Refuse To Regain

Is Your Irisin A'Risin?

by Barbara Berkeley, MD

The latest chemical substance to get scientists into raptures is irisin, a hormone that is produced in muscle cells but exerts its effect on fat.  We've all figured out that exercise and weight are somehow tied together and that this means that muscle and fat must communicate. Unfortunately, we've showed a woeful lack of imagination in tryng to come up with the mechanism. For decades, we've persisted in trying to jam the same puzzle piece into a space that doesn't fit.  We are determined to prove that the connection is calories.  It seems so logical.  If we burn calories through working out we must lose weight, right?  And yet the evidence that this is so remains annoyingly equivocal.  

While readers will occasionally write to me about great weight loss successes from becoming physically active, it is rare to observe this in clinical practice. The more common experience is to see people who have added exercise, but have not achieved anything more than a minor result.  As I've mentioned in the past, I have taken care of many very athletic people, even marathoners, who were clinically obese.  Could they have just been eating enormous amounts of food?  Of course it's possible.  But most of them were trying to lose weight by modulating their diet.  One would think that these prodigious amounts of exercise would force weight loss, but in their cases it did not.

On the other hand, it is observationally obvious that maintainers who exercise have a higher rate of success at keeping weight off.  This observation has been confirmed by data from the National Weight Control Registry, a large study which monitors those in maintenance.  While the NWCR subject pool is limited to maintainers who volunteered themselves (and thus are probably highly motivated), the data shows that successful study maintainers are exercising a lot (on average, about 1 hour daily). 

Irisin is a hormone that is produced from the breakdown of a protein that is produced when muscles are exercised.  In rodents, it's injection appears to turn white fat into the more metabolically active brown type.  Humans do not have very much brown fat, so it is difficult to speculate whether this finding is meaningful for us.  Even rats who made more brown fat did not lose weight when injected with irisin.  So why the flurry of interest?  Because high levels of irisin appear to improve the way the body metabolizes food, making it less insulin resistant and more weight stable.  The following is from a recent NY Times article on irisin:

But while irisin appears to have a critical impact on metabolism, it does not appear to play any discernible role in the effects that exercise has on the heart or the brain. And various issues remain unresolved. Why, for instance, if exercise increases levels of irisin and irisin increases the body’s stores of energy-burning brown fat, does exercise so rarely produce significant weight loss? The mice injected with irisin lost little weight. On the other hand, Dr. Spiegelman notes, they resisted weight gain, even on a high-fat diet, and their blood sugar levels remained stable. So it would seem that exercise, through the actions of irisin, can render you healthy, if not svelte.

As I have repeatedly said in this blog, research results only become important when they are repeatedly reproduced.  The irisin story is obviously in its very earliest chapters.  But the existence of such a hormone may well help to explain why exercise is so important during maintenance, and relatively ineffectual during weight loss.  For those who are currently losing weight, I don't discourage exercise, but I ask you not to rely on it.  Weight loss is about forcing the body to burn itself (which it would prefer not to do) through caloric restriction.  Think of your exercise as a way of rebuilding and retuning your muscles for later use.  Once you reach maintenance, these irisin producing factories will be fired up and ready to go--giving you a much improved shot at maintaining the body you've earned. 

A Calorie Just a Calorie? No Way

by Barbara Berkeley, MD

 A calorie is a calorie.

This is my least-favorite dietary mantra.  Why?  Because in the real world of real people and real weight loss, it isn’t true.

In scientific terms, a calorie is a specific measure that refers to the amount of heat needed to raise the termperature of 1 gram of water 1 degree centigrade. We can measure the amount of heat contained in any substance by burning it in a machine called a calorimeter.  Using this narrow definition, there is no question that calories are all the same.  One calorie of lettuce will raise 1 gram of water by one degree.  So will one calorie of M&Ms.

But the colloquial usage of “a calorie is a calorie” (let’s call this C=C) bears no relation to the scientific definition.  What's usually meant is this: diets that contain the same number of calories will have the same effect on your weight loss.  It doesn’t matter if those calories come from chicken breast or chocolate cake. 

Those who claim that any calorie we eat is equal to any other calorie,  routinely invoke the First Law of Thermodynamics as evidence.  This argument is a real show-stopper.  It’s hard to argue with the basic laws of universe!

But a deeper look at the thermodynamic argument reveals many holes. The First Law says that energy cannot be created or lost, only transformed.  C=C  proponents interpret this to mean that any calorie that goes in has to be balanced by a calorie that goes out.  If the balance is tipped one way or the other, you will either lose or gain weight.   But  the equation for the First Law was designed to represent energy in a closed system, not in a biological system that exchanges energy with the outside world. It would be much more true if the body acted like a perfectly consistent machine and burned all calories with equal efficiency.  While all calories may be the same, the way in which the body burns calories is not.  This variation depends on the package which surrounds those calories.

The calories in food don’t stand alone.  They are intertwined with the other properties of foods… their protein, fat and carbohydrate contents for example. These properties have absolutely no effect on a calorimeter, but they have profound effects on the human body. 

This leads to an important omission in the thermodynamic argument.  While those who believe in C=C support their contention with the First Law of Thermodynamics, they never mention The Second Law.  (There are four, but only two apply to the physics of food). This Law states that when energy goes through a transformation, there is always some loss of energy as heat.  This dissipation of calories is a function of the efficiency with which the calories are burned.

In a 2004 paper on this topic Dr. Richard Feinman offered this useful analogy (the italics are mine):

 The efficiency of a machine is dependent on how the machine works and, for a biochemical machine, the nature of the fuel and the processes enlisted by the organism. A simple example is the inefficiency of low-test gasoline in high compression gasoline engines. If a "calorie is a calorie" were true, nobody would pay extra for high test gasoline. (The calorimeter values of a gasoline will be the same whether or not it contains an antiknock compound).    

This dovetails nicely with what I have observed clinically for many years;  that our body loses fat, works better and is less hungry when we feed it “primary” or ancestral foods.  I believe that these foods are our biological “high-test”.  As I often say to first-time patients, “Your body is a Ferrari but for years you’ve been putting kerosene in the gas tank”.  

Feinman’s article posits a “metabolic advantage” to low carbohydrate foods.  There are many studies that show that at equal calorie levels low carbohydrate foods promote greater weight loss than high carbohydrate foods.  While a single calorie of each of these foods will look exactly the same to a calorimeter, it doesn’t look the same to the body.  One possible reason for the difference in weight loss? The brain needs a certain amount of glucose, or blood sugar, to run.  On a low carbohydrate diet, the food we eat may not provide enough.  The body has to manufacture its own sugar via a process called gluconeogenesis.  This process uses energy and therefore burns calories.  Thus, the net available energy from a low carb calorie is lowered simply by the fact that it provokes another, heat-generating, bodily process.

A low carb calorie may be very different from a higher carb calorie in other ways.   It appears to suppress appetite better. A 2011 study in the journal Obesity reported that dieters who were fed a low carb diet for two years had significantly less hunger and a statistically significant decrease in cravings for sweets and starches when compared to those on a low fat diet. 

A diet that is higher in protein may have the same calories as another diet, but the protein content may cause increased thermogenesis…the loss of calories that occurs through digestion. This effect and others are laid out in a paper in the Journal of the International Society of Sports Nutrition http://www.jissn.com/content/1/2/21.

And then there is this important consideration: many of us who eat the SAD (standard American diet) have developed insulin resistance.  This is a condition in which insulin is produced in response to elevated blood sugar, but fails to work properly.  The muscles, which normally would burn off some of this sugar, have stopped responding to insulin.  Instead, there is diversion of calories into fat.  For people with insulin resistance, calories from sugar and starch provoke a very different bodily response than do protein or fat calories.  They should be avoided.

Perhaps the issue is not whether a calorie is a calorie.  It is the understanding that a calorie is not ONLY a calorie.  When it comes to food, the body reacts to myriad elements of the food package and calories may be only a minor part of that.  Even for those who already believe that calories are just a single aspect of food, the answer to the question of perfect diet remains elusive.  Much of the literature refuting the C=C position comes from scientists who support low carbohydrate diets. When designing studies that pit low carb against low fat diets, they tend to use the Atkins diet as the low carb choice. While I am firmly in the low carb camp I believe in low carb in the context of Primarian (or ancient-style) diet.   In our clinic, we see all of the benefits of very-low carb diets like the Atkins induction (brisk weight loss, decreased hunger, correction of metabolic abnormalities).  We achieve this, however, with Primarian plans which are less restrictive and easier to follow.  Unfortunately, there are few studies that have looked at the effectiveness of ancient-style eating for weight and health.  

The moral is this: calories are not the be-all and end-all we’ve been led to believe.  While lowering calories is key to weight loss, the type of calorie you’re consuming is equally—if not more—important.

 

Controlled by a Cookie: When Foods Become Drugs

by Barbara Berkeley, MD

Do you take medicine to treat your blood pressure?  Once you swallow your pill, can you control your blood pressure via sheer willpower?  While such feats of bodily control are reported by swamis and other advanced body-mind practitioners, they are not in the average person's repetoire.  And a good thing too, because the power of drugs to take over ailing body systems is the reason they work. Medicinal drugs are substances which enter from the outside and take control of inner processes.  They cause chemical changes that in turn change those who take them..hopefully with positive effect.  But, as we well know, drugs can have negative effects too, especially when their chemical properties are used to create pleasure.

Consider these two definitions of the word "drug":

1. a chemical substance that affects the processes of the mind or body.  

2. a substance used recreationally for its effects on the central nervous system, such as a narcotic.

 

Every overweight person I've ever encountered recognizes that certain foods have drug-like properties. During an intake visit, a new patient will generally put his finger right on the foods that are submarining him.  He or she will often use the language of addiction to describe these foods:  "I'm addicted to sweets",  "I'm a chocoholic", "I just can't stop eating bread."  It's not coincidence that such language should leap to the lips.   Foods DO alter the processes of the mind and/or body.  Foods ARE substances that are used recreationally and which do have effect on the central nervous system.  In fact, certain foods can be viewed very much as drugs.  Despite this, we believe that once ingested, we can control these particular "drugs" by sheer willpower. 

Perhaps you do not agree that food and drugs are similar.  After all, we are designed to eat food and even if ingesting food does cause changes within the body, they should be natural, expected changes.  Until recently, this has certainly always been the case, but let me suggest two reasons why things may have changed.

First: There can be no question that eating food is a natural behavior that provokes natural responses. I would make the case, however, that in a very real way we no longer eat "food".  Processed foods that are chock full of preservatives, colors, and chemicals have little resemblance to what our body is equipped to handle.  Foods that hit us with enormous punches to the insulin system---the sugar and starch foods---are also very new to human experience.   

Second: Many of us who eat the western diet or SAD (Standard American Diet) have developed inappropriate reactions to eating these newer foods.  This is especially true for those foods that turn into sugar after digestion (the sugars themselves and the starchy carbs like grain, cereal, pasta, flour based foods and potatoes).  If we have begun to develop a "broken" reponse...in the form of what we call insulin resistance... we will react in a new and negative way to eating.  We will experience more hunger, more craving and less ability to control these foods.

 

Recent research into the modern epidemic of insulin resistance suggests that those of us whose insulin is no longer properly interacting with our body may also have a problem with insulin's role in the brain. The brain's form of insulin resistance occurs when insulin-related signals which normally tell us to stop eating are blunted.  Thus, foods that cause insulin release are no longer equipped with the satiety safety valve that nature intended.  Indeed, these foods may make cause more hunger rather than less.   And who among us has not experienced the inexplicable carbohydrate craving that follows a day of bread, pasta and cookie consumption? 

 

Thus, my hypothesis is that foods become drugs when our body no longer tolerates them well.  As a child, you might have been quite able to eat a cupcake and simply stop.  As an adult, one doughnut might lead to an entire box.  When drugs are at the helm, you can forget willpower.  Be they medicines in pill form or cookies that are decorated like Grover, your physiology is co-opted and someone else is driving the bus.  

 

Sometimes I use the following analogy in the office:  think of your trigger foods as concealed aliens. Remember the movie Men in Black?  An innocuous shop-keeper might look harmless, but was actually a man-eating cockroach!  Drug-foods are like that.  They look attractive, luscious, and controllable, but allow them past your lips and you are under their control.  You can bemoan your lack of willpower all you want, but if you've given yourself over to the aliens you are likely to spend quite some time doing things you didn't intend. 

 

Many people simply can't understand how something as small as a cookie could cause them to abandon all resolve.  But there is the error!  A cookie isn't small at all.  The chemical signals and bodily changes that start the moment a susceptible person sees and smells that cookie are quickly overwhelming.  Eat that cookie and it is very possible that---diet-wise---all is lost. 

 

This illustrates  the problem I have with advice that suggests that it's ok to eat everything in moderation.  Yes, if you are a person whose food-processing systems are all in good shape, this may be a fine strategy.  In fact, if this works for you, you might well be unable to understand why it wouldn't work for everyone.  But most people who are overweight have gotten heavy because food has become drug-like for them.  To me, this is part of a larger picture which includes fundamental physiological changes in the way their body handles that food (mostly the starches and sugars).  If you have been wrestling with willpower and blame yourself for being weak, I advise you to start seeing the true nature of your trigger foods.  Start with a healthy respect for their power and a strategy of avoidance whenever possible.  Remember, if you don't take a drug it can't own you. 

 

 

 

Sugar. Cholesterol. JAMA. Finally.

By Barbara Berkeley, MD

Scientists are supposed to be curious. Weren’t they once the little boys and girls who peppered their parents with a zillion questions about how the world worked? Didn’t they once want to solve the riddles of the universe?  

But then the scientists grew up and like all the rest of us, they became less open minded.  Perhaps they were influenced by powerful figures. Or perhaps they became so immersed in their own hypotheses that they stop looking at others. 

In no area has this been so true than in the reluctance of researchers to look at the negative role of sugars in our modern diet. In 1970, Ancel Keys, a professor of physiology from the University of Minnesota, published the first results of a study that would change science for decades. The Seven Countries Study was a research project that looked at diet and heart disease throughout the world.  It concluded that there was a strong association between the amount of saturated fat people ate and their cholesterol levels and subsequent chance of developing heart disease. 

The Seven Countries study has arguably been one of the most influential forces on our modern American diet. Keys was a big, loud voice in the scientific community. Beginning in the 1960s, he and others had begun convincing much of America to start eating more polyunsaturated fats and fewer saturated ones. It was around this time that my mother banned the Breakstone butter tub from our table and substituted that fabulously healthful product - margarine - made completely from corn oil. Americans stopped frying in lard and started consuming tons of vegetable oils instead. As the years went on, things got more confused. All fat became the enemy and the fat free craze was on with a vengeance. Carbs good. Fats bad. Dutifully, I switched to a diet of vegetables, grains, pasta,  and bread with fat free Entenmanns cookies for dessert. It was all completely fat free.  But, for the first time in my life, I started to gain weight as if it was going out of style. I chalked it up to being 40. My diet was obviously pristine

But holes began to appear in the Seven Countries Study. (For more on this, see Gary Taubes’ book, “Good Calories, Bad Calories”) Critics noted that Keys had omitted data from countries in which results contradicted his preferred hypothesis. At the same time, Dr. Atkins popularized a diet which had pretty much no carbohydrates.  Cholesterol levels fell on this diet. How could that be if fat raised cholesterol? For years, people like Weston Price who studied the anthropology of diet had noted that the inclusion of large amounts of carbohydrate in native diets was linked to modern disease. Yet science refused to be swayed from its single-minded pursuit of fat as villain.  Clinicians who spoke out against sugar and starch consumption, and those who wrote about it were sidelined as kooks. 

Despite the fact it is clinically obvious that cholesterol falls when patients are placed on low carbohydrate diets, other doctors still look at me as if I’m nuts if I suggest that sugar has anything to do with lipids. Even more importantly, we now know that our levels of total cholesterol are only one, very generalized,  piece of the puzzle. Equally, if not more important, are the types of lipids we have. We’ve gone beyond just the “good” cholesterol and the “bad” one. We now know recognize vital subtleties.

Bad cholesterol turns out to exist in two forms: a light, fluffy, innocuous form and an irritating, small, dense and dangerous form.  Dense LDL predisposes us to coronary disease. Standard lipid tests do not say anything about the size of LDL particles, but doctors can guess if we have them by looking at levels of two other lipids,  triglycerides and HDL. If the ratio of these two elements is above 3.8, that is a strong indication that there is small, dense LDL. We call this type of lipid profile “dyslipidemia” and it is highly correlated with vascular disease.

Are these changes entirely brought about by the fat we eat?  Absolutely not.

On April 21, 2010,  with absolutely no fanfare, the Journal of the American Medical Association published an uber-important study ( JAMA study). Here is how the authors introduced it:  "Dietary carbohydrates have been associated with dyslipidemia, a lipid profile known to increase cardiovascular risk.  Added sugars...are an increasing and potentially modifiable component in the US diet.  No know studies have examined the association between the consumption of added sugars and lipid measures.

  
Isn’t it incredible that with all the research on diet and heart disease that has been going on for the past 30 years, this is the first study to directly test the possibility that sugars impact lipids??

So here’s what the study showed.   It looked at 8,495 US adults over the age of 18 who were part of our ongoing national nutritional survey (NHANES, 1999-2006).   Excluded from the study were those on cholesterol medicines or diabetics---so two of the populations that theoretically might have shown the greatest correlation of lipid levels with sugars were not considered.    The study also looked only at the added sugars people consumed, in other words, the extra sugar, high fructose corn syrup or other sweeteners that were included in the foods they ate, not at the total carbohydrate composition of their diets.  

Results: Good Cholesterol levels, which should be high, fell as the consumption of added sweeteners increased.  Triglyceride levels rose significantly, meaning that the ratio between the two went up (suggesting more dense LDL) as sweetener use did.  In women,   total LDL (bad) cholesterol rose with increased sugars as well. 

Interpretation: Sweetening agents directly affect cholesterol and triglyceride levels  (or at least are highly correlated with them). If this study is correct,  eating more sugars increases your risk of vascular disease. Finally, It’s not just about fat anymore. 

How much added sugar do we consume? On average, about 16% of our calories are coming from this completely unnecessary source. Recently, the American Heart Association jumped on the anti-sugar bandwagon with the recommendation that women consume no more than 100 calories in added sugar per day (150 calories for men). How likely is this to happen? Well, one can of coke has 140 calories from sugar. A Starbucks blueberry scone has 460 calories, 96 of which come from added sugars, and a small pack of M&Ms has about 130 calories of added sugars. Eat any one of these and you are done with sugar for the day and that doesn’t factor in the hidden sweeteners that are added to restaurant foods, canned foods, and just about everything else. How many sugars should we truly eat? In my world, the answer would be: just the sugars contained in natural foods. 

Finally, this study just skims the bare surface. It opens the door to the thought that too many sugars can be just as dangerous for your heart as too many of the wrong fats.  But the name of the game is gestalt—or totality. If we get bogged down in running after sugars as we’ve gotten bogged down in running after fats, we will find ourselves at the end of another blind alley. Each and every one of these studies confirms the very same priniciple, that the further we depart from the diet that was original to man, the more we mess things up. Clumsy attempts to “correct” the problem only reveal our ignorance. Remember that margarine my mother switched to? Turned out that it was full of corn oil, which is high in omega 6—or pro-inflammatory—fats. Also turned out that margarine was just a tub of trans-fat, one of the most dangerous substances for the heart. And all of those Americans who switched to vegetable oil?  They vastly raised the ratio of omega 6 to omega 3 fats in their diet, putting them at risk for inflammatory problems.   Is it such a fringe idea to suggest that we need to revamp our entire idea of diet to bring it back into line with what kept us healthy in the past? I certainly don’t think so.

But for today, I will celebrate the JAMA study and be glad that science has started to expand its view.  Maybe I’ll try re-reading it while eating the peculiar concoction that I’ve recently been enjoying for lunch:  some  sardines mashed up with a good mustard, a salad, and an avocado.  Lots of omega 3, completley Primarian, and not a sugar in sight. 

The Talented Mr. Warburg

By Dr. Barbara Berkeley

I have this thing. Maybe it’s genetic, I don’t know. I sometimes become intensely interested in certain things, foods, people, microcosms. I can eat the same meals, order the same kind of coffee, read the same book, watch the same movie a zillion times. It’s not so much that I get stuck in a loop as that I enjoy things more with repetition.

When I was about 10 years old, this intense focus landed on an unlikely candidate: Amelia Earhart. I spent a whole summer with my sister and my best friend researching and writing little books about Amelia. We spent days in the library when we could have been swimming at the Boulevard Pool. We discussed the details of Amelia’s life with the same fascination star-gazers usually reserve for celebrity gossip mags. We were endlessly intrigued by her life story, particulary her marriage to George Palmer Putnam, which we judged to be loveless.

Recently, my odd propensity for intensity has landed on a new subject: Otto Warburg. Warburg was a Nobel prize winner who was born in Germary in 1883. As a German biochemist living in the mid 20th century, he got to hang around with some pretty impressive company: people like Albert Szent-Gyorgyi and Hans Krebs, the guys who figured out the Krebs cycle (a cellular process, the memorization of which torments med students to this day). Otto’s career in science went on hold when he joined the cavalry in WW I. He loved anything equestrian (he never married and had no discernible love-life). His devotion to the cavalry made his family worry that he might remain in the army permanently. He was persuaded to return to research by a friend of his father’s who knew a bit about science: Albert Einstein.

It was a lucky thing that Warburg traded horses for the laboratory. He made a major discovery, known to this day as the Warburg Effect. To understand this discovery, you first need to know that all bodily cells make their own energy; in other words, they self-create the fuel they need to stay alive and to do their particular work. This fuel is called ATP. 

You probably recall that cells have a kind of gel inside called cytoplasm. Within this cytoplasm are small organelles…tiny factories that have special jobs. Normally, cells make a bit of ATP by burning up some glucose, or blood sugar, in the cytoplasm. That process throws off a molecule called pyruvate which is then taken up by mitochondria (which are organelles). Once in the mitochondria, a complex process turns the pyruvate into lots more ATP. Warburg’s fascinating discovery was the following: cancer cells aren’t able to make fuel by this normal pathway. In cancer cells, the mitochondria are not working and cannot process pyruvate. Thus, cancer cells are left having to make all of their fuel from glucose in the cytoplasm. This takes a lot of glucose. Essentially, cancer cells are obligate sugar burners.

This is not the case for normal cells. Normal cells can burn other fuels, in particular, chemicals which are made from the breakdown of fat. We all know about this because we all know about the Atkins diet. When sugar in the diet is reduced to nothing and most of what is consumed is fat and protein, the body soon begins to run on ketones. It does just fine on this fuel. Many of us believe that we will die unless we have glucose, but there are only a couple of areas in the body that must use glucose as fuel. Enough glucose to feed these areas can be created within the body. We don’t have to consume it. For proof, we can look at the native diets of people like the Inuit, who survived in excellent health on little more than fish, meat and blubber and the Masai, who eat mostly meat, blood and milk. For an excellent discussion of Inuit diet and health, see this article in Discover Magazine.

Warburg first articulated his hypothesis in the 1920s and the Warburg Effect has been widely accepted for many decades. The PET scan, which is a test which identifies active cancer cells, is based on the fact that tumor cells use up glucose so avidly that they can be spotted this way. On the other hand, one aspect of Warburg’s work has remained highly controversial.

Warburg believed that cancer itself was caused by the damaged mitochondria. As we all know, cancer cells have many mutations and appear damaged. It was Warburg’s belief that this DNA damage occurred as the result of the switch to an unnatural cellular fuel production method. As the years progressed, most cancer scientists researches came to believe that damage to DNA came first and the damage went on to cause the mitochondrial problems Warburg observed.

Warburg was aware of the slipping acceptance for his hypothesis about the cause of cancer. He never wavered in the belief that he was correct. As he said at a meeting of Nobel laureates in 1996, “…the prime cause of cancer is the replacement of the respiration of oxygen in normal body cells by a fermentation of sugar." Further, Warburg felt that the refusal to accept his hypothesis was delaying research into treatments which might work on restoring mitochondrial function and thus cure, prevent or slow down cancer. He himself became obsessed with dietary carcinogens as he became older and insisted on eating only organic foods.

So why am I so interested in Warburg? You guessed it! The sugar connection!! Since it is my belief that ancient diets which are low in glucose-producing foods (starches and sugars) are the best for health, Warburg’s work makes a nice fit. In doing some research on suggested diet for a patient who recently developed cancer, I came across Warburg. I was hooked. Two questions immediately came to mind:

1. Can consuming a very low glucose-producing diet slow down cancer? If cancer cells can’t burn alternate fuels, this would seem to make sense.

2. Does continuing to eat a low glucose-producing diet perhaps inhibit small cancer “areas” that we may develop from time to time? If that were true, would we see less cancer in those who eat such diets?
Interestingly, Warburg’s hypothesis is getting a new look. The treatment of cancer with agents that might restore mitochondrial function or block the abnormal sugar burning process are now being investigated. Here is one such attempt, reported yesterday in Science Daily. This drug works by “choking off the sugar supply” to tumors.

But can we do something similar with diet? To find out, I wrote to Dr. Thomas Seyfried, a biology professor at Boston College. Dr. Seyfried is among those who believes that cancer is a metabolic disease, as Warburg did. He is conducting research on very low carb, ketogenic diets in the management of brain tumors. In other words, he is trying to starve the tumors by forcing them to burn fuels that they cannot use. Seyfried says that it is the number of calories (very low) and not the composition which is most important. The research is not yet advanced enough to draw conclusions, but Dr. Seyfried believes that such an approach may work. When combined with other agents, it may work even better.

As to the answer to question two, one can only speculate. We know that animals who are calorie restricted have slower aging, less cancer and chronic disease. Might this be related to a lower sugar environment? I guess you know what I think. Stay tuned.

Sanjay Gupta Pedals Backward….Then Forward

By Barbara Berkeley

The first episode of public backpedaling on vitamin supplementation probably occurred during Sanjay Gupta’s segment on CNN’s Situation Room Wednesday evening. Reporting on the results of a recent study that associated multivitamin use with an elevated risk of breast cancer, Gupta dared to venture that we should be cautious about vitamin use. He spoke to the fact that the great majority of the many studies on vitamins do not show benefit. He also said something that made me cheer: removing a vitamin from its food source and concentrating it many times may not work; may even be harmful. Bravo for Sanjay.

But by later that day, the CNN website had thought better of Dr. Gupta’s comments. After warning readers about the shortcomings of this study (and there certainly are many), it carefully decided to cover all bases.

First, it took one side:

“The National Institutes of Health have said that "some of the roughly 75 million Americans who buy [multivitamins and supplements] may not need them."

Then, the other:

"At the end of the day, it's always better to see someone taking a vitamin than not. The benefits outweigh the risks," advises Dr. Kent Holtorf, medical director of The Holtorf Medical Group, who was not affiliated with the study.

"The bottom line is a patient is not a population," says Holtorf. "It's better to take a vitamin than nothing, but your best bet is to find out if you're deficient in anything and then treat those deficiencies in an individualized way."

This article equates information from the NIH with the opinion of Dr. Holtorf. Since I had never heard of the Holtorf Medical Group, I Googled them. They are a practice in California that deals in natural supplementation for a whole host of conditions from menopause to “adrenal fatigue.”

They also use supplements for anti-aging medicine. This is not exactly an academically rigorous discussion of the issues raised by the study.

But we shouldn’t be surprised. The media does a generally poor job of covering complex issues like medical studies and treatment. America is hooked on the idea that supplements are a magic wand that can erase our dietary indiscretions. Very little science supports this view. The American Journal of Clinical Nutrition study is challenging because it provides the springboard for discussion and for a re-evaluation of supplementation. We should pick up that gauntlet rather than ignore it. Time to take a look.

It’s particularly interesting that the people who defend supplements most vigorously are those who believe in natural solutions to health. There may be a basic misconception here. Is supplementation with vitamins and minerals which are extracted from food sources natural? Time to take a look.

Even if vitamins are useless but harmless (they make very expensive urine, as a professor of mine used to say), there is potential damage from relying on them as a kind of magic feather that allows us to eat all kinds of bad stuff and assume we’ll be saved. We use medicines like cholesterol lowering drugs and blood pressure pills the same way. Time to take a look.

In the meantime, I’m personally putting my money on original, whole foods from sources that (I hope) I can trust. I remain suspiciously paranoid about ingesting anything made in a factory or deemed to be healthy be dubious experts. We just don’t know enough about that stuff. We do, on the other hand, know an overwhelming amount about the positive benefits of living clean.

Stuck on Fill: The Faulty Metabolism Myth, Part Two

By Barbara Berkeley

In my last post, I tried to debunk the idea that those who have trouble losing weight have something wrong with their metabolisms. Even if that information struck a chord with you, you might have been left wondering the following: “Your explanation tells me why I can’t lose weight, but what about my tendency to gain if I do so much as look at a doughnut? If I don’t have a damaged metabolism, why do I gain weight so easily ?”

When I suggest that most overweight people have normal metabolisms, I’m often met with angry and dismissive responses. Of course there’s something wrong, I’m told. Actually, I completely agree. There is something very wrong, it’s just not metabolism.

Part of the answer lies in our misuse of the term “metabolism .” This word has become something of a catch-all that is employed by just about everyone without much of a definition. What’s generally meant by “I have a slow metabolism” is “There is something really wrong with the way my body reacts to food.” Since we don’t have a specific explanation for what that “something” is, we tend to chalk it up to metabolism.

In medical terms, metabolism refers to the number of calories your body burns each day. These calories are expended by your daily life processes, things like breathing, circulating your blood, digesting, and the microscopic work of cells. Calories are also burned when you move around. It takes fuel to to walk, run, shiver, blink and so on. If we measure only the calories that are burned in basic work, we are measuring Resting Metabolic Rate. When we add on the calories burned with physical activity, we are calculating Total Metabolic Rate. Most studies of overweight and obese people confirm that, far from burning fewer calories, they actually burn more calories than normal weight people. In the graph below, from The Obesity Society, you can see this demonstrated.

 
Why would this be? First, because large people have more mass that needs to be carried each time they move. They therefore burn more calories in doing so. An SUV is going to burn more gas than a Mini Cooper. Secondly, calories are burned more actively by muscle tissue and overweight people have more muscle. This muscle is gained when new fat tissue is manufactured. It provides the scaffolding that holds up that tissue. The greater muscle mass is responsible for a larger daily calorie burn.

So, for most overweight people, there certainly is a problem with the way their bodies react to food, but it’s rarely “metabolism” as we know it. It’s actually more of a food partitioning problem, a derangement in the way the body stores food calories. For lack of a better descriptor, let’s call this “Stuck on Fill.”

When we are confronted with food, our body has a choice as to what to do with the calories. It can burn them (generally by sending them to muscles and other active tissues) or it can store them by filling up the fat cells. This is meant to be a subtle balancing act that works perfectly without our knowledge or intervention. (I’ve written about this before in a previous post on IBM.) Every element that we take into the body is controlled by a similar balance mechanism. Unless some piece of the balance machinery gets broken, the mechanism will continue to work seamlessly. 

Here is an example. A huge overdose of potassium can stop your heart, but you can eat bananas and other high potassium foods day and night without being endangered. A silent mechanism is measuring, balancing and correcting your blood potassium from moment to moment. The ability of the body to control all of its elements within a narrow range is called homeostasis. Our bodies have insistent demands regarding balance. Homeostasis keeps us alive. But one of the components of the balance mechanism for potassium is the kidney. The body relies on the kidney to either hold back or excrete more potassium depending on levels in the blood. If the kidney fails, potassium balance also fails. Suddenly, we humans have to take action by measuring and checking potassium and by adding medicines to control it.

The evidence for a homeostatic mechanism regarding weight is all around us. Just look at the people you know who have never been heavy. With few exceptions, they do not monitor calories or record exercise minutes. How is it that they can weigh the same on December 31st as they did on January 1st? The answer must be that the body is silently and elegantly making decisions that keep weight stable. It is burning more calories on one day and filling the fat cells on another. Just enough to keep things steady.

What about the easy weight gainer? If we think of the burn/fill mechanism as a switch, it is my contention that they are “stuck on fill .” Their bodies have lost the ability to efficiently burn calories and instead are sending  mostly everything into fat storage. This may look like a slow metabolism, but it’s actually quite a different problem.

Since insulin is the mega-hormone that deals with burning and storing calories, it makes sense to look for a failure there. What we know about insulin dovetails neatly with the “stuck on fill” hypothesis. We know that it is very common for people on western diets to develop insulin resistance, a condition in which the muscles stop listening to the signals sent by this hormone. Essentially, the burn part of the equation gets shut down. We also know that people who are insulin resistant are still able to make a lot of fat. Essentially, things are tilted toward fill. Insulin resistance develops with increasing age and gets worse as people get fatter. The heavier you are, the more resistant, the less you can burn. Eventually, your lever gets stuck on fill, and most food is going into storage. It’s a vicious cycle unless you can figure out a way to unstuck the switch.

So how do you fix the problem? By looking at the elements of the mechanism that are broken and the parts that are amenable to repair. Here’s what you can do…and these fixes really do work:

1. If we force the body to lose weight, it becomes less insulin resistant. Once insulin starts working properly, there is a better burn/fill ratio. (But to lose weight, you must be tough and consistent. See my last post).

2. Exercise helps sensitize the muscles so they can “hear” insulin better. It gives us a hedge against resistance and is very important, particularly for maintainers.

3. (And most controversial). It is my firm belief that the switch gets weakened and finally stuck when insulin is asked to overperform day after day, and year after year. As most of my readers know, I believe that our obesity epidemic comes from eating a diet we weren’t genetically designed to consume. The largest difference between our modern diet and our ancient one is the huge load of insulin-requiring foods that we eat. In order to keep a damaged insulin switch oiled and supple, we need to cut back on these foods. The amount of cut-back has some individual variation, but the foods we need to be concerned about are starches and sugars, including bread, pasta, rice, potatoes, cereals, grains, honey, syrups and sugars of all kinds. If you find yourself becoming “stuck on fill” after a weight loss, look to a reappearance in your diet of these foods.

Why am I making a big deal about all of this? Because there is nothing you can do about a “slow metabolism .” It’s simply something you’ve inherited and there’s nothing to do but curse your bad luck. On the other hand, if your problem is a stuck switch, you’ve got some exciting repair work to do. Loosen up that switch by vastly taking the load off insulin, forcing your body to lose pounds, and exercising faithfully and vigorously on most days. Let me know how it goes.

The Faulty Metabolism Myth

By Barbara Berkeley

“Why can’t I lose weight? There must be something wrong with my metabolism. “ 

This question and its seemingly logical answer must be among the most commonly stated beliefs of overweight people. But an answer that appears to be correct is not necessarily so simply because it has been stated repeatedly. As long as we keep asking this question and answering it in the same way, I believe we will not move an inch toward solving our obesity problem.

What if we looked at this question in an entirely new light, starting with a different kind of assumption? What if we began with the fact that the act of trying to lose weight intentionally is most likely an unnatural behavior for humans.

Why do I say this? Until very recently, there was arguably no time in man’s history when he would have thought of forcing his body to give up fat. Since humans lived close to nature, their relationship to food was more like that of other living creatures out in the wild. Fat storage, if it occurred, would have been beneficial, an insurance for lean times. There are very few lions on weight reduction plans.

The evidence for the unnatural nature of forced weight loss can be seen in our body’s response to calorie restriction. When we stop eating, our body does not just start happily burning fat. What it actually tries to do is to avoid losing weight. It does this by going into a sort of “economy” mode. To better understand this, imagine a situation in which you were cash poor with a cold winter approaching and a full tank of heating oil sitting in your backyard. Eventually, the cold sets in. You have that tank of oil, but you’d rather not use it since you are facing a winter of uncertain length. So you wisely decide to go into economy mode. You turn down the heat in your house and wear sweaters instead. You close off some rooms rather than burn fuel to keep them warm. You wait and hope that winter will pass. Meanwhile, your storage tank stays untouched, a hedge against true emergency.

This is exactly what your body does when you try to lose weight. Your genes don’t know that the food shortage they are experiencing is called “Weight Watchers” or “Jenny Craig.” They only know that they are suddenly facing a famine. Ancient responses shift the body into economy mode, dialing down the energy used for heat (the reason many dieters feel cold) and slowing down less vital processes. We call this “lowering the metabolism”, but basically it is the body’s attempt to keep weight stable during a food crisis.

Doesn’t the body want to rid itself of harmful fat? Paradoxically, the answer seems to be no. There is a perplexing propensity for the body to ignore its fat, almost to fail to realize that it’s there. Overweight people experience this every day when they deal with elevated levels of hunger. Why should the body continue to generate strong hunger signals when it is full up with fuel? The answer appears to lie in a disconnect between fat and the brain. Signals which should tell us that we have enough stored fat and that we should stop eating, simply fail to reach their mark. Something inherent in the very process of gaining weight acts as a disruptor to the normal signals that control fat and appetite. When it comes to weight loss, the body seems relatively determined to avoid burning its stored calories unless it is really pushed.

 We are taught that the fundamental truth of weight loss is: burn more calories than you take in and you will lose weight. We are told that this is an immutable law of physics and that if it isn’t working, we must be doing something wrong. But all dieters know that this central tenet of weight loss is simply wrong. Adding more exercise often doesn’t lead to weight loss, nor does restricting calories. What is the problem here? The answer is quite simply the body’s ability to change the game by shifting into economy mode. This is maddening for dieters who often feel unable to lose an ounce when they cut back on food. But that problem reflects a simple truth: when you eat less, your body will run on less. A lot less. This is the beauty of our construction, a metabolic balancing act that allowed us to survive for millions of years. Yes, it’s frustrating. But here’s the good news. A solid understanding of this bodily behavior can help us figure out how to get around the problem.

In my experience, the biggest impediment to successful weight loss is something I call “calorie summarizing.” Americans are hooked on calorie theory, which is peculiar because calorie counting is nearly impossible and doesn’t work very well at all. But more on that another time. When people diet, they tend to look at days or weeks as a block. At the end of each block, they summarize what they ate. They see that, when the days are lumped together and on average, they ate far, far less than what they had been eating before their diet. They exercised far, far more. According to prevailing calorie theory, this should guarantee weight loss. Then they get on the scale. Shriek! They’ve lost a couple of ounces, or nothing at all. They throw up their hands and let out that eternal wail: “There’s something horribly wrong with my metabolism!” Often, they abandon their attempts to lose weight. How could they possibly succeed when they are so metabolically challenged?

But what has really occurred? Far from being metabolically flawed, their bodies have simply been doing their job, protecting their clients from the ancient threat of famine. From the point of view of the dieter, the problem was an inconsistent attempt to “scare” the body into using its stored fuel. On one day, this dieter ate more because she’d been good on another. Because she was so strict all week, it seemed fine to have that piece of birthday cake or that dinner out. Because the week’s total calories were lower than they had been, it seemed fine to have a treat here and there. In doing this, this dieter played right into her body’s hands. She gave the body just enough to get by in economy mode and too much to force it into significant fat burning.

A terrific study that appeared in the New England Journal of Medicine a few years ago supports this hypothesis. In this study, researchers compared average weight losses after one year on a number of different diets, including Atkins, Weight Watchers and the Zone. They showed that the average loss was quite small, just a few pounds. Initially, that looked pretty discouraging. But on closer inspection, researchers noted that not every dieter was average. Some actually gained weight, while some lost very large amounts. What differentiated them? In a stroke of brilliance, the researchers decided to look at their data through a new lens. They asked each subject how consistently they had followed their diet on a scale of 1 to 10. What developed was a perfect curve, the same for each and every diet that was studied. Weight loss began to occur at compliance levels of 5 or better. The largest amounts of weight loss were seen in those people who had been almost perfect in following their diet plan.

It probably matters very little which diet plan you follow as long as you don’t try to alter or make up the rules yourself. What seems to be fair, what seems to be scientifically correct, what seems to make sense, is often not the case during weight loss. What is the case is that your body will economize and run itself on less until you force it to do otherwise. Consistency, toughness and sticking with the plan – not just most of the time, but 90-100% of the time – are the behaviors that work. We must respect the fact that we are asking our body to do something it would rather not do. All the diet commercials in the world can tell you how easy it is, how you can lose weight without really dieting, how you can do it without giving up the foods you love. None of these assurances provide a hedge against the facts of life.

Please note that this particular post is not a maintenance post. While consistency remains very important in maintenance, some degree of off-plan eating can be offset by exercise. This is not the case during weight loss. Unless you are very big (people with lots of fat to lose will generally lose weight with less effort, at least at first), complete consistency is the key. Now you know why. If you have been trying to lose weight and have been bemoaning your slow metabolism, try rededicating yourself to the project by assessing your success from moment to moment rather than summarizing calories over time. Keep food records and measure yourself by how well you stuck to your guns each and every day. Convince your body that there is serious and ongoing food shortage in its environment and it will burn fat to take care of you.

BMI: Tool or Tyranny?

 by Barbara Berkeley, MD

The patient in front of me is Mr. C, a 308-pound man who has been sent by one of my favorite referring doctors. This doctor truly cares about the health of his patients and it shows. In fact, Mr. C’s physician is a triathlete, eats for health and practices what he preaches. He’s never been overweight. His clients are devoted to him and Mr. C is no exception. But Mr. C. is worried. He genuinely wants to lose weight but the doctor he so much wants to please has told him that he needs to reach 170 pounds: the white or “healthy” zone of the BMI chart. “Doc,” he says earnestly. “Is that possible? I’ve never been that light, not even in high school.”

Twenty years ago,the term BMI was part of the foreign language of doctors, a measurement that was recorded on the chart and remained obscure to patients. Today, nearly every dieter understands, (and sometimes obsesses about), his or her niche on the BMI chart.

BMI, or Body Mass Index, is a shorthand that describes the relationship between your body height and weight. The measurement first saw the light of day in the mid 1800s, invented by a scientist named Adolphe Quetelet. In order to compare peoples' masses, Quetelet proposed a method which divided weight by height squared. Current BMI figures are still based on the same equation: weight in kilograms/ height in meters squared. Today, high BMIs denote overweight and obesity.  The cut-offs are as follows: BMI of 25 or less = normal, BMI of 25 to 30 = overweight, BMI of 30 to 35 = obese, BMI of 35 or greater = morbid obesity. On many BMI charts, the obese weights are colored red, the overweight weights yellow and the normal weights white. (You can find a typical BMI chart on my practice's website: www.weightmp.com).

Because BMI looks at weight without distinguishing whether it is coming from fat, bone, or muscle, people with denser bone structure or those with large muscles masses can have high BMIs. I am frequently asked by patients whether a weight that increases or fails to drop might be coming from a new muscle-building gym regimen. Alas, the answer is generally no. Unless you are built like Dwight Howard or Arnold Schwarzenneger, the amount of muscle you gain in the average gym is not causing your BMI to rise. This is especially true for women, who can get great toning and definition from lifting, but are generally not capable of building large amounts of new muscle mass.

However, the major problem with BMI is not that it is inaccurate for the Greek gods among us. The major problem is in its low end, where it sets the bar for “normal”. The BMI chart, with it’s white, yellow and red sections shouts unequivocally that certain weights are unhealthy. These arbitrary divisions are at odds with the advice that obesity societies routinely give patients: that weight loss of 5-10% of current poundage can greatly reduce medical risk. So which is it? Do we need to lose just a bit or do we need to get ourselves all the way to the Promised Land….the white zone???

In my book, Refuse to Regain, I reference the work of Dr. Walter Willett of Harvard School of Public Health. Dr. Willett has been in charge of the comprehensive Nurse’s Health Study for some years, a study which shows that the risk of diabetes, hypertension, gallbladder and coronary artery disease starts to rise at BMIs that are far below the 25 we consider “just overweight.” Dr. Willett has said that this data was known, but ignored when committees set the “normal” cutoff for BMI. He believes that the reason is simple. If normal BMI were lowered to somewhere around 22, the vast majority of America would be classified as overweight.

While Dr. Willett is one my dietary and medical heroes, I have a somewhat different take on BMI. Yes, we know that weight gain impacts our health negatively. We know that even small amounts of weight gain put us at risk. But what happens once the horse is out of the barn? Once we have gained that weight, incurred that new risk, what then? Are the rules for “healthy” BMI the same after gain has occurred? This question brings us to a larger and more fascinating issue: Is there some permanent change that occurs within us once we have been overweight that changes those rules?I believe the answer is yes.

What I call POWs (previously overweight people) seem to be quite different from NOWs (never overweight people). As someone who was a NOW in my earlier years and is now a POW, I can attest to the fact that my physiology has changed. Can I prove this scientifically? No. We have now crossed over into the area of observation and opinion. Read on with that knowledge.

In my view, weight gain occurs when the normal mechanism that controls and stabilizes weight is damaged by over-exposure to elements of the SAD (standard American diet). Once the damage is done, I believe that we remain prone to weight gain. We can prevent this by avoiding the foods that caused the damage in the first place, but we must be extra careful. Most POWs cannot eat mindlessly anymore.

This tendency to weight regain may also have to do with fat cells which remain in the body, but which no longer contain fat. No one knows if depleted, empty cells signal the brain or cause other kinds of hormonal havoc. So what does this have to do with optimal BMI? When we gain weight, the body has to manufacture new fat cells to store the oily triglycerides which are being created. These cells are supported by a scaffolding of connective tissue and muscle. After weight loss, the fat cells are emptied, but some of the tissue may remain. Many POWs find that they simply cannot lose enough weight to reach the white area of the BMI chart. This may well be because the BMI chart is based on the weights of those who have never been heavy, in other words, the weights of NOWs. Since they have never manufactured new fatty tissue, their baseline weights are lower.

I love what I do, but I have written before about the one part of my job I don’t enjoy. That would be the very last phase of a patient’s weight loss. Almost without exception, my patients are unhappy with their final weights. This happens even when they have lost 60, 80, or 150 pounds. Each one longs to to get down “just a little more!” Each one feels like a failure for not reaching the white zone. This is the point at which BMI charts become tyrannical, and for no good reason. The rules for optimal BMI in the POW are different, just as pretty much everything else is different for POWs. Since there are no established guidelines for optimal weight in the POW, I can only offer my own take.

1. If you have been significantly overweight, a loss of 20% of your pounds is highly successful and is what I usually target. If you’ve lost more, great!!

2. Your optimal BMI should be the one at which you have eliminated or greatly minimized any weight related medical issues (especially blood pressure, diabetes, and lipids). In some people, remnants of the problem will remain, but the vast majority can expect significant improvement and decrease of medications.

3. Your optimal BMI should be one at which you can comfortably maintain.

Number three is probably the most important guideline, because weight loss is of no consequence if it ends in regain. POWs who push themselves to very low weights often do so at the expense of muscle tissue. If you start to look wasted, your vital muscle mass may be dissipating. At such low weights, and without muscle to help out with calorie burning, you will have to make do with what I call “two peas and a bean”. That’s not fun, that’s not life, and that’s not sustainable.

Are BMI charts important at all? Yes. They remain vital for judging the weights of NOWs, like our kids, young adults and that minority who remains at normal weight. If we can prevent them from converting to weight gainers, they will not have to deal with the permanent changes that dog the rest of us. As parents, educators, doctors and public citizens, this is a worthwhile goal and one that our health care system should be targeting. But for the rest of us? Shoot for maintenance, comfort, health, mobility. These will stand you in good stead whatever your zone or color.      

“Lost”….and What Else We Might Lose

By Barbara Berkeley

My daughter and her friends have been posting excited messages on Facebook for weeks. “Lost”, ABC’s blockbuster mystery-on-an-island, is back for its final season! This is an occasion for special t-shirts, viewing parties and intense discussion. For fans of faux-terror, “24” is also back. “American Idol” has returned fueling speculation about its life without Paula and about who will replace Simon. Television takes up time. A lot of time. The SuperBowl is coming up. There’s a war going on for late night supremacy. And if you live in Cleveland, as I do, there are weekly hours of obligate viewing as LeBron, Shaq, and the Cavaliers continue their domination of the NBA.

Believe it or not, I am actually able to remember a time when television DID NOT EXIST! My father had a friend who owned a local furniture and appliance store and as a result was able to get one of the first TVs on the block. Most of the time there was a test pattern on the screen when you turned it on. Later, there was Milton Berle, Sid Caesar and Ding Dong School. Not much else. As time passed, the broadcast schedule grew and television watching became a family activity. This seemed to culminate in my preteen years when the whole family gathered to watch shows like Man from Uncle, The Defenders and Dr. Kildare. But television was still not primary in our lives. School activities, playing out in the street in front of our house and congregating on the stoop took up a lot more time and were a lot more fun.

When I first moved to Cleveland over 20 years ago, I remember being invited on a house tour that included some of the fanciest homes in the neighborhood. I remember being shocked by one house in particular which had TVs in just about every room and not a single book. Now, my own house has multiple TVs in many of the rooms and that includes one of those big flat screen babies…the better to watch every detail of every Cavs game.

So the question is: is all this TV good for us? In January, a study from Australia announced some sobering findings. Researchers studied 8,800 adults for a median time of 6½ years while looking at things like exercise, smoking, weight and television viewing time. Amazingly, each daily hour of television was associated with an 18% increase in death from heart disease and an 11% increase in death from all causes. This translated to a whopping difference between those who watched less than two hours of TV per day and those who watched over four. In fact, the big time viewers were 80% more likely to die of heart disease and 46% more likely to die of anything than those who showed viewing restraint! (By the way, a person’s weight was not a factor in this study.) The study authors postulated that this significant risk came from sitting still for prolonged periods. That interpretation is certainly possible, but is it necessarily true?

When we read the results of studies as reported in the news, it’s tempting to accept them at face value. But it is important to understand that epidemiologic studies like this one can prove association only…not causation. In other words, we can see that TV viewing and shortened life exist together, but not that one caused the other. Nevertheless, we must be intrigued by the relationship. It would have been interesting to look at those people who watched TV while on a treadmill or at those who frequently jumped around while watching (like certain basketball fans!). This might shed some light on whether it’s the sedentary behavior that causes the problem or something inherently unhealthy about living life vicariously through little images on a screen. Do Ph.D. candidates who spend hours in the library live shorter lives? Are some sedentary activities – say, writing poetry or meditating for extended periods – more conducive to health than others? We simply don’t know.

In the meantime, I doubt that this study will stop anyone from turning on the tube. For those of us of a certain age, though, its results remind us poignantly that there once was a world where playing on the street and sitting on the stoop seemed far preferable to parking yourself in front of an electronic gadget.