Ketosis v.s. Ketoacidosis: Insulin makes the Difference

Ketosis is a word which you may have seen recently in print and online media, usually in material about a very low carbohydrate diet in which most calories come from fat and protein. One recent headline alluded to a plan by the Pentagon to increase military fitness by imposing the “keto diet” on some of its soldiers. But you might also have the impression that there is some controversy around the diet, and that ketosis, whatever it is, might not be good for you. After all, it is very similar to that word ketoacidosis which is associated with poorly controlled diabetes, the problem that put your friend’s daughter in the hospital ICU for a week. In fact, both ketosis and ketoacidosis refer to physiologic body states that occur when come chemicals called ketones are produced from normal metabolic processes that produce energy from the body’s own fat. The circumstances surrounding ketone production determine whether ketones cause ketoacidosis (bad) or ketosis (not so bad but maybe not so good over a long period of time).

How your body produces energy

Most of the time you are utilizing at least some fat to create energy and producing ketones in small amounts as the fats are metabolized. At the same time, the bulk of your energy is derived from the carbohydrates you eat, all of which, even the “healthy” grains, vegetables and fruits, become a simple sugar called glucose in the process of digestion. That is correct – for the most part, you burn sugar to produce energy. Under normal circumstances, with sufficient food and regular eating schedules, some glucose is burned immediately by all parts of the body for energy production. Any remaining glucose gets shuttled off to the liver and muscles to be clumped into long chains called glycogen and stored for use between meals. These reserves last for about 24 hours at which point your metabolism switches over to fat burning, and to breaking down a little protein, mainly from muscle, to supply the liver with building blocks for making more glucose.

The brain has special needs

At this point, you must eat again or rely on free fatty acids from the triglycerides stored in your body fat. The brain, however cannot burn free fatty acids. But it can burn some of the ketones, called ketone bodies, that come from the breakdown of triglycerides. By about three days of starvation, the brain is a ketone burning organ, supplemented by a little glucose constructed in the liver from amino acids given up by proteins.  The body is in a state of ketosis, with excess ketones exhaled, giving the breath a fruity odor, and released in the urine, turning a dipstick stick test positive.

Acidity makes the difference

Ketosis is not ketoacidosis. Ketoacidosis appears when the acidity rises in all the body’s tissues while it is in a state of ketosis. Acidity is measured as pH, and a fall in the body’s pH signals rising acidity. Outside a narrow range of pH, the body’s metabolic workings begin to fail.  Rising acidity produces symptoms like rapid breathing, nausea, vomiting, abdominal pain, low blood pressure, mental impairment, lethargy, heart arrhythmias and ultimately, if uncorrected, death. In otherwise healthy people, diets that promote ketosis by restricting carbohydrates do not appreciably change the body’s pH, despite the acid nature of ketones and other breakdown products of triglycerides. What keeps severe acidity and its dire consequences at bay?  In short, insulin, the central hormone of metabolism.

Insulin keeps the brakes on fat burning

Insulin is secreted by the pancreas in response to eating carbohydrates. In fact insulin is such a reponsive hormone that a burst appears from the pancreas in response to anything sweet in the mouth (the so called cephalic insulin response that prepares the gut to receive expected incoming carbohydrate, even when the sweetness is artificial and no carbs arrive in the stomach).  In addition to its role escorting glucose into cells for energy production, insulin keeps the brakes on fat burning. When insulin circulates at normal or high levels in response to carbohydrate ingestion, triglycerides remain locked in fat cells, unavailable for energy production. As night falls and eating ceases, the liver and muscles break down their glycogen to glucose to keep the supply up. When this supply dwindles, insulin levels fall, unleashing fat burning. Free fatty acids and ketones appear in the blood, but in a controlled manner, unless insulin disappears altogether. Then the brakes come off fat burning, fatty acids and ketones flood the system, and their acidity begins to drop the body’s pH.

Ketoacidosis comes from insulin’s diappearance in type 1 diabetes

Type 1 diabetics are the most at risk for ketoacidosis because immune attacks against the insulin producing cells in their pancreases severely diminish or obliterate insulin production. Their blood sugar levels  rise because sugar cannot get into cells. Fat burning comes to the rescue for energy production, and, with little or no interference from insulin, free fatty acids and ketones pour out into the blood. In new Type 1 diabetics, before treatment with insulin, major weight loss is very common – as is presentation to an emergency room in a state of profound ketoacidosis, requiring intensive medical care. Once patients are stabilized, urinary ketones are a useful guide for adjusting insulin dose– their appearance means more insulin is needed.

Type 2 diabetes is a different problem

Type 2 diabetics have a different problem, called insulin resistance. Their cells do not allow insulin to bring glucose in from the blood.  In an attempt to compensate, their pancreases make more insulin. Blood glucose levels rise, but at the same time high levels of insulin block fat breakdown, preventing the release of large amounts of potentially acidifying fuels, and diminishing the risk of ketoacidosis. But if a crisis such as trauma, infection, or surgery occurs, sugar levels can rise to extraordinary levels in Type 2 diabetics, causing huge amounts of water to be lost in urination as the body passes the sugar out through the kidneys. Severe dehydration and electrolyte abnormalities make this condition, called hyperosmolar hyperglycemia, a crisis requiring intensive care, even without acidosis. When insulin production begins to fail in Type 2 diabetics, ketoacidosis does occur and type 2 diabetics account for 20-30% of ketoacidosis cases in hospitals. One class of Type 2 diabetes drugs, the SGLT2 inhibitors known as gliflozins, has been reported to trigger ketoacidosis.

The caveat about ketosis as a dietary strategy

There is some concern, from epidemiological research, that when a very low carbohydrate diet is continued over the long term, chronic ketosis may trigger insulin resistance, the underlying problem in type 2 diabetes. Insulin resistance is not well understood, but it is associated with a cascade of health problems associated with metabolic problems.  If chronic ketosis does somehow trigger insulin resistance,  the enthusiasm for deliberately inducing ketosis to lose weight and improve fitness will wane. The word ketosis will fade back into the scientific world.

Fever: Resetting the Thermostat


Humanity has but three great enemies: fever, famine, and war; of these by far the greatest, by far the most terrible, is fever.
―William Osler, MD

    In Dr. William Osler’s world of the late 1800s, doctors had not yet seen antibiotics rescue people from death caused by infectious diseases. Osler, one of the founders of Johns Hopkins Hospital routinely saw children die from meningitis, scarlet fever and diphtheria. He watched adults die from wound infections and cholera and the threat of mortal infection loomed over every surgical procedure. Fever was an unwelcome herald of trouble that often ended in death.

However, since antiquity fever was also thought to be therapeutic for some ailments of the brain, including melancholy and seizures. In the 1920s, a German psychiatrist, Julius Wagner-Jauregg, attempted to use the recurring high fevers of malarial infection to treat syphilis, then an incurable disease that eventually robbed patients of their minds and motor coordination.  Wagner-Jauregg was a eugenicist and later a Nazi sympathizer, and gave his patients malaria without their consent, but the fact that six of his nine patients recovered earned him the Nobel prize in medicine in 1927. He remains the only psychiatrist ever to be so honored in that discipline. Fever asylums popped up in many locations on both sides of the Atlantic in the 1930s, but were relegated to history by the discovery of antibiotics in the next decade.

How does the body temperature rise?

Fever begins when a “pyrogen” – some kind of viral or bacterial protein, or a protein made by the body as part of an inflammatory response — stimulates a tiny, deep part of the brain called the hypothalamus.  There, “warm sensitive neurons,” normally responsible for keeping the body temperature stable, act as if the temperature has fallen and slow their firing rates, triggering physiologic responses throughout the body that produce more heat. The incipient fever sufferer feels cold and sometimes begins to shiver. Blood vessels in the skin clamp down, sacrificing their flow to the core of the body in an effort raise the temperature. Heart and breathing rates go up, core temperature rises and the forehead begins to feel warm to the touch, even though the patient still feels chilled.

Definition of normal and abnormal body temperatures

Normal body temperatures vary over the course of the day and from individual to individual, within a degree above or below 98.6°F (37°C). Oral temperatures are about a degree lower than ear and rectal temperatures.  Fever is defined in adults as 100.4° orally or 101°F (38.3°C) rectally, and 101° orally in children. These elevated temperatures seem to work, along with the body’s immune system, to undermine the success of an invaders like viruses and bacteria……up to a point. Temperatures rising to 103-104° begin to have deleterious effects on cells, making their membranes unstable and triggering faults in the workings of cellular machinery. Organ failure can result, complicating already serious illness with kidney and liver problems.

Why do babies and little children get fevers so often?

Babies and small children, who are at the beginning of their life experience with infections, develop fevers more often than adults do. Their fevers may be the first or only symptoms of illness, and the illness may be brief and self-limited. Fevers which indicate worrisome problems in children are accompanied by other symptoms like rash, stiff neck, lethargy, breathing difficulties or abdominal pain.

Adult fevers 

In adults, other symptoms of trouble often come before a fever and point to a body part in some kind of trouble.  When fever occurs along with GI symptoms like abdominal pain, nausea, vomiting and diarrhea, a significant abdominal problem requiring medical or surgical attention may be present. Fever along with cough and sputum production may mean a bacterial pneumonia. Fever that develops as a part of the flu is usually accompanied by profound fatigue, muscle aches and pains and headache.

What causes fever?

About 75% of elevated temperatures come from infections. What causes account for the other 25%?  This “non-pyrogenic category” includes fevers from some cancers, from inflammation of all kinds, from brain injuries like hemorrhages and strokes, and from major bodily injuries with crushed or otherwise damaged tissues. In addition, overactive thyroid glands elevate body temperatures. Some drugs, particularly the neuroleptics used for depression and other psychiatric disorders can cause fever, as can some genetic problems.  Familial Mediterranean Fever comes from mutations in genes that control inflammation responses. Malignant hyperthermia, a potentially fatal rise in temperature in response to anesthetics, comes from a muscle gene mutation.

To treat or not to treat fever?

Treatment of fever is straightforward – body temperature drops in response to an antipyretic drug such as acetaminophen (Tylenol) or aspirin. But fever appears to be an evolutionary response in almost the entire animal kingdom, aimed at protecting the body from invasion by other living forms. In other words, fever induced by infection may be helpful.  Why try to normalize the temperature during the illness?

Most of the time, with temperatures in the 101-102 range, treatment beyond making the patient comfortable is not necessary. But the deleterious effects of raising body temperature begin to show up in the 104 range, and perhaps sooner in people who have underlying medical problems that affect their ability to tolerate higher heart and breathing rates or to maintain adequate hydration. Fever makes demands upon the body that young and otherwise healthy people can tolerate, but older, sicker people may not. Elevated temperatures in heat stroke from a hostile environment or from excessive exertion without adequate hydration serve no useful purpose and should always be treated promptly, with external cooling and hydration.

In the modern age of medicine, antibiotics have reduced Osler’s greatest enemy to a symptom of illness. But it is a symptom that deserves respect. When fever is present, something is wrong and the wrong thing usually involves and invasion of the body by another living form, or a significant area of tissue inflammation or decay. Careful evaluation of other symptoms is the first priority in discovering the cause of fever, for that is what needs treatment more than the fever itself. Should we overuse antibiotics and render them ineffective against our most common infections though, Osler’s great enemy will regain its fearsomeness.

Sleep Debt: The Hidden Costs

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

The biological clock

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

Setting the clock

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

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

Why the clock matters

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

Lack of sleep wreaks havoc on hormones

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

Lack of sleep and obesity

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

Sleep debt is all around you

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

Managing the sleep budget: factors under your control

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

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

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

Chilly Treatment

Large scale studies of survival after cardiac arrest have produced dismal statistics, with survival to hospital discharge of 17.6% when the patient is already in the hospital at the time of the arrest and only 6.1% when the arrest occurs outside the hospital.  The development and widespread deployment of portable automatic external defibrillators (AEDS) in public places has increased the number of people who make it to the hospital after cardiac arrest.  However, the survivor’s longer term outcome depends in large part on how much brain damage occurs during the arrest and whether or not the restoration of circulation damages the brain further, a phenomenon called reperfusion injury.  Because the odds of initial survival have improved, and because lowering the core temperature of the body appears to lessen reperfusion injury, the subject of hypothermia has emerged as a vibrant area of research and therapeutics.

Therapeutic hypothermia is an old idea

Hippocrates (460-370B.C.) recognized the value of cold temperatures in the outcome of soldiers with head injuries and in people suffering from tetanus. In the 1800s, Napoleon’s surgeon used ice to prepare limbs for amputation because it numbed pain and reduced bleeding. Over much of history, miraculous recoveries were reported in victims of cold water submersion. But not until the late 1950s did therapeutic hypothermia become a routine part of some surgical care, when experiments in animals demonstrated its value in protecting the brain during the open-heart surgery.  Despite some attempts to cool patients for other problems such as cardiac arrest, strokes and head injuries, the number of problems encountered in during cooling and in the re-warming phase put a damper on the use of the technique. Now, however, we are in the middle of a revival of interest in therapeutic hypothermia.

How does cold help?

Cold protects the brain because the biochemical reactions that sustain life are influenced by temperature. If the heart stops, the brain runs out of fresh supplies for energy production in two minutes. A downward spiral toward brain cell death begins unless blood flow is restored within the next two minutes. When blood flow is restored (reperfusion), a cascade of potentially damaging chemical reactions begins in cells that have been deprived of oxygen. The longer the period of arrested circulation was, the more damaging these reactions are.

The body at different temperatures

Changing the body’s temperature changes the speed and efficiency of its chemical reactions.  At temperatures over 105 many processes fail completely. As body temperature falls below normal, chemical reactions slow down.  Between 92 and 89.6  the damaging chemical responses that come after blood flow returns are blunted enough to improve outcomes significantly.  By 90, pulse and respirations slow and peripheral circulation shuts down. By 86 the patient may still be alive, but looks dead. This level of deep hypothermia is used for some long, difficult cardiac and neurosurgical procedures.

Lowering temperature is now routine, sometimes

Since 2005, the American Heart Association has recommended therapeutic hypothermia as a routine part of patient care after a cardiac arrest in circumstances that depend on the reason for the cardiac arrest, the speed of the resuscitation, and the state of the patient after circulation is restored.  Some medical centers are also experimenting with the technique in the treatment of certain types of strokes and head injuries.

How do you lower someone’s core temperature?

How do you cool a body that normally maintains a constant temperature that hovers within a few tenths of a degree of 98.6?  Any environment with a temperature less than body temperature provides a gradient for heat loss.  Deliberately making someone hypothermic means increasing that temperature gradient. In the presence of a gradient, heat radiates away from the body. Heat is also conducted away when the body is in contact with any colder substance; when the colder substance such as air or water is in motion, heat is lost even faster, by convection.  Heat is also drawn away by evaporation of perspiration on the skin’s surface, where the sweat keeps the microclimate humidity at 70% even when you think you are dry.   Heat also dissipates when warm moist air is exhaled from the lungs.

Several internal and external ways of changing the temperature gradient  exist: ice packs applied to the head, neck, axillae, groin, where large blood vessels are close to the surface; cooling blankets that house cold water circuits; closed catheters through which cold saline circulates inserted into large blood vessels; ice water balloons in the bladder.    These methods are directed at the core temperature of the body – the temperature of the internal organs and the brain. They do not cause problems like frostbite, seen commonly with accidental hypothermia, because the ambient temperature is not freezing and the skin is protected from direct exposure to ice packs being used for cooling.

The body resists lowering the temperature

Normally, we protect ourselves from falling temperatures by putting on more clothes and increasing activity, and by shaking and shivering, which produce heat.  A patient who has suffered a cardiac arrest will not engage in the normal behavioral responses, but he will shiver and perhaps become agitated, both of which are counterproductive to getting the temperature down. Sedation and even muscle paralysis are therefore necessary for the period of cooling.

Despite problems,  therapeutic hypothermia is here to stay

Current therapeutic hypothermia protocols call for maintenance of temperature between 32-34 (89.6-93.2) for 18-24 hours, followed by passive re-warming over the next 24 hours. Overshooting and undershooting of temperature are both common, as are difficulties maintaining electrolyte and sugar balance. Some complications like pneumonia and bleeding problems are more common than in similar patients not being treated with cold temperatures. Much work remains to determine the best timing for induction and maintenance of hypothermia after cardiac arrest, but it is clear that “the sooner the better” is the general rule and that the revival of interest in therapeutic hypothermia is here to stay.

Human Foie Gras: The New Plague of Fatty Livers

 “M. Apicius [Marcus Gavius Apicius, a first century AD Roman gourmet] made the discovery, that we may employ the same artificial method of increasing the size of the liver of the sow, as of that of the goose; it consists in cramming them with dried figs, and when they are fat enough, they are drenched with wine mixed with honey, and immediately killed.”

— Pliny the Elder, The Natural History, Book VIII, Chapter 77

For thousands of years, humans have created a tasty delicacy called foie gras from the livers of certain animals. Foie gras, which means “fatty liver” in French, is made by force-feeding animals, usually geese or ducks, a mash consisting of fat-soaked grain. Fatty livers are most easily induced in animals that regularly store extra fat for energy before migration. Humans also store energy easily, and modern lifestyles, including diets heavy in fat-soaked carbohydrates, have inadvertently created an epidemic of fatty livers in people. Some researchers estimate that the problem now affects one-third of the US population. 

Alcoholism was the main cause of fatty livers in the past

Doctors have long been familiar with fatty livers in alcoholics, in whom a combination of the toxicity of alcohol and dietary deficiencies converts liver cells into fat-laden bubbles. This condition is known as alcoholic steatosis and is the first step along a road that can lead to cirrhosis and liver failure. Alcoholic steatosis can be reversed if the patient stops drinking. If not, it can become progressively worse, leading to inflammation of the liver called alcoholic steatohepatitis. Ultimately this inflammatory degeneration can lead to a scarred and shrunken liver (cirrhosis) and to liver failure.

Non-alcoholic fatty liver becomes a new diagnosis

By 1980, the appearance of fatty livers and the kinds of problems that are associated with them in nondrinkers forced doctors to devise a new diagnosis—nonalcoholic fatty liver disease (NAFLD). As in alcohol fueled liver disease, NAFLD can also lead to inflammation, a condition called nonalcoholic steatohepatitis (NASH), and to cirrhosis and liver failure in some patients. Progression from NAFLD to NASH seems to require the additional effects of viral hepatitis or of toxic substances, like certain medications, both of which also play a role in some alcoholic liver disease progression. 
…..and becomes a serious problem

Since the 1980s, the prevalence of NAFLD has been climbing in parallel with the numbers of people affected by the metabolic problems of obesity, insulin resistance, and type 2 diabetes. Like these problems, NAFLD is now affecting younger people, even children. By 2006, NAFLD and NASH were the leading reasons patients were referred to liver specialists. They were also the leading cause behind diagnoses that led to 4 to 10 percent of liver transplants. While it is very difficult to make accurate estimates about the overall prevalence of NAFLD, by now it is clear that it is very common in people who have abdominal obesity, insulin resistance, and type 2 diabetes—perhaps affecting as many as 75 percent of such individuals.  
Why fat in the liver is bad for you

In a state of good health, the liver functions silently. Tucked up under the ribs on the right side of the abdomen, it is the size and shape of a deflated football and is the second largest organ in the body (the skin is the largest). The liver coordinates energy storage and regulation and makes proteins and cholesterol necessary to the health of all cells in the body. It also makes and secretes bile to absorb fats from the intestine and filters toxins from the blood to destroy them or ship them out with bile. The liver also stores vitamins and regulates the blood’s ability to clot in a fine-tuned range.  
 If necessary, the liver stores fat in its cells. Generally, this is a temporary state, and the fats are transported back to the body for use as an energy source or for storage in fat tissue. Obesity, insulin resistance, and diabetes, however, work together to keep fat in liver cells. Despite the stored fat the liver can continue to function well, producing no symptoms, unless other factors produce inflammation and scarring. NALFD is often discovered incidentally, because of abnormal liver function blood tests from inflammation, or a scan of the abdomen for other problems. 

Fat plus inflammation can trigger liver failure

When fat accumulation in the liver is accompanied by inflammation or occurs in someone who already has a scarred liver from other problems, like heavy alcohol use or hepatitis, liver failure and cirrhosis ( shrinkage from scarring) may follow. It is estimated that 20 percent of those with NAFLD have inflammatory changes in their livers, moving them from a diagnosis of NAFLD to a diagnosis of steatohepatitis, or NASH, which increases their risk of developing liver failure and cirrhosis. Unfortunately, there are no easy tests to determine the presence or absence of inflammation in the liver, and patients may have no symptoms. Liver function tests may remain normal, and although liver biopsy provides a definite diagnosis, it carries some risks and thus is not a suitable screening test for patients who have no symptoms or findings. 
Symptoms of liver disease

Symptoms of liver disease can be very vague until liver scarring and failure are well advanced. Fatigue, vague abdominal pain, and digestive complaints, as well as enlargement of the liver are early indicators. Jaundice (yellowing of the skin and eyes), fluid in the abdomen, poor clotting, and bleeding from the intestinal tract are late symptoms. Most people who have fatty livers will not go on to this degree of failure, just as most alcoholics do not, but there is no easy way to know who will and who won’t. 

What can be done?

In the presence of NAFLD it is important to avoid liver toxins such as alcohol and many drugs. With gradual weight loss, it is possible to reverse the accumulation of fat in the liver and to reduce liver inflammation, particularly if the weight loss program includes significant exercise to improve insulin sensitivity. Even in transplanted livers, NAFLD can recur as long as obesity, diabetes, and insulin resistance remain. Obesity surgery appears to reverse some of the liver problems in affected people and may yield new insights into the mechanism of insulin resistance. While researchers are striving to develop drugs that improve insulin resistance and alter fat transport and storage mechanisms, prevention, as always, is the best advice. This will require education, patience, self-discipline, and hard work, and it is particularly important for young people. While foie gras from a goose is tasty, its development in humans is undesirable. 

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.


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.

American Society of Metabolic and Bariatric Surgery ( Access to readable, professional information regarding bariatric surgery. Support group website for patients contemplating surgery or looking for related information

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.

Walking or Running For Fitness? Both.

Karl is a friend who hikes a local trail almost every day. The trail is not easy, ascending 300 feet in the first quarter mile alone. Uphill stretches push the pulse and breathing rates up; downhill stretches require strength, flexibility and balance. Karl is 83 and he has maintained his physical fitness with functional activities like hiking and skiing. His old friends in the valley no longer hike with him.  “It is sad,” he says, shaking his head. “They didn’t need to stop and now they can’t do it anymore.”  He is right – fitness requires doing.

Why bother staying fit?

Physical fitness is worth preserving. It makes aging easier and more enjoyable, prolongs independent living and accessibility to many pleasurable activities, and lessens dementia risk. It raises insulin sensitivity, reduces blood pressure, cuts weight and improves cardiovascular risk factors.  You needn’t be an athlete to be fit and, as Karl demonstrates, fitness does not require gym memberships, classes or travel to and from a sports facility. And as many researchers have demonstrated, simple activities such as walking and running have positive effects on body and mind.

What does running do for you?

Much information about the beneficial effects of running comes from studies done in high level athletes. This sports oriented literature can be bewildering, leading into a thicket of terms like periodization and lactate thresholds and specialized measurements like aerobic capacity and heart rate variability. But buried in the details of these studies are useful facts that, when simplified, provide guidance that will improve the fitness of beginners and people who already have a stable exercise habit.

Why walk too?

While running promotes faster weight loss than walking, both lower blood pressure and improve heart and lung function. Walking requires more of the shin muscles and running more of the gluteals and quadriceps. Both are worth incorporating into a fitness program because of these different patterns of leg muscle use. Balancing the strength of lower and upper leg muscles and improving flexibility of all of them lessens strain on knees.

How much of each?

The balance between walking and running in an exercise plan depends on beginning fitness level and on goals.  For a sedentary individual unaccustomed to exercise, regular walks will be enough to increase fitness, at least in the beginning. For someone who has run in the past but not recently, a combination of walking and running is a good way to start. And for someone who has a good level of fitness and a long running history but is getting older and accumulating aches and pains, the addition of walking balances leg muscle groups.

Short periods of intense effort pay off

For all groups, the introduction of short bouts of more intense walking or running into a regular exercise program is perhaps the most important aspect of maintaining and improving fitness. These “intervals” provide the challenge that the heart and lungs need to stimulate their capacity to provide blood to working muscle more efficiently. A recent study from Denmark provides good evidence that a very small amount of time spent running faster improves fitness. It also decreases blood pressure and makes routine running more efficient. In the study, the addition of an interval program of faster activity, performed twice a week, was not only well tolerated but study subjects stuck with it and benefited more than they did from other seemingly more difficult programs.

In the Danish program, a short warmup is followed by two five minute segments separated by a 2 minute rest, and followed by a short cool-down walk or run. The five minute segments consist of running comfortably for 30 seconds, harder for another 20 and as fast as possible for another 10 seconds, and repeating this pattern 4 more times. A walker could try the same pattern, with effort judged by breathing rate and difficulty and by the ability to complete the 5 minute segments. As improvement occurs the segments cover more distance.

Change the terrain

Other ways to increase effort include walking or hiking uphill and climbing stairs. The important thing is to build in some segments of exercise that require more effort and cause faster breathing into at least two periods of exercise a week. In addition, going “off-road” on dirt and rock and sand requires use of little balancing muscles and improves strength and balance.

How much is enough?

How much weekly exercise is necessary? One figure quoted frequently is 150 minutes – less than half an hour a day. The payoffs though, depend on demanding more of the heart and lungs during those times than during routine life. Ambling up the street at the same pace as you walk between the couch and the TV will have less effect than but walking briskly, to the point of feeling slightly short of breath.

Can people who have arthritis walk and run for exercise? For the most part stiff joints feel better with movement. If walking or running gets easier as the joint is “warmed up,” the joint stiffness and discomfort are most likely related to shortened muscles and tension on their tendons, not to joint pathology that will get worse with activity.

Make sure you remain able to get up and down from the ground

For overall fitness, some time also needs to be devoted to strength and flexibility exercises. Pilates exercises, yoga practices, weight lifting and core muscle strengthening exercises like the TRX programs all improve muscle strength and flexibility, enhance walking and running ability and contribute to improving balance. The ability to get up and down from the ground indicates a lot about these non-cardiovascular aspects of fitness, and every effort should be made to make certain this ability is preserved over time.

Mind over matter

The most difficult part of beginning or sticking to an exercise plan is often in the mind rather than the muscles. When Karl says his friends didn’t need to stop hiking, he means that they stopped pushing themselves before there were any compelling physical reasons to stop, and then one day they no longer had the ability which he has so far maintained. His example is inspiring.

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 18th 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.

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


Beef and chicken liver*

Whole milk, eggs, cheese

Carrots, spinach, yellow vegetables and fruits
Vitamin B1 Thiamine 1.2 mg


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
5.0 µg-10 µg Dairy products, salmon, tuna Fortified cereals
Vitamin E Tocopherol and
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

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