Why is my weight loss diet not causing me to lose weight?
New patients to my practice often say that they can't lose weight no matter what they do. They chalk this up to a bad metabolism or to something that must be extremely dysfunctional about them. Over the years, however, I'm hard pressed to remember anyone who was not able to lose weight once they began an effective diet. No matter how impossible weight loss had seemed, it became possible once the diet was properly adjusted. Naturally, this result assumes that the dieter follows the diet as prescribed.
Why then the frustration and why do diets seem to fail? Here is what I've come to believe (followed by some suggestions that may help):
1. Diets Fail Because We Fail to Understand What They Are
I like to think of dieting as a completely unnatural act. If you could revisit ancient times, you would not find any humans forcing themselves to lose weight. Having a bit of extra fat would have conveyed a survival advantage, so why would anyone have wanted to get rid of it? Our twenty-first century bodies still behave this way. In fact, they seem to completely ignore weight as we gain it.
Knowing the body's propensity to correct imbalances, one would think that increasing fat would cause the appetite to shut down, or prompt the release of a cascade of hormones that would dissipate the excess. But that doesn't happen. Perhaps the reason is this; since it was always a good thing to store extra fat, we never developed any mechanisms for aborting weight gain.
Since the body ignores our fat, how can we create weight loss? We do it by recreating the ancient situation that would have forced the body to notice its own fat. That situation would be a significant food shortage. In actuality, a modern weight loss diet is simply the process of tricking the body into believing that there is a famine in the outside world. Once the body gets the idea that there is very little food coming in, it suddenly wakes up to the presence of stored fat and starts to use it up. This state of awakening was doubtlessly designed as a survival response hundreds of thousands of years ago. Let's call this bodily state: "The Ancient Famine Response."
Next, let's think about what would have constituted normal eating for these same ancestors. Since they hunted and gathered, they probably had ample food one day and very little another. To adjust to this, human bodies developed a very flexible system for using food. If food is in short supply, the body can slow down , burn fewer calories, and be more efficient. If we eat more, the body can speed up. These mechanisms allowed our ancestors to stay at stable weight even when food intake fluctuated. Let's call that the "Normal Ancient State".
Most of us start a diet with all intentions of following the rules exactly. That works! We lose weight because we are consistently telling the body that there is very little food coming. We've mimicked the “Ancient Famine Response." But we soon start to get creative. We eat things which seem to be minor, but aren't on plan. We eat a bit more than we should. Or, we don't eat on some days and eat more on others. All of these behaviors put us back into the "Normal Ancient State". It's true that we are eating less than we did before the diet, but we are not losing. That's because food intake is intermittent and not sufficiently restrictive. The body adjusts, lowers its burn and keeps weight stable, just as it's programmed to do.
Suggestion: Pick a diet that you can follow to the letter. Stay as compliant as you possibly can. Resist the temptation to go off the diet on some days and resume on others.
2. We Don't Have a Way to Get Calories Low Enough
In our practice, we create weight loss with a diet that has approximately 1200 calories. Larger women and/or men may use 1500 calories or so. This sounds simple, but it isn't. Calorie counting is complete guesswork in the modern world. Using packaged foods which have known caloric content can help. Once you start eating out in restaurants, as most of us do, counting becomes impossible. Although I do not like processed foods, dieting may be a good time to use them. If you can construct a diet from bars, supplements, frozen diet entrees, low fat dairy products and other foods which have calories already listed, you can be pretty sure of the number of calories you are getting.
In our program, we use three diet shakes or bars (each 160 cals) per day and have patients eat a dinner which is composed of a small piece of lean animal protein (chicken, fish, meat), a large mixed vegetable salad, a big portion of cooked green vegetables, a piece of fruit, and a 100 cal fat free pudding. You can work out your own plan, but knowing that you are getting the right calorie count is important.
Suggestion: If You Aren't Losing, Check Your Calories. Make more use of foods which have calorie labels. Try to avoid eating out if it is scuttling your weight loss.
3. We Don't Get Our Insulin Low Enough
Insulin is a mega-important hormone for dieters because it stores fat. It not only puts fat away into the fat cells, but it also stands guard outside the cells to make sure the fat stays put. Only by lowering your insulin levels can you break down fat. Imagine insulin as a jailer that keeps the prisoners trapped. Put him to sleep and they can escape.
Insulin is made whenever we eat starch or sugar because those two things turn into blood sugar once they are absorbed. (Insulin's other job is to control the levels of blood sugar). Dieters have already intuited the role of insulin. What is the first thing they do when they start a diet? They begin with salad and chicken breast. They eliminate bread, pasta, crackers, rice and dessert. Insulin goes to sleep and weight loss follows. But before long, the carb addiction begins to howl. That piece of pita doesn't have that many calories. That rice cake is a diet thing, right? Wrong. This part isn't about calories. Wake up your insulin enough and you won't lose weight.
Suggestion: Keep starch and sugar to a bare minimum when dieting. (This works for maintenance too!).
4. We Rely Too Much on Exercise as a Weight Loss Creator
Exercise is great. I love it! But alone, it will not cause weight loss (unless you are running the ultra-marathon or something). Remember the Ancient Famine Response: unless you create a consistent state of calorie reduction, you won't lose. In my practice I have many skilled tennis players, marathon runners, volley ball enthusiasts, and other athletes. If exercise caused weight loss, they would not be visiting me to get off the 30 extra pounds they've accumulated. Be especially careful with the temptation to over-exercise. This can create hunger and entitlement (as in, "I earned that bag of M and M's"). Exercise by all means, but during weight loss, put most of your faith in calorie reduction that is consistent and calculable.
Suggestion: During weight loss, think of exercise as secondary to caloric reduction.
Remember this: magazine covers would lead you to believe that weight loss is simple and that pretty much everyone in America is having their pounds "melt off". This is the big lie. Weight loss is tough and takes a tough effort. What remains true is that the rewards for this effort are great; the endpoint incredibly worthwhile. So keep at it and always congratulate yourself for taking on such an important and challenging task.
What if you could cloak yourself in a defensive shield that warded off disease and extended your life? Would you do it? Would you take a pill that could do it for you? Many of us are already trying to, by swallowing tablets of antioxidants and resveratrol, swigging acai and pomegranate juice and downing loads of vitamins of uncertain benefit. But a growing body of research suggests that the solution may be as seamless and elegant as nature itself. It’s possible that we can activate just such a defensive shield this very moment…simply by eating less.
As readers of this blog know, I am especially interested in the role of food choice in life extension. I am also deeply convinced that the hormone insulin is the central “superhormone” which mediates fat storage, obesity, inflammation and longevity. Whenever you read any research about overweight and its related conditions, you will find the fingerprints of insulin all over it. I also believe that a broken or poorly functioning insulin system is the reason that the vast majority of us develop modern disease. We don’t need to have diabetes or even elevated blood sugar to have a struggling insulin system. Defects in insulin signaling can be going on for years before we can detect them. This doesn’t mean that our bodies are not suffering.
Now, in a paper that is due to be published in Nature, “Hungry Immune Guardians Are Snappier: Nutrition Has a Direct Influence on the Immune System,” German scientists have shown that we have a second defensive system which acts independently of our classic immune system. When we go without food for awhile, this system switches on. Surprise, surprise…. the hormone which is responsible for flipping the switch is insulin. Once the system is activated, cells produce proteins which are capable of destroying harmful microbes and defending us against invasion from the outside. According to the the study director, “This happens every minute every day. What is fascinating about this is that a function of the immune system directly depends on how much and what we eat.” In other words, slightly stress your cells by making them hungry and your shields will go up.
This, and other research studies, provides a great deal of non-caloric food for thought. We know that obesity and the diseases it spawns lead to increased inflammation in the body and can result in reduced life span. We also know that uncontrolled inflammation is bad. Might it be that the habit of affluent societies to eat continually results in a chronically lowered defense system? If more invaders are able to penetrate our outer barrier, we would likely respond with aggressive inner defenses, in other words: inflammation!
One of the strategies for weight maintenance that I suggest in my book and that I continue to suggest to patients is that we spend parts of each day in the non-eating state. This allows insulin levels to fall. We now know that these lower levels can active the FOXO transcription factor; the messaging system which turns on defense genes.
So put up those shields and rethink that grazing habit. As those of us who are maintaining weight know, the body does best on small amounts of highly nutritious foods. Our miraculous physical plant is finely tuned and we may be best off if we stop trying to second guess it with pills, potions and manipulations. More and more, we are coming to know that a return to simple basics and realignment with our genetic priorities is the only way to put nature to work for us.
All living things are the same. Life is complex, achingly beautiful, and enduringly mysterious. Sometimes it's hard not to be amazed by its toughness. Life goes on, stubbornly, even after disasters occur.
But life, while incredibly durable in recovery, is fragile while it exists. That is because the conditions for life are so specific. All organisms have optimal environments and internal balances which cannot be breached without disaster. In the bloodstream of humans, a minor decrease or increase in potassium levels can be fatal, as can blood which becomes too acidic or alkaline. Life is a walk on a tightrope with the balancing pole handled by a master wire-walker. Life's corrective mechanisms, however, are meant to work within a narrow range of challenge. A hurricane will blow even Phillipe Petit off the high wire.
All life is the same. Oceans. Animals. Humans. It is our failure to understand this, our hubris about our superiority as a species that has gotten us into what is rapidly becoming fatal trouble. As I listen to the increasingly depressing news coming from the Gulf of Mexico, I am continually reminded of the parallels to be found in our own personal pollution.
The rapid development of technology in the 20th century has led us to a dark place. We have come to believe that we can control nature, even create it. We have come to rely on technology as a way to repair the damage we have done to ourselves and our planet. The fragility of life is unimportant. We can do what we please, consume what we please, and fix it all later. The message of the Gulf should be one we take personally. Just as the Gulf is dying, so are we.
In the Gulf, BP extended the reach of its technology beyond its powers. In order to produce the oil we gulp like thirsty infants, pipes have been placed into the very heart of our tender earth. Did we ever think about the fact that we had no equipment to address a problem at that depth? Did we ever consider the extent of the disaster that would occur if things went wrong? No. When consumption and gluttony are primary, questions of stewardship become secondary.
Now we find, to our horror, that life can be easily extinguished by our errors. Because of our supposed scientific prowess, we always felt we could stem the tide, mop up the mess. As of this morning, a machine that looked like a pair of ragged lobster claws was trying to hack away at BP's spewing oil pipe. This resembled nothing so much as an attempt to stop a ruptured aorta with a pair of pliers.
So too is it with us. Because all life is the same, we are the Gulf of Mexico: a gorgeous, fragile ecosystem that should be preserved at all costs. Instead, we have allowed endless pollutants in the form of manufactured foods, additives, pesticides, carbon monoxide, sugar loads, preservatives, ad infinitum, into our inner marshes. We gasp when a blood test shows that we have diabetes, when a CAT scan reveals a cancer. We turn to technology to fix us: pills, stents, injections, surgeries...only to find that these are roughshod solutions, about as precise and effective as the aforementioned pliers.
Like the people of coastal Louisiana, we should be angry that we have trusted those who told us that all this was safe. When we stop connecting with who we are, with what our planet is; when we focus more on what feels good for the moment, we become vulnerable to the talk of people who want to sell us the things we crave.
For the past 20 years, my extended family has visited the Bahamas and has enjoyed its pristine beauty. It is a place that is dear to our hearts. The photo above was taken in January. What will this beach look like next year at the same time? I found myself having the very same thought as I stood behind a mother and her daughter in Starbucks this morning. The mother was very overweight, fairly bursting out of her jeans, and having some difficulty walking. Her daughter was about 16, a bit too heavy and very pretty. Her mother offered her a large chocolate frappacino with extra syrup and encouraged her to add whipped cream. The barista happily made it up. Starbucks contentedly collected the six bucks. It was 7 am.
All living things are the same.
My path to becoming both a doctor and a writer began one fall afternoon in 1963. JFK was President and the world seemed like a very youthful, modern place. I had just turned 15 years old. Despite living in what seemed to be a golden time, I had two major fears: I was afraid of nuclear war for one. Everyone was in those days…the years of bomb shelters and air raid drills. My second fear was the worry that something might happen to my parents. My parents were 45 and 50 years old, and despite the fact that they both smoked, they seemed incredibly healthy. But a number of events had conspired to make me nervous. My closest cousin had lost her mother at a young age. Soon after that, my Grandmother died of a heart attack. And most recently, a friend of mine had returned from the movies to find that her father had suffered a cardiac arrest while on the living room couch. While most adolescents have a feeling of immortality, I no longer believed that either I or my family was invincible.
On the particular day in question, my parents, my sister and I were eating a lunch of hamburgers and French fries at our tiny kitchen table. I remember that my father stopped in the middle of helping himself to the ketchup. He got a strange look on his face. My mother sensed something was wrong immediately and asked what was going on. My father didn’t know. He had a strange pressure in his chest though. Not a pain really, he said. Just a tight feeling. But within moments he began to sweat and said he was going upstairs to lie down. This was odd indeed. My father was known for bounding around, taking the stairs in our house two at a time. We had never seen him taken ill suddenly. My mother threw a few reassuring words our way and followed him upstairs. Within a few minutes, my mother was on the phone to our family doctor and then was hurrying out the door with my father leaning on her arm. “Dr. Shapiro thinks that Daddy may be having a heart attack.” Was all she said. “I am taking him to the hospital. I’ll call you when I know what’s going on.”
My sister and I were left at home. We weren’t old enough to drive yet so we sat around waiting for the phone to ring. We were terrified. All I could think about was the night that my Grandmother had gone to the hospital with her own heart attack. At three that morning, the phone had rung. My mother had answered and I had heard her crying. My grandmother had not survived the night. From this I learned that a heart attack was a frightening, unpredictable, dangerous thing.
But my father was lucky. Dr. Shapiro decided that he had suffered only a minor heart attack. This sounded ok until my sister and I finally got to the hospital. We found my father in an oxygen tent, a contraption that looked like a plastic bag with a zipper that sat around his head and shoulders. The distorted view through the plastic, the distance it put between us and the uncertainty on my father’s face started a fresh wave of worry. My mother told us that he would need to be in the hospital for a couple of weeks. This was how things were done in the 60s. A heart attack meant complete rest. There was no such thing as cardiac rehab, surgical fixes, or fancy medicine.
For days, I camped out in my father’s hospital room, coming right after school and staying until visiting hours were done. My homework suffered because it was tough to concentrate. But at least I wasn’t worried about English class. Although I was taking a college prep class, the school had assigned it to a teacher who had never worked with college bound students. Her assignments tended to be boring and easy. One evening, shortly after the heart attack, I sat in my father’s hospital room anxious and unable to think. I was supposed to be writing an essay entitled, “Why We Study English” and it was due the next day. I opened my notebook, dashed off two pages that were pretty trite and called it quits. It was the best I could muster at the time. The gist of my essay was that language was important and knowing how to use it was important too. We underestimated what we could accomplish by communicating, I wrote. To make this point, I quoted the proverb: the pen is mightier than the sword.
A couple of days passed. I went to class by day and continued my hospital vigil at night. At the end of English period, I was summoned by my teacher and asked to stay after class. My teacher took me aside. “Where did you hear the phrase, the pen is mightier than the sword?” She asked. She seemed belligerent. I couldn’t answer. It was simply a proverb I knew. I thought everyone did. (By the way, the derivation is incredibly obscure. According to Wikipedia: “The pen is mightier than the sword" is an adage coined by English author Edward Bulwer-Lytton; in 1839 for his play Richelieu; Or the Conspiracy.) When I could not produce a source for this quote, my teacher went on to tell me that this proved that I must have plagiarized my entire essay. In fact, she claimed to have the source for the original essay and said that she could produce it. (This would have been a neat trick since the entire paper had been concocted in under 20 minutes in my father’s hospital room!!!) If I didn’t immediately fess up to my crime, she went on, I would face severe consequences. To say that I was dumbfounded is quite an understatement. I fairly sputtered. I explained about writing the essay on the fly while my father sat under the oxygen tent. She refused to believe me and also refused to produce the essay she claimed to have. Instead, I was sent directly to the school disciplinarian, a fearsome presence in our high school and was threatened with several months of detention. The whole matter became an escalating horror that lasted for weeks. This incident taught me about the power of false accusation, particularly when you are in a subordinate position to the accuser. In the end, the principal, my mother, and a whole cadre of my ex-teachers became involved. It was all hushed up, but the teacher was never disciplined and the incident remained an unresolved blot on my high school experience. For me, the incident is inextricably bound up with the story of my father’s heart attack. While the whole mess was awful and unfair, but it became suddenly less important when, in the same English class that November, a classmate burst through the door with the news that John F. Kennedy had just been assassinated in Dallas.
After my father came home from the hospital, my mother decided to do whatever she could to make him well. For her, that included a complete revamping of his lifestyle. Although there was less known about the prevention of coronary disease then, my mother was savvy enough to figure out an effective plan. Gone were the cigarettes, and gone were the fried and fatty foods. Prior to his MI, my father had hated fish and refused to eat it. Now my mother became insistent, and fish appeared on our menu. So did chicken, which was a huge departure for my red-meat-eating Dad. Then there was the exercise. My mother got my father walking 2 miles a day, a habit he continued well into his 80s.
My mother’s plan changed and prolonged my father’s life for sure, but he remained affected by his coronary artery disease. Today, thanks to her, he is 96 but he still needed a coronary bypass operation and several stents to go this distance. Once a disease process is established, it is easier to control than to eradicate. Ironically, I am watching an example of this principle break on CNN as I write this. Bill Clinton has just been admitted to the hospital to have stents placed in his coronaries. He needs these despite having had earlier bypass surgery. The message here is that medicine and surgeries can only get us so far. We are best off…by far….if we prevent heart disease from ever getting started. And that is quite possible. Blocked arteries are not inevitable. In fact, coronary artery disease is a condition that was largely unheard of until we started eating the modern diet and stopped using our bodies to do physical work.
Prior to my father’s heart attack, I thought the world was fair. After my father’s illness and my plagiarism experience, I found out that fairness was not guaranteed. But through my mother’s interventions with my father, I learned that there was hope. You could do something to help yourself, to change the odds. I became interested in medicine and in finding ways, as my mother had, to prolong life through disease prevention. Rather than being discouraged from writing, the false accusation emboldened me to use writing to get a bigger voice. So I suppose you might say that these two experiences converged and started me on the path that led to this very moment. Here I am, writing to people all over the world about heart disease.
So what can we do about coronary disease? First and foremost, we should try to prevent it from happening in the first place. Heart attacks occur when the small vessels that feed our heart become inflamed, damaged, and blocked. To avoid this, we should keep our waistlines trim (fat around the middle secretes chemicals that start off inflammation in our vessels and promote coronary blockage). We should eat a diet that does not resemble the standard American diet. Mediterranean is good. Ancient may be even better. If our cholesterol numbers are high, we shouldn’t fear taking medicine. Cholesterol lowering drugs are among the safest and they also decrease vessel inflammation. We should do everything we can to avoid damage to our precious arteries. Damage comes from sugar that is too high (above 100 when you’ve fasted overnight), from blood pressure that is too high (in the 120s or below is best) and from blood fats (cholesterol and triglycerides) that are too high. We should make physical activity a priority. Our heart is a muscle, and like all muscles it benefits from a work out.
Please join me in thinking about ways that you can treat your heart better. Find ways to encourage the same changes in those you love. And share the word. Thanks Mom, for figuring this out 47 years ago. And thanks, Daddy for following the program.
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 ten 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.
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 scientist’s research came to believe that damage to DNA came first and the damage went onto 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 Professor of Biology at Boston College. Dr. Seyfried is among those who believe 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 that are calorie restricted have slower aging, less cancer and chronic disease. Might this be related to a lower sugar environment? So, I guess you know what I think.
The first episode of public backpedaling on vitamin supplementation probably occurred during Sanjay Gupta’s segment on CNN’s Situation Room. 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. http://pagingdrgupta.blogs.cnn.com/2010/03/31/can-your-multivitamin-give-you-cancer/ 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 AJCN 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.
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?
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.
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.
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 1980 (take note of this date), Ancel Keys, a professor of physiology from the University of Minnesota, published 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 late 60s, he 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. With the advent of the Seven Countries Study, 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, much generalized, piece of the puzzle. Equally, if not more important, are the types of lipids you 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 you to coronary disease. Standard lipid tests do not say anything about the size of LDL particles, but doctors can tell if you have them by looking at levels of two other elements, triglycerides and HDL. If the ratio of these two elements is above 3.8, it’s a strong indication that you have small, dense LDL. We call this type of lipid profile “dyslipidemia” and it is highly correlated with vascular disease.
Is this all about 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. “Caloric Sweetener Consumption and Dyslipidemia Among US Adults.”
Here is how the authors introduced it:
Dietary carbohydrates have been associated with dyslipidemia, a lipid profile known to increase cardiovascular disease risk. Added sugars…are an increasing and potentially modifiable component in the US diet. No known 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 even consider 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 principle; 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 good mustard, a salad, and an avocado. Lots of omega 3, completley Primarian, and not a sugar in sight.
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.”
With the advent of the internet, interactive tools like BMI calculators have become familiar to dieters. Twenty years ago, BMI was part of the foreign language of doctors. The measurement was recorded on the chart and remained obscure for patients. Today, nearly every dieter understands, (and sometimes obsesses about), his or her niche on the BMI chart.
BMI, or Body Mass Index, is 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 people’s 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, with the cut-offs being as follows: BMI of 25 or less =normal, BMI of 25 to 30=overweight, BMI of 30 to 35= obesity, 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 website at 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 Schwarzenegger, 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 its 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’s 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 an 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 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.
“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 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.
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? In the answer appears to lie 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. 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, they’ve lost a couple of ounces, or nothing at all. 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.
The common wisdom tells you to build it. Most people think they don’t have enough of it. Fitness experts tout it as something almost magical. But what’s the real deal with muscle?
I have the strange habit of reading certain research papers repeatedly. The tendency to read things over and over may be inherited. My father loves to read certain books dozen of times. We have a copy of Shogun at my house that is literally falling apart; ditto Prizzi’s Honor, Lonesome Dove, and The Godfather, but research papers? I can only say that there are just some articles that I enjoy as much as a novel. When I found myself re-reading my favorite paper on muscle, it occurred to me that perhaps I should share the love.
My dog-eared, underlined, thinning favorite paper is called “The Underappreciated Role of Muscle in Health and Disease.” It was published in the American Journal of Clinical Nutrition in 2006 and is one of the only reviews I’ve ever read that focuses on exactly what muscle does. We talk an awful lot about muscle, but its real importance - the vital role that muscle plays - is virtually never discussed.
The story of muscle starts and ends with protein. Proteins, made up of various amino acids, are the material that build our organs and repair the damage we incur every day just from living. We cannot survive without a steady supply of proteins because this daily wear and tear causes unavoidable organ breakdown. Proteins repair this damage. Think of yourself as a building that is exposed to the environment 24/7. As your paint starts to wear away and your façade starts to weather, there are workmen who are constantly repairing the damage. They are fixing you up with buckets of protein.
Eating foods with proteins provides a flood of amino acids to your body. These are reassembled into new combinations to form the exact proteins needed for that day’s repair. The need for amino acids is a 24 hour-a-day situation. So here’s a question: Where do amino acids come from if you’re not eating or if you are asleep? The answer is: from muscle. Muscle is a bank. Your body withdraws protein from muscle to accomplish repairs. When you eat, most of the protein you ingest actually goes to replace what’s been “borrowed” from your muscle in the hours before.
People who are obese actually have larger stores of muscle than lean people. Studies have shown that these big banks of muscle can keep protein levels normal after as many as 60 days of fasting! On the flip side, when muscle shrinks to about half of its normal amount, life can no longer be supported. Observation of people who have undergone starvation conditions has shown that it is the critical loss of muscle mass that leads to death. Once there is no longer enough protein in the bank, repair ceases, and so does life.
Muscles are even more important protein “lenders” when we suffer from conditions that greatly accelerate the body’s need for protein. Injuries, illnesses, operations, burns, cancer, chemo, and other physical stresses greatly increase demands for repair proteins. Sometimes, a seriously ill person can have protein needs that can be as much as four times those of a healthy person. These can’t be met through diet alone, so the muscle bank is accessed for massive withdrawals. Those who start out with a large amount of muscle mass will have a greater likelihood of getting through such an event.
Since our muscular bank account is so vital, we need to worry about that fact that we can lose muscle as a consequence of aging. Loss of muscle is called “sarcopenia” (sarco=muscle, penia=impoverished) and is it a common problem for older people. Sarcopenia is estimated to occur in about 30% of those over 60. Sarcopenic people are frail, tend to have more falls, and have more difficulty with daily activities. As we saw above, a decrease in muscle mass not only means weakness, but an inability to fight off serious illness.
What about the much touted ability of muscle tissue to burn calories? Muscle burns calories when it remodels itself by either adding to or breaking down its mass. These processes take energy and, as we’ve discussed, are constantly occurring because of the withdrawal and redeposit of protein which is normal operating procedure. However, larger muscle masses have higher rates of turnover and calorie burn than smaller masses. A young man, for example, might have about 80 pounds of muscle which burns 485 calories per day. An elderly woman is likely to have just 30 pounds of muscle, providing only 120 calories of burn. This calorie burn is independent of exercise, by the way. It is part of the “resting metabolism;” calories which are burned when we simply sit still. You can see that the metabolic difference between the young man and the older woman is quite large. Now you know why your 17 year old son can eat seemingly endless amounts of food without weight gain. You can also understand why building extra muscle might help you to maintain weight loss. Even at rest, the extra muscles and their turn over will burn extra calories for you. The problem is that building extra muscle is not all that easy, especially if you are a woman or are older.
When people become obese, they do not gain fat alone. They also gain muscle which supports the heavy fat tissue. This can potentially be used to the overweight person’s advantage. Theoretically, if this extra muscle can be preserved during weight loss, the calories it burns will make weight maintenance more likely. We also know that we can increase the rate of muscle turnover by providing a stream of amino acids in the diet. These amino acids start the muscles to work, but the fuel the muscle uses to build and rebuild itself actually comes from FAT. In fact, fat is “the preferred energy substrate of resting muscle”.
Thus, we have the rationale for recommending higher protein diets for weight loss. Theoretically, the hefty amount of amino acids gets that big muscle mass turning over. Turn-over then contributes to fat burning. In addition, dietary protein keeps muscle mass from disintegrating as weight is lost. The idea is to get fat to burn preferentially while leaving the dieter with a hefty amount of calorie-burning muscle. In our clinic, we use high-protein liquid drinks and one dinner meal to get weight loss. We find that the combination works very well, perhaps for this reason. We might also extrapolate that continuing to eat diets that focus on goodly amounts of protein will stimulate muscle to maintain itself, turn over actively, and burn fat calories in the process.
Muscle also plays a pivotal role in insulin resistance, which can lead to diabetes. Normally, insulin tells the muscles to accept sugar from the blood. This is one of the ways that insulin keeps blood sugar controlled. As weight gain progresses, many people develop insulin resistance; an inability of the muscle to take up sugar when insulin calls. The body compensates by making too much insulin which in turn leads to high blood pressure, cholesterol and triglyceride problems, and eventually, high sugar in the blood.
The question is why should muscles become resistant to insulin? While we’re still not sure, this paper notes that people with insulin resistance have muscles which have become filled with fatty globules, visible on MRI. This inappropriate fat storage seems to be linked to insulin resistance and may reflect a problem with the muscle mitochondria, small cellular engines which normally burn fat. Instead of fat being burned, it is being deposited within the muscle. Physical activity seems to tell the mitochondria to work properly. “[…] As little as a single bout of exercise […] can transiently reverse insulin resistance,” the paper reports. This is crucial information for those of you who either have or have experienced insulin resistance. Keep exercising to keep your mitochondria burning fat rather than storing it. This will lessen resistance problems.
What about ways to preserve or build the muscle mass you have? Once you become sarcopenic, it is very hard to reverse the loss. Efforts should focus on preserving the mass you have as a young or middle aged person. Remember that the goal of exercise should not be simply to grow big muscles. The effect that exercise has on getting the muscles to work efficiently at a cellular level is just as important even though it can’t be seen with the naked eye.
What’s the bottom line?
No one seems to have exact recommendations for protein intakes. Don’t be afraid to add some low calorie protein shakes or bars to your regimen if you are trying to build and maintain muscle. Make sure that you are getting adequate protein, particularly if you are vegetarian and most specifically if you are vegan. Keep up your exercise, not only to preserve the muscle you have, but to assure that it works properly. Keep exercising throughout your life in order to minimize your chances of sarcopenia as you age. Maintain muscle at good levels in order to give yourself the best chance of weathering unintended storms like illness or injury.
Like most of our body parts, muscle is not as simple as it seems. We will benefit greatly by feeding it, building it and taking care of it.