Sleep Apnea

In ancient Greek, pneuma meant the breath of life and apnea meant the cessation of that breath. Pneuma in modern medicine is only a fragment of many words related to breathing but apnea has made the transition from the ancient lexicon unchanged. It means no breathing. Sleep apnea is a condition in which breathing halts over and over during sleep, sometimes hundreds of times a night. The resulting disruption of sleep and respiratory physiology triggers chronic health problems like high blood pressure, cardiovascular disease and strokes. Other negative results are psychosocial and accidental, stemming from chronic daytime sleepiness. Motor vehicle accidents are but one example.

My first exposure to someone with sleep apnea was during childhood, in my grandparents’ house, where visiting grandchildren were divvied up among the adult rooms for sleeping. My grandmother was a Camel smoker who read the New Jersey tabloids late into the night. I knew she was finally asleep when her snoring began, at first softly with a regular cadence, and then gradually increasing in volume and depth, building to a crescendo that would suddenly end…in silence. I tried holding my breath as long as she held hers, but seldom made it to the point when she would suddenly snort, inhale in a ragged fashion and then settle back into the snoring rhythm, building up to another period of no breathing. I gave up worrying about whether or not she would restart, because she always did. I wondered why my grandfather, a Lucky Strike smoker snoring away in an adjoining bedroom, breathed steadily, never stopping like she did.

The upper airway is the problem

While smoking can cause snoring, my grandmother stopped breathing intermittently because her upper airway was anatomically different from my grandfather’s and it became obstructed when the muscle relaxation caused by sleep made her throat go slack. In 1965, upper airway obstruction was finally discovered to be the cause of the marked daytime sleepiness that often affected obese people, whose airways collapsed under the excess neck fat when they lay down and fell asleep. Charles Dickens made this kind of hypersomnolence famous in the 1800s by his creation of the character Joe the Fat Boy in The Pickwick Papers.

Sleep research begins

The discovery of the cause of daytime sleepiness in obese people happened to coincide with the development of interest in and funding for research into sleep disorders. The first sleep lab was begun at Stanford University in 1964. Prior to that time not much was known about normal sleep, let alone disordered sleep. By the 1970s the hundreds of awakenings interrupting the sleep of people with upper airway obstruction had been demonstrated. Sleep cycles were continuously disrupted in these patients, and sleep apnea was on its way to being tagged as a common disorder with serious consequences in terms of morbidity and mortality.

Risk factors

Who suffers from sleep apnea? According to one estimate, approximately one quarter of people between 30 and 70. Despite the increased awareness of sleep apnea in the last few decades, experts also estimate that 70-80% of people who suffer from the condition remain undiagnosed. Men are about four times more likely than women to be affected. Obesity is the largest risk factor because increasing body fat encroaches on the upper airways. Smoking irritates sensitive tissues, making them swell and further narrowing the throat. In some people, the jaw shape and position are anatomical culprits. Sleeping medicines and alcohol consumption can also alter breathing patterns in sleep and contribute to sleep apnea.

Snoring is the first symptom

Not every snorer will develop sleep apnea, but snoring is the first phase of the condition. When the snoring becomes associated with breathing cessation, problems begin. Apnea causes an immediate fall in blood oxygen and a rise in carbon dioxide. Rising carbon dioxide triggers the respiratory drive center in the brain. The sleeper wakens in order to breathe, though he may not be aware of it. Multiple awakenings interfere with normal cycling through progressively deeper stages of sleep back up into lighter stages of dreaming sleep, cycles that are necessary for mental and physical health. Over time, lack of normal sleep cycles takes significant physical and mental tolls. Levels of inflammatory markers and hormones associated with stress rise; the vascular changes that lead to heart disease speed up; heart rhythms become erratic; blood pressure goes up and stroke risk rises. Profound daytime sleepiness results in attention deficits, errors of omission, motor vehicle accidents, mood disorders and memory problems.

Other clues

Might you suffer from sleep apnea? If people complain about your snoring, if you awaken with headaches and feeling unrested, if you are lacking in energy though not ill and if you cannot stay awake once you are not physically up and about – for instance when you sit down to read or watch TV, you might want to talk to your doctor about the possibility of sleep apnea, especially if you are also overweight.

Diagnosis

The definitive diagnostic test for sleep apnea is an overnight stay in a sleep lab, where polysomnography – multiple measures of physiologic function including electroencephalography or brain wave testing are monitored while the subject is sleeping. Treatment will depend on the severity of the findings. How many awakenings occur per hour? Are there associated heart rhythm or brain wave abnormalities during the apnea?

Treatment works

In mild cases, lifestyle treatments such as weight loss, cessation of smoking, alcohol and sleeping pills, and avoidance of sleeping on the back are all that will be advised. In other cases, the addition of a mask and device that pumps continuous positive air pressure (CPAP) into the upper airway is necessary. CPAP treatment is very effective, and improvements occur rapidly. Less commonly, mouthpieces to alter jaw position, or surgery to increase airway space are advised.

I never noticed daytime sleepiness in my grandmother. She weighed no more than 100 pounds and was an Irish whirlwind of housekeeping activity. Until she developed an autoimmune disease in her 70s, she was, to all appearances, healthy, despite the ever present cigarettes. Sleep apnea is a medical condition on a continuum, dependent not on just the upper airway obstruction component but on other aspects of the sufferer’s health. As with all physical problems, differences in disease severity reflect differences in the whole people in which the problems occur.

Posted by medical plaintalk

Physician turned medical writer.

Iron: Too Little and Too Much

Poison is in everything, and no thing is without poison. The dosage makes it either a poison or a remedy.
Paracelsus. Swiss-German physician (1493-1541)

Iron is present in abundant quantities in the earth’s core and crust, in the sun, the stars and meteorites – and inside all living things. In humans, iron carries oxygen to all the body’s cells, carries carbon dioxide back to the lungs, enables many chemical reactions related to energy production, and binds oxygen inside for use in muscle cells. It is a vital nutrient – a substance that must be part of the diet, but also one which the body cannot excrete except by losing blood and skin cells. Both too little iron and too much iron present us with problems.

Where the body puts iron

Iron is absorbed from food in the upper part of the small intestine. Specialized proteins
carry it in the blood and store it in the liver and other organs. Ten percent of total body
iron is attached to myoglobin in muscles, 25 percent is stored in the liver and in specialized cells throughout the body, and the major portion, 65 percent, is bound to hemoglobin inside red blood cells. Hemoglobin-bound iron is constantly recycled as old red blood cells are destroyed and new ones are made.

Iron absorption from food – a tightly regulated process

Iron must be bound to proteins or it excites free radical damage in cells. When all of the protein binding sites for hemoglobin in the body are filled, the liver sends a signal to the small intestine to decrease the amount of iron taken in from food. This regulation of iron absorption is a very sensitive and tightly regulated process in which a message is sent to the intestines conveying how much iron is already in the body. That amount determines how much or how little iron is absorbed from food. This feedback loop is necessary because, beyond minor blood loss and regular shedding of skin and bowel cells, the body has no way to get rid of extra iron. Most health problems related to iron come from too little iron in the diet, from too much iron, delivered intravenously in the form of blood transfusions, or from genetic defects in the feedback loop that tells the intestines how much iron to take in.

Too Little Iron

Deficiency of iron in the body causes weakness, fatigue, and shortness of breath because of inability to carry enough oxygen in the blood and failure to produce required energy. Skin and nail beds are pale because mature red blood cell production is limited (iron deficiency anemia). Dizziness and fainting upon standing up can occur.
Iron deficiency comes about because dietary iron is insufficient to make up normal losses of iron through menstrual blood loss , or abnormal losses that might occur chronically, such as from an unsuspected stomach inflammation, an intestinal tumor or abnormally heavy menstrual bleeding.

Who becomes iron deficient?

Dietary iron deficiency is very common, especially in people who restrict calories, avoid meat or have poor diets. Women of childbearing age, children and the elderly of both sexes are the most at risk. Dietary deficiency can also be aggravated by increased need for iron, as in pregnancy and childhood growth. While many foods contain iron, it is better absorbed from animal sources like beef, chicken liver, fish and mollusks than from plant based sources like spinach and beans. Iron absorption also requires an acid environment, which acid relieving drugs block.

Iron deficiency in post-menopausal women or in men of any age group always raises suspicion of low grade, unsuspected blood loss, which usually comes from the gastrointestinal tract. Causes are gastritis (often from use of anti-inflammatory drugs), ulcers, colitis, diverticulitis, tumors and rare vascular malformations are all causes. Black, tarry and metallic smelling stool is often a clue.

Replenishing iron stores

Treatment of iron deficiency requires improving diet and finding and correcting sources of blood loss. Iron is better absorbed by the stomach from food than it is from pills. Red meat is the best source. But iron supplements are necessary when iron deficiency has caused symptoms. Several different versions of iron supplements may have to be tried – ferrous sulfate is the most commonly prescribed, but can be hard on the stomach. Ferrous gluconate may cause less nausea and stomach upset. Ferrous fumarate contains more iron per pill. The addition of Vitamin C to the diet helps absorption of iron supplements and iron can also be delivered by injection if dietary methods and oral suuplements fail.

Too Much Iron

Iron overload is called hemochromatosis and its symptoms come from damage to the cells in which iron is stored once the normal iron binding proteins can hold no more. The damage is very slow and cumulative and the liver and the heart bear the brunt. Testicles and thyroid gland are also storage sites. Skin storage may cause the patient to look inappropriately tanned, but weakness, lassitude, weight loss, shortness of with breath and abdominal pain typically bring the patient to the doctor.

Transfusion-related iron overload

Hemochromatosis can be caused by repetitive transfusions of blood. Transfusion related hemochromatosis afflicts patients with bone marrow diseases such as myelofibrosis and multiple myeloma. Repeated transfusions are the treatment for severe anemia in these patients and each unit of packed red blood cells delivers enough iron for six months. Iron overload begins to develop quickly.

Hereditary hemochromatosis

Hemochromatosis can also be caused by a genetic problem in which too much iron is absorbed. This hereditary version of hemochromatosis occurs in about 5 in 1000 people in the US. Caucasians are more susceptible than other races. While men and women are affected equally, men typically develop symptoms in their 30s or 40s, a decade or two earlier than women, because women are able to shed iron on a monthly basis until menopause.

Hemochromatosis is treated by regular bleeding, performed in the same way that blood donations are collected. But bleeding is not suitable treatment for patients whose severe anemia is the problem that forces them to receive repeated blood transfusions. The only option for them is chelation of the iron with drugs that bind iron in the blood and carry it out of the body, a difficult and time consuming process, but one that lengthens survival time. A new oral drug may soon make the process easier. At this time in medical history though, using iron as a remedy is easier than treating iron as a poison.

Posted by medical plaintalk

Physician turned medical writer.

Chronic Fatigue Syndrome Gets Renamed

Imagine the way you felt the last time you had the flu. You were flattened, devoid of all energy. Staying upright to get dressed was more than you could handle. You slept – and slept – and slept – and still experienced none of the normal refreshment that a good night’s sleep provides. A fog descended on your mind and fuzzed up memory, destroyed drive and made your head ache. You could not concentrate on simple mental tasks like reading. Though you were doing nothing physical, your muscles ached. Then it all went away and you forgot about it.

But now imagine that it didn’t go away. The same misery persists and dramatically alters your life. You cannot work. You move from bed to couch and back to bed. You go to doctor after doctor and they find nothing wrong. Routine blood tests, X-ray and scan results are normal. Someone prescribes an antidepressant, confirming the suspicions of family, friends, and some doctors that your debilitating physical symptoms are “all in your head.” Eventually, you find your way to a doctor who makes a diagnosis. You have CFS which stands for chronic fatigue syndrome, and which, as of early 2015, has been renamed system exertion intolerance disease or, in our acronym-laden age, CFS/SEID.

A long history, with different names

CFS/SEID has probably been around for more than 200 years, making its appearance in the medical literature as “neurasthenia,” a term applied to patients who were lacking in physical, emotional and cognitive energy without any discernible disease to account for their malaise, without any improvement over time and without any progression that brought them to a worsened state. They were mostly ladies, whose frail constitutions prevented them from exerting themselves and who mysteriously took to their beds for weeks at a time.

The Yuppie flu

British doctors in the 1950s christened the symptom complex myalgic (painful muscles) encephalitis (inflammation of the brain), even though there was no evidence for inflammation to account for the headaches, difficulty concentrating and memory problems patients experienced. In the US in the 1980s, the syndrome was dubbed the Yuppie Flu because it seemed to follow viral infections like infectious mononucleosis and occurred in cities where young urban professionals (“yuppies”) congregated. When reported from other settings as well, the name was changed to chronic fatigue syndrome.

No apparent cause, but a real illness

Because no single infectious, hormonal or immunologic cause for CFS emerged from many attempts to identify its cause, because it was impossible to measure the subjective complaints constituting the syndrome, and because some improvements occurred when antidepressants were prescribed, CFS was, for decades, viewed as a psychological disorder. But this view became more and more untenable as it became clear that the illness hit people who had no history of depression or inability to cope with life. Many CFS patients continued to be very productive, learning how to manage their lives within the limitations of their fatigue and mental fog. Laura Hillenbrand, author of Seabiscuit and Unbroken is one outstanding example. Though no cause has yet been identified for the illness, the name change from chronic fatigue syndrome to systemic exertion intolerance disease signals that the illness is one rooted not in psychology but in an, as yet, unidentified physical cause.

Epidemiology and diagnostic criteria

It is estimated that there are about 1 million patients with CFS/ SEID in the US at any given time. There is no evidence that its incidence is increasing, but it is quite possible that some cases are hidden on among the legions of people who have been diagnosed only with depression. CFS/SEID is more common in women than in men. Sometimes it follows directly upon an acute flu-like illness, but at other times appears out of nowhere. The diagnostic criteria at this time include 6 months of unexplained, life-altering fatigue and orthostatic intolerance, which means the inability to stand for more than very short periods. Four of eight other symptoms are also required and these include disturbances in memory and concentration, persistent sore throat, tender lymph nodes, muscle pain, joint pain, headache, disturbed sleep patterns, and malaise following even minimal exertion. Additional symptoms may include increased sensitivity to tastes, odors, temperature and noise.

A relapsing illness

A small minority of CFS/SEID patients get completely better and never suffer a relapse. The majority suffer relapses for prolonged periods of time, perhaps the rest of their lives. Relapses are triggered by infections, surgery, temperature extremes and stressful events. Another minority are severely affected from the beginning of their illness and require support in the activities of daily living for the rest of their lives. Deterioration, though, is unusual and suggests the diagnosis of CFS is wrong and further attempts to find the correct diagnosis are indicated.

Problems in mitochondrial energy production?

While there is no identifiable single cause for CFS/SEID, poor energy production seems to be at the root of the many symptoms in this illness, which has focused some researchers’ attention on mitochondria – the powerhouses of all cells in the body. Mitochondria must continuously recycle the molecules they use to produce energy and there is some indication that this process is impaired in people with CFS/SEID. Perhaps this is why experience has taught many CFS/SEID patients to pace their lives, always allowing significant time for recovery from exertion.

Boosting energy production

In addition to pacing life to allow recovery time, lifestyle alterations that seem to help CFS/SEID patients minimize relapses also happen to be useful in maximizing mitochondrial function. These include avoidance of drugs and environmental toxins, avoidance of processed foods with high carbohydrate and sugar concentrations, addition of whole foods containing plenty of antioxidants and high quality protein, correction of hormonal problems, especially of the thyroid gland, and decreasing chronic inflammation associated with obesity and allergies. Gradual and graded programs of exercise, outdoors with some sun exposure help prevent the loss of muscle associated with inactivity and improve Vitamin D levels, with positive effects on immune function. Continued research will most likely show that CFS/SEID has many causes, all of which result in impaired mitochondrial function.

Posted by medical plaintalk

Physician turned medical writer.

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