessment of obstructive sleep apnoea (OSA) in children: an update. Acta Otorhinolaryngol Ital 39, 289-297, doi:10.14639/0392-100X-N0262 (2019).
  27. Benumof, J. L. Obstructive sleep apnea in the adult obese patient: implications for airway management. J Clin Anesth 13, 144-156 (2001).
  28. Benumof, J. L. The elephant in the room is bigger than you think: finding obstructive sleep apnea patients dead in bed postoperatively. Anesth Analg 120, 491, doi:10.1213/ANE.0000000000000461 (2015).
  29. Benumof, J. L. Mismanagement of obstructive sleep apnea may result in finding these patients dead in bed. Can J Anaesth 63, 3-7, doi:10.1007/s12630-015-0513-x (2016).
  30. Urman, R. D., Chung, F. & Gan, T. J. Obstructive Sleep Apnea and Ambulatory Surgery: Who Is Truly at Risk? Anesth Analg 129, 327-329, doi:10.1213/ANE.0000000000004217 (2019).
  31. Coleman, L. S. Four Forgotten Giants of Anesthesia History. Journal of Anesthesia and Surgery 3, 1-17 (2015). <http://www.ommegaonline.org/article-details/Four-Forgotten-Giants-of-Anesthesia-History/468>.
  32. Salvatore, A. J., Sullivan, S. F. & Papper, E. M. Postoperative hypoventilation and hypoxemia in man after hyperventilation. N Engl J Med 280, 467-470, doi:10.1056/NEJM196902272800903 (1969).
  33. Coleman, L. S. in apsf Newsletter Winter 2009-2020 (Anesthesia Patient Safety Foundation, Administrator, Deanna Walker Anesthesia Patient Safety Foundation Building One, Suite Two 8007 South Meridian Street Indianapolis, IN 46217-2922 e-mail address: [email protected] FAX: (317) 888-1482, 2010).
  34. Coleman, L. S. A call for standards on perioperative CO(2) regulation. Can J Anaesth, doi:10.1007/s12630-011-9469-7 (2011).
  35. Overdyk, F. J. postoperative Opioids Need System-Wide Overhaul. Anesthesia Patient Safety Foundation Newsletter (2010).
  36. Overdyk, F. J. Postoperative opioids remain a serious patient safety threat. Anesthesiology 113, 259-260; author reply 260-251, doi:10.1097/ALN.0b013e3181e2c1d900000542-201007000-00041 [pii] (2010).
  37. Bromage, P. R. 50 Years on the wrong side of the reflex arc. Reg Anesth 21, 1-4 (1996).
  38. Cannon, W. B. The wisdom of the body. (W.W. Norton & Company, 1939).
  39. Blitt, C. D. Monitoring in Anesthesia and Critical Care Medicine. (Churchill Livingstone, 1985).
  40. Anand, K. J., Hansen, D. D. & Hickey, P. R. Hormonal-metabolic stress responses in neonates undergoing cardiac surgery. Anesthesiology 73, 661-670 (1990).
  41. Anand, K. J. & Hickey, P. R. Halothane-morphine compared with high-dose sufentanil for anesthesia and postoperative analgesia in neonatal cardiac surgery. N Engl J Med 326, 1-9 (1992).
  42. Anand, K. J. & Maze, M. Fetuses, fentanyl, and the stress response: signals from the beginnings of pain? Anesthesiology 95, 823-825 (2001).
  43. Anand, K. J., Sippell, W. G. & Aynsley-Green, A. Randomised trial of fentanyl anaesthesia in preterm babies undergoing surgery: effects on the stress response. Lancet 1, 243-248 (1987).
  44. Lowenstein, E. et al. Cardiovascular response to large doses of intravenous morphine in man. N Engl J Med 281, 1389-1393 (1969).
  45. Raja, S. N. & Lowenstein, E. The birth of opioid anesthesia. Anesthesiology 100, 1013-1015 (2004).
  46. Monk, T. G., Saini, V., Weldon, B. C. & Sigl, J. C. Anesthetic management and one-year mortality after noncardiac surgery. Anesth Analg 100, 4-10 (2005).
  47. Cullen, D. J. & Eger, E. I., 2nd. The effect of extreme hypocapnia on the anaesthetic requirement (MAC) of dogs. Br J Anaesth 43, 339-343 (1971).
  48. Koestler, A. The ghost in the machine. Danube edn, (Hutchinson, 1976).


Lewis Coleman, MD, FAIS is a board-certified anesthesiologist who completed his BS degree in biology at Ohio State University, earned his MD degree from New York Medical College, and completed his surgical internship and anesthesiology residency at UCLA, followed by 40 years in private practice. Coleman’s basic sciences instruction at NYMC miraculously coincided with the two-year sojourn of Dr. Johannes Rhodin, a famous Swedish pioneer of electron microscopy who was retained by the school to upgrade its curriculum. Dr. Rhodin was an expert on the stress theory of Hans Selye. His stress theory lectures devastated the dogma of classical physiology and convinced Coleman that stress theory represented the future of medicine. Many years later, these lectures miraculously enabled Coleman to identify Selye’s long-sought stress mechanism. Thus identified, the stress mechanism enables Selye’s “Unified Theory of Medicine” that promises a new era of health, longevity, and freedom from the eternal curse of disease. Its implications exceed the bounds of medicine and confer a “unified theory of biology” that explains embryology, extinction, evolution, ethology, intelligence, anatomy, taxonomy, the Cambrian explosion, and dinosaurs, and resolves the disparities of Darwin, Lamarck, Baldwin, and saltation. Its distant implications reside in the realm of science fiction. His website http://www.stressmechanism.com is dedicated to stress theory and offers relevant materials free of charge. His book, 50 Years Lost in Medical Advance: The Discovery of Hans Selye’s Stress Mechanism, is available on Amazon.


Contentment Magazine

The dictionary defines “content” as being in a state of peaceful happiness.  The AIS magazine is called Contentment because we want all of our guests and members to find contentment in their lives by learning about stress management and finding what works best for each them.  Stress is unavoidable, and comes in many shapes and sizes that makes being in a state of peaceful happiness seem like a very lofty goal.  But happiness is easy to find once you are able to find ways to manage your stress and keep a healthy perspective when going though difficult times in life.  You will always have stress, but stress does not always have you!

Subscribe to our FREE magazines and begin your journey to a happier, healthier and longer life!