Cholesterol Phobia

Cholesterol research is difficult, esoteric and accessible in journals that seldom make it beyond their target audience – other people doing the same type of work. One theory about the relationship of cholesterol and heart disease has dominated medical practice for over half a century, but there has always been dissension in the ranks of scientists, some of whom labor away in obscurity, slowly building a case that may one day topple the current dogma. I have attempted to make this subject accessible to a non-medical audience because the current paradigms for thinking about heart disease and treating it affect everyone who sees a doctor, listens to the news or reads the popular press – even children, because they eat what their parents believe is healthy for them.
Cholesterol phobia: is the end in sight?

Cholesterol earned a villain’s reputation because it got caught at many criminal scenes where victims succumbed to heart attacks. It was found lurking in the walls of arteries too narrowed by “plaques” to allow blood passage. Even in young healthy men, cholesterol- laden “fatty streaks” were surprise findings at autopsy after accidental or war-related death. Experimentally, fat choked arteries were easy to produce in experimental animals by feeding them food pellets saturated with fat – even olive oil worked. The laboratory work bolstered attempts to show that different populations consuming different amounts of fat had different rates of heart disease. Though both the laboratory and epidemiology studies were fraught with contradictory results, and the dietary cholesterol theory of heart disease was initially rejected by the American Heart Association, the personalities and scientific politics involved eventually catapulted the theory into the lives of all Americans, over 20 million of whom are now on potent drugs to combat the evil substance.

The dietary theory of heart disease

After more than half a century of war on cholesterol, the dietary theory remains just that – a theory – no matter how many commercials remind you that you need to lower your cholesterol. You may be surprised to hear that cholesterol could be absolved of its villainous status, within your lifetime. But don’t expect your doctor to agree, at least not yet. The cholesterol theory has a grip on our culture that is almost religious. The current dogma, advertised everywhere, is simple: there is good cholesterol, labeled HDL, and bad cholesterol, labeled LDL and anyone who cares a whit about his health will do whatever it takes to get those numbers in line with the current recommendations of the American Heart Association –eat a low fat diet, exercise, and take the right drugs.

Inconvenient facts

Inconvenient facts have always dogged the theory. Cholesterol levels plummet in seizure patients treated with high fat, no carbohydrate diets. Heart attacks occur despite normal cholesterol levels. Low fat diets raise cholesterol levels -President Eisenhower was one of the most famous examples. And buried in the literature of the last half century are many clues pointing a blaming finger away from cholesterol and toward the complex lipoproteins that ferry it around the body. As more and more questions are raised about the efficacy and dangers of drugs that reduce cholesterol, more attention may turn to these lipoproteins. After all, like cholesterol, they have been part of the statistic most closely associated with heart disease – the LDL (low-density lipoprotein) cholesterol.

What are lipoproteins?

Total cholesterol measures cholesterol attached to lipoproteins. Lipoproteins are combinations of phospholipids (fats that dissolve in water) and specialized proteins that fit like keys into receptors on cells. Lipoproteins function like cargo ships, carrying fats to cells for fuel, to fat tissue for storage, and back to the liver for reprocessing when demanded. More or less cholesterol crowds aboard each boat depending on the number of boats available. The size of the fleet, in turn, depends on the amount of triglycerides (another type of fat), awaiting shipment – not on the amount of cholesterol.

Triglycerides rule

Triglycerides and cholesterol are very different fats. Triglycerides provide the fatty acids that fuel most cells and are stored in fat tissue for later energy demands. Cholesterol yields no energy at all. It is a building block, used in the construction of all cell membranes and in the making of hormones and bile. Not all cholesterol comes from fat in the diet. The brain makes its own, and the liver and skin make whatever the body needs – raising production whenever dietary intake is low. Cholesterol and triglycerides attached to lipoproteins are like citizens of two different countries travelling together on one of the country’s boats. That country that builds the boats belongs to the triglycerides. The more triglycerides present in the body, the more lipoproteins in the fleet.

The varying density of lipoproteins

Lipoproteins fully loaded with cholesterol and triglycerides are fluffy and buoyant (fat floats) and called very low density lipoproteins, VLDL for short. They dock at cells in need of fuel or cholesterol, unload some cargo, lose some buoyancy, and become a little denser. Eventually they become low-density lipoproteins (LDL) and , with no energy or building material left to give up, they return to the liver for recycling. Another particle type called high-density lipoprotein (HDL) is even less buoyant – and less well understood. In contrast to cholesterol bound to LDL and VLDL, the cholesterol carried by HDL particles, like the cholesterol carried away from the intestines by chylomicrons (very large lipoproteins) does not contribute to the storage of fat in any tissues so is not associated with plaque formation in arteries. Normal to high levels of HDL cholesterol are associated with lower risk of heart disease.

What do the anti-cholesterol drugs do?

The widely prescribed statin drugs block the body’s ability to make cholesterol, which makes less cholesterol available to be loaded on to the lipoprotein boats. But boat making proceeds apace because it is driven by the amount of triglyceride awaiting transport- and the triglycerides, remember, come from dietary carbohydrates. Lowering cholesterol manufacture does not lower lipoprotein production – the lipoprotein boats will simply carry less cholesterol per lipoprotein particle, making each particle smaller and denser. Will this magically keep cholesterol out of artery walls? Not a good bet. Lipoprotein research labs have identified seven different particle types within the LDL fraction of total cholesterol. Heart risk appears to be correlated with the smallest and densest sub-fraction – the kind carrying the least amount of fat per molecule. (The anti-cholesterol drugs do have an independent anti-inflammatory effect which may be the way they diminish risk of a cardiac event in people with heart disease.)

Take-away message

So how does this complicated information change your life? Triglycerides, the stimulus for VLDL and LDL production, are a product of carbohydrate processing – especially of sugars and refined grains. Lowering VLDL production and hence LDL production requires lowering dietary carbohydrates – not fat, not cholesterol. Blood cholesterol isn’t even a good marker for total body cholesterol, which includes cholesterol squirreled away in artery walls. Cholesterol in arteries behaves much like cholesterol stored in fat tissue. It is responsive to the entire array of interconnected feedback loops involving not only fats, but carbohydrates and insulin and all the other hormones. It is time to respect its complexity and quit expecting that coaxing the body to make less cholesterol by taking drugs to block its production, or by eliminating it from the diet will end the scourge of heart disease.

Posted by medical plaintalk

Physician turned medical writer.

A Case History *

Today, just for laughs in a world where medicine and a few other subjects make us worry unnecessarily, a case history.
Case history

13 month old, ambidextrous WM presents with chief complaint of “something wrong with legs,” noticed by his aunt. History obtained from caretakers, as the patient does not speak English.

HPI: Several weeks ago, the patient switched suddenly from four point locomotion on hands and knees to upright posture and ambulation on legs. His caretakers were pleased with this event and recorded his progress to share with interested parties. Upon viewing one recording in which the patient was hurrying to catch up with his mother, his aunt, who works in a health field, noted that “something is wrong with his legs.” There has been no sign that the patient is uncomfortable with his new choice. In fact he seems to revel in it and consistently pushes away the hands of those who attempt to support and assist him. He does not appear to be uncomfortable when he loses his balance and falls, which happens less and less frequently as he practices his new skill. Initially he reverted to 4 point locomotion when he seemed eager to reach his destination, as if valuing speed over the upright posture. Of course this is an inference, because, as noted previously, the patient does not speak English (aphasia might also be considered). Now, however he chooses to ambulate in the upright position most of the time. He has also demonstrated increasingly frequent and increasingly more skilled ability in squatting and rising, picking things up and carrying them – and other more subtle indications that he is multitasking with his motor system while engaging in his new form of locomotion. And he is able to rise from sitting to the upright posture without using his hands or shifting to his knees, a skill that eludes many people who have used the upright posture for many years – a skill that some believe correlates well with life expectancy.
ROS: Of note and possible relevance is the fact that he is incontinent and as a result wears a bulky diaper and rubber pants.
PE: 1. Examination of the video in question reveals a small male at some distance from the camera. As he comes into clearer view it is evident that he is walking unsupported in bare feet on uneven ground. He uses gross motor groups of the trunk and hip to move his weight from one foot to the other, leaning from one side to the other as he unweights the new balancing leg to move it into the new planting position, slightly in advance of the weighted leg. His base is broad and his toes point outward. The aforementioned diaper and rubber pants may slightly exaggerate these two features. He also moves rapidly and since his build includes relatively short legs and large head, he appears a bit ungainly and off balance, as though he might topple over (prompting the aforementioned but usually spurned offers of help). His timing appears somewhat irregular, and he plants his feet without any finesse, leaving the observer with an overall impression of unsteadiness (recall Lurch, of the Adams Family).

2. Physical examination several weeks later and in the patient’s usual environment was remarkable for its normality. Neurological evaluation revealed a similar gait pattern, but with an appreciably narrowed base, and less outward deviation of the feet in forward motion (see supplemental video). He does remain aphasic, but responds appropriately to non-verbal accompaniments of speech (at times this leads to the conclusion that he understands some words, but unless the response occurs in a vacuum of other elements of communication this is hard to evaluate precisely).

Impression: Reversible gait dysfunction indicative of incomplete development of the cortico-cerebello-pontine pathways
Treatment plan: 1. Encourage patient to get on with getting older

2. Practice, practice, practice

*This post is not based on an Elks Magazine column, but written in response to a request for advice

(Video removed for privacy. Available on request to friends and family)

Posted by medical plaintalk

Physician turned medical writer.

Partners: Fiber and Bile

Everyone knows you need fiber in your diet. Everyone knows fiber comes from plant foods. And everyone knows that fiber helps move food through the system – just like a lot fiber in grass and hay help move a horse’s food through its unusually long and tortuous bowel. Fiber in the human diet helps package waste in softer, bulkier bowel movements, and a high fiber diet reduces constipation, which in turn reduces the risk of hemorrhoids, diverticulitis and even colon cancer.

More than a laxative

What is not obvious is just how a diet high in fiber lowers cholesterol levels and improves the other cardiovascular risk factors associated with the metabolic syndrome (obesity, high blood pressure and diabetes). How can the indigestible component of food, which releases no energy and is not absorbed into the body, affect metabolism? And how does moving food through the body with greater ease and efficiency alter body chemistry? The answers are interesting and worth knowing, since they provide impetus for even the unconstipated to pay attention to fiber intake.

What is fiber?

By definition, fiber is the indigestible component of food. Both cooking and chewing break fiber-rich food down in size, but fiber is impervious to stomach acid and digestive enzymes. The stiff portions of the plants – the parts that that give them shape and cover– are carbohydrates called cellulose and lignins. Since this type of fiber doesn’t even dissolve in water, it is called “insoluble fiber.” Insoluble fiber is what most people think of when they read about the virtues of a high fiber diet. It is like the horse’s hay and grass.

The softer plant parts provide a different kind of fiber which does dissolve in water and is therefore “soluble.” Soluble fiber is made up of carbohydrates called pectins, mucilages and gums. Because it attracts water, soluble fiber helps ease the passage of food by making it softer and bulkier. So far, then, this kind of fiber seems like nothing more than a softer version of insoluble fiber. But along with water, soluble fiber attracts bile, making soluble fiber much more than a passive factor in the transit of food. The bile connection is the key component in the role of dietary fiber in cholesterol metabolism.

What is Bile?

Bile is a solution of chemical compounds called bile salts that act like detergents in breaking down fat and making it ready for absorption from the intestine. Using cholesterol as the main building block, the liver makes about 4 cups of bile a day, storing it in the gall bladder until food arrives in the stomach. The gall bladder then squirts bile into the small intestine. Without bile we could not absorb necessary fats and fat-soluble vitamins. The liver also uses bile as a shipment device for the fat soluble debris and toxins it filters from the bloodstream, especially the breakdown products of hemoglobin. Bile is the trash hauling contractor for the liver.

Elimination or recycling?

Bile breaks down once it has completed its digestive work. Its pieces get absorbed in the last part of the small intestine and carried back to the liver via the blood – or it escapes the body via the waste in the colon (bile imparts the color to bowel movements). Like the oil in your car, which accumulates dirt and get sluggish, bile that is re-circulated concentrates more and more fat-soluble waste. Escaping bile takes the waste along with it. And the less bile returned to the liver for recycling, the more cholesterol the liver has to use in the bile manufacturing process – making less cholesterol available for clogging up arteries.

In the small intestine, soluble fiber also sops up other carbohydrates, slowing their digestion and the absorption of sugar into the blood stream. This function appears to improve insulin sensitivity, making soluble fiber beneficial to people who have type 2 diabetes. Slowing carbohydrate absorption indirectly improves fat metabolism as well.

Soluble fiber and the colonic environment

Once soluble fiber reaches the colon, it begins another phase of its work. The colon, unlike the sterile small intestine, contains numerous bacteria. Bacteria need to eat, and they take whatever they can from the food passing through. Soluble fiber, for bacteria, is eminently digestible. They chew it up and produce short-chain fatty acids, creating an environment favorable for the absorption of minerals like calcium and iron. Some researchers think the acid environment helps slow cancer development.

Getting enough fiber

Is it hard to get enough fiber in your diet? Yes. Not because it is not available, but because we opt for easy food – easy to get, easy to prepare, and easy to eat. On average adult Americans get about half the 25-35 grams of fiber a day that they need, and children only about 20%. Constipation is a cardinal sign of a fiber poor diet. Bowel movements that are hard and dry, with frequency of less than once every three days, and the regular need to strain to evacuate the bowels are all signs of constipation. Constipation is also made worse by inactivity. Other results of a fiber deficient diet are less visible and occur over the long term: development of outpouchings of the colon wall called diverticuli, inflammatory changes in the colon lining, cancerous changes in colon cells, and the possible contributions to the metabolic syndrome and heart disease.

The best sources of insoluble fiber are the plant foods with tough structures: vegetables and whole grains. Soluble fiber comes in the form of oat bran, fruits, nuts, beans, and peas. The most useful fiber shopping rules are to stay as far as possible from manufactured foods and to choose liberally from the fresh produce section of the grocery store. Fiber supplements? Studies of their metabolic effects are contradictory, but supplements such as psyllium, guar gum and pectin appear to do no harm. If they produce satisfactory results in terms of easing bowel symptoms, they are probably helpful.

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.

Mind-Body Medicine

If the mind, that rules the body, ever so far forgets itself as to trample on its slave, the slave is never generous enough to forgive the injury, but will rise and smite the oppressor. Henry Wadsworth Longfellow

In the 1600s, philosopher René Descartes gave the world the concept of mind-body dualism. The body was composed of physical substance, visible, weighable and measurable. The mind was something else. Over the next three centuries, as scientists deconstructed the body to discover its secrets, the mind reclaimed its place as an inseparable part of the body. (Soul is another matter, not open to scientific inquiry.) Some rudimentary examples of the mind-body connection are the blush of embarrassment, the adrenaline rush following a near miss accident or the receipt of bad news, and the cotton mouth that accompanies emotional distress. The mind perceives and the body reacts. The mind decides and the body acts. Not only are mind and body inseparable, but most often the body responds to a vast subconscious system rather than to the aware part of the mind known as consciousness.

The powerful subconscious mind

In Sigmund Freud’s (1856-1939) introductory rendering, the unconscious mind was a cauldron of seething resentments that gave rise to neurotic behaviors and bad dreams. Modern research softened this view and today the unconscious mind seems more like an executive secretary who relieves the boss of routine work. It sorts through incoming information, keeps track of the environment and runs the motor system that operates the body, all with such subtlety that much of the time you, the boss, think you are in charge. But if you have an electrode placed in your brain recording the action of the nerve cells that put your arm in motion, the recording will show activation of those cells before you are consciously aware of your decision to reach for that candy bar. Before you “know” it, the choice has been made in your subconscious mind. But this doesn’t mean we are automatons – after all, you can still decide not to eat the candy.

The neuropeptide network: connection of mind to body

The subconscious mind may have even more power than we suspect. The same chemicals that transmit information in the brain are found in virtually every organ of the body. This neuropeptide network, discovered around 1980, bridges the gap between the brain and the body, making a psycho(mind)somatic(body) connection. Since the time of Freud, the word psychosomatic has a bad reputation, often synonymous with “hysterical” or “without physical cause.” All symptoms, however, are technically psychosomatic because they arise in the body and are perceived in the mind. The discovery of the chemical interplay between brain and other body organs forces us to consider whether the flow of information goes the other way too. Can the mind cause diseases to happen? Can it help heal disease?

Placebo effect

Eastern medical practices have always regarded the body/mind as one entity. Since the 1950s, Western medicine has acknowledged the mind’s influence over the body by taking into account the placebo effect in studies of new treatments. The placebo effect is the relief that happens when a patient believes he has received a real treatment, despite the treatment being a sham. The phenomenon may reflect the power of belief or it may reflect the fact that many disease processes get better on their own – the only way to tell is to add a third, no-treatment group to each study. The fact that the placebo effect occurs in more than 30% of patients in many studies demonstrates the mind’s significant role in disease and health.

Conventional medicine takes a look at the alternatives

Western medicine’s gradual acceptance the mind/body connection culminated in the establishment of a National Center for Complementary and Alternative Medicine (NCCAM) within the National Institute of Health (http://nccam.nih.gov/) in 1991. The center conducts controlled studies on subjects such as the effect of regular meditation on chronic pain, anxiety, high blood pressure, cholesterol, health care use, substance abuse, post-traumatic stress syndrome in Vietnam veterans. It offers objective descriptions of Eastern medical theories which for which science has no proof. Part of the NCCAM’s mission is also to educate the public to become discerning customers within the vast alternative care and wellness industries that capitalize on the tantalizing possibility that good health may be a byproduct the “right” frame of mind.

The alternative and the conventional medical industries operate side-by-side, sometimes, but not always complementing each other. Conventional medicine is increasingly fragmented, with care delivered on an organ by organ basis. The whole person and his mind- body relationship can get lost in the process; unwanted side effects occur, and sometimes treatments hurt more than they help. But conventional methods save many lives and provide much needed comfort. Alternative practices that teach wellness via mind-body wholeness also do much good, mostly in preventing disease by emphasizing the back- to- basics factors: nutrition, sleep, exercise, relaxation, relationships and environment. Importantly, most of them do no harm except if they keep patients from seeking conventional help when necessary.

The importance of habits

In this century, the commercial spotlight is trained on the role of the mind in sickness and in health, which may obscure an important fact: most of the mind’s effects on health are subconscious, embedded in long years of mental and physical habits and not amenable to conscious adjustment over short periods of time. The right thinking and attitudes will help only insofar as they can work their way into the subconscious underpinnings of the mind by the diligent practice that leads to habit formation. Whether the mind-body practices are called meditation, yoga, Tai-chi, guided imagery, art and music therapy, biofeedback or acupuncture, they should be undertaken as long term projects requiring persistence, just like all those other low-tech habits that promote good health. The mind may be the body’s master, but it cannot change the laws of nature that govern all biologic systems. There are no quick and easy fixes.

Interesting Reading

Blink: The Power of Thinking Without Thinking, Malcolm Gladwell, Little Brown, Boston, 2005

Anatomy of an Illness as Perceived by the Patient, Norman Cousins and Rene Dubos, W.W. Norton & Co., NY, 1979.

Posted by medical plaintalk

Physician turned medical writer.

Gout and Girth: A Sweet Relationship?

At Hampton Court, one of King Henry VIII’s sixteenth century palaces outside London, tour guides regale visitors with tales of Henry’s obesity and the miseries he suffered during flare-ups of gout – exquisitely painful episodes of arthritis that come from the buildup of uric acid crystals in joints. Gout was known as “the king’s disease,” because it afflicted wealthy people who could afford the meats and sea foods that trigger uric acid crystal formation. The guides also point out the “confectionary,” a corner room near the kitchen wing, and describe the sugar-rotted royal teeth produced by the then scarce sweetener. The guides do not link Henry’s gout to the royal sweets, but perhaps they should. Sugar is composed of equal parts glucose and fructose, and scientists are now beginning to link increased fructose intake not only to obesity and type II diabetes, but also to increased uric acid in the blood – a risk factor for gout.

What is uric acid

Some uric acid in the blood is normal, because every cell in the body makes uric acid out of purines, chemical compounds that come from the regular breakdown of DNA and RNA as cells recycle themselves. Purines also come from many foods, but are particularly concentrated in red meat, organ meats like liver, many fish and shellfish, and yeasty beverages like beer and red wine. Uric acid in the blood is not bad – it serves as a powerful antioxidant. However, in some genetically susceptible people, uric acid levels become too high because they make too much, or because their kidneys don’t excrete enough into the urine.

When uric acid crystallizes

Abnormally high uric acid levels in the blood, a condition called hyperuricemia, can be present for 10-20 years without any symptoms. But just as minerals crystallize out of water in caves and form stalagmites and stalactites, uric acid can crystallize out of fluids in the body, forming microscopic deposits in tissues, especially kidneys, joints, tendon sheaths and skin. The painful part comes with the inflammation that ensues when the body attempts to eliminate the crystals. The classic case of gout, also known as podagra, begins suddenly with exquisitely painful, bright red swelling in the joint space between the foot and the big toe. Symptoms last from days to weeks.

The swelling comes from inflammatory fluid in the joint space. Diagnosis of gout depends on withdrawing some of this fluid through a needle and examining it under a microscope, where the uric acid crystals show up as pointy spicules which bend light waves in an identifiable way. Fluid withdrawal can also relieve some of the pain, but the mainstays of treatment during acute attacks are anti-inflammatory drugs such as Indocin, ice and or heat, and plenty of water. Prevention of attacks depends on efforts to lower uric acid levels, by diet, weight loss and use of medications that block uric acid production or increase its elimination in the urine.

Fructose is a building block for uric acid

For centuries, dietary advice about gout has revolved around foods high in protein. But as numbers of gout cases climbed steadily over the last forty years and average uric acid levels in people without gout also increased, a correlation with increased sugar consumption began to emerge. Scientists are now studying the relationship of sugar intake to uric acid and gout and also attempting to tie uric acid to hypertension, obesity and heart disease.

Sugar consumption was once rare to non-existent. Table sugar, a mixture of the two simple sugars sucrose and fructose, came only from sugar cane, which originally grew only tropical regions. Sugar’s spread around the world followed trade routes, and accelerated markedly after the discovery of the beet as a sugar source in the 18^th C. But the most dramatic rise in sugar consumption followed the invention of high fructose corn syrup (HFCS) in the 1970s. From work done so far, it appears that sugar’s fructose is a bigger culprit than its glucose in aggravating the metabolic syndrome (obesity, high blood pressure, heart disease and diabetes). And the metabolism of fructose actually produces uric acid.

When the glucose/fructose mix of sugar enters the body, glucose is transported directly into cells for use, but fructose requires processing. This requires energy, provided by ATP (adenosine triphosphate), and ATP breakdown produces uric acid. Eating fructose regularly also makes fructose easier to metabolize because it “induces,” or makes the body produce specific enzymes required to break it down. For someone prone to overproducing uric acid, or someone whose kidneys excrete it inefficiently, a diet chronically high in fructose may not only provide the building blocks for uric acid, but also speed its production.

Cutting fructose may help – and will do no harm

Cutting purine-rich foods down in a diet helps many susceptible people remain gout free. There is no data yet on the effectiveness of limiting fructose intake on gout or hyperuricemia, but such a diet can do no harm. Limiting fructose sources to whole fruits would dramatically lower total fructose intake for most people. Fructose is the major sugar in fruits, but it is combined with fiber and vital nutrients and present in much lesser quantities than in sugar-sweetened beverages, soft drinks, baked goods and many processed foods. Even ketchup contains HFCS.

When dietary modification is not enough to keep people gout free, drugs that block uric acid production or increase its elimination help. Ideally, uric acid levels should be in the range of 3-6 mg/dl. Diet is important not only for those who have suffered acute gout attacks, but also for those who have high uric acid levels without any symptoms. Hyperuricemia warrants a good look at the amount of dietary fructose.

Henry VIII’s confectionary was a clue to the relationship of girth to gout. As uric acid research progresses, blood tests for uric acid will probably become routine, because high levels often precede the development of high blood pressure and Type II diabetes, even in people not susceptible to gout.

Other Gout Facts

Many diuretics in common use raise uric acid levels and can trigger gout, especially the thiazide group.

Gout attacks commonly follow trauma or surgery because tissue breakdown produces purines.

Cancer treatments may also raise uric acid levels as tumor cells break down.

Uric acid levels increase in women after menopause and women rarely suffer from gout before then.

Uric acid levels in men rise at the time of puberty.

Posted by medical plaintalk

Physician turned medical writer.

Vitamins: Is Nature’s Magic Enough?

When I was a medical intern I watched my supervising resident perform an immediate and visible cure and in that moment understood the appeal of vitamins to our pill-loving culture. We were laboring over an old gentlemen brought to the emergency room from Boston’s Commons – a park that was home to many people whose diets came largely from brown-bagged liquor bottles. Our patient was agitated and confused. Try as we might we could not get his eyes to move in any direction. My resident disappeared and returned with a tiny syringe filled with a Vitamin B1, also known as thiamine. He injected the liquid into the patient’s vein and, as if he’d waved a wand, our patient’s eye movements returned and he calmed down. Here was a miracle drug, and it was something nature made for us.

Vitamin deficiency

The magic of our patient’s recovery was a clear example of the function of vitamins. In minute amounts, they act as facilitators of chemical reactions necessary for energy production and cellular maintenance of all kinds. Our patient had a textbook case of vitamin deficiency, the result of a very bad diet or failure to absorb vitamins from the stomach and small intestine, or both. Alcoholism is the most common setting, but vitamin deficiencies occur with other severe gastrointestinal problems and in the malnutrition associated famine or devastating illness like cancer and AIDS. Sometimes medical treatment itself is the perpetrator, in the form of anticancer drugs or bypass surgery for morbid obesity.

Vital nutrients

For thousands of years, people have understood that certain foods contain substances vital to human life. The ancient Egyptians recognized that night blindness was cured by eating liver. In the 1700s, seagoing men found that lime juice prevented scurvy – the aches, skin rashes and loss of teeth from painful gum disease that occurred when men attempted to live for months without fresh food. When the nature of food’s magic yielded to chemical analysis, scientists found complex molecules with many active forms that acted as co-factors or triggers in energy-producing chemical reactions in all cells of the body. They were also involved in cell maintenance and reproduction.

Naming the magic

Chemists named the indispensible compounds vitamins (vita: root word for life; amine: a chemical group containing nitrogen, which early studies suggested all vitamins contained) and tagged them with letters as well as chemical names (see list below). Vitamins F – K eventually became part of the large Vitamin B complex group, and some vitamins were downgraded to “vital nutrients.” Synthetic vitamins appeared on store shelves, joining age-old remedies like cod liver oil, yeast and wheat germ. But even in our times, the best source of vitamins remains the whole foods in which nature embeds them with other factors that we may not yet recognize as important.

Water soluble vitamins

The B vitamins and Vitamin C dissolve in water. They aren’t stored in the body and can be lost or inactivated by cooking. These water-soluble vitamins find their way to their target cells, get used, recycled a bit, and then find their way out of the body in the urine. They need to be eaten on a daily basis. You cannot overdose on B vitamins in food, but very high doses of B vitamin pills can damage the nerves.

Fat soluble vitamins

Fat-soluble vitamins (A, D, E and K) accumulate in liver and fat tissue, ready to be used when necessary, but damaging if too much is stored. Some Arctic explorers died of brain swelling from consuming polar bear liver, very high in Vitamin A. Too many carrots (source of carotenes, or pre-Vitamin A) cause yellow skin. Too much Vitamin D raises blood calcium levels, producing weakness, lethargy and kidney stones. Vitamin K can interfere with Coumadin, a medicine used to prevent blood clotting, so patients are cautioned to eat only small amounts of very flavorful greens like Kale and collards.

If you are not alcoholic or malnourished from serious illness, if you live in a western countries where vitamin fortification (enrichment) of common foods is the routine, if you eat well-balanced meals drawing fresh food from plant and animal sources, if you are meeting your energy needs and not trying to lose weight by restricting calories, and if you get enough sun exposure, you do not need any vitamin pills. Vitamins are best absorbed from real food.

Vitamin supplements?

In our current eating culture, however, a couple of vitamins do warrant concern. Folate (Vitamin B9) consumption, vital to cell replacement, is inadequate when fruits and vegetables are not chosen or hard to come by. Vitamin D deficiency, which became rare when fortification of milk began, is again on the rise, producing rickets (malformed bones) in children, weakened bones in adults, and weakened immune systems in all age groups. Cholesterol phobia makes people avoid good Vitamin D sources like whole milk and egg yolks. Sun exposure of head and arms for just 15 minutes 2 or 3 times a week makes enough Vitamin D in skin to our needs, but effective sunscreens and lack of outdoor activity have put serious dents in sun exposure.

What about Vitamin C, the wonder vitamin? Most plants and animals make it. We do not. Linus Pauling, Nobel prize-winning chemist, speculated that our intake should be much higher than the small amount required to prevent scurvy. Apes, who’ve also lost the ability to make Vitamin C, consume 10 -20 times as much as we do. Goats, who make Vitamin C in huge quantities, make even more when stressed. Does Vitamin C help prevent colds, strengthen our connective tissue, and get used up faster in times of physical stress? Maybe. We just don’t know. But in the meantime, large doses, up to several thousand milligrams per day, appear to do no harm. (Smokers do need extra C.)

Take advice with a grain of salt

What are we to think of all the articles we see extolling the virtues of this vitamin or that in preventing this disease or that? Be wary of these words: suggests, indicates, may be, could prevent. If any of the putative effects were as clear as our emergency room patient’s revival, or the salvaging of sailors’ gums and teeth, or the cure of the Egyptians’ night vision, we would not be using tentative words. Keep your focus on a fresh food diet that excludes no food group, and on the physical activity that enables you to eat enough food to get everything you need without getting fat. Take Vitamin C if you want to, and add a multivitamin from a reputable company if you are dieting or restricting your diet in any way, or don’t like vegetables and fruit.

Major Vitamins and Some Food Sources

Vitamin name	Chemical name	(RDA) Recommended daily allowance (male, age 19–70)	Animal Source	Plant Source
Vitamin A	(retinol, retinoids and carotenoids)	900 µg (micrograms)	Beef and chicken liver* Whole milk, eggs, cheese	Carrots, spinach, yellow vegetables and fruits
Vitamin B1	Thiamine	1.2 mg (milligrams)	Pork*, lean meats, fish	Brewer’s yeast, wheat germ, whole grains Enriched grains, legumes, nuts
Vitamin B	Riboflavin	1.3 mg	Eggs, lean meats, milk	Brewer’s yeast*, cereals, nuts, leafy greens
Vitamin B₃	Niacin	16.0 mg	Lean meats, poultry, fish, eggs	Beets, Brewer’s yeast*, peanuts, other nuts, sunflower seeds, green leafy vegetables, coffee, tea
Vitamin B₅	Pantothenic acid	5.0 mg	Calf’s liver*, eggs, yogurt	Brewer’s yeast*, whole grains,sunflower seeds, mushrooms, squash, cauliflower, broccoli
Vitamin B₆	Pyridoxine	1.3-1.7 mg	Liver, egg yolks, poultry, fish	Wheat germ, whole grains, peanuts, walnuts, bananas, avocados
Vitamin B₇	Biotin	30.0 µg	Eggs yolk, liver	Brewer’s yeast, wheat bran cauliflower, avocado
Vitamin B₉	Folic acid	400 µg	Beef liver*, egg yolk	Fortified cereals*, leafy green vegetables, citrus fruits
Vitamin B12	Cyanocobalamin	2.4 µg	Meat, eggs, dairy products, shellfish, salmon	Fortified plant milks and cereals only. No natural plant sources.
Vitamin C	Ascorbic acid	90.0 mg		Citrus fruits*, tomatoes, berries, green and red peppers, broccoli, spinach
Vitamin D	Ergocalciferol and Cholecalciferol	5.0 µg-10 µg	Dairy products, salmon, tuna	Fortified cereals
Vitamin E	Tocopherol and Tocotrienol	15.0 mg		Wheat germ oil, almonds, hazelnuts,sunflower seeds and oil, safflower oil
Vitamin K	Naphthquinone	120 µg		Broccoli, Kale, Swiss chard, soybean oil, canola oil, olive oil

*excellent source

Posted by medical plaintalk

Physician turned medical writer.

Alzheimer’s Disease: A Power Failure?

Like Willy Sutton, the bank robber famed for his explanation of why he robbed banks (because that’s where the money is), Alzheimer’s disease researchers have aimed most of their efforts at the well-known, visible pathology of the disease, the collections of debris scattered among the dying cells in the brains of patients suffering from the dementing illness. Made of a protein known called beta-amyloid, these plaques are the cause of the progressive death of brain cells and consequent loss of mental function – or so it has been thought. Research focus on amyloid plaques has been disappointing, though, yielding neither effective treatments nor preventive strategies. Moreover, the dramatic rise in the incidence of Alzheimer’s disease (AD), from 2% of people over age 85 in 1960 to 50% in 2000 indicates that something else is in play, something other than bad genetic luck that supposedly causes beta-amyloid to accumulate and nerve cells to die.

Energy production in the brain

As attention has turned to other potential causes of AD, older research findings seemingly unrelated to AD have assumed new importance, particularly discoveries related to brain energy metabolism. The preferred fuel for the brain is glucose. Until the 1980s, researchers thought that the brain, unlike other organs, did not need use the hormone insulin to allow glucose to enter its cells. But in the 1970s insulin receptors were discovered in brain cells and insulin was found in the spinal fluid, implying that the brain did indeed use the hormone. Because progressive resistance to insulin and difficulty getting glucose into cells to provide energy are the hallmarks of type 2 diabetes, and because the rise in AD incidence paralleled rising rates of type 2 diabetes in the last few decades, researchers began to wonder if AD might be rooted in insulin resistance and impaired energy production in brain cells. Insulin resistance in the brain might also explain the results of glucose metabolism studies in the brains of people at high genetic risk for AD, showing as much as 25% decrease in the use of glucose in areas concerned with memory and learning – long before any symptoms suggestive of AD have appeared.

Insulin resistance

By 2005, the idea that insulin resistance in the brain plays a significant role in the development of AD gained traction. Since not all type 2 diabetics get AD and not all AD patients have type 2 diabetes, insulin resistance cannot be the sole cause of AD. But a high blood insulin level is one of the two biggest risk factors for the disease. The other is a genetic factor – the gene for the E4 version of a protein called apolipoprotein B (apoB). Like insulin, apoB’s function is moving the building blocks for energy production into place in the various cells of the body. ApoB is like a delivery vehicle, packed with fats and cholesterol which are necessary for building the cellular machinery in the brain and providing fatty fuel for use when glucose is unavailable.

The tie between glucose, insulin and amyloid

Does impairment of glucose metabolism in the brain have any relationship to the classic pathological components of the disease – the amyloid plaques littering the brain, the destruction of nerve cell architecture, and the non-specific inflammatory changes? There are tantalizing clues. In the brain amyloid protein is a normal waste product. What is not normal is its accumulation in clumps around nerve cells. Beta-amyloid is usually broken down by an enzyme called IDE, insulin destroying enzyme. IDE breaks down insulin much more readily than it does amyloid proteins and when insulin is present in high amounts, the amyloid waits longer to be cleaned up and precipitates out of solution, forming clumps. Uncleared amyloid also prevents insulin from attaching to nerve cells to let more glucose in, depriving them of fuel.

Competition for IDE may not explain beta-amyloid accumulation completely, but it is a link between insulin, glucose metabolism and AD. In addition, high levels of glucose in all parts of the body prompt the development of abnormal collections of proteins/glucose combinations called advanced glycation products which trigger inflammatory damage to tissues in all organs. The brain is no exception.

A link between poor sleep and AD?

Sleep is another subject beginning to gain attention in the prevention and treatment of AD. Lack of good sleep contributes to the development of the metabolic syndrome, including type 2 diabetes, though disruption of normal hormonal rhythms. In normal people and in people with sleep apnea, sleep deprivation produces measurable impairments in working memory, thinking speed, attention, vigilance, and higher cognitive functions – the same functions affected by dementing illnesses such as AD.

Reasons for optimism

Do changing theories about AD have any practical consequences? Indeed. First, there is more reason for optimism about the future. If AD rates have risen because of changing dietary habits and lifestyles, we can change them again. The factors known to produce the metabolic syndrome are weight gain, lack of exercise and poor diet. Regular exercise is recognized as a deterrent to the development of AD. Some people are beginning to feel that the low fat dietary recommendations must also be changed since they have resulted in diets high in processed foods and carbohydrates, and low in foods with high amounts of antioxidants which counter inflammation. Fat metabolism, abnormal in the metabolic syndrome, is also important in the brain, which contains 25% of the body’s cholesterol. It needs sufficient healthy fats in the diet for normal function.

The second practical implication of the changing view of AD is the application of known drug treatments for type 2 diabetes, both for attempted prevention and for treatment of AD. Clinical studies in AD patients are already under way, using medications that improve insulin resistance. Intranasal insulin has also been tried. It is delivered directly into the brain, without fear of lowering body glucose levels and has shown some promise in improving AD symptoms. These approaches are entirely new and evidence of shifting focus in research. If Willy Sutton were an AD researcher he would be changing his targets.

Terminal Lucidity and Lucid Intervals

Caregivers of Alzheimer’s patients have long reported episodes of the patient returning briefly to “themselves,” for periods of hours to days. Some dramatic cases of such returns have been reported in the terminal phases of life. All of these cases have fallen into the “we don’t know why that happens” category of clinical observations. The concept of brain cells failing to function because of lack of energy is one that fits the appearance of lucid intervals better than a theory of the disease that implicates cellular destruction alone as the underlying cause of symptoms.

Arch Gerontol Geriatr. 2012 Jul-Aug;55(1):138-42. doi: 10.1016/j.archger.2011.06.031. Epub 2011 Jul 20. Terminal lucidity: a review and a case collection.

Nahm M¹, Greyson B, Kelly EW, Haraldsson E.

Posted by medical plaintalk

Physician turned medical writer.

Concussion: Temporary Power Outage

One of the most dramatic conditions in medicine is the concussion – the total and immediate paralysis of brain function that follows a blow to the head. Typically, the victim loses consciousness and all reflexive muscle activity for seconds to moments. Blood pressure and heart rate may fall and breathing might stop, effects that are usually brief and unnoticed but which on rare occasion cause immediate death. As consciousness returns, the victim seems confused. He does not recall the fall or the blow. Depending on the seriousness of the injury, he suffers a variable period of time during which he remembers nothing new. He asks repetitive questions about what happened and may seem aggressive or out of character. Normality may reassert itself quickly after a concussion, but sometimes several weeks or months of irritability, insomnia, mood change, headaches, and dizziness follow. In other cases, a period of normality, the lucid interval, may be followed by headache, confusion and drowsiness, indicating more severe trauma to the brain and its surrounding tissues.

Concussion of some degree occurs in almost all “closed head injuries,” defined those in which there are no skull fractures or penetrating injuries to the brain. Depending on the trauma involved, symptoms vary from momentary stunning to prolonged coma, but the mechanism of initial paralysis of brain function is always the same. Understanding that mechanism makes it easier to understand delayed worsening and persistent symptoms that sometimes occur afterwards.

How concussions happen

Concussions happen because the brain has the consistency of Jello and is only loosely tethered inside the rigid skull, mainly at the base. When the head accelerates after a blow, or decelerates because of a fall, the brain keeps moving after the skull has stopped. First the cerebral hemispheres slam into the skull in one direction, and then they rebound in the opposite direction. The temporal lobes, where memories form, are particularly vulnerable to impact damage.

Loss of consciousness, however, comes from movement of the tiny brain stem, which emerges from beneath the two large cerebral hemispheres and connects them with the spinal cord. As the heavy cerebral hemispheres above move, the brainstem bends, rotating first in one direction and then in the other. Inside the midbrain, the top part of the brainstem, a group of cells called the reticular activating system reacts with shock and shuts down all communication between brain and body. The power failure lasts anywhere from seconds to weeks, depending on the degree of rotational force in the midbrain and the amount of stretching and shearing of nerve cell connections.

Added Problems

Prolonged symptoms, however , usually indicate more widespread damage to the brain in the form of contusions (bruises) and hemorrhages, which cause delayed swelling and worse symptoms. In addition, bleeding from small veins on the surface of the brain (subdural hemorrhage) or between the skull and the dura mater, the tough fibrous lining around the brain (epidural hemorrhage) can occur after seemingly minor concussions. The bleeding stretches, then ruptures more blood vessels, and the growing accumulation of blood puts increasing pressure on the brain. In 2009, the actress Natasha Richardson died from this kind of complication, soon after a relatively minor fall while skiing. Ronald Reagan suffered much slower development of a subdural accumulation of blood following a fall from a horse. Surgical evacuation of the accumulated blood returned him to normal.

After The Concussion

After a head injury, it is very important for the victim to be accompanied by someone who knows him, in order to alert medical personnel to subtle changes in personality or cognitive ability. Most people suffering loss of consciousness will undergo CT or MRI scans, though this is probably unnecessary in mild cases in which the victim has returned to normality quickly. But even after a normal scan, observation, including waking and checking the victim every few hours at night for the first 24 hours, is prudent. If confusion persists after a concussion, the victim should be hospitalized until it clears, and observed carefully after discharge for 24-48 hours.

Most post concussive symptoms like headache, insomnia, irritability and lightheadedness resolve over a few months, requiring only simple medications like ibuprofen and sensible habits such as avoiding alcohol, eating well, sleeping enough, exercising and managing stress.

Repetitive concussions over a lifetime, as suffered in a sport like boxing, clearly damage the brain, producing decline in memory and cognitive abilities, as well as slurred speech and motor symptoms resembling Parkinson’s disease. Recent research suggests that brain injuries may induce progressive change some brain proteins, producing, over a long period, an Alzheimer’s like deterioration in function. The recent attention to the long term effects of other sports related head injuries, especially in professional athletes, stems from this research.

Do Helmets Help

Do helmets protect people from concussions? Helmets do reduce brain damage from trauma in sports like biking and rock climing, but they do it by protecting the skull from fracturing. To dampen the movement of the brain within the skull – the mechanism of injury in concussion- the diameter of the helmet would have to be so large that it would be impossible to wear. I have heard many people express surprise about concussions they experienced while wearing helmets in sports like skiing. But if you understand that the skull stops moving in a fall before the brain inside does, you understand that, no, a helmet does not stop a concussion from happening.

Posted by medical plaintalk

Physician turned medical writer.

No more posts.

Posted by medical plaintalk

Posted by medical plaintalk

Posted by medical plaintalk

Posted by medical plaintalk

Posted by medical plaintalk

Posted by medical plaintalk

Posted by medical plaintalk

Chemical name

(RDA) Recommended daily allowance (male, age 19–70)

Animal Source

Plant Source

Posted by medical plaintalk

Posted by medical plaintalk

Posted by medical plaintalk

(RDA) Recommended daily allowance
(male, age 19–70)