The Doctor Weighs In

"Most heart attacks in women are preventable," is the headline of an article posted on NBC.com.  The article describes a study, published in the Archives of Internal Medicine, that was done by the researchers at the Karoinska Institute in Sweden.  Dr. Agneta Akesson and colleagues looked at the diet and lifestyle patterns of almost 25,000 postmenopausal women.  At the time of enrollment none of the women had heart disease, diabetes or cancer.

The researchers asked the women to fill out "food frequency" questionnaires to identify how often they ate 96 different foods.  The researchers analyzed the data and found four major dietary patterns:

• Healthy - vegetables, fruits, and legumes
• Western/Swedish - red meat, processed meat, poultry, rice, pasta, eggs, fried potatoes, and fish
• Alcohol - wine, beer and some snacks
• Sweets - sweet baked goods, candy, chocolate, jam, and ice cream

Other information collected included family history of heart disease, education level, physical activity, and body measurements.

The women were followed for an average of 6 years.  During that time, 308 women had heart attacks.  The investigators found that two of the dietary patterns (healthy and alcohol) were associated with a decreased risk of heart attack.  Women who drank less than a quarter ounce of alcohol daily (that is just a splash in the bottom of your glass) and ate lots of veggies, fruit, whole grains, legumes, and fish had a 57% lower risk of having a first heart attack.  That is a whopping big difference.

If women added three other healthy lifestyle habits into the mix (not smoking, being physically active, and avoiding too much weight gain), they had a 92% lower risk of heart attack.  In other words, most heart attacks in women are preventable by making healthy lifestyle choices.

Now, it is one thing to say, eat healthy, drink in moderation, exercise and maintain a healthy weight.  It is quite another thing to actually do all of those things over the course of an entire lifetime.  On the other hand, if you look at the amount of money the US (and, indeed, the entire world) spends to treat cardiovascular disease, I believe you would find there is enough there to buy each and every person a personal cook and a personal trainer (I believe this is the secret to Oprah's weight loss and maintenance).

I say this tongue in cheek, but it does make the point that we aren't spending our "health" care dollars on the right things.  We spend generously to fix disease, but we are very stingy when it comes to funding health.   It is time to get this right.  There aren't enough dollars in any treasury to treat all of the heart disease we are going to see as a result of the global epidemic of obesity and physical inactivity.  This must be  a top priority of policy makers and health reformers.  Studies, like the Karolinska study, should be used to promote changes in public policy - such as healthy school foods, ensuring that all neighborhoods have access to fresh fruits and vegetables and that they have safe places where kids and adults can move their bodies (without worrying about getting shot in the process).

Every politician, health reformer, and policy wonk ought to know about this study and others that prove that healthy lifestyles mean fewer heart (expensive) attacks - not just in women, but in men as well.  The bottom line is most heart attacks are preventable!

by Bill Besterman

The underpinning for much of the death and disability from arterial vascular disease in this country is the metabolic syndrome. One of the real authorities on the metabolic syndrome is a Dr. Ralph DeFronzo.  I particularly like his description of this collection of disorders as a “complex metabolic web.” 

The patients who have this diagnosis are burdened with multiple chronic conditions: hypertension, high LDL or bad cholesterol, high triglycerides, low HDL or good cholesterol, and high blood sugar ultimately resulting in type 2 diabetes. These patients routinely have vascular systems where the vessels are inflamed and the blood more likely to clot.

Early in the condition the arteries are thicker and less distensible than in people without the syndrome; progression of the arterial disease is the norm. Many of affected individuals also have gout. More recently, the metabolic syndrome has been called the cardiometabolic syndrome because this name underscores the impact of these conditions on the heart and the rest of the vascular system. Metabolic syndrome patients have an increased risk of coronary artery disease, cardiac enlargement and congestive heart failure.  Type 2 diabetes is the late stage of the syndrome

Dr. DeFronzo highlights a very important clinical reality in describing the cardiometabolic syndrome as a complex metabolic web. "Job one" of the clinicians who treat these patients is to unravel that complex web using every medical and lifestyle tool in the medical toolbox.

Only 7% of these patients have all of their risk factors (hypertension, blood sugar, and cholesterol) simultaneously controlled to the most conservative goals. For each risk factor that is controlled, using the proper interventions, the risk of all adverse outcomes is reduced by roughly 50%. So, the task of the clinician is not just to control hypertension or diabetes, but rather to control all risk factors to goal at the same time.

That is where the focus, skill and training of your provider come into play. The particular medical choices that are made are critical for success. For three decades now I have heard physicians blame patients for not being “compliant:”

 “Mrs. Brown is diabetic and she does not listen to a thing I tell her. She just stuffs herself with anything she wants and she continues to gain weight.”

Here is the reality. Every medication commonly used for the treatment of type 2 diabetes causes weight gain with the exception of metformin (Glucophage) and the Byetta-type medications. The new drug Januvia is weight neutral. Most patients do not have their sugar controlled to goal using a single medication. Most patients require multiple drugs and even then progressive loss of glucose control is the norm. Weight gain not only makes control of the sugar more difficult—the metabolic syndrome is itself worsened by increased abdominal weight—weight gain also makes controlling pressure, cholesterol, triglycerides and gout more difficult.

The patient that receives a prescription for two shots of NPH insulin a day will gain 10 pounds in a year. The patient that uses glyburide plus a single shot of NPH gains 9 pounds. The regimen combining  glyburide, metformin and a single shot of NPH, produces a similar weight gain. Metformin added to a single injection of NPH at bedtime produces no weight gain, the best control of the blood sugar and the least number of hypoglycemic attacks. The doctor with the prescription pad is producing this result—not the patient. These are impressive weight changes and they make a big difference over time. I have treated 450 type 2 diabetics for nearly 10 years with a regimen based on metformin and a long-acting insulin injection with durable control in most patients.

The treatment of high blood pressure hides the same kind of traps. Until very recently beta blockers like propranolol (Inderal), metoprolol (Toprol) and atenolol (Tenormin) were recommended as first line therapies for the treatment of hypertension.  Many patients continue to be on these medications for the one purpose of treating high blood pressure. These medications have important metabolic effects:

• Propranolol increases triglycerides by 25%, decreases HDL by 10%, increases total cholesterol by 9% and increases insulin resistance by 33%
• Metoprolol increases triglycerides by 30%, decreases HDL by 7%, decreases total cholesterol by 1%, and increases insulin resistance by 21%

Tricor (fenofibrate) is prescribed to treat the lipid or cholesterol abnormalities that go with the metabolic syndrome decreases triglycerides by 29%, increases HDL by 11%, and decreases total cholesterol by 18%.  When we prescribe propranolol and fenofibrate simultaneously, we have simply cancelled the lipid effect of two drugs.

The prescription of propranolol makes it 28% more likely that the patient will develop diabetes. Choosing an ACE inhibitor makes it 33% less likely that a patient will develop diabetes. These are critical metabolic issues. There is a newer beta blocker carvedilol, with dramatically improved metabolic effects relative to the older drugs.

The point of all this is that treatment of these patients is very complex if it is done properly. 95% of type 2 diabetes care is provided by primary care doctors who are under tremendous pressure to see patients at the rate of 5-6 per hour. They are required to be experts in the whole massive knowledge base of medical practice We need focused clinics of the type described by the Institute of Medicine to treat metabolic syndrome patients. The providers in these clinics will need to be very expert in the coordinated, integrated management of metabolic syndrome patients and the resulting complications. Until that happens, we will continue to produce the same poor levels of risk factor control and pay a terrible price in lives, disability and treasure.

A few weeks ago (May 9, 2007) we posted a comment on Gina Kolata’s article in the New York Times (May 8, 2007) The article basically laid the blame for the obesity epidemic afflicting us at our genes. Kolata reviewed work suggesting that genes are involved in obesity, with the implication that a fight to lose and maintain a lower weight is not only excruciating, it is practically futile.

That simply didn’t sound right. At least 10 genes have been discovered thus far that are involved in obesity and diabetes; more are bound to be discovered. We also know that the US population is fast approaching the 50% mark of overweight (BMI 25-29.99) or obese (BMI > 30). These genes presumably are not recent mutations. Why is it then, that only relatively recently did these genes express themselves to cause the outbreak of obesity? I think the answer is quite obvious: we have here a classic case of genetic/ environmental interaction. The genes have been there all along; they haven’t changed. The new elements that caused such a massive upward shift in BMI are the invention of the car, television, computers, all leading to a sedentary life style. Couple this with profound changes in our dietary and eating habits, resulting in a significant increase in caloric intake, and you’ve got an inescapable outcome: weight gain.

Don’t go shopping for food when you are hungry

I don’t know who first pronounced this maxim, but I am sure many of us rediscovered it many times, independently. What we actually discovered is that hunger is such a powerful physiological drive that no rational, moderating influence can keep it in check.

The hunger drive

Our gut reaction, so to speak, to hunger is primarily hormonal. Fat cells secrete a hormone, leptin (leptos means thin, in Greek), that travels to the brain, and signals a message of satiety; the more leptin, the less hunger. Another hormone, called ghrelin is secreted from the stomach when it is empty, and its signal to the brain is hunger; the more ghrelin, the more hunger. This description is obviously a vast oversimplification, but the basic mechanism is clear: our sense of hunger or satiety is a balance between hormones with opposing influences on the center in the brain that controls feeding. This area, called the hypothalamus has neuronal connections to two other important areas: the amygdala, and the nucleus accumbens. Activation of the amygdala, when the hypothalamus senses hunger, causes a sense of alarm, sometimes accompanied by aggressiveness, easy irritability and other hard-edged feelings. On the other hand, a sense of satiety and fullness activates the nucleus accumbens, which is the seat of all the warm and fuzzy feelings, like reward and pleasure. The neurotransmitter that mediates this sense of pleasure is dopamine.

The cocaine connection

It turns out that dopamine is also secreted in the nucleus accumbens in response to cocaine, amphetamines and other recreational drugs. In fact, the response of the cells that carry the dopamine receptors to the sudden rise in dopamine concentration is to reduce the number of receptors, so as to keep the stimulus within manageable bounds, so to speak. This phenomenon is called receptor downregulation. To keep the pleasurable sensation at its previous level one needs to take even more cocaine, which in turn causes even more downregulation. You can readily see the neurobiological downward spiral that we call addiction.

Lo and behold, the same pattern is seen in brain scans during binge eating: Surfeit of dopamine, activation of the nucleus accumbens, and downregulation of dopamine receptors.

The brain’s “adult supervision”

Of course, being civilized creatures we could not let ourselves be governed by such “primitive” drives as pleasure and reward on the one hand, or anxiety, aggression and rage on the other. Indeed, evolution endowed us with a highly developed area in the brain called the prefrontal cortex. This is the seat of judgment and rational decision-making. It weighs the messages arriving from the reward and anxiety centers and renders judgments that find their expression in what we call behavior.

However, this Solomonic wisdom does not always prevail. When exceptionally strong messages arrive from one center, they overwhelm the messages from the other, and the judgment of the prefrontal cortex becomes skewed, or completely overwhelmed by the flood of the incoming powerful signals. Each one of us, after along period of fasting, must have felt an overwhelming desire to binge-eat. Only when we are finally disgustingly stuffed, do we ask ourselves: what am I doing? In neurobiological terms, the storm of signals from the amygdala (hunger to the point of anxiety) and the nucleus accumbens (“how sweet it is”, and the hell with the diet!) subsided, and the ever stern, judgmental prefrontal cortex reasserts itself (“have you no shame?”).

So, is it genes or addiction?

I believe that the addiction model is a more plausible explanation of the overeating epidemic that is afflicting us now. It also explains the extreme difficulty in “kicking the habit”, losing weight and maintaining it over a long period of time. As any recovered drug addict will tell you: one never really kicks the habit; it is a constant battle, and one is always on the brink.

The encouraging aspect of this grim picture is that addiction is susceptible to therapeutic intervention. There are drugs that can blunt the addictive urge. For instance, the drug naloxone reverses the effects of morphine. Interestingly, naloxone also blunts the hunger drive and reverses binge-eating.

Dov Michaeli, MD, Ph.D

If you enjoyed reading this, you may also want to read:

• Obesity:  The devil made me do it
• Genes and food -- good and genes

The April 12, 2007 online edition of Science (www.sciencemag.org/cgi/contrent/abstract), has important news from the field of obesity/diabetes type 2 research.

Is FTO the culprit?

FTO is an obscure gene that was discovered in mice who were born with fused toes (hence the name), and since that earthshaking discovery nobody bothered to study it, or find out what its function is, or in which pathway it participates.  In other words, the gene is, well, totally obscure.

And so it lay dormant until a group of scientists from nine institutions in Britain and one in Finland examined the genomes of 38,750 adults and children. Lo and behold, FTO stood out like a sore thumb (or toe)—people who had 2 copies (alleles) of a variant (or mutation) of the gene were 67% likelier to have a BMI of 30 or higher, and the ones who had only one allele of the mutation had a 37% likelihood of being obese (BMI of 30 and higher). Furthermore, the fat distribution was interesting: the gene was associated with both higher weight (regardless of differences in height) as well as wider waists and thicker concentrations of fat mass. These parameters are associated with increased incidence of heart disease and diabetes type 2.

What to make of it?

Before we shout Hallelujah, let’s examine it more carefully:

•  The study is indeed credible; a large sample size, reputable scientists in excellent medical institutions. But I can recall at least 4 other genes that were touted as the “obesity genes”, and later turned out to be totally unrelated. The science was good, but the field of genome-wide analysis is still in relative infancy, and interpretation is rife with pitfalls.
• Even if further studies corroborate FTO as a culprit in the heartbreak of obesity, it is unlikely to be the only one. Obesity and diabetes type 2 are multigenic diseases; and the interaction between them will add even more complexity to the picture.

The promise

But if FTO turns out to be the real thing, then several benefits will come out of this research:

1. A diagnostic test can be developed quite rapidly, to alert people who are at increased risk of metabolic syndrome.

2. Identifying the function of FTO will allow the development of drugs that will counteract the effects of the mutated gene.

Can I then go and pig out?

Alas, no. First, development of such a drug will take a minimum of 10 years, more likely even longer.

But even more important: genetics is only part of the story; the environment (read lifestyle) is just as important. Even if you don’t have the genes for obesity—abuse your body long enough, and your girth will tell all.

What to do?

The answer to this question is quite simple: eat less, exercise more. Regardless of genetics—it works! In some people a lot slower, a lot more painful; in others (whom we all envy) it's  “no sweat”. But barring some rare metabolic diseases, it is within our control. No excuses!

Dov Michaeli, MD, Ph.D

Photo from USA Today, by Jeff Mitchell, Getty ImagesAccording to a front page story in USA Today, there has been a “mind-boggling” increase in the number of people who are severely obese (aka morbid obesity). A study, published in the journal Public Health, by RAND Corporation researcher Roland Sturm, documents that there are 2.6 million more people with a body mass index of 40 or higher than there were just five years ago. Overall almost 25% of people are now considered obese, up from 20% in 2000. A staggering 66% of people in the US are either overweight or obese.

To help us visualize what this means, USA Today published a chart to accompany the article. Here is what it takes to be obese or severely obese:

Height                    Obese                    Severely Obese

5 foot 4                             174                                             232

5 foot 10                          209                                              278

George Blackburn, associate director of nutrition at Harvard Medical School is quoted as saying the increase in the percent of severely obese people is a catastrophe.

All this fat is not going to melt away without effort — effort on the part of individuals, communities, and society as a whole. For Americans to lose all that weight and get physically fit will require both personal and collective responsibility.

We need more bike paths; attractive, easy to use stairwells; safe neighborhoods; availability of inexpensive healthy foods; PE in schools; exercise breaks at work; and, in general, an American lifestyle that makes it easier to do the right thing for our health and well-being, than the wrong.

Failure to make significant changes in our work and family lives will indeed lead to a health catastrophe – more and more childhood and adult obesity, epidemics of diabetes, heart disease, high blood pressure and abnormal lipids and other obesity-linked diseases.

So, let’s get on with it…let’s work together to get the lifestyles we want and need.  I really hope I am not writing about severe obesity levels of 30% in 2012.

Pat Salber

We all know the devastating statistics:

· 13.5 million people in the US suffer from coronary artery disease

· 8 million people have diabetes type 2.

· 95,000 people are diagnosed every year with colon cancer, and a sedentary lifestyle increases the likelihood of getting this disease by 40%.

· People who don’t exercise have about a 60% increase in osteoporosis; 250,000 suffer from hip fracture every year.

· 50 million suffer from hypertension.

· More than 60 million people in the US are overweight.

You might conclude from the last bullet that obesity is the culprit. You’d be only partly right. Lack of physical fitness is the other culprit, regardless of percentage of body fat. Even if we take people with a high % of body fat (more than 25%), the relative risk of death from all causes in the fit person is half that of the unfit.

Exercise and the body.

The effects of exercise on the body are well known:

· Exercise increases HDL, the good cholesterol, by an average of 4.6%. This, in turn, results in a decreased risk of coronary artery disease.

· Exercise increases insulin sensitivity, reducing the risk of metabolic syndrome and diabetes type 2.

· Exercise strengthens the heart muscle, improving its function.

· Exercise increases bone size and density, reducing bone loss due to aging and osteoporosis.

· Exercise increases muscle strength, coordination and reaction time. Result: improved balance and stability; reduction in falls and bone fractures.

What about mind?

This is a truly fascinating story, and you can read about it in more detail in an article in Newsweek, March 26, 2007 , by Michael Craig Miller, MD, from Harvard Medical School . Here are the salient points:

· Exercise has been known for many years to give, during and after exercise an “endorphin high”. This is the feeling of satisfaction, well being, and increased self-esteem that many people experience. This effect is short term, on the order 1-2 days in duration.

· Aerobic exercise increases blood supply to the brain, thus increasing oxygen and nutrient supply to the neurons, and removing metabolic waste materials from the brain.

· Aerobic exercise increases the production of neurotrophic factors in the hippocampus.

What are neurotrophic factors?

When the nerve cells are getting organized to form the organ that we call ‘brain’ (a process that doesn’t end at birth, it actually continues until about age 20), they do it under the direction and control of peptides and proteins that are secreted by the nerve cells themselves. But the job of these factors doesn’t end there: they continue to shape, modify, and re-shape several areas of the brain. They are essential for the formation of new neurons from stem cells—a process called neurogenesis. They also are important in the formation of new connections between existing neurons—a process called neuroplasticity. These two processes are important because they are the basis for learning and memory; everything we know and remember is stored in neuronal circuits. Furthermore, the thicker the connections between the neurons the faster the flow of information in the circuits—very much like the broadband required for fast transmission of electronic signals. The brain factors cause this thickening as well.

There are several known neurotrophic factors that have been shown to increase in concentration due to a sustained, long term exercise regimen:

· BDNF (Brain-Derived Neurotrophic Factor).

· NPY (Neurpeptide Y).

· VEGF (Vascular Endothelial Growth Factor).

The fact that we can identify specific brain peptides that increase neurogenesis and neuroplasticity is interesting enough. But what makes it even more fascinating is where in the brain this increase happens.

Enter the Sea Horse.

In the temporal lobe of the brain there is an area, called the hippocampus, because it is shaped like a sea horse. This area regulates emotions and stores memories. In fact, it has been known that in aging brains and in depression, two situations in which neurogenesis and neuroplasticity are reduced, the hippocampus gets smaller. Furthermore, electroshock therapy and antidepressants caused an increase in the size of the hippocampus, apparently due to increase in neurogenesis and neuroplasticity.

It was especially gratifying to read in the latest Proceedings of the National Academy of Sciences (PNAS, vol. 104, p. 4647, 2007) the report by Warner-Schmidt and Duman. The unequivocally demonstrated that the antidepressant drug fluoxetine (Prozac) and the pain-control drug desipramine (Norpramine, Pertofran), cause a large increase in VEGF in a specific area of the hippocampus (The subgranular zone). Interestingly, desipramine’s action is inhibition of pain signals ascending through the spinal cord to the brain; in other words, it inhibits the perception of pain.

Not surprisingly, aerobic exercise does the same thing. We even know how this happens on the molecular level—through the action of the very same brain factors: BDNF, NPY, and VEGF.

The take home lessons

· We now know beyond the shadow of a doubt that aerobic exercise increases the feeling of well being, increases learning capacity and improves memory.

· Aerobic exercise ameliorates depression and is becoming an additional tool in the treatment of this disease.

· Aerobic exercise reverses the effects of aging on the brain.

· Aerobic exercise may reduce the perception of pain—an important implication for people suffering from chronic pain, such as arthritis.

One final note: to all you Yoga practitioners, iron pumpers, and assorted other exercise enthusiasts—these effects on the brain were demonstrated only with aerobic exercise. Sorry.

Dov Michaeli, MD, Ph.D

It isn’t often that you get a good chuckle while reading a medical journal. But today I did. I am on a plane again (not United Airlines, thank heavens) .  I am flipping through some recent issues of the Journal of the American Medical Association (JAMA). One article catches my eye. It describes the case of a woman with polycystic ovary syndrome (PCOS).   I decided to read it in detail to see if there was anything new in the cause, diagnosis, or treatment of women PCOS since I last wrote about it – there wasn’t.

PCOS is one of the most common causes of anovulatory infertility. Women with the condition have irregular periods, and cycles where they don’t ovulate. They also have physical findings related to hyperandrogenism (excess hair growth, acne), and they are frequently overweight or obese. Many are insulin resistant and some will go on to develop Type 2 diabetes. PCOS is risk factor for that condition.

As I read through this case study, I found that I didn’t really agree with the physician expert’s take on the case. The patient, “Ms R,” was worried because she had gained weight despite a pretty rigorous exercise regimen (she bikes 20 miles a day and swims regularly). She was described as 59 inches and 122 pounds with a BMI of 25. Did I do the math right? That means she is quite short to be packing around 122 pounds. She says she eats the same as she always has, but at the ripe old age of 27, she finds that she has gained weight.

The doctor discussing this case kept saying it was good that Ms R was “normal” weight, but we never learn whether she is slender or. in fact, is “abdominally” obese. And, he doesn’t mention whether he actually assessed how much she eats in a typical day or if he just believed her uncritical self-assessment. Before I started logging my food intake, I probably would have told you that I ate the same amount of calories as I did when I was thirty and thin. But once I started weighing and measuring and counting and recording my intake, surprise, surprise, I was actually quite an oink-oink. The weight started dropping when I decreased my intake to a caloric amount more appropriate for my height.

This article also does not mention Ms R’s ethnic background. Asians and South Asians can have abdominal obesity (and associated insulin resistance) at BMIs that are considered “normal.” It isn’t the BMI that is the problem, it is the abdominal, and in particular, intraabdominal or visceral fat – that is the problem. (I am willing to bet Ms R has plenty of fat around her middle.

Although her most recent fasting glucose level is normal, this woman is at risk for Type 2 diabetes because her father had it. And, as the doctor discussant pointed out he didn’t test her to see if she was glucose intolerant. You have to do a glucose tolerance test (drink a sugary substance and have blood drawn at regular intervals after that) to detect this type of insulin-resistance-related abnormality in glucose metabolism.

So I am already a little annoyed by the way this case is being discussed, but then, on the last page, this doctor says that he would counsel the patient that she appears to have a mild case of PCOS (not sure if this is the equivalent of doctors who tell their patients that they have a “touch of sugar.”) He recommends she keep on taking birth control pills that help her have regular periods and counteract the hair growth and acne cause by the increased androgen levels characteristic of PCOS (I agree). He enthuses that Ms R has “done an admirable job at weight control.” Yeah? But he did say he would refer her to a dietitian for further counseling on diet.

And then, comes the comic bombshell: He says, “I would counsel her against excessive “Googling” of PCOS on the web. I kid you not…I can hear it now, “No excessive googling, dear, you might learn something I don’t agree with?”

I have already written about Google’s ability to diagnose. This doctor has taken “Googling” to a new level by including this admonition in his case discussion in a respected medical journal. What a hoot.

Pat Salber, MD, MBA

USA Today reports that newly minted heart surgeons are having a hard time findings jobs. According to an article in the Annals of Thoracic Surgery, 12% of 88 cardiothoracic residents surveyed, received no job offers in 2004. Bummer. It takes 10 years of training after med school to become a heart surgeon. Not so long ago, cardiothoracic surgery was a ticket to an exciting and lucrative career.

A major reason for the decline in CV opportunities is a change in the way heart disease is treated. More and more folks with coronary artery disease are having stents placed by cardiologists instead of chests cracked by CV surgeons. That’s a good thing, right?

The story might be even better if we spent as much energy and money on primary prevention of heart disease (you know, healthy diet and vigorous exercise on a regular basis) as we do on treating the end-result of too much fat, too many cigarettes, and too little movement. Oh, well. I think we’ll get there eventually.

Meanwhile, never fear, all you unemployed CV surgeons, the article points out that older heart surgeons are bound to retire soon and us boomers are entering our prime heart disease years. Keep those scapels sharpened.

A reader takes issue with my positive presentation of VBLOC. Read on:

"Pat - I am surprised you would be advocating for VBLOC that is in the same category as bariatric surgery and does not "require any change in diet or exercise"! I personally believe that most chronic illnesses and conditions such as obesity are emotion-based - including my own, Crohn's - and that drug/technology interventions -are ineffective or short-lived solutions....of course I am not mainstream in this thinking...”

I think many of you who follow my TDWI posts know I am a strong advocate of diet and exercise. Sometimes, I feel like the diet and exercise nag. But I am also a pragmatist who recognizes that some people can't/won't/will never be successful in achieving a healthy weight with diet and exercise as their only options.”

There are alot of reasons why people fail good old fashioned lifestyle change. Some people have a physiologically stronger appetite drive than others and yes, some people with the thrifty genotype may be better at storing excess energy as fat. Some people preferentially store bad fat (aka visceral fat) and end up with the complications of cardiometabolic syndrome. And some folks have socioeconomic factors that make it harder to lose weight via life style changes alone - they live in unsafe neighborhoods, work long hours, and don't have easy access to healthy foods like fruits and veggies.

I think we make a mistake when we send a message that there is only one right way to lose weight; that is, eat less and exercise more. Yes, we should all do that if we can. But, medical and surgical approaches, including bariatric surgery are viable and valuable options for some people.

"Memoirs of a Fat Broad" by Wendy Hanawalt is a powerful story that opens your eyes to how hard it is to live with fat and its metabolic consequences. Wendy describes in detail what it is like to be really, really fat and she tells us how a doctor who suggested gastric by-pass saved her life. She was suffering so many complications of her obesity that she had contemplated suicide. That is not to say she didn't have problems after her surgery, she describes her life after her gastric by-pass surgery in a follow-up article to her Memoirs....nothing in life is completely free after all but compared to her life before, she says, post-by-pass and post-weight loss, the changes in her life are "miraculous."

So, diet, yes. Exercise, absolutely. But, if you can't get where you need to be without adding something more aggressive, I say keep your options open. Scientifically-proven medical adjuncts to weight loss may help you get to goal.

Pat Salber, MD, MBA

An article in the NY Times declares that one in eight adults in NY City has diabetes. That is 12.5% of the population or 700,000 people. Lest you feel relieved that you don’t live there, let me remind you that the rest of the country is not all that far behind. Overall, about 10.3% of Americans have diabetes and about a quarter of them don’t know it (yet). 

An additional 24% of adults in NY (and in the rest of the country) have abnormally high blood sugars that have not yet reached diabetic levels.  This condition is known as pre-diabetes.

Not too many years ago, the diabetes rate was 6%--half of the current NY rate. But our self-indulgent ways have caught up with us. Too little exercise, too many calories plus too much stress adds up to an epidemic of obesity, particularly abdominal obesity.  Abdominal obesity, especially visceral obesity, is linked to the development of Type 2 diabetes in genetically predisposed individuals.

It’s just a “touch of sugar.” Why all the concern? Because diabetes and it precursor, pre-diabetes, are the most familiar manifestations of a constellation of metabolic changes, known as cardiometabolic syndrome. Other manifestations of this syndrome are high blood pressure, dyslipidemia ((high triglycerides and low HDL (“good”) cholesterol)), clotting abnormalities, and problems with inflammation. People with cardiometabolic syndrome, even if they haven’t yet developed full-blown diabetes, have an increased risk of heart attacks and strokes.

Cardiovascular disease, strokes, and peripheral vascular disease are all very expensive conditions to treat in our technologically sophisticated health care system. These conditions already occupy some of the top slots when it comes to where our health care dollar are spent. So imagine what is going to happen now that the rates of diabetes have doubled (with no end in sight).

So, this epidemic of diabetes and pre-diabetes is not just a health care issue that burdens individuals and their families living with the disease. It is a looming societal problem that threatens to bankrupt our already fragile health care system. It could cause health care insurance premiums to escalate even further, impacting not only employers who provide coverage, but also public payors, like Medicaid and Medicare.

It is time to get deadly serious about doing something about prevention. We need to rapidly move to institutionalize regular exercise programs in school and at work. And we need affordable, easily accessible healthy eating options. That means we must be willing to regulate, legislate, and maybe even implement taxes (oh, oh, the tax word!) that can get us to where we need to be. Failure to do something now will almost certainly result in huge adverse financial consequences that will ripple through society in the not too distant future.

My son Jason, the radiologist, sent me an article from the American Journal of Roentgenology.  It is called, "Impact of Obesity on Medical Imaging and Image-Guided Intervention."  It is a treatise on what radiologists need to know about providing imaging services to obese people.   Here are some of the key questions addressed in the article:

• Is it possible to transport the patient from the hospital room to the radiology department?
• Can the patient fit into the machine?
• Can you get good images that help with the diagnosis?
• Can you get good images without exceeding recommended allowances for exposure to radioactive substances?
• Can interventional radiology procedures (e.g., imaging-guided biopsies) be done safely and effectively?

Too big to fit?

It turns out there are weight limits for both transportation equipment and imaging machines that can preclude a very obese individual from being able to get in a wheelchair for transport and from fitting into, say, an MRI machine.  Most hospitals currently have equipment that accommodates individuals up to about 450 pounds, although one type of MRI, called a vertical field MRI, can accommodate individuals up to 550 pounds.  If you try to put someone heavier into the machine and it is damaged as a result, the cost of the damage won't be covered by the manufacturer's insurance.

But it isn't just about weight, obese individuals may also be too big to fit into the opening of the imaging machine.  To save obese patients the embarrassment failing to squeeze into an MRI or CT scanner and to save precious time on the part of the radiology department, the article counsels that staff should ask about the patients weight and girth before scheduling the appointment.

Manufacturers are responding to the obesity epidemic by producing hospital equipment and imaging machines that can accommodate larger people.  But this equipment is expensive, particularly the imaging machines which can costs more than a million dollars.  We can expect that smaller hospitals and hospitals that serve populations that are un- or under-insured are not going to be able to afford to replace existing equipment quickly enough to keep up with demand.

Quality of the image

The increased body thickness of obese individuals requires the X-ray beam to travel farther than it does in a normal weight person.  This means increased exposure time and introduces the possibility of motion artifact (this is similar to what happens when you use long exposure times on your camera).  The result can be images that do not provide enough clarity to help with a diagnosis. 

Sometimes, obese people are so big that you need to use more than one radiograph cassette or, in the case of nuclear imaging, you need to give high doses of the radionuclide used to obtain the images.  Sometimes, even administering the maximum allowable dose of radionuclide is inadequate to obtain optimal images.

Can you do the biopsy safely?

There are lots of problems performing imaging-guided interventions on very obese people.  They may have compromised airways making conscious sedation (the person is awake, but doesn't feel or remember the procedure) unsafe.   Further, proper positioning of the patient for the biopsy may be difficult requiring extra staff people to accomplish.  Pillows and sometimes sandbags may be required to hold the person in position.  Longer than normal instruments may be necessary to reach the site to be biopsied.   These problems posed by obese patients may dictate that the obese person has to go to the operating room and have a surgical procedure instead of the less invasive imaging-guided procedure.

The AJR article provides information not only on the challenges of imaging obese individuals, but it also provides detailed suggestions for how to successfully address these challenges.  But, in the end, there is no question that if you are obese, you may likely have an imaging problem. 

This will be added to TDWIs growing list --  "Yet another reason to lose weight:"

Spending more on gasoline?  Yet another reason to lose weight

Obese people earn less, yet another reason to lose weight

Escape from prison:  yet another reason to lose weight

Pat Salber, MD, MBA

We have known for a long time that the distribution of fat in the body is important in determining important health risks, such as type 2 diabetes and cardiovascular disease. “Apples” (or the abdominally obese) are at much greater risk than pear-shaped people who tend to deposit their fat in the hips, thighs and butts.

More recently, researchers have determined that one type of belly fat, called visceral fat, is worse than belly fat just below skin.  Visceral fat is deposited the omentum, the tissue that drapes around the intestines and other abdominal cavity organs (or viscera). You don’t have to be obese to have visceral fat. One the other hand, not all people who are obese develop significant amounts of this “bad fat.”

An article in the San Francisco Chronicle reports that recent research suggests that abdominal fat is related to the release of the stress hormone, cortisol. According to UCSF’s assistant professor of psychiatry, Elissa Epel, an expert on the physiological effects of stress, cortisol which is released when people are under stress, seems to interact with the pancreatic hormone, insulin, to create visceral fat. At the same time, cortisol stimulates a craving for “comfort foods” – the sweet stuff and the stuff high in fat. This is a double whammy – you desire and, as a result, often consume high calorie foods and you deposit those excess calories as bad fat in your belly.

To test the hypothesis that stress is related the deposition of visceral fat, researchers at the University of California San Francisco are recruiting 50 overweight women to participate in a study on the impact of stress relief techniques on body fat, particularly visceral fat. The study is not designed to help the participants lose weight per se, rather it is designed to reduce stress and stress-related eating.

The 50 women will be divided into two groups. One group will start stress reduction classes right away, the other won’t start these classes until after 6 months have passed. The classes will teach women stress reduction techniques and will also teach them how to recognize triggers that prompt stress-related eating. They will also be taught “mindful eating.”

I described mindful eating in my recent post “Getting in touch with your feelings…about raisins.” In that post, I describe a “raisin exercise” developed by the author of Soul-Full Eating, Maureen Whitehouse. This approach to eating involves really engaging with the foods you eat. As opposed to gulping them down as many of us do in the course of our hectic lives, you are taught to visually examine the food and then explore it with your fingers and hands. When you put it in your mouth, you explore it with your tongue and chew it, ever so slowly, letting the flavors linger in your mouth and in your mind.

According to a co-researcher on the UCSF study, Jennifer Daubenmier, a postdoctoral fellow with the UCSF Center for Obesity Assesment, Study and Treatment, mindful eating helps participants to think about how and why they eat. The goal of the UCSF program is to ultimately help the participants make better, smarter food choices. Although weight loss is not the goal, it is hoped that the program will result in a reduction of bad belly fat.

To qualify for the study, women must weigh less than 300 pounds and have apple-shaped figures. They must be between 21 and 50 years old. They must not be recently pregnant, diabetic or have heart disease. If you fit these criteria and are interesting in participating in the study, send an email to ucsfcalmmstudy@yahoo.com. If you want to learn more about what it means to participate in a clinical trial, click here.

Not too long ago, my husband and I vacationed in Israel.  We had dinner with some Israeli friends.  One of them, Avinoam told us a story about his brother, a lawyer, David.  David is in his late 50s, a hard-driving attorney who pays attention to everything but his own personal health. 

Avinoam describes his brother as a "big man."  In fact, his description places him squarely in the severely obese category.  He can barely move, never walks if he can help it, and he smokes cigarettes, as do way too many Israelis.  Recently, he went to see a doctor for the first time in many years. 

No surprise.  David was diagnosed with diabetes, high blood pressure, and early kidney disease.  David, from a medical perspective, is what we clincians call "a walking time bomb."  He is at high risk for coronary artery disease, stroke, peripheral vascular disease, kidney failure, nerve damage and diabetic eye disease.   Doctors sometimes refer to patients like this as potential "train wrecks."

David has gone from taking no medications and being blissfully unaware of his medical problems to a high risk patient.  He now takes, per Avinoam, seven different types of pills.  Despite his diagnosis and risk status, he is still smoking. 

Unfortunately, there are way too many people in the US and around the world who are just like David.  They eat too much, exercise too little, smoke, and are ignorant of their risk factors.  Given the high prevalence of obesity, diabetes, pre-diabetes, and metabolic syndrome around the globe, the impact of these time bombs is enormous.  No wonder the former Surgeon General of the US, Dr. Richard Carmona, recently referred to obesity and the associated problem of type 2 diabetes "the terror within."

In addition to proper diet and exercise, I believe everyone should know their risk of developing health problems when they get overweight.  Some of these risks include having a family history of type 2 diabetes, having high blood pressure, abnormal lipids, insulin resistance, glucose intolerance or frank diabetes. 

Women with a history of gestational diabetes, big babies (greater than 9 pounds), or polycystic ovary syndrome also have increased risk.  Risk of type 2 diabetes increases with increasing age as does habitual inactivity.  Certain racial and ethnic groups have increased risk of type 2 diabetes, including Native Americans, Latinos, African Americans, Asian Americans and Pacific Islanders.  Type 2 diabetes is now occuring in very young children who are overweight or obese, a phenomenon that is relatively recent.

If you are at risk for type 2 diabetes or its precursers (metabolic syndrome or pre-diabetes), here are some things you can do.

• Lose weight.  If you are normal weight, initiate lifestyle changes that will assure you maintain this weight throughout your life. 
• Increase your physical activity aiming to eventually achieve 30-60 minutes of moderate to vigorous physical activity most days of the week
• Know your numbers.  See a health professional or attend a health fair to learn your diabetes risk statistics:
  • Weight, BMI, waist circumference
  • Blood pressure
  • Fasting glucose
  • Fasting lipid panel
• If you smoke, stop!

If any of your numbers are out of the normal range, talk to a health professional about developing a plan to bring them into an acceptable range.  The plan should establish specific goals for you to achieve (e.g., blood pressure of less than 130/90, HDL greater than 50).  It should also include recommendations for lifestyle changes (weight loss and increased physical activity).  It may include medications.  There are good medical studies that show that lifestyle changes (and some medications) can improve diabetes control and, if you are pre-diabetic, prevent progression to type 2 diabetes. 

My mantra for every one at risk for type 2 diabetes is simple:  "know your numbers, reach your goals."  Your life depends on it.

Dr. Bill BestermanWelcome, Dr. Bill Besterman, Guest Blogger for TDWI.   Bill is the President of the Cardiovascular Center of Excellence program under the auspices of the Consortium of Southeast Hypertension Control. He is currently in the process of moving to Holston Medical Group in Kingsport Tennessee to establish a Cardiovascular and Diabetes Center in that practice.

The American people have the power to determine the way medical care is delivered. The people decided they wanted to choose their own consultants and would not put up with gatekeepers and dramatic restriction on specialty care -- and there are no longer gatekeepers. Evidence-based care in cardiovascular diseases has the potential to improve health and save money. It is time that the people demanded consistent application of evidence-based care from the people who pay the bills -- employers and the government. One need look no