A Slip of Memory: Transient Global Amnesia

Search the internet for drugs that cause memory problems and you will immediately become familiar with a fascinating syndrome called transient global amnesia (TGA). A website at the top of the list of results opens with these words: My personal introduction to the incredible world of transient global amnesia (TGA) occurred six weeks after Lipitor was started during my annual astronaut physical at Johnson Space Center.  TGA is not listed as an adverse effect associated with cholesterol lowering drugs, but with 12 million Americans now consuming these products, recognition of this peculiar syndrome by patients and doctors becomes important.  Beyond the tightly controlled world of pre-market drug approval studies, unexpected symptoms need to be noted.

Transient global amnesia is a short–lived problem, over in less than 24 hours. It involves all aspects of new memory formation. Nothing gets recorded during the event and the sufferer fails to remember anything from the event after it is over. To appreciate the disconcerting nature of the syndrome, imagine suddenly losing your ability to put any information into your memory. In addition, you lose access to a few hours or days or even years of past memory, but not to information about yourself. You look around but cannot identify why you are where you are. Depending on how much access to the past you’ve lost, your current situation might be totally unknown to you. With great urgency you question the people around you. “What am I doing here?” How did we get here?” What’s going on?” Someone answers and for about 30 seconds you can hold on to the information. But your ability to put that information into memory has gone offline. You forget that you just asked the question. You ask again, and again, and again, with obvious anxiety. All your other mental capacities work. You can speak, read, write – even drive and problem solve. Except for your anxiety, you are the same person as always. Then the confusion ebbs. You start to encode information again. Your past gradually returns, in chronological order. Once again you are tethered to time and place, but you will not ever remember what went on while you were cut loose and for a little while you might complain of a little headache.

The first descriptions of this odd set of symptoms appeared in an obscure medical journal in 1956. More cases came to light, and by the early 1990s there were a few epidemiological studies that suggested that TGA occurs in about 10/100,000 people, or as many as 25-32/100,00 in the peak age group of 50-80. Far from being a harbinger of impending stroke or evidence of seizures, these episodes seemed to have no correlation with any problems other than a history of migraine and left no problems in their wake. They recurred in somewhere between 5 and 25% of the cases, with one patient having over a dozen recurrences. No definite cause has ever been found, though many physicians have associated them with immediately preceding, physically or emotionally strenuous events.

Very rarely, underlying brain problems like tumors involving the deep middle and frontal areas, where memory formation takes place, turn up in TGA cases, but careful examination of these cases inevitably reveals some deviation from the typical clinical symptoms, or some type of abnormality on neurological examination. TGA research studies, using sophisticated scanning and EEG techniques, suggest that there is decreased activity in areas of the brain involved in memory formation, but give no clue about the mechanisms involved.

In 1990, criteria for diagnosis of the syndrome were published (listed below), and when a diagnosis of TGA strictly adheres to these criteria, it is almost always safe to predict that there is no underlying neurologic or vascular problem. Nevertheless, when a patient appears in an emergency room with TGA symptoms, good practice still requires a CT or MRI scan and an EEG at some point to rule out the remote possibility of an underlying tumor, hemorrhage or seizure disorder.

Reports like those of Dr. Duane Graveline, the astronaut/physician author, are considered anecdotal and not of the same value as information gleaned from statistical analysis of controlled studies .  The cholesterol lowering drugs are in widespread use and considered very safe by most physicians. However, there have been cases of muscle and nerve problems, as well as cases of decline in cognitive function attributable to the drugs, possibly mediated by damage to mitochondria, the power houses of all cells in the body. Since the drugs are viewed as valuable additions to the battle against heart disease and are likely to be used over long periods by increasing numbers of people, it is important to understand and catalogue their unintended consequences.  Once drugs reach large populations outside medical studies, more problems emerge, sometimes beginning as odd, single cases.  In the meantime Dr. Graveline has died after a progressive illness which resembled Lou Gehrig’s Disease (progressive loss of muscular strength and bulk). His memory, however, remained good.

Diagnostic Criteria for Transient Global Amnesia

  1. A witness must be present to describe what happened.
  2. The patient must be unable to form new memories of any kind (anterograde amnesia).
  3. The patient must have full knowledge of his identity and an unclouded state of consciousness.
  4. All other mental functions are normal, including speech.
  5. There are no other neurological symptoms or signs.
  6. There are no signs of a seizure.
  7. There is no history of seizures within the last 2 years, or of recent head injury.
  8. The patient is back to normal within 24 hours.

 

 

 

The Gratitude Attitude: Five Best Days

Gratitude is an attitude that mental health professionals say promotes mental well-being. They advise practices such as noting three good things about each day and writing them down at night. Studies actually show that such habits durably improve mood. In the giving spirit of the Christmas season I would like to share with you one of our family traditions that, in retrospect, I realize promotes the gratitude attitude over the course of each year.

We began taking our boys to Colorado to learn to ski when they were very little. Economic and time constraints meant one week a year, determined by my husband’s surgical on-call schedule. That week included the turn of the year on New Year’s Eve. Children’s skiing torchlight parades, followed by dinner at a Chinese restaurant and early bedtimes gradually gave way to a movie (usually laughably bad) followed by dinner at a locals’ Italian restaurant with paper-covered tablecloths and crayons for doodling. The family expanded to include our boys’ friends – first as children and teenagers along for a vacation, then as young men who worked as ski instructors. Somewhere along the way we began the habit of discussing our five best days of the year over New Year’s Eve dinner.

The crayons and the paper table covers are very convenient – everyone begins jotting down their five best days, in order, almost as soon as the menus arrive. The entire dinner time winds up devoted to going around the table in five rounds, hearing from each person about what made each wonderful day and how they decided where to rank it in the list. The choices are life stories in snapshots, changing with growth and priorities. They are funny, poignant and surprising. We also hear from people who have been with us on past New Year’s Eves, calling, e-mailing, or texting their top five days, sometimes accompanied by pictures. They all get heard.

The reason this tradition promotes gratitude is a very practical one. If you know you are going to have to come up with your five best days of the year on New Year’s Eve you learn pretty quickly that memories are weak. You cannot cram for this test. You have to start noticing potential top five days as they happen over the course of the year. You start writing them down. Pretty soon you actually have a little journal and it contains good stuff. The good things that happen in life start to break into your awareness and compete with danger-surveillance program that runs continually in the background of your mind. All good, with none of the side effects of mood enhancing drugs (which fail in the long run anyway).

Just as a matter of historical interest, we traced this tradition back to its origins. It actually began with my husband’s surgical training at Massachusetts General Hospital. The surgical interns and residents on the general surgery service met at the end of each day and were asked to talk about the cases they helped with and to explain what they had learned. The practice helped everyone process what they had done and learn from their experiences. As a family, we were always sit-down dinner people,  with candles even when there was still a high chair at the table. Like the surgery residents, we  always talked about everyone’s day. Skiing days included lots of bests. Best fall, best jump, best run, best lift ride. The evolution to a summing up of bests at the end of a year was inevitable. What is a surprise is the way the practice has continued and spread from our families to others. Maybe you would like to give it a try.

Human Diversity: A Mind Thing

(A version of this essay was published in Minnesota Medicine in March, 2005.)

The first snowy egret I ever saw was standing in a shallow pool, a beautiful white creature with a wispy headdress floating in a gentle breeze. When he lifted off, trailing his long black legs, I was startled by a flash of bright yellow – he looked like he was wearing a child’s rubber boots, designed to hug a bird’s clawed feet. He did a loop around the pond in  flying low in a peculiar, non-aerodynamic position. His legs hung down rather than stretching out parallel to his body. He dipped closer to the water and his dangling yellow feet brushed the surface. He’s landing, I thought. But he didn’t. He repeated the maneuver four times.  He’s afraid to land, I thought. But then he touched down with hardly a splash, and dipped his beak to catch a fish, then another, and another. In a moment of bird-watching epiphany, I realized that his feet were like a fisherman’s lure. He’d rounded up his lunch. 

I looked around the pond. I’d just watched a bird with bright yellow feet use them to attract the curiosity of his prey. Across the water was a bird with a lower bill that expanded into a pouch to collect fish as he skimmed, openmouthed, over the water. Perched high above was another, just about to dine on a large fish he’d  skewered with  fearsome talons. What an impressive display of diversity!  If people were this diverse, New England fishermen would grow waterproof, blubber lined hands, typists would develop extra fingers, and mothers really would have eyes in the backs of their heads.  

But people are pretty much the same as far as their bodily equipment goes.  Five fingers on each of two hands, ten toes divided between two feet, two eyes, upright posture, and a narrow range of physical abilities, notwithstanding the spread between ordinary and Olympian. The traits we associate with human diversity are superficial – hair color and texture, skin color, facial appearance. Almond shaped or round, eyes still see. Long, elegant skeletal frames and short squat ones all support bodies against the universal force of gravity. Skin pigmentation protects the body covering from the sun, more or less depending on the power of the sun in the areas of the world where the people originated. We are much more like each other than we are different in our biology. The birds have it all over us in the diversity contest.  

After my egret experience, I packed up my binoculars, got on my bike and headed home, humbled a little by the thought that all of the talk and concern about diversity among people is overblown, maybe just another representation of man’s abiding sense of self-importance. But along the way I passed bikes and cars, houses and stores, a radio broadcast tower, and a museum.  I crossed a bridge between two islands and waved to a fisherman in his boat. And I realized that each of these man made things  I passed began as an idea, somewhere, some time, in somebody’s head. We might not differ much in anatomy and physiology, but no two of us have identical thoughts. The mind is the site of the real diversity among humans. The mind is plastic and ever developing. It records, collates, recalls, communicates, and combines unrelated information in new ways. Yellow feet catch the eye, but minds change the world.

Why We Cry..and How We Make the Tears

 

 

“It is such a secret place, the land of tears.” The Little Prince, Antoine de Saint-Exupery

Do animals cry? Probably not. Indian gamekeepers told Charles Darwin stories of elephants that shed tears of sadness, and dog lovers have tales of canine tears, but the emotional tears of humans are unparalleled in the animal kingdom.

We are always making tears

All land dwelling animals, including people, make tears constantly. Eyes are windows on the world, and baseline tears are constant window washers. The window pane is the cornea, a thin panel of collagen, containing very few cells, no blood vessels, and more nerves per square inch than any other part of the body. These nerves signal alarm and summon an army of reflexive tears in response to a speck of dust, a cold wind, or a whiff of an onion. Reflexive tears, which are just a lot of baseline tears, wash out intruders and fill in dry patches on the cornea, keeping it clear and moist to focus light entering the eye. Emotional tears appear in humans during infancy, but not immediately. The crying that infants first do to signal their needs is much like the crying of little chimpanzees – tearless. Emotional tears come later, just like talking. Both are outward expressions of the lives of our minds, and they take a while to learn.

What tears are made of

Tears are much more than little beads of salt water running down your face. They are a three layer sandwich. The oil-containing molecules in the outer layer tighten up the surface of the watery middle layer to keep it from spilling over eyelid and sliding off the surface it protects. The oil floats on the watery middle layer and smooths its surface, optimizing the passage of light through to the eye’s interior. The third part of the sandwich, inside and closest to the eye, is the mucinous layer, kind of a gluey protein that helps tears stick to the eyeball. The mucinous proteins capture and kill biologic intruders like bacteria and viruses, and soak up some of the watery layer to help transfer nutrients, oxygen and moisture to the cornea. Both the oil and mucin slow evaporation of tears as blinking spreads them over the eye.

Evaporation and drainage

Dry spots appear on the cornea after just fifteen non-blinking seconds – easy to do while concentrating or daydreaming. Even with blinking, tears evaporate, or they drain out from the eye into the nose via two tiny lacrimal ducts on the upper and lower eyelids near the nose. If these ducts become scarred or blocked by infection, tears overflow. Six to 10% of babies are born with tear ducts not yet open, but 95% of these will open by age one without any attempt at surgical repair. Conversely, one way of treating dry eyes is to block these ducts with small plastic pellets.

Dry eyes

Too few tears, tears with abnormal composition, and decreased blinking cause dry eyes that itch, sting, burn, get red, and cause blurred vision. Dry eyes are an increasing problem in our air-conditioned, airline-traveling, contact lens-wearing, Lasiked, medicated and aging society. The list of drugs that dry eyes includes many commonly prescribed classes: decongestants, antidepressants, antihypertensives, antihistamines, beta-blockers, hormones, diuretics, ulcer medications, acne drugs, and oral contraceptives. Other causes of dry eyes are infections and immune diseases like rheumatoid arthritis and Sjogren’s syndrome as well as  radiation and radioactive iodine treatment can also damage the tear producing cells. All of these conditions damage the tear producing cells  – the machinery for tear production. 

Remedies for dry eyes 

Treatment of dry eyes is always aimed at removing offending problems and increasing lubrication. The usual tactics include artificial tears, wind protection, air humidification, cessation of unnecessary medications, and treatment of underlying diseases and infections. Excessive tearing often means allergies, or blocked lacrimal ducts leading to poor drainage of baseline tears into the nose.

 

The tear producing machinery

The medical conditions mentioned above shut down tear production and cause pain and swelling in the lacrimal gland, a spongy little structure tucked up under the upper outer corner of the eyelid. The lacrimal gland is the tear producing factory, aided by the oil-producing Meibomiam glands near the eyelashes, and a cluster of mucin-producing cells in the eyelid lining.

The controls for the machinery

When the lacrimal glands get a call for more tears, either reflexive or emotional, the messages come through the autonomic nervous system, which oversees the automatic functions of the body. Reflexive tears spring from messages sent from the eye and nose. Emotional tears come from messages sent by the limbic system, the deepest and oldest part of the brain, the part that conjures up feelings.

What are emotional tears?

What are emotional tears? Are they just more voluminous baseline tears? Or does emotional crying rid us of “humors of the brain,” as Hippocrates thought? In Roman times, mourners used small glass vials called lachrymators to collect their tears for burial with the one for whom they cried. In today’s laboratory, emotional tears are almost as hard to come by as research money to investigate them. Some dedicated men such as Professor William H. Frey II (Dept. of Pharmaceutics at the U. Of Minnesota) have learned enough to suggest that tears of grief rid the body of some of the products of stress, supporting the claim that crying makes people feel better. Compared to reflexive tears, emotional tears contain up to 25% more proteins, of classes related to stress. Why? No one knows – yet. Emotional tears are still a land of mystery, part of the unique expression of inner life that separates the human animal from the others.

 

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.

Polar Moods

Bipolar disorder, previously called manic-depressive disease, is a not a new diagnosis. But it is one being made with increasing frequency, particularly in children and young adults. In psychiatry diagnoses are legion, but they all fall into one of three categories: disorders of mood, thinking, or personality. Bipolar disorder is a problem in the sphere of mood, described in the 1880s by Emil Kraepelin, the German psychiatrist whose Compendium der Psychiatre was the world’s first systematic classification of mental disorders. At the time, psychiatrists recognized separate illnesses called mania and melancholia, but Kraepelin was the first to see that some patients cycled between these opposite poles of mood. Over time, the term cyclical insanity gave way to manic-depressive disease, and finally to bipolar disorder, type I or type II (the milder variety). Melancholia is now called unipolar depression and mania is no longer a diagnosis but rather a  behavioral symptom in all kinds of psychiatric disorders.

Normal ups and downs in mood

 

Everyone has ups and downs in mood. Mood involves both  subjective feelings and  outward behaviors. It is clear from “normal” mood  swings that both internal and external factors influence ups and downs. Many of those factors, such as sleep, stress, physical activity, diet, and abuse of alcohol, nicotine and drugs, also affect general health.

The definition of mood disorder

Normal ranges of mood vary greatly from person to person, so the psychiatric definition of “mood disorder” rests on the degree to which disrupted behavior interferes with carrying out the normal activities necessary for functioning at a given stage of life. Clearly abnormal symptoms like hallucinations, which define the thinking disorder schizophrenia, may also appear in bipolar type I. New genetic work suggests that mood and thinking disorders are not as separate as our classification systems try to make them, so it is not surprising that symptoms at times overlap.

The down side of the mood spectrum

Depression, the low side of the mood spectrum, robs a person of interest and joy in his activities. He has little energy, sleeps more than usual, or may be unable to sleep through the night, waking up anxiously at two or three AM. He may gain or lose weight. He tends to ruminate, repetitively chewing over negative thoughts. Sadness permeates his world. Of course these  same symptoms  can be completely appropriate responses to terrible life events that cause profound grief.  A depressed mood becomes abnormal when it occurs or persists unrelated to circumstances, blocks the activities necessary for normal life, and/or includes persistent thoughts of death or suicide.

The up side

At the other end of the mood spectrum, mania, the mind speeds up. Thoughts are rapid, distractibility is high, speech is pressured, and ideas become grandiose. Sleep isn’t necessary. The manic person engages in risky behaviors and feels invincible. He undertakes grand schemes, spends money with abandon, and becomes obsessed with projects or ideas. When the exuberant moods are still under some control (hypomania), they can be very productive. The afflicted individual seems lively and charismatic, the life of the party. But when mania spirals out of control it can become life threatening. As mentioned above, mania not confined to bipolar disorder. It is a symptom that can happen in mood, thinking and personality disorders.

Bipolar: more down than up

Most patients with true bipolar disorder spend far more time on its depressive side, experiencing few manic phases. In fact, it is now felt that many cases unipolar depression, with no history at all of hypomanic or manic episodes, actually represent bipolar mood disorders, making diagnosis tricky. Correct diagnosis is important. In unipolar depression, the response to conventional antidepressant therapy takes weeks, but in bipolar depression, the same drugs can tip the patient into a manic state quickly. It is possible that the reported cases of suicide shortly after antidepressants are started may be related to this phenomenon.

The danger of wrong diagnosis

In our current medical and economic climate, the threshold for using antidepressants is very low. Frequently the drugs are prescribed by non-psychiatrists, without concurrent talk or behavioral therapy, and without adequate follow-up. So it is imperative for patients who are given antidepressants to understand that a rapid response, within days to a week, and feelings of agitation or irritability might mean that the diagnosis of unipolar depression is wrong. For bipolar patients, the drug of choice is a mood stabilizer, which calms manic states and can prevent return of depression.

Stabilizing the mood

The most effective mood stabilizer is lithium. Lithium is a simple chemical element in the same family of elements as sodium, potassium, calcium and magnesium, rather than a complicated molecule like other psychoactive drugs. Its mechanism of action remains elusive, though it is thought that it makes the neurochemical transmitter norepinephrine less available and less effective in the brain. Lithium must be monitored carefully, with urine levels performed regularly. Toxic side effects include diarrhea, tremors, thirst, weight gain, drowsiness, and impairment of kidney and thyroid function.
If lithium is ineffective or poorly tolerated, drugs normally used for treatment of seizures may work as mood stabilizers. One, valproate, is particularly effective for people who also have substance abuse problems, a not uncommon occurrence. Antidepressants may also be necessary at some point, but not without concurrent use of mood stabilizers. Bipolar disorder is a lifelong problem that requires careful monitoring, variable amounts of drug therapy, and simultaneous counseling aimed at development of cognitive skills and habits that help blunt the effects of mood swings on behavior.

Are we creating more lifelong psychiatric problems with drug treatment?

Some psychiatrists feel that the widespread use of antidepressants and other mood altering drugs to treat poor behavior or reactions to life’s inevitable problems changes brains enough to change the way true psychiatric problems now evolve. These days, we have increasing numbers of bipolar diagnoses. Compared to past decades, bipolar patients now cycle more rapidly between highs and lows. While the increasing frequency of bipolar disorder diagnosis may represent increasing labeling of behavioral problems, we also must consider the disturbing possibility that temporary alteration of brain activity with drugs is leading to long term psychological and behavioral changes. Readers who are interested in more extensive discussion might want to read Anatomy of an Epidemic: Magic Bullets, Psychiatric Drugs, and the Astonishing Rise of Mental Illness in America by Robert Whitaker, Broadway; (August 2, 2011).

Sleep Debt: The Hidden Costs

Everyone has a sleep bank. Each night your accounts get credited with 7-8 hours of the physical and mental benefits of sleep and each day the accounts pay out those benefits in the form of emotional, intellectual and physical energy. Just like in any bank account, withdrawals can’t exceed deposits without incurring debt. Sleep debt, though, is easy to ignore because physical activity keeps alertness high. As long as you move around instead of reading or watching TV, you won’t nod off and you can keep thinking that 5 or 6 hours of sleep a night meets your needs. But covering the debt with activity is like keeping a bank balance out of the red by borrowing money and paying interest. Sleep debt exacts a toll on the body that goes beyond depressed mood, irritability and lack of ability to concentrate and learn, not to mention the potential for causing motor vehicle accidents.

The biological clock

As sleep debt mounts, the body’s biologic clock goes awry. This clock, located deep in the brain, controls circadian rhythms – regular ups and downs in behavior, body temperature, appetite, hormone production, alerting mechanisms, and the urge to sleep. When the clock malfunctions chronically, the results show up in the form of weight gain, high blood pressure, diabetes and diminished immunity to infection.

Setting the clock

Regular periods of darkness are required to set the brain’s internal clock to keep the body in synch with the 24-hour day set by the sun. Sleep researchers have shown that, when living in a research setting where there are no external clues about time of day or night, subjects’ internal clocks actually work on a 25-hour cycle. Normal peaks of sleepiness and alertness work themselves into the wrong time of the  24-hour day and night outside the sleep lab, producing weeks of daytime sleepiness and nighttime insomnia in the research subjects. Over time, the peaks cycle back into synchrony with day and night producing several weeks of normal daytime alertness and nighttime sleepiness.

Laboratory settings may exaggerate these patterns, but most people know that during some weeks they simply perform better during the day and sleep better at night  than during other weeks, indicating that in the modern, artificially lit world, the 24-hour day is more like a 24-25 hour day as far as the body’s natural rhythms are concerned. This clock drift is very sometimes very evident. Cyclical insomnia and daytime sleepiness are in common in blind people, in people at very high latitudes where the summer sun circles the sky for almost 24 hours, and in shift workers who are up all night in brightly lit environments. These problems, while distressing, respond to maintaining regular sleeping schedules and closing out all light during sleep periods, which resets the clock.

Why the clock matters

The internal clock is easily disrupted by one or two day episodes of sleep deprivation that people experience for reasons as varied as extra work loads, exams, brief periods of emotional upheaval, or any of the other myriad problems that keep people awake, but studies have repeatedly demonstrated that a few days of “catching up” on sleep restore the body to normal rhythms, contributing to a widely held impression that sleep deprivation, while responsible for serious accidents, doesn’t cause real health problems.
However, bigger problems do come from disturbing circadian rhythms more chronically. In recent years research attention has shifted from short term sleep deprivation to the chronic, partial sleep deprivation that is so common in our modern society, where nodding off during monotonous and sedentary activities like reading or watching TV are almost expected. Many people think they need no more than 5-7 hours of sleep at night, but while a few truly short sleepers exist, most people require around 8 hours of sleep each night to achieve maximal alertness throughout the day. Chronically shortchanging sleep by even an hour a day changes the timing and levels of multiple hormones, causing other metabolic changes and weakening the immune system.

Lack of sleep wreaks havoc on hormones

One of the first hormonal changes produced by chronic short sleep involves cortisol, the stress hormone produced by the adrenal gland. Normally cortisol levels decline during late evening hours, but without enough sleep, production continues unabated, Cortisol then begins to contribute to immune stress and to insulin resistance, which leads to diabetes and fat deposition. A second contributor to insulin resistance is a change in growth hormone secretion from one large burst during sleep to two, smaller bursts before and after sleep. A third change comes from failure of the pituitary gland to produce its normal night-time rise in thyroid stimulating hormone, the stimulus for the thyroid gland to produce more thyroid hormone. All of these changes are consistent with the fact that as little as one week of 4 hour sleeping nights can convert healthy young people to a pre-diabetic state. Observational studies do show higher rates of diabetes in chronically sleep-deprived women.

Lack of sleep and obesity

If these hormone changes are not enough to convince a short sleeper to turn out the lights earlier, studies on the appetite influencing hormones leptin and ghrelin, produced by fat tissue and the stomach respectively, might help. Leptin, which signals when to stop eating, diminishes markedly after 6 days of four- hour sleeping nights, despite no change in caloric intake. Ghrelin, which stimulates appetite, particularly for high carbohydrate foods, goes up when sleep is short.

Sleep debt is all around you

    All of these hormonal factors are significant in society where people lead overscheduled lives in stimulating, loud and bright environments without regard to natural day and night. We do not need sleep studies to tell us that we are in an age of significant sleep debt – just count the number of people, including children, asleep on planes and buses, over books and newspapers, and on couches in front of TVs. If you fall asleep regularly under these circumstances, you are in chronic sleep debt. Given the increase in obesity and diabetes over the last few decades, sleep is another potential therapeutic avenue – a fruitful and inexpensive area of health over which we have considerable control.

Managing the sleep budget: factors under your control

Environmental
1. Take the television out of the bedroom.
2.Darken the room completely, or wear a comfortable, opaque eye mask.
3. If noise is a problem were soft ear plugs.
4. Keep the temperature low at night and invest in a comfortable mattress that does not move.

Behavioral
1. Keep the biologic clock in sync with the sun by getting outside regularly.
2. Get regular exercise like walking, but avoid exercise in the last 3-4 hours before bedtime.
3. Keep naps short – 45 minutes or so – and confined to early afternoon hours.
4. Avoid heavy meals and alcohol in the last 4 hours before sleep.
5. Aim for the same bedtime every night, well before midnight, and develop a quiet bedtime ritual

Internal factors
1. Empty your bladder right before getting in bed.
2. Seek medical treatment for heartburn if causes frequent awakening. Ditto for urination.
3. Evaluation for sleep apnea is a must for someone who snores and suffers from daytime sleepiness.
4. Treatment of arthritis with exercise, physical therapy and medications, if necessary.
5. Try to get weight down to normal: sleep apnea, heartburn, and arthritis pain all benefit

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