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.

Why Cancer Happens

According to Greek mythology, Cancer was the crab that the goddess Juno immortalized in the night sky after the lowly creature sacrificed himself in a fabled battle between Hercules and the nine-headed Hydra. Since Juno was stingy with the number of stars she allotted to the crab’s constellation, the amateur astronomer often looks in vain for a body with claws. Nevertheless, first century physicians, searching for picturesque language to describe their patients’ ailments, found in the crab constellation a name for hard masses covered with tortuous veins – particularly those that seemed to burrow deeply into the body. And so we came to know cancer, the disease that inspires today’s most sophisticated research in cell biology, by a name that has no scientific meaning whatsoever.

The biggest risk factor: age

Cancer is a problem of birth, growth and death of cells, and occurs because our bodies are in a constant state of renovation, from development as tiny embryos until death many decades later. At first we grow and change shape. Then shape becomes fixed but body maintenance requires cell replacement on a regular, repetitive timetable. The master plans laying out instructions for regular destruction and reconstruction of cells lie in the DNA coiled into chromosomes. Just as job-site blueprints get smudged, torn and stained, DNA accumulates damage over time. External agents such solar, cosmic and X- radiation, toxic chemicals, some hormone use, and some viruses add to the innate wear and tear. In some people DNA code errors are built in from birth, handed down from one generation to the next. Errors in the blueprint lead to the imperfect cells which give rise to cancer.

Errors in cell reproduction are visible everywhere. We call them signs of aging. Crinkles around the eyes, sagging skin, “liver” spots, bunions and so on – all are external, visible reminders that internally, similar changes are underway. It is no coincidence that tobacco smoking, single-handedly responsible for most cancer deaths, also produces conspicuous, premature aging. The most remarkable thing about cancer is that it occurs so infrequently despite billions of cycles of error-producing cell reproduction in each person. Fortunately for us, DNA also contains numerous safeguards for getting rid of error-ridden rogue cells before they get out of control.

What makes a cancer diagnosis

While cancer cells are identified under microscopes by changes in their appearance, looks alone do not make a cancer diagnosis. Until abnormal cells acquire the ability to grow unchecked, and to travel to other parts of the body (to metastasize), they are precancerous. In many cases, pre-cancerous cells never make the transition to cancer, but we are unable to predict with 100% accuracy which ones will and which ones won’t. A large number of breast abnormalities detected on mammograms will not go on to run wild, but few women will comfortably forgo treatment without 100% accurate prediction of the growth potential of their abnormal cells.

Difficulties in prediction

In addition to the breast, the prostate gland in men and the colon in both sexes are the sites of cell growth abnormalities that can, but do not always, result in cancer. Prostates enlarge with age and develop nodules of cell growth called adenomas. Colons develop polyps – enlargements of the lining protruding into the colon on flat or narrow stalks, with or without adenomas on their surfaces. Intuitively, it seems as if detecting these abnormalities and removing them before they have a chance to become cancerous is a good idea. This thinking drives the screening studies aimed at early treatment of cancer. But many of these common cancers are very slow and indolent in their growth and epidemiologic studies do not bear out the intuitive bias. Unless a patient is young at the onset of a slow growing cancer, treatment does not necessarily lengthen life. Routine prostate cancer screening has fallen out of fashion because, while removing a cancerous prostate may prevent death from prostate cancer, treated patients do not outlive untreated ones. Decisions about treatment have to be weighed carefully, with attention paid to age and the potential for harm and diminished quality of life that can go along with cancer treatment.

While all cancers begin slowly, some escape the body’s control mechanisms more easily and become aggressive and difficult to treat. Primary brain, liver, pancreatic and ovarian cancer fall in this category. Toxic external factors that alter DNA may render cancer cells more resistant to the body’s methods of keeping slower growing cancers in check. Lung cancer from smoking, blood cancers secondary to radiation and some viruses, ovarian cancers stimulated by hormone use, and asbestos-induced lung tumors gallop along compared to the slow movers like prostate and colon cancer.

Treatment

Currently cancer treatment consists of removing cancers surgically and/or intervening with drugs or radiation to kill the abnormal cells. Both approaches leave something to be desired. Surgery removes a tumor already developed, but not the underlying biology that produced the tumor. Chemotherapy that seems effective at first is often followed by a relapse in which the cancer is less responsive – not surprising since the cells surviving the first rounds of treatment are resistant to the drug’s actions. Radiation induces cell damage in all exposed tissues and accounts for cancer development years later in people who have survived the first bout.

The new paradigm for thinking of cancer is as an age and genetics related derangement of cell growth that is also influenced by environmental factors. Effective, tolerable treatments require understanding of the individual biology of each person’s cancer. As the interior of living cells give up their secrets to researchers, we are beginning to see some real successes with drugs such as Gleevec (used for chronic myelogenous leukemia) – drugs aimed at specific pathways in the life of microscopic cancer cells – and also with immunotherapy in melanoma. Perhaps we will eventually be able to retire the image of the crab to his home in the sky.

Factors in cancer development

Under your control	Not under your control
Avoiding tobacco	Your genetic makeup
Using sunscreen	The passage of time
Maintaining normal weight	Cosmic radiation
Choosing high quality foods, low in sugar	Accidental radiation exposure
Eating and exercising enough to avoid constipation (avoiding slow transit of waste through the colon)	Exposure to carcinogenic agents not currently recognized as carcinogenic
Minimizing post menopausal hormone use	Bad luck

Posted by medical plaintalk

Physician turned medical writer.

A Sweet Decision: Artificial Sweetener or Sugar?

“I would feel more optimistic about a bright future for man

if he spent less time proving that he can outwit Nature

and more time tasting her sweetness and respecting her seniority.” E. B. White

Little packets of faux sugar sit beside all convenience store coffee pots. Grocery store shelves are lined with lo-cal, no-cal, and no-sugar foods. Authorities assure us that these staples of modern life are safe. Nevertheless, unease persists. Should millions of people, including children, be engaged in an attempt to “outwit Nature?” In deciding whether or not to participate in this vast modern experiment, there are two questions to answer:

1. Are artificial sweeteners necessary for me?

The first question has an easy answer. Artificial sweeteners are not necessary for anyone at any time. But for someone struggling with weight problems or diabetes, artificial sweeteners can add some “better living through chemistry.” Bear in mind, though, that the only studies showing any positive effects on weight loss by the addition of artificial sweeteners are those involving serious attempts at long term dieting – the kind that involves lifestyle change. Casual, habitual users of sweeteners typically weigh more and gain more than non-users. In addition, frequent consumption of sweetened foods and beverages aggravates the sugar addiction that drives so many poor food choices. Artificial sweeteners also contribute to elevated insulin levels. As soon as the tongue perceives sweetness, a quick burst of insulin begins the body’s preparation for an influx of sugar (the “cephalic insulin repsonse”). When no real sugar appears, insulin falls back quickly, stimulating hunger. Or if food accompanies the diet drink, the insulin helps make any excess calories into fat.

2. What is the likely harm if I choose to use them?

The question of potential harm is difficult to answer. Wading through the contradictory literature on safety studies of non-nutritive sweeteners is a confusing trek that exposes the influences of politics, power, money and fear on science. FDA approval of food additives, or designation of them as “GRAS” – generally recognized as safe – does not make safety questions disappear. Saccharin (Sweet’N Low) for instance, is known to produce bladder cancer in rats, but human population studies show only “a trend” toward more bladder cancer if more than 6 packs a day are used.

Widespread use of any substance is very hard to tie to small changes in physiology or upticks in disease processes for which there are no clear, single causes. For instance, one of the worries about aspartame (NutraSweet, Equal) was its ability to cause brain tumors in rats. There was a rise in human brain tumor rate that coincided with the introduction of aspartame in the early 1980s. But the increase may well have reflected better diagnosis due to the introduction of the CAT scan. A more recent increase in brain tumors of high malignancy prompted some scientists in 1996 to call for a reevaluation of aspartame’s role, but other opinions prevailed.

Safety testing

Safety testing of individual sweeteners in bacteria and laboratory animals involves huge doses over months to years. But only when the products reach the market does the most important test begin – long term consumption under varying circumstances by large numbers of people who have not been prescreened for other problems. To make sweeteners more palatable, manufacturers often combine them in foods, exposing the consumer to chemical mixes never tested in the lab. Anyone using artificial sweeteners regularly is a volunteer in long term safety experimentation, so wisdom dictates having at least a rudimentary understanding of the most common ones.

Saccharin

Saccharin, a petroleum derivative, is one of the oldest sweeteners. Time on the market has given it an aura of safety, but it has been used sparingly in soft drinks, making it less used than aspartame. A persistent group of scientists still rings the warning bell about saccharin’s carcinogenic potential and about its unstudied effects on fetuses and children. Even a weak carcinogen, they say is of concern over a lifetime of use.

Aspartame

Aspartame is dogged by the most complaints, including legitimate ones like headache and mood disorders and skin rashes, and unproven ones like links to Alzheimer’s disease and brain tumors. Rare people with an inherited condition called phenylketonuria cannot tolerate one of the amino acids from which it is made. In 2002, a new version of aspartame without that that amino acid (Neotame) was approved but is not yet widely used.

Splenda

Sucralose (Splenda) has the shortest track record. Better taste, heat stability that enables it to be used in cooking, and masterful marketing as “made from sugar” and “not absorbed” gave Splenda 60% of the sweetener market by 2006. Eleven per cent of prepared foods on the grocery shelves are now sucralose sweetened. The additive does start out as sugar. Chemical alteration replaces three parts of the sugar molecule with chlorine atoms, making a “chlorocarbon” that is structurally most similar to insecticides – but still called “natural.” On average, about 15% of Splenda is absorbed into the body. (The legal definition of “unabsorbed” applies if at least 80% of the product passes through the intestine unchanged.) Test rats wound up with enlarged kidneys and livers, but so far, the large pool of human subjects seems to be tolerating the sweetener. Splenda is also not quite free of calories. While the chlorocarbon compound at the heart the sweetness has no calories, the added bulk needed to stabilize it is a mixture of carbohydrates – which contain about 12 cal/ teaspoon or 96 calories per cup.

Acesulfame

Acesulfame-K(Sunette) is bitter tasting sugar substitute seldom used alone. It has undergone safety evaluation multiple times since the 1980s and is considered by some to have a poor test record

Before you make your decision, consider one more thing. Eating real, whole fresh food rather than artificially flavored processed versions revives dormant taste buds. Smaller amounts are more satisfying, allowing room for a few extra calories from naturally sweetsources.

Addendum: What about the “natural” sugar substitutes?

Stevia, a no-calorie sweetener chemically extracted from plant leaves was in exile in health food stores since an anonymous complaint to the FDA in the early 1990s. Some say this was political exile since Stevia requires no patent. The beverage industry subsequently developed Stevia flavored products and the FDA changed its stance in Dec. 2008. There is already a long history of Stevia use in Japan and China, but expect to see it combined with other sweeteners to improve its vaguely licorice-like flavor.

Nectresse is the Splenda manufacturer’s entry into the natural market. It is derived from the monk plant and is 300 times sweeter than sugar, but must be combined with molasses and a sugar alcohol to make it work. It interferes with sugar absorption and the alcohol can ferment in the gut causing gas production. And yes, these plant derived substances have some calories – the FDA allows up to 5 cal/.5 tsp. in its definition of “no-cal.”

Posted by medical plaintalk

Physician turned medical writer.

Parkinson’s Disease: a New Research Era

In the 1980s, a designer street drug* derived from the narcotic Demerol appeared in California and caused immediate and irreversible Parkinson’s disease in the young heroin addicts who used it. At that time, scientific research into Parkinson’s disease had plateaued. The excitement surrounding the use of the drug L-Dopa to treat the disease in the 1960s had faded as the long term problems with its use became apparent. But the Demerol derivative, called MPTP (short for 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) gave researchers a new tool. For the first time in history they had the ability to create an animal model of the disease. A new flurry of research began, providing hope for all patients with the progressive and debilitating disease.

The clinical picture

Most people know someone who has Parkinson’s disease because it is a relatively common ailment, affecting approximately one out of every 100 people over the age of 65 in all parts of the world. To doctors, Parkinson’s disease is a “doorway diagnosis,” meaning that when all of its core components have developed, and there are no unusual features, the diagnosis can be made from the first sight of the patient.

The typical Parkinsonian patient sits quietly, with none of the spontaneous gestures or shifting of the trunk or extremities that most people exhibit when confined to a chair. His face is smooth and expressionless, and he looks slightly wide-eyed, blinking only 5-10 times a minute, about half the normal frequency. Both seated and standing, he has a forward flexed posture of head neck and trunk. His hands shake rhythmically unless he is using them, a problem known as a resting tremor.

When he gets up to walk he does not make preliminary movements to adjust his foot position. Walking seems hard to start, but once started, his upper body may move ahead of his feet, and his steps “hurry up” to catch up to the body, a “festinating” gait. His gait is simultaneously “shuffling,” since his feet barely clear the floor. His elbows are bent with arms held slightly forward of his body. They do not swing as he walks. Should someone tap him on the chest, he does not make any quick postural adjustments such as stepping back with one foot, and he may topple over if someone does not catch him.

His voice is soft and monotonous, and his words are hurried. While he has normal muscular strength, he cannot generate any speed, so an action like clapping appears weak. All of his motions are slow, a phenomenon called bradykinesia.

Parkinson disease begins most commonly in the sixth decade and is rare before age thirty. Many of the characteristics of the disease, in minor form, are also characteristics elderly people: forward flexed postures, shorter step lengths, softer voices, and slower, less forceful movements. But these signs in people who have Parkinson disease appear earlier and progress enough to impair normal activities within about 10 years. Parkinsonian symptoms can also be side effects of drugs used in the treatment of some psychiatric disorders.

Where the symptoms originate

The symptoms of Parkinson’s disease come from nerve cell death a tiny area in the brain stem called the substantia nigra. These cells contain neuromelanin, a substance similar to the pigment in the skin, and they produce a chemical neurotransmitter called dopamine. When the cells die, the substantia nigra loses its black color and dopamine levels decline. The drugs that improve symptoms in Parkinson’s disease either raise dopamine levels or make it more effective at the junction between nerve cells where dopamine works to transmit information from cell to cell.

Replacing the lost dopamine

However, the pharmacologic treatment of Parkinson’s disease has limitations. Initially, the drugs that elevate dopamine levels work in most patients, but sooner or later they became less effective and dose increases produce unwanted movements called dyskinesias. The drugs also have a peculiar tendency to produce an “on-off effect,” causing symptoms to reappear random times. Nevertheless, L-Dopa (in the form of Sinemet) and drugs that improve dopamine’s actions (like Eldepryl) remain the mainstays of treatment, supplemented by a few other drugs that alter the levels of another brain chemical called acetylcholine. Drug treatment of Parkinson disease requires patience and close attention to timing of doses, with frequent adjustments of schedules. Since dietary protein can interfere with the drugs, many doctors also suggest confining dietary protein to the evening meal.

The limitations of pharmaceutical treatment spurred a number of different surgical procedures aimed at restoring balance to the complicated interplay of brain signals that, under normal circumstances, control balance, speed and fluidity of movement. These procedures involve destruction of tiny localized areas in deep centers of motor control (pallidotomy), or stimulation with tiny electrodes of other nearby areas. Implants of dopamine-producing fetal stem cells have caused devastating side effects in some patients and enthusiasm for this approach has waned.

How the ‘frozen addicts” advanced Parkinson’s research

Because Parkinson’s disease does not run in families, researchers have long suspected that it is triggered by some type of environmental factor. They have examined the role of neurotoxins such as heavy metals and fertilizers because Parkinson disease is more common in industrialized countries and also in agrarian areas, but they have never been able to pin blame on any specific substance. Now, though, they know that the California street drug MPTP destroys the dopamine producing cells in the substantia nigra by damaging their mitochondria, the power houses of all cells. Mitochondria are susceptible to damage by other toxins. They also contain DNA, with all its variations from person to person, perhaps explaining why some people might be more susceptible to toxic damage than others.

New ideas for treating the disease pharmacologically will eventually emerge from animal models of Parkinson’s disease. For interested readers, the medical mystery posed by the young people who developed Parkinson disease after using MPTP is recorded in a fascinating book, The Case of the Frozen Addicts. ** The research born from their tragic losses will someday help all Parkinsonian patients.

*a drug produced by modification of the chemical structure just enough to make it no longer identical to drug regulated by the FDA

** The Case of the Frozen Addicts, by J. William Langston & Jon Palfreman, New York, Pantheon, 1995.

Posted by medical plaintalk

Physician turned medical writer.

The Air Connection: a Tour of the Lungs

Before birth the lungs are not inflated. Oxygen and carbon dioxide enter and exit through the mother’s blood via the placenta. In the first 10 seconds after birth, a dramatic changeover begins, and from that point until the last breath is drawn the lungs connect us to this world. The first gasping breath of a newborn baby signals the beginning of the body’s most vital and most tenuous relationship with this world – that with air, or more correctly with the 21% of air that is oxygen.

Breathing is something we do without thinking, adjusting rate and depth of respiration to the demand for oxygen by the tissues. Healthy hearts and lungs rise to the demand, increasing blood flow as needed. In a sedentary person, exercising muscle has to be trained in order to be able to utilize the increased oxygen delivered. Unhealthy lungs, however, fail to meet the increased demands of exertion, and may eventually fail to meet oxygen demands at rest. Then, breathing is always rapid and even speaking is laborious.

Decoding lung symptoms

A huge number of problems affect the airways, but only a limited number of symptoms result. They are: 1. shortness of breath, especially with exertion. 2. cough – either dry and unproductive, or productive of sputum which is either clear, red and frothy, yellow or green, foul smelling, or bloody. 3. chest pain, often associated with the chest wall movement. 4. wheezing. In addition, lung tumors can cause a variety of peculiar symptoms outside the lungs – the most common is weight loss; the most exotic are peculiar neurological symptoms.

Because the lung is a living record of the air inhaled over time, a complete patient history is the first step in decoding symptoms. The second step is almost always an imaging study. X-rays, CT and MRI scans are so good at revealing chest pathology that a skilled chest examination is a dying art. Technology also uncovers lung scars and nodules in patients who have no symptoms. Bronchoscopies and biopsies define abnormalities further. Often, but not always, such findings are benign, evidence of old encounters with fungus spores or of unknown cause. Autopsies also uncover unsuspected lung pathology like mild to moderate emphysema (see side bar) and evidence of long term exposure to pollution and smoke. Lungs of modern city dwellers are speckled with black particles from polluted air. Smokers’ lungs are black and shiny, as if smeared with tar. Smoking avoidance would be the single most effective way to improve many people’s respiratory problems, but a pristine lung at the end of a long life would still be a virtual impossibility. Breathing is often very dirty work.

The bronchial tree – air’s roadway

The work of breathing begins with muscular contraction. The diaphragm, a muscular sheet lying horizontally between the abdomen and the chest, contracts downward and expands the chest cavity. The short muscles between the ribs – the intercostals – assist by pulling the chest walls outward. Like a bellows, this chest expansion pulls air into the lungs by means of negative pressure. Air rushes from the nose into the trachea, down hollow tree-like branches called bronchi, into tinier branches called bronchioles, and finally into millions of tiny expandable sacs called alveoli. The bronchial tree is elastic, expanding on inhalation and collapsing back to baseline diameter on exhalation. In asthmatics, the fine muscles in these tubular walls respond irritably to allergens and constrict the passages. Inflammation from infection or inhalation of toxic substances and even rapid breathing of cold dry air can also trigger tightening of the bronchi, called bronchospasm. Airflow resistance rises in bronchospasm, making the sufferers of asthma and bronchitis cough and wheeze. Treatment of both conditions aims at dilating the airways by using drugs that relax the smooth muscle fiber and at reducing inflammation of the bronchial lining with steroids and antibiotics.

The alveoli – where the work gets done

Air flow rushing down the bronchial tree dead ends in the alveoli, expanding them until they resemble very soft Styrofoam. Fine capillaries course through the thin walls of the alveoli, picking up oxygen and delivering carbon dioxide for exhalation. Airborne particles settle out in the moist alveoli, though they only get that far by surviving the cough reflex and the cilia -the tiny hair-like projections that constantly sweep dust and foreign bodies up and out of the bronchial tree. Alveoli are also the site of pneumonia – infections with either bacteria or viruses that set up shop in thin alveolar fluid. The organisms excite inflammation and increased secretions, which impair gas exchange and cause shortness of breath, fever and coughing. Patients with pneumonia look and feel terrible. Pneumonia can also involve the pleura, the lining over the lung, adding the misery of pleuritic pain with each breath, and causing fluid to accumulate between the lung and chest wall – a problem called a pleural effusion.

Fluid accumulation in the chest

Pleural effusions sometimes accompany heart failure. Less often, they are blood tinged accompaniments of pulmonary emboli – clots that reach the lung from leg and pelvic veins. Small clots in the lung block oxygen exchange in their vicinity; large ones kill suddenly, with no warning, by blocking major blood vessels bringing blood to the lungs. Shortness of breath and coughing producing blood tinged sputum are warnings to be heeded, particularly if they occur after a prolonged period of bedrest or sitting without getting up – situations that promote clot formation in the legs.

Sputum- the stuff that gets coughed up

Blood-tinged sputum can be less serious a symptom, since it is a common result of a bloody nose above. But when associated with cough and weight loss, it is a telltale sign of lung cancer. Yellow and green sputum usually indicate infection. If foul smelling, it may come from a lung abscess. Pink frothy sputum is a sign of edema in the lungs, usually from heart failure, but also from altitude sickness, and is always accompanied by severe shortness of breath.

The last breath

At the end of life, breathing usually ceases not because the lungs fail, but because the drive to breathe that made the newborn gasp its first breath ceases. All those breaths in between are like footprints left behind. Use them well.

Addendum: Alveoli Gone Wrong

Over a lifetime, especially when chronic airway disease impedes airflow, the alveoli change. They merge making larger spaces with fewer capillaries for air exchange. When severe, even getting enough oxygen in at rest is difficult. This condition is called emphysema, most commonly a problem in chronic smokers, but also a genetic disease in rare people. Oxygen delivered by a mask helps the symptoms for a while, but the condition inevitably progresses.

If alveoli rupture, as they can in emphysema or in congenital conditions that produce enlarged pockets, they leak air into the chest cavity. Air builds up between the lung and the inner chest wall an emergency condition called a pneumothorax that is very painful and potentially life threatening, requiring insertion of a chest tube to drain the air and restore negative pressure to keep the lung inflated. Similarly, a penetrating wound in the chest wall sucks air into the chest cavity, collapsing the lung. Covering the chest wound tightly to prevent air from entering can save a life.

Posted by medical plaintalk

Physician turned medical writer.

The Sweet Tooth: Pathway to a Broken Heart?

For the last half a century or more we have believed the dietary cholesterol theory about heart disease, a hypothesis (idea to be tested by experiment) that found favor with researchers, grant makers, doctors and drug makers. What if this theory is wrong? What if cholesterol in artery walls has less to do with dietary fat than with the way the body processes carbohydrates? What if refined sugars and grains are the dietary culprits? Could insulin, the master hormone at the center of all energy processing, be a better marker than cholesterol for heart disease?

What is blood sugar?

The first thing to understand about sugar is that the blood sugar is not the same thing as the sugar in your pantry. Or the sugar in soft drinks or the sugar in fresh fruit. Blood sugar is a simple molecule called glucose – a product of plants’ ability to convert the energy of the sun into starches, long chains of glucose linked together. When you eat a starch, the digestion process breaks down the chains into simple glucose molecules which circulate in your blood. Glucose is used by every cell in the body for energy, and is also made into glycogen for storage in liver and muscle.The sugar in your pantry is sucrose extracted from plants, specifically cane grasses and beets, by a refining process that concentrates and crystallizes it. Each sucrose molecule is a combination of one glucose molecule with another of fructose, a chemically different plant sugar molecule.

The taste for sweetness is innate and possibly addictive. Before the advent of refined sugar, indulging the sweet tooth was difficult. The only edible sources were berries and fruits and small amounts of honey guarded by nasty bees – all confined by climate and geography. Sugar made its way into the human diet slowly, spreading from the East to the West as the secret of this “liquid gold” made its way along routes of commerce.

Sugar and the diseases of civilization

With time and commerce, consumption of sugar and refined grains skyrocketed. The diseases of civilization – diabetes, heart disease and obesity – followed refined sugar, flour and rice around the world, appearing wherever old dietary staples were replaced by these “white” foods. By the 1920s, the Americans averaged 110-120 pounds of sugar per person per year. We inched up to 124 pounds by the late 1970s. Then came the Japanese chemical innovation that made high-fructose corn syrup (HFCS) a dietary staple. By 2000, HFCS bumped sugar consumption up to 150 lbs. per year, largely in the form of sweetened drinks.

High fructose corn syrup

HFCS differs from sucrose because the ratio of fructose to glucose in corn syrup is 10% higher than in table sugar – 55:45 instead of 50:50. Some scientists believe that it is the remarkable increase in fructose consumption in modern times that correlates with the appearance of the metabolic syndrome – abdominal obesity, high fasting blood sugar, high triglycerides, abnormal lipoprotein levels and high blood pressure. If so, a 10% increase in fructose combined with a recent, large jump in overall sugar consumption may spell real trouble.
How can fructose cause trouble? Isn’t it the primary sugar of fruits? Yes, but eating an apple with a small amount of fructose combined with absorption-slowing fiber hardly nudges blood sugar up – a far cry from the blood sugar spike after 20 ounces of an HFCS sweetened beverage. Drink a coke, and about 60% of the glucose in the HFCS goes directly into the blood for immediate use, and 40 % into the liver for storage as glycogen. The fructose all goes to the liver for conversion into fat – released into the blood as triglycerides. The higher the fructose in the diet, the higher the triglycerides in the blood. Fructose is a “lipogenic” or fat-producing sugar, and long term consumption also raises LDL or bad cholesterol.

The problems with too much sugar

Once sugar consumption exceeds the small amounts nature provides without refining techniques, trouble begins. The different ways the body processes fructose and glucose combine to produce very efficient fat production. A rise in blood glucose prompts the pancreas to put out insulin to help ferry glucose into cells for energy use or storage. Insulin, like fructose, is “lipogenic” because it helps move fats into storage depots in three areas – the liver, fat tissue, and the walls of arteries. And as triglycerides are formed from fructose, insulin busies itself shuttling them around the liver and out into the blood. The pancreas then produces even more insulin to take care of the glucose – this is the phenomenon known as insulin resistance, part of the metabolic syndrome associated with heart disease.

Is it the cholesterol or the sugar?

The theory that cholesterol in dietary fat is the direct cause of cholesterol deposits in arteries requires a leap over the metabolic pathways that process simple sugars and are intimately involved in fat formation and storage – and over the fact that many people with low cholesterol levels have heart disease. Over the last half century, many researchers and doctors made the leap because they believed the theory. Just as important to widespread acceptance, though, were less scientific influences like the cheap availability of a test for blood cholesterol, the difficulty and expense of measuring insulin, and the dominance of researchers devoted to the dietary cholesterol theory over those who questioned it.

Medical history books contain an embarrassing array of once-unassailable theories and practices that have fallen by the wayside. Despite a modern sense of scientific invincibility, current medical ideas are not immune from error. Sugar and refined carbohydrates are not yet the poster children for the scourge of heart disease, but they may be a far better target than cholesterol. If the dietary fat theory gives way to the sugar theory, the massive push to lower cholesterol by diet and drugs may go into the books as one of those once-unassailable ideas that eventually fell.

Posted by medical plaintalk

Physician turned medical writer.

Thyroid Failure:Hashimoto’s Disease

When I was a resident in medical training a woman arrived in the emergency room in a coma. She had been living alone and, according to neighbors, sitting in a chair in her apartment for weeks. Her clinical state was like one of hibernation, with very low pulse, blood pressure and temperature. Her hair was like thin and brittle, her skin scaly and dry, her face puffy and her legs thickened by a waxy swelling called myxedema. She was in the final stages of thyroid gland failure, myxedema coma. Early in the course of her illness, when symptoms were probably mild and ill-defined, no one had realized she was “hypothyroid.” Later, when thyroid hormone levels had fallen to dangerous lows, she was too slow mentally and physically to seek help. By the time she arrived in the ER she was on the brink of death from Hashimoto’s disease, an autoimmune inflammation of the thyroid gland, or thyroiditis. Hashimoto’s disease was the first recognized disease caused by the immune system attacking some part of the body, and is the most common cause of thyroid gland failure in the USA.

Hashimoto’s disease affects at least one in every 1000 people in the US, women more frequently than men. Though the thyroid disease was first described in 1912, and is now known to be caused by the production of antibodies against thyroid hormone producing enzymes and proteins, there is still no known way to prevent it. The only risk factor is a family history of a similar problem. Some environmental factors such as high iodine intake and viral infections may play a role in triggering the process in genetically susceptible individuals. In Hashimoto’s disease, the antibodies gradually destroy the gland’s hormone producing follicles. Most often, the thyroid gradually and irregularly enlarges as the follicles are replaced by inflammatory tissue. While the bumpy neck bulge created is similar to a goiter, the latter is smoother and more regular in shape and a sign of an overworking but non-inflamed thyroid gland which is getting insufficient dietary iodine.

In Hashimoto’s disease, subtle physical symptoms often precede the development of an enlarged thyroid gland. Since thyroid hormone facilitates all metabolism and energy production in every part of the body, inadequate amounts of the hormone cause a host of vague symptoms which are often excused as simply the byproduct of life style inadequacies such as too little sleep, poor diet, lack of exercise and stress. The symptoms include fatigue, weight gain, depression and anxiety, inability to stay warm, joint and muscle aches and pains, constipation, slow pulse, coarse and thinning hair, puffiness, irregular menstrual periods, and inability to conceive. In some people, gland enlargement never occurs. And though the underlying problem is inflammatory, the thyroid gland is not tender.

Because of the vague nature of the symptoms that bring a patient with Hashimoto’s thyroiditis to the doctor, because the thyroid gland may not be enlarged and because the screening blood test for total thyroid hormone level may fall within a normal range, many other diagnoses are often entertained before the correct one is made. These include depression, anxiety, chronic fatigue syndrome and subclinical infection. In addition, because hypothyroidism drives cholesterol and weight up, attention gets diverted to heart disease and other components of the metabolic syndrome.

But once suspicion of Hashimoto’s has been raised, the problem is easily identified by blood tests for antibodies to an enzyme called thyroid peroxidase and to a thyroid hormone binding protein called thyroglobulin and a test for a pituitary gland hormone called TSH, or thyroid stimulating hormone. TSH rises as thyroid function fails and the pituitary gland attempts to stimulate it to keep producing thyroid hormone.

Some patients need thyroid scans and biopsies of any suspicious gland areas to rule out the very rare possibility that a lump in the gland is cancerous. A general medical evaluation is also helpful since low thyroid hormone can accelerate cardiovascular disease and since the autoimmune dysfunction underlying Hashimoto sometimes occurs in association with other autoimmune disorders such as celiac disease, Type 1 diabetes, adrenal gland insufficiency, autoimmune gastritis with Vitamin B12 deficiency, rheumatoid arthritis, lupus, and some clotting disorders that may cause either bruising or clot formation in blood vessels.

If other autoimmune problems are not found, the therapy for Hashimoto’s thyroiditis is as easy as taking one pill a day, usually a synthetic thyroid hormone called levothyroxine. Prior to the development of synthetic thyroid hormone, a desiccated powder made from pig thyroid glands was the only treatment available and it is still preferred by a significant number of patients. A controlled study done in 2013 to determine whether there was any scientific evidence for treatment preference showed that both synthetic thyroid hormone and desiccated thyroid hormone are equally effective in raising thyroid hormone levels and returning TSH levels to normal, but that desiccated thyroid hormone resulted in slightly greater weight loss.

Our myxedema coma patient survived, though her management was difficult because of the severity of her hypothyroidism. Under the autoimmune attack of Hashimoto’s thyroiditis, the thyroid gland is a victim of a very slow war of attrition as more and more of its structure is replaced by inflammatory cells and scar tissue. The fall-off in hormone production is slow, and the body adapts to lower and lower levels of thyroid hormone until all systems finally begin shutting down. At that point, re-introducing high levels of thyroid hormone can be dangerous to heart function. The correction must occur gradually, as the decline did, underscoring the importance of detecting thyroid gland failure early, before it takes such a metabolic toll. Even when discovered early, the establishment of appropriate hormone dose and the reversal of symptoms may take some time and patience. The hormone must be taken for the rest of a long and otherwise normal life.

Posted by medical plaintalk

Physician turned medical writer.

Iodine: An Unfinished Story

In these days of high tech medicine it is easy to forget that some of the most effective and efficient health interventions are simple and cheap. One example is the addition of iodine to salt, an idea which began in the early 1900s with experimental trials in schoolchildren living in what was then known as the “goiter belt” of the USA. In that region surrounding the Great Lakes, many children developed enlarged thyroid glands called goiters. A goiter is a sign of iodine deficiency. So successful were the trials of iodine-supplemented diets that, by the 1930s, 90% of residents of the Great Lakes region used iodized salt and goiter rates in the region had plummeted. Now, 70% of the world’s population uses iodized salt.

Iodine as an essential element

When iodine is in short supply, thyroid glands grow large in an attempt to harvest as much of the vital element as possible from the blood. Iodine is necessary for making thyroid hormone and thyroid hormone is crucial for normal development and metabolism. Pregnant women who have low iodine levels and insufficient thyroid hormone often miscarry their babies or produce babies who are deaf, mentally-retarded and stunted in growth. In children and adults, iodine and thyroid hormone deficiencies cause fatigue, weight gain, lowered IQ levels, mental apathy and numerous metabolic abnormalities. Regular intake of iodine is a simple preventive measure for a host of serious problems.

Unequal distribution

Iodine exists in an inorganic form in soil and water and makes its way into the plants and animals that we consume by combining with larger carbon-containing molecules. In its inorganic form, iodine is a water-soluble salt which washes out of soil easily, especially in areas where the land is rocky and exposed. Where soil is iodine deficient, so are crops, unless supplemented with iodine containing fertilizers. In contrast to its variable presence in soil, iodine is much more uniformly distributed in salt water seas. Algae, kelp and other seawater plants, as well as saltwater fish and shell fish are the most reliable natural sources of dietary iodine, while iodine concentrations in land based plants depend on the amount of iodine in soil that supports them. Terrestrial animals supply iodine proportional to the iodine in their food sources. Egg yolks are a good iodine source, because, like people, chickens develop goiters, and chicken feed is supplemented with iodine. Dairy products are also good sources. Cattle feed was originally supplemented with iodine to prevent hoof rot, and and because of the supplemented feed, iodine is secreted in the milk the cows produce.

Iodine and breast tissue

Milk contains iodine because mammary gland tissue, like thyroid gland tissue, accumulates iodine. The fact that iodine is found in human breast tissue, where it has no known function, has prompted studies of the element’s relationship to breast health. Japanese women have low rates of breast cancer and fibrocystic breast disease compared to American women, and their regular iodine consumption via seaweed is high, perhaps 25x higher than the recommended daily iodine consumption in the US. Studies on the treatment of fibrocystic breast disease with iodine supplements have been promising but so far a direct relationship between breast disease and iodine consumption has not been proven.

Iodine supplementation?

Even if high dietary iodine content has something to do with low breast cancer rates among Japanese women, translating this information to attempts to prevent breast cancer is not a straightforward task. While it is clear that iodine supplementation prevents goiter, hypothyroidism and cognitive impairment, it is also clear that increasing iodine intake is not risk free, particularly in people who are accustomed to low levels of dietary iodine. The thyroid gland, when faced with insufficient iodine in the blood, becomes a ruthless scavenger, extracting every last iodine molecule it can find. When iodine levels in the blood suddenly increase because of supplementary iodine intake, some thyroid glands will actually grow in size, pump out excessive thyroid hormone and even develop cancerous nodules. It may be that Japanese women can tolerate high amounts of iodine because it has never been in short supply for them. Caution and careful follow-up are always advisable when supplementing the diet with iodine in the form of tablets, drops or multivitamins.

Dietary iodine in the age of dietary angst

Obtaining enough iodine through the diet should be possible in almost all circumstances, especially because of the wisdom of public health policies regarding iodine. Nevertheless, some eating trends in health in the closing decades of the 20^thC have again raised public health concerns about iodine intake. Assessments of body iodine content are made by measuring urinary iodine levels, since the body extracts as much iodine as it needs and excretes the rest in urine. But individual measurements are so variable that averages of all people tested are used to estimate the iodine status in a given geographic area. Between 1971 and 2001, American iodine intake dropped dramatically then leveled off at half of the 1971 levels.

What happened over the last few decades? Americans began getting much more of their salt in the form of the un-iodized salt in processed foods. Many people began avoiding salt altogether, some quite unnecessarily. Sea salt appeared on the grocery store shelves as part of the natural and organic food trends. It is also possible that the 1971 levels of iodine consumption were artificially high. Studies in the 1970s showed that iodine-containing sanitizers were raising iodine levels in cows’ milk. Practices changed and milk iodine levels returned to normal. Between the 1960s and 1980s, iodine was used in dough making and bread supplied 25% of the iodine consumed during that period.* Perhaps the baseline measurements of iodine intake in the early 1970s were unnecessarily high. Perhaps intakes in 2001 and since are adequate, at least to prevent goiters from developing. But the fact that Japanese people ingest far higher levels of iodine from whole food sources without ill effect suggests that we can tolerate more. Stay tuned.

*Note: Iodine in the Nuclear Age

In the wake of the atmospheric nuclear testing period, the government mandated the use of iodine containing oxidizing agents for dough conditioning in commercial baking. The iodine in the bread competed in the diet for uptake into the thyroid gland with radioactive iodine isotopes generated in the wake of atmospheric nuclear testing. Saturating the thyroid gland with normal iodine is standard practice when radioactive iodine in the atmosphere is a threat, as it was after the Chernobyl disaster. Taken within 8 hours after, or 48 hours prior to a nuclear disaster, iodine can prevent accumulation of radioactive iodine in the thyroid gland and thus prevent radiation damage to the gland. Pills to be taken in the event of a nuclear catastrophe are simply potassium iodide.

Posted by medical plaintalk

Physician turned medical writer.

Thyroid Ups and Downs

Early in her husband’s presidency, first lady Barbara Bush began to lose weight. Her eyes became, in her own words “horrible and puffy” looking.” She had developed an autoimmune thyroid gland problem called Graves’ Disease. A few months later, the Bush‘s dog Millie came down with another autoimmune disease – lupus. The next spring, the president became ill with weight loss and a rapid, irregular heartbeat. Like Barbara he had Graves’ disease. Conspiracy theorists blamed Saddam Hussein for this outbreak of autoimmune disease in the White House, but thyroid experts saw nothing but coincidence. They admit, though, that they do not know what triggers antibody attacks against the thyroid gland, the most common cause of thyroid disease.

The many and varied symptoms of thyroid disease
Symptoms of thyroid disease most often involve effects of the hormones the gland makes. Thyroid hormone stokes the fire of metabolism, setting the rate of energy usage in every cell of the body and determining the basal metabolic rate (number of calories burned at complete rest).
Too much thyroid hormone causes hyperthyroidism; too little creates hypothyroidism. Extreme cases of either problem are easy to diagnose, but milder excess or deficiency states are much trickier and more common (an estimated 7-10% of adults have thyroid abnormalities). Hyperthyroid patients lose weight, become intolerant of warm environments and sweat profusely. Hair becomes thin and fine. The heart beats too fast and blood pressure rises, while muscles feel weak and hands shake. Sleep becomes elusive. On the hypothyroid end of the spectrum, lack of thyroid hormone banks the metabolic fires and drops the heat. Patients feel cold and become constipated. Incoming energy gets stored as fat; weight and cholesterol levels climb. Lethargy encroaches on daytime hours, and ambition and mental quickness decline. Both under and overactive glands can be enlarged and even visible as swellings just under the Adam’s apple.

Diagnosis
The confirmation of the thyroid gland’s role in symptoms comes from blood tests that measure thyroid hormone levels. Extreme cases are easy to diagnose. Milder cases, with less impressive symptoms and “borderline” blood tests are trickier. Mild symptoms overlap many of life’s normal patterns that are unrelated to thyroid hormone: weight, blood pressure and cholesterol tend to go up with age; sedentary people frequently feel cold and constipated; women at menopause would sometimes like to abolish indoor heating, and physical and mental energy are always subject to lifestyle, happiness, and drug effects. The opinion of an endocrinologist is particularly helpful in interpreting borderline thyroid symptoms and lab values.
Thyroxin or T4 (with four iodine molecules) comes from the thyroid gland. Tri-iodothyronine (T3) comes from T4 when one iodine molecule is split off. Thyroid stimulating hormone (TSH), made in the pituitary gland, is like a thermostat that regulates how much T4 the thyroid gland makes. When T4 is too high, TSH goes down. When T4 is too low, TSH goes up. So hypothyroid patients have high TSH and low T4, and hyperthyroid patients have low TSH and high T4.
Symptoms suggesting hyperthyroidism, combined with high-normal T4 and T3 and low- normal TSH prompt further tests to look directly at the thyroid gland. Thyroid scans employ radioactive iodine and distinguish between glands that overproduce in all areas, ones that have nodules of overproduction, and enlarged glands that no longer make any hormone. Measurement of three different types of anti-thyroid antibodies further narrows the diagnosis.

The problems with the tests
Not all labs use the same ranges of normal values. Some rely on broad TSH ranges found in a random selection of apparently healthy people (0.32 -5.0 µIU/ml). Other labs use a much narrower range (.34-2.5µIU/ml) found in people who have been screened to rule out thyroid disease. So if you see a doctor who uses the first range and your TSH is 4.5, you might be told just to watch your weight, get better sleep, take a little blood pressure medicine and be rechecked in 6 months or a year. A doctor using the second might would give you a prescription for thyroid hormone. Treatment of hypothyroidism in these gray areas might normalize the blood tests without producing any clinically identifiable benefits. Nevertheless, it is wise to follow up on iffy test results because, over time, thyroid conditions may declare themselves further.

Autoimmune thyroid disease
Graves Disease and Hashimoto’s thyroiditis, caused by different types of antibodies, are the most common causes of thyroid problems and tend to run in families. In Graves ’ disease, the antibodies may also attack eye muscles and make them swell, producing the characteristic bulging eyes that Barbara Bush complained about. Graves disease most often begins with a hyperthyroid state that requires treatment to suppress overproduction of thyroid hormone or to obliterate the gland by radiation, producing hypothyroidism that requires treatment; sometimes Graves’ improves on its own but then goes on to hypothyroidism. Hashimoto’s disease most commonly bypasses the clinical hyperthyroid phase altogether and is the most common cause of hypothyroidism.

Iodine deficiency
Lack of dietary iodine once caused many cases of hypothyroidism. The word cretin (slang for dunce, idiot) originated in a mountainous French region where iodine deficient soil and lack of iodine-rich seafood resulted in a high incidence of mental and physical retardation from hypothyroidism in babies. Thyroid hormone and the dietary iodine required to make it are critical for normal growth and development, especially of the brain. In modern societies babies are screened and treated for hypothyroidism, and iodized salt makes this essential element easily available so this once frequent deficiency is much less common.

Treatment
Oral, synthetic versions of T3 and T4, or “natural” versions made from batches of pig thyroid glands make failing thyroid glands easily treatable. Synthetic versions are easier to regulate than are the natural ones. Finding the proper dose to return the blood tests to the normal range is often much easier than finding the dose and timing of pills that improves symptoms. The latter process is an inexact science that sometimes results in too much hormone effect.
Overactive glands are treated with medicines that shut them down, sometimes with radioactive iodine that kills the glandular cells and sometimes with surgery to remove the entire gland. The latter two treatments always produce hypothyroidism which then requires treatment with replacement hormones.
One study on thyroid disease prevalence estimates that there are 13,000,000 Americans with undiagnosed thyroid problems. Thyroid tests are now part of routine blood work, more problems will be caught and treated earlier, and more will be learned about triggers for autoimmune thyroid problems – eventually putting at least one conspiracy theory to rest.

Notes on less Common Thyroid Conditions

Lumps in the thyroid: These are common and most are benign nodules or cysts; sometimes they produce thyroid hormone and cause hyperthyroidism.

Viral thyroiditis (also known as sub-acute thyroiditis): self-limited illness with several weeks of hyperthyroidism, followed by several weeks of hypothyroidism, and then recovery of normal function.

Thyroid cancer: Uncommon. Rarely produces thyroid hormone so usually the diagnosis results from evaluation of lump in the neck or hoarseness; results from radiation exposure – as once was the practice for treating acne.

Pituitary Gland Tumors: Pituitary failure to produce TSH causes hypothyroidism; very rarely the pituitary overproduces TSH and causes hyperthyroidism.

Dietary Hyperthyroidism: At least one outbreak of hyperthyroidism came from meat contaminated with animal thyroid glands. Another rare cause is sudden, excessive iodine supplementation in a patient with underlying thyroid disease .

Posted by medical plaintalk

Physician turned medical writer.

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