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.

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

Posted by medical plaintalk

Physician turned medical writer.

When Diets Fail: Bariatric Surgery

“A Roux-en-Y gastric bypass is the strangest operation I have ever participated in… (It) removes no disease, repairs no defect or injury. It is an operation that is intended to control a person’s will and to manipulate a person’s innards so that he will not overeat again.” Dr. Atwul Gawande, Complications, 2002.

Human evolution occurred in a world of varying food supply. The body’s ability to store some fat insured survival when food was scarce. For most of us now there are no lean times when a few extra pounds disappear, so getting rid of them means voluntarily diminishing food intake to amounts less than we require for normal activity. This is easy if we haven’t strayed more than 10-20lb over normal weight. Above this level, gains and losses tend to become cyclical – weight that comes off reappears easily, and tends to increase with each round of dieting. When obesity becomes “morbid” – in the neighborhood of about 100 excess pounds – weight loss by conventional means is all but impossible.

A surgical way to restrict calories

So far, bariatric (from Greek words bari:heavy weight, iatr: physician, ic: pertaining to) surgery has provided the only long-term solution to morbid obesity, by restricting the amount of food entering the stomach and by altering the route the food takes through the small intestine. Patients who undergo bariatric surgery often see immediate results. Pounds finally melt away and, surprisingly, so do many previous food compulsions. Many patients maintain losses of 60-65% of their excess weight for many years. Most interesting is a profound effect on diabetes that appears before any significant weight disappears. This rapid reversal of impaired glucose control that the surgery triggers has opened a whole new frontier of research. But weight loss surgery is a drastic measure, and no one knows the results of living 30 to 50 years with this type of intestinal re-routing.

Early attempts

Beginning in the 1950s, pioneers in bariatric surgery, doctors and patients alike, learned from early negative experiences. The first approach, stapling the stomach to reduce its size, made patients lose weight, but long term results were poor. Tiny stomach pouches stretched, staple lines broke down and patients were able to eat their way back to obesity. The next approach blocked absorption of food by rerouting its path from the stomach to distant portion of the small intestine, bypassing the upper small intestine where much nutrient absorption normally occurs. Early procedures bypassed too much small intestine and caused malnutrition, foul smelling diarrhea and a very unpleasant set of symptoms called the dumping syndrome (cramps, nausea, faintness and diarrhea). Refinements of technique resulted in fewer symptoms, though patients require supplementary vitamins and minerals, and some dumping symptoms still occur.

Modern Procedures

Today, gastric “banding” with an adjustable silicone noose placed around the upper stomach and a procedure called vertical gastric banding are the least invasive and most reversible of the commonly done bariatric procedures. They are also the least effective in terms of amount, speed and persistence of weight loss. The best operation for treating obesity is the Roux-en -Y procedure, the type of surgery most commonly meant when the term gastric bypass is used.

Understanding the Roux-en-Y

Under normal circumstances, food travels from the mouth, through the esophagus and into the stomach, which is about the size of two fists. There, it sloshes around for about 20 minutes before passing through a valve to the first part of the small intestine (the duodenum), where it mixes with bile and pancreatic enzymes. After Roux-en-Y surgery, incoming food finds only a tiny pouch of stomach, 5% of its original size, opening directly into the second part of the intestine (the jejunum). Surgical rerouting has separated 95% of the stomach and the the entire length of the duodenum from the food stream and plugged the end of the duodenum back into the system farther down the jejunum. The small amount of food tolerated by the tiny stomach bypasses several feet of small intestine before it meets up with bile and digestive enzymes.

After Surgery

Under the best circumstances, weight loss following Roux en Y surgery is prompt and long-lasting. Initially patients can eat only an ounce or 2 at a time. They must schedule meals and plan content carefully in order to meet their protein and fluid needs and to avoid constipation. Over time they can begin to eat a little more at one sitting. Most patients lose 35-40% of their bodyweight over 12-15 months, and maintain that for at least 15 years. Diabetes is cured in over 80-95% of patients. Hypertension, sleep apnea, acid reflux, arthritis, infertility, stress incontinence, fatty liver, and leg infections also disappear or are significantly improved.

Candidates for Surgery
Given all of these positive results, why not offer this type of surgery to less than morbidly obese patients who struggle to lose weight? Currently weight loss surgery is limited to patients with BMIs (Body Mass Index) of 40, or 35 if the patient already suffers from obesity related diseases like hypertension or diabetes. BMI is a calculation of weight divided by height squared, with measurements expressed in kilograms and meters. A BMI of 30 qualifies a patient as obese; 19-24.9 corresponds to appropriate weight. Statistical analysis of risks and benefits of bariatric surgery set the acceptable range for surgery. Surgical candidates must also undergo extensive medical tests and psychiatric analysis, and have made serious attempts to lose weight. They must understand that gastric bypass is drastic and usually permanent, that complications can be bad, and that success is not guaranteed. Some patients manage to regain all their weight and then some.

Oversight

Bariatric surgery is regulated by American Society of Metabolic and Bariatric Surgery, which sets professional standards for hospitals and surgeons, establishes centers of excellence, and promotes research and data collection about the procedures. In 2007, surgeons performed over 200,000 surgeries for obesity, up from around 16,000 in 1992. Advances in laparoscopic surgery have made recovery faster and less uncomfortable. The best surgical mortality rates are 1% and peri-operative complication rates 10% – acceptable numbers given the worse risks of morbid obesity.

Complications and Long Term Results

Possible complications of bariatric surgery include blood clots travelling to the lungs, heart attack, respiratory compromise, suture line leaks, hernias, ulcers, GI bleeding, bowel obstruction, and gallstones. Calcium iron and some vitamins are not well absorbed and they require life-long monitoring and supplementation. All bariatric surgeons emphasize that long term success depends on patient cooperation with major eating and lifestyle changes forever. This is especially important when the choice of procedure involves only change in stomach size, as is the case with the gastric banding procedures.

Clues about metabolism and diabetes

Sheer calorie restriction accounts for some of the success of all types of bariatric surgery. When the surgery also bypasses a segment of small intestine, more is at work than meets the eye. The rapid disappearance of diabetes before significant weight loss occurs and the remarkable loss of previous cravings are clues to unappreciated biochemical and hormonal complexity of the intestines. The surgical assault on obesity appears to have much to teach us about energy metabolism and diabetes. One day, hopefully, such strange surgery will be unnecessary.

Resources:
American Society of Metabolic and Bariatric Surgery (http://www.asmbs.org/): Access to readable, professional information regarding bariatric surgery.
http://www.obesityhelp.com/: Support group website for patients contemplating surgery or looking for related information

Posted by medical plaintalk

Physician turned medical writer.

The Obesity Epidemic: Blame it on Science Too

When I was a child I thought my grandfather and Jackie Gleason were two of the fattest men in the world. Last year I happened on a rerun of The Honeymooners and was taken aback by Mr. Gleason’s modest girth. And an old movie of my grandfather shows, at most, a size 40 waist – practically svelte these days. What’s happened to us? We’ve become accustomed to widespread obesity in men, women and children. Is this one of the prices we pay for our market-driven, entertainment-loving culture? Look at all the factors conspiring to load the scales: escalating inactivity, a vast snack and soft drink industry, supersizing, frenetic lives, fast food restaurants, the demise of the family-centered, home-cooked meal and its replacement with eating anywhere and everywhere, all the time. There is blame aplenty to go around, but this is a medical column, so we’ll stick to the role of science. Why pick on the medical science? Because we need to know how the expert advice we rely on plays out over time and if well-intentioned advances lead us astray.
Taking fat out of the diet
In the 1950s, medical researchers took on the epidemic of heart disease that had begun around 1900. Fatty streaks in the aortas of young soldiers dead in the Korean War made pathologists think that heart disease actually began early in life. They created an animal model for study, feeding rabbits cholesterol dissolved in vegetable oil instead of lettuce and carrots. When fat showed up in the rabbit arteries, the dietary theory of heart disease came to life. Some scientists quibbled, claiming that the problem was more complex, that other dietary factors like sugar might be equally to blame, but they lost the debate. Dietary cholesterol became the enemy, and over the next half-century the public learned to view the egg as a toxic substance, despite its near perfect protein and yolk full of valuable vitamins.

Along came the observation that Mediterranean populations had little heart disease compared to Americans. They also walked more, ate regular meals in family settings, didn’t snack, doused all but breakfast in olive oil, and scoffed at tasteless, pre-packaged food. But what we saw was lots of pasta, with not an ounce of cholesterol in it. Pasta was the ideal candidate to replace fat. We embraced the carbohydrate age, and turned a blind eye to the fact that, for years, we had managed to turn cattle fat by feeding them carbohydrates.

The national waistline ballooned, but can we at least say that the dietary agenda paid off in terms of heart disease? The answer is murky, because there were other, simultaneous prongs of attack: a fruitful campaign against tobacco use; drug treatment of high blood pressure; drugs that keep the body from absorbing or making cholesterol and drugs that calm the heart. Galloping technological advances allowed doctors to ream out plugged coronary arteries, prop them open with metal struts, or bypass them altogether. Nevertheless, cardiovascular disease remains our leading cause of death and the total number of patients with the disease has increased. Only the death rate from heart attacks has fallen and that statistic is attributable to the interventions and drugs and declines in smoking. The effect of the officially sanctioned diet on the epidemiology of heart disease, if any, is hard to discern. Now we face even more cardiovascular disease as epidemic abdominal obesity brings with it more diabetes, high blood pressure, and inhibition of physical activity.

A contribution from chemistry: artificial sweeteners

Science contributes to the obesity epidemic in other, more subtle ways. Through chemistry, we possess the magic of intense sweetness without a caloric price. An enormous rise in artificial sweetener use parallels the obesity epidemic. Well, is that a surprise? Everyone’s trying to lose weight. But what if, in addition to failing to stem the tide of weight gain, non-nutritive sweeteners are contributing to it? A few studies raise this unsettling possibility, and no study shows any significant effect of these chemicals on the process of weight loss, unless they are used in conjunction with a disciplined program of eating and exercise.

How could something with no caloric value contribute to obesity? Perhaps by raising levels of insulin, hormone which promotes fat storage. At least one artificial sugar (Xylitol) stimulates enough insulin release in dogs (who ate the stuff accidentally) to cause profound hypoglycemia and death. Do “non-nutritive” sweeteners cause release of insulin in people as well? This hasn’t been studied well. Artificial sweeteners were developed for Type I diabetics, who lack insulin altogether, so there wasn’t any point in measuring the hormone. But there is an insulin burst from the pancreas within thirty seconds of sweetness arriving in the mouth (the cephalic insulin response), and most people who use non-nutritive sweeteners do make insulin, which efficiently converts any extra calories in the meal accompanying the drink to fat. Some studies do suggest that insulin levels are higher in regular artificial sweetener users than non-users.

Tipping the scales while fixing the mood?

Chemistry also gives us the drugs that make people happy – or at least less unhappy. Over the last 30 years, antidepressant use for life’s inevitable miseries has skyrocketed. We are engaged in the very new practice of using these drugs in children. One side effect, perhaps more common than advertised, is difficulty withdrawing from the drugs. Another is weight gain. Some depression requires drugs, and antidepressants or antipsychotic agents don’t always cause weight gain. But the drugs are in such widespread use that you probably know someone who has packed on 20 pounds in the course of a divorce or other life stress that prompted antidepressant use and someone else who accepts the weight gains because they can’t stop the drugs.

Will science solve the obesity epidemic?

Should we look to medical science or to the mega-million dollar diet industry to reverse our big obesity problem? To the development of new surgical procedures, more appetite suppressing drugs, sterner diet and exercise prescriptions, or new versions of deprivation diets (which rarely lead to permanent weight loss)? I think not. And who knows what unexpected consequences might come along for the ride. For a significant statistical improvement in the obesity problem, the answers will have to come from all of us and from our choices about how we act and what we value – from the culture, not from science. For too long we have treated food as an enemy, taking the joy and taste out of eating, without much to show for our efforts. Heart disease is still the number one killer, obesity is epidemic, and diabetes is hot on its heels. Extra weight comes off for good in the same slow, sneaky way it crept on – a few hundred calories a day out of balance with caloric needs. That’s just one dessert, or a beverage or two. Or a brisk walk instead of an hour of television. Every day we make the choices that determine our energy balance – elevator or stairs? TV or a walk? Coke or water? Vote for the guy who wants to put PE back in school or the one who doesn’t care? Yes, extra weight takes a very long time to lose, but next year will come around before you know it, no matter what you do. The choices will have added up, one way or the other. Every choice counts. In an epidemic, every person counts.

Posted by medical plaintalk

Physician turned medical writer.

Holding the Line: Stop Gaining First

One of the most remarkable failures of modern medicine is its inability to combat obesity and its associated ills. Obesity is not a new human condition, nor will it ever completely disappear. But since the 1970s, something has changed in the environment and culture to make the condition epidemic, despite sophisticated medical research, a multi-billion dollar diet industry, and constant media attention. The most effective solution remains not gaining excess weight in the first place, but that is no longer an option for over 60% of the population, many of whom are veteran dieters.

The body wants to keep the fat

Diets depend on adherence to a long-term plan for eating that fails to meet the body’s need for energy. In response to this semi-starvation, the body mounts a defense. Hair and fingernails grow more slowly. Heat generation declines and the dieter feels cold and is less inclined to move around. Cells throughout the body ramp down their energy needs. Within a few days, even sleeping burns fewer calories. Caloric requirements remain suppressed long after the target weight is achieved. Upward weight creep begins as soon as vigilance about food intake and exercise declines, and happens at a lower calorie intake than in the pre-diet days. So begins the yo-yo dieting cycle, unless the dieter just gives up.

Stop the upward creep first

Giving up the attempt to starve away the pounds will eventually bring the metabolic rate back up, but only as the pounds re-accumulate. At this point a tactic other than a repeat diet attempt may be in order. The most reliable way to achieve weight loss that lasts is by burning slightly more energy than is consumed on a daily basis over a long period of time – a sneak attack rather than a frontal assault. Such long term daily commitment requires habit formation, and habit formation requires patient repetition of actions over long periods of time. Holding weight stable- just simply trying not to gain any more for at least 6-12 months- is the first preparation for mounting a sneak attack.

Going on defense

In contrast to the coordinated offense of a diet plan, not gaining any more weight requires defensive tactics. Mindfulness – thinking before eating – is the primary tool. Each day presents dozens of choices that might contribute to weight gain – or not. The only concern is reacting to choices presented. Reacting correctly to just a few of them every day adds up over time. At the end of 6-12 months of no weight gain, you are better off than at the end of another diet cycle that winds up on the upside of the starting weight. You’ll have the habits of a person who maintains stable weight, and you will be ready to lose weight slowly and permanently by undershooting energy requirements just a little each day – but not enough to put your body into energy conservation mode.

Learn from the people who succeed

People who maintain stable weight often have some sensible guidelines for themselves. A common behavior is refusal to buy larger clothing sizes. Another is the choice of clothes with zippers and buttons and belts. If clothing becomes uncomfortable, they cut the sweets and alcohol back and pay more attention to activity level. A weekly weight check keeps others on track. These people know better than to obsess about daily weight fluctuations, but 3-5pound gain in a week gets their attention. While a common mindfulness tactic is procrastination of eating to sort out true hunger from urges of emotional origin, people who maintain stable weight also do not go long periods without eating. The body begins to downshift into a lower energy gear if no food appears to break a fast of more than 6 hours.

Choices, choice, choices

Easily digestible carbohydrates in the modern diet, especially those combined with fats, make good targets for people seeking stable weight. Carbohydrates trigger surges in insulin. Insulin blocks fat usage for energy needs, and hunger recurs much sooner after a high carbohydrate snack or meal than after one containing more protein and fat. Choose to keep insulin levels down: eggs instead of cereal; one slice of bread on a sandwich instead of two; one M&M instead of a handful; nuts instead of M&Ms; half the normal spaghetti serving – or eat just the meat sauce; drink water instead of juices or soft drinks, even diet ones. (The taste of artificial sweeteners also triggers a burst of insulin, even though they have no caloric value.) Put off eating something that you really don’t need – distract yourself with an activity or task. Practice self-control in other areas of life. Self-control is a “transferable skill” and any practice helps build it.

Activity choices abound. Park far away from your destination. Walk if the trip is less than a mile (get a pull cart for groceries if you are lucky enough to live near the store). Skip the elevators. Make dates for walking instead of eating. Keep your hands busy and mind busy (mental activity takes energy too). Sit on an exercise ball instead of a desk chair. If you have a wireless printer, put it far away from the computer – on another floor if possible. Mow your own lawn. Shovel your own snow. Buy a pedometer and watch the steps add up. Engage in some strengthening activities to build high-energy demanding muscle tissue.

Stay in the present

Dieting to lose weight is always focused on the future. Weight maintenance is a present-moment task. There will never be a better time than now to go on the defense and begin to stop gaining weight. Now is the only time you have in which to take action – all the rest of time is either a memory or an imaginary future.

Posted by medical plaintalk

Physician turned medical writer.

The Problem with Sugar: Insulin

This article is about insulin, not diabetes. Diabetic or not, you need to know about insulin. My epiphany about the importance of this hormone occurred when one of my children brought Micah, a friend with Type 1 diabetes, home for dinner. We had a healthy “Mediterranean” dinner – pasta tossed with olive oil, chicken, fresh tomatoes, and cilantro, with accompanying salad and French bread. And birthday cake. Fresh from life in a college dorm, the young friend ate with gusto – at least two helpings of everything. We all did. Later, I found him groggy and in need of two to three times his normal insulin dose. The epiphany was this: all the non-diabetics at the table that night required a lot of insulin to cover hefty carbohydrate intakes, but we were blissfully unaware of the consequences of over-indulgence. We did not have to fill syringes with extra insulin. Our pancreases did the work behind the scenes.

Awash in Insulin

Why was this realization an epiphany? Because we live in an age of excess, consuming large amounts of refined carbohydrates and frequently eating more than our energy requirements demand. We are awash in insulin of our own making and need to understand this hormone’s central role in metabolism. More and more research links insulin to the chronic diseases of civilization: high blood pressure, heart disease, obesity, and Type II diabetes (the variety in which insulin is too plentiful and doesn’t work properly, as opposed to Type I, in which the pancreas fails to produce insulin).

How insulin works

Insulin is the hormone that moves sugar from the blood into all the body’s cells. Blood sugar comes from carbohydrates in food and from glycogen made by liver and muscles as a way to store a twelve-hour supply of sugar. When glycogen stores run out and little food is coming in, as in starvation or very low calorie diets, we make sugar, first from our muscle proteins and then from our fat. The main goal of all metabolism is to keep blood sugar in a tight range – just right for the brain’s needs, because sugar is the only fuel the brain uses under normal circumstances. (It will resort to using ketone bodies, formed from fat in the liver during prolonged fasting or total carbohydrate restriction, but if sugar is available it is the preferred fuel).

Incoming dietary sugar elicits a burst of insulin from the pancreas. Insulin’s job is ferry the needed sugar to cells and to squirrel away extra sugar as glycogen and fat. Insulin is a lipogenic, or fat-producing hormone. Every time we overindulge, insulin goes into high gear to produce fat. It also raises triglyceride levels and lowers high density lipoproteins, exactly the changes in blood lipids that are associated with heart disease.

When insulin fails to work

Insulin is also mysterious. For unknown reasons, many people – one in every three of us – have a tendency to become “resistant” to insulin’s effects. Their pancreases put out more and more insulin to handle routine blood sugar levels. No one knows what makes the insulin inefficient, though fat accumulation in muscle cells may be part of the problem. This stage of “insulin resistance” goes unnoticed for years because there are no symptoms. Blood insulin levels are expensive to measure and difficult to standardize, so they are not part of any kind of routine, preventive screening.

Insulin promotes fat storage

High levels of insulin make fat storage and weight gain easier. Weight gain, particularly around the middle, promotes insulin resistance, and the pancreas responds with yet more insulin. A vicious cycle is underway. Insulin resistance can become so pronounced that blood sugar escapes control and spills into the urine. Insulin resistance is now Type II diabetes, treated with medicines that help insulin work, and ultimately, with shots of yet more insulin. Before this happens, and even afterwards, weight loss and exercise can reverse insulin resistance, leading medical researchers to believe that insulin resistance has something to do with abnormal energy processing in muscle cells. They’ve found that the muscles of some lean, healthy relatives of Type II diabetics show insulin resistance long before there is any fat in muscle, or abnormality in blood insulin levels.

Epidemic

In our sedentary age of super-sized, sugar-laced, low fiber meals, we produce far more insulin than our ancestors did. In addition, the genetic make-up of many people, particularly Hispanics, Native Americans and some African-Americans makes their insulin less effective. We don’t measure insulin levels routinely. Instead, we concentrate on easily-measured cholesterol and fret about fat in the diet. At the same time we are in the middle of an epidemic of insulin resistance and on the verge of an epidemic of Type II diabetes, which is no longer just a disease of middle and older age. For the first time in history, type II diabetes is appearing regularly in children, teens and twenty year olds.

The average American fast food diet sets people on the road to obesity, insulin resistance and type II diabetes. Lack of exercise keeps them there.In a world of easily available food that requires little or no work, the only defense against overeating is mental. Education and self- discipline are the weapons. Insulin-requiring, Type I diabetics like Micah know how much insulin has to be paid out for a big meal. The rest of us have to visualize that syringe full of extra insulin and imagine tucking away excess calories as fat. We have to see ourselves requiring more and more insulin as time goes on and becoming unable to produce enough to meet the needs of an insulin resistant body. It’s enough to make that second helping seem less desirable and regular exercise more attractive.

Keeping insulin levels under control:

Avoid weight gain
Lose any extra weight
Exercise 30 minutes per day.
Eat regular, small, balanced meals, and 25-30gm/day of fiber
Avoid the “white stuff:” Flour, sugar, white rice
If you are overweight and/or have relatives who have diabetes do all the above, and see if your doctor thinks a glucose tolerance test is warranted.

Posted by medical plaintalk

Physician turned medical writer.

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