The Doctor Weighs In

by Pat Salber, MD

The cabbie who drove me from the airport to the hotel on my last business trip probably weighed 400 pounds.  We made small talk during the trip.  He told me he was hoping to leave Nevada soon and move to Oregon.  But, he said, it was tough getting the time and resources to make the move.

He works 12 hours days, six days a week.  The cab company deducts chunks of his pay  for their share of his revenues and to cover his health insurance premium and a tax on his tips.  His take home pay is $500 every two week pay period.

As we started talking about his health insurance, the conversation naturally drifted to health.  He is prediabetic, he told me, and his brother is a type 2 diabetic who has already had some toes amputated.  He knows he is facing the same future if he doesn't lose weight, but how can he do it?

When you drive a cab 12 hours a day, you often eat on the run.  That means fast food, high fat, and lots of calories.  Also, how do you fit in exercise?  Should he try to walk before the 12 hour shift or, perhaps, go out in the middle of the night when his shift is over? 

I found myself wondering what I would do if I were his doctor.  Of course, I would recommend he lose weight, alot of it.  And, I would tell him to get moderate to vigorous exercise 30 to 60 minutes a day.  I would prescribe any needed medications.  And, I would tell him to join WeightWatchers, or better yet an on-line weight loss support program, like PEERtrainer (www.peertrainer.com).

Chances are, in my 15 minute office visit, I wouldn't have learned about the challenges presented by his daily schedule.  I wouldn't understand that my recommendations were unlikely to be followed -- not because he wouldn't, but rather because he couldn't.

If something doesn't change, his prediabetes will most likely become diabetes.  He will probably have a heart attack or stroke or maybe, like his brother, he will end up with toes or feet amputated -- all potentially preventable if he could change his lifestyle.

At the end of the ride, all I could think of to say was that he needed to get a new job -- one that is less stressful and would allow him to exercise and eat better.  But I knew this too would be a daunting task given the long hours he already works and the meagerness of his financial resources.

I keep mulling over his story and wondering, how could you help this man?  I haven't come up with an answer.  Can you?

This is an oldie, but goodie, first published on TDWI September 15, 2006

by Brian Klepper

I routinely hear well-intentioned people say that, if Americans, and most particularly kids, would just become more responsible for their own health and start eating right, then our obesity and diabetes epidemics would turn around.

I don't think this is going to happen, at least not anytime soon. The blunt truth is that, to a large degree, we have an obesity epidemic because Congress ensures that the food industry has free rein with their marketing practices.

Late last year, Pat Salber wrote a post – she had a corresponding video commentary on Medscape – on advergaming. An important study had been released on the Kaiser Family Foundation website that detailed how food companies were using the Web to influence kids' eating behaviors, building on their TV advertising tactics. Here's a quote from the press release:

The report, “It’s Child’s Play: Advergaming and the Online Marketing of Food to Children,” found that more than eight out of ten (85%) of the top food brands that target children through TV advertising also use branded websites to market to children online. Unlike traditional TV advertising, these corporate-sponsored websites offer extensive opportunities for visitors to spend an unlimited amount of time interacting with specific food brands in more personal and detailed ways. For instance, the study documents the broad use of “advergames” (online games in which a company’s product or brand characters are featured, found on 73% of the websites) and viral marketing (encouraging children to contact their peers about a specific product or brand, found on 64% of sites). In addition, a variety of other advertising and marketing tactics are employed on these sites, including sweepstakes and promotions (65%), memberships (25%), on-demand access to TV ads (53%), and incentives for product purchase (38%).

In 2005, Consumers Union issued a report on the food industry's advertising campaigns. That press release headline read:

Certainly, the data say we're losing the war on obesity. Data from two National Health and Nutrition Examination Surveys show that the prevalence of obesity in adults (aged 20–74) more than doubled between the end of the 1970s to the early 2000s (from 15.0% in the 1976–1980 survey to 32.9% in the 2003–2004 survey).

Children and teens also grew significantly plumper. The prevalence of obesity in children 2–5 years rose 2.5 times, from 5.0% to 13.9%; for those aged 6–11 years it nearly tripled, from 6.5% to 18.8%; and for the 12–19 year olds, it more than tripled, from 5.0% to 17.4%.

It's worth noting that, while obesity has intensified throughout the country over the last several decades, certain areas, like the South, are consistently worse than elsewhere. This is traceable in part to regional dietary habits that, of course, long predate the food industry's influence, as well as to the role of poverty.

Percentage of Obese Americans - 2005

BMI > 30, or ~ 30 lbs. overweight for 5'4" person

Source: Centers for Disease Control, Behavioral Risk Factor Surveillance System, 20006 

(If you're interested in seeing the CDC's 20 year (1985-2005) annual trend data on overweight by state, go to http://www.cdc.gov/nccdphp/dnpa/obesity/trend/maps/index.htm, and look for the link that says "Download the Obesity Trends Map." Play the slides in quick sequence. It's very alarming to watch as the entire country lights up, reflecting how quickly we're getting fatter.)

The reality is that most of us are susceptible to the marketing, and can't withstand the barrage of enticements. And they're everywhere. Every day, Americans are bombarded by come-ons for fast, prepared and junk foods. This diet has become part of many people's regular routine. The industry now vies to subsidize school districts in exchange for the unrestricted ability to advertise, put in vending machines and have their products available in cafeterias. They have developed books for very young children with appealing characters to create brand loyalty early on,

And except for the unhealthy part, what's not to like? These foods are cheap, readily available and, lets face it, all that salt and fat taste really good. Only the most optimistic among us can imagine that, unless something dramatic changes, we'll be able to reverse our love affair with bad food. Nor will any of the other developed and developing countries that all have the same problem.

The food industry has virtually unrestrained promotional access because Congress has willfully ignored their role in the obesity problem, preferring instead to argue that if people were just more responsible as individuals, they'd get this under control. (A quick glimpse of our Congressional representatives shows that, when they preach restraint and self-control, they're talking about us, not themselves.)

 The threats are to the national health and the national pocketbook. At the moment, for example, diabetes and related conditions alone cost Americans about $165 billion a year, about 8 percent of the national health care spend. And we're just getting going. As the population gets fatter, this is going to be a blockbuster national health care problem. Nobody will be able to afford what, in today's terms, we'll be expected to pay to keep all these people alive, semi-well, and consuming.

Congress has good reason to advocate for the food industry, in the form of millions of dollars in lobbying funds that go to buy influence. Skeptical? Go to www.opensecrets.org, the site of the Center for Responsive Politics, a non-partisan group dedicated to accountability in government, and do some checking yourself. Big dollars from the food, beverage, candy and restaurant industries to Congress, part of the larger $2,5 billion dollars that were distributed in 2006 to our 535 representatives. This is the way it is with virtually all special interests. Most effective groups lobby. Why? Because it works!

There are, of course, precedents for change. Congress decided that the tobacco and alcohol industries would be limited in where and how they could advertise, actions that have had profound impacts on America.

It's absolutely in the national interest to turn this problem around. But unless we have dramatic change from elsewhere – chemical concoctions that make junk food taste as good but have no ill effects, or some miraculous national consciousness-raising (Not impossible. Check out the teen fitness program Dance Dance Revolution or consider how the green movement is sweeping across the globe.) – we won't change our obesity and chronic disease problem. To fix that, we'll need a change in how the food industry behaves. And to get that, we'll have to change how our government works.

(The same is true, by the way, for health care reform, but that's another post.)

Brian Klepper is a health care analyst based in Atlantic Beach, Florida. You can reach him at bklepper@gmail.com.

Alli (pronounced "ally") was approved by the FDA in February and will hit the shelves tomorrow.  About half of people in clinical trial studies were able to lose approximately 5% of their body weight in six months.  The medication is supposed to be taken three times a day and will cost about $50 per month. 

Sounds good?  Yeah, but the devil is in the details -- or, in this case, in the side effects.  

This "fat-buster" may not become a blockbuster for its manufacturer, GlaxoSmithKline.  Here's why from an "oldie, but goodie" TDWI post from February 7, 2007:

If you can deal with the "icky" factor, Alli may help you lose weight

Pat Salber, MD

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Is "Accomplia" the next silver bullet in weight control?     (Note:  On February 13, 2007, a U.S. Food and Drug Administration panel Wednesday unanimously rejected Acomplia, a weight-loss drug from Sanofi-Aventis  on concerns the drug increases the number of psychiatric events like depression and suicidal thinking among users.

Yesterday’s New York Times ( May 8, 2007 ) carried a front page article by one of the paper’s premier science reporters, Gina Kolata. The article, titled “genes take charge, and diets fall by the wayside”, is an excerpt of her newly published book “Rethinking thin: the new science of weight loss- and the myths and realities of weight loss”. In the article she reviews the succession of studies started in the late 1950’s by Dr Jules Hirsch at Rockefeller University , which culminated in recent studies demonstrating conclusively that the tendency to weight gain and obesity is genetically determined. Ms. Kolata describes the heartbreak of dieting, a constant struggle of losing weight, trying to maintain, gaining, dieting again, and so on and so on. Psychological testing showed the toll this struggle can take; people are perpetually unhappy, many are chronically depressed, some are suicidal.

One of the major conclusions Kolata cites is that each body has a metabolic “comfort zone”, and dieting to go below this zone is painful, metabolically unsound, and essentially futile.

I admit I haven’t read the book yet, but if the excerpt reflects the message of the book, I strongly disagree.

Why?

For several reasons:

· Yes, a metabolic range specific to each body makes a lot of intuitive sense. But to accept it we need to see the genetic/molecular/physiological mechanisms. The evidence is still not in. Having been around the block a few times, I never cease to marvel at nature outsmarting us, and upending our ‘no brainers’ and ‘slam dunks’.

· The fact that genes control our metabolism does not mean that they are the sole players. Genes interact with the environment, and the outcome of this interaction is all important. The old debate of nature vs. nurture set up a false choice; nature and nurture operate together in biology. The best example is diabetes type 2. An individual may have the genes that predispose to this disease. But it will be expressed clinically only if that individual overeats and exceeds a certain BMI.

· The most obvious evidence that genes are not the final word in weight regulation is the recent obesity epidemic. If  "obesity genes",which undoubtedly have been with us for eons, were such an all-controlling factor, why is it that only in the last few years did this epidemic break out? The answer is well-known: we take in a lot more calories, and we exercise a lot less. Yes, the genes were there all along, but they were not expressed.

I believe that research into the genetic basis of obesity and diabetes is absolutely essential. But it should not become an excuse for the fatalistic attitude of “it’s beyond my control”. Counteracting and ovecoming the genetic dictate may be unpleasant, tough, exasperating—but it beats the alternative.

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

Geneticists postulate that the human genome has changed very little in the last 10,000 years. In the Stone Age, our ancestors had to work hard to hunt and gather food. Life then involved cycles of feast and famine, but also cycles of intense physical activity and rest.

Physically fit individuals could hunt and gather more food. And, individuals who could efficiently store and use energy from food were better able to survive periods of famine. That meant they were more likely to survive to pass on their genes to the next generation. So, over time, thrifty genes became more and more common.

Unfortunately, the same genes that conferred a survival advantage on our ancient ancestors are creating havoc in the Space Age. For most of us, high caloric foods are easy to come by and opportunities to burn calories in the course of our work-a-day life are increasingly scarce.

Have you ever finished a day at the computer (coffee and donut at hand) and felt like the only part of you that moved all day was your fingers? If so, you aren’t alone. It is estimated that at least 70% of the US population experiences less than 30 minutes of moderate intensity physical activity per day. And, although, we likely consume fewer calories than in the distant past, our energy balance is out of whack and the pounds pile on.

It is important to remember that the problem is not just consuming too many calories, it is also about a physical activity deficiency. In fact, scientists have documented an independent effect of diet and exercise on weight loss.

According to Manu Chakravarthy and Frank Booth in the Journal of Applied Physiology (2004), we must reintroduce physical activity in modern society in order prevent a stall in the feast-famine and activity cycle of modern Western society. They go on to state that “given the unlimited food supply, modern humans in developed countries are unlikely to be exposed to famines. They will also likely not be able to tolerate drastic caloric reductions [they didn’t have to tell me that!] Thus, the logical way to ensure the {healthy} cycling of metabolic processes is by providing an adequate threshold of physical activity."

Pat Salber, MD, MBA

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.

Our immune response is usually characterized as the recognition of “self” from “non-self,” or as the response to “danger signals.”  Although there are some subtle distinctions between the two, we will not concern ourselves with them here. Rather, we’ll examine how the immune response works, why it is important to our survival and how we can boost its function.

How does immunity work?

There are two ways our immune response can protect us from foreign invaders like viruses and bacteria. One is through white blood cells known as T lymphocytes or T-cells.  T-cells have the uncanny ability to tell a normal cell from a cell which had been invaded by pathogens.  When T-cells find cells that are not normal, for example, cells that are infected, they eliminate the offending cells. This is called cell-mediated immunity or CMI.

The other way T lymphocytes protect us is by reacting with another type of white blood cell called B lymphocytes. These cells are veritable factories of antibodies, which are proteins that circulate in the blood looking for the infectious organisms, binding with them and ‘neutralizing’ them.

The most amazing attribute of T lymphocytes or antibodies produced by the B lymphocytes is their exquisite specificity. That is to say, if a T lymphocyte or an antibody is designed to attack a flu virus of a certain strain-it will attack this strain, and only this strain. This is, by the way, why we have to get a different flu vaccine every year- the virus mutates and therefore requires an antibody with a different specificity to neutralize it.

The T cells are formed in the thymus an organ that is prominent in the neck area of young people, but shrinks to unnoticible proportions in as we age.  T lymphocytes get their name from the thymus. 

In an early stage of their development, they are ‘naïve.’  That means they have not yet acquired their specificity .  As these lymphocytes mature, however, they acquire a specificity, for example, against a specific flu virus strain.  This occurs because of an actual encounter with the virus or some part of it. The result of this interaction is an "educated" T lymphocyte --a lymphocyte that can perform its function in protecting us against the flu virus.

In the human body, as in the rest of life, no resource is infinite.  This is true for the pool of naïve (or non-specific)lymphocytes as well. Starting at about age 30, the thymus, where the T lymphocytes are being formed, begins to shrink (this is called involution of the thymus).  As a result, the supply of naïve T lymphocytes progressively diminishes.

What that means is that older people slowly lose their capacity to mount an immune defense against new pathogens if they have not already "educated" T Lymphocytes at a younger age. To give you a real world example: 70-80% of people between the ages of 16 and 65 will be protected from the flu if they get vaccinated; but only 30-40% of elderly people will be protected.

So what does it have to do with longevity?

In a word: everything. The main reason for the improved longevity since the 18^th century (the age of Enlightenment) is the "discovery" of the scientific method.  It started with the discovery of the microscope by the Dutch scientist von Loevenhook.  Then there was the discovery, by a French scientist, of the connection between bacteria and disease and ways to kill them by pasteurization (yes, you probably guessed his name -- Pasteur).  Another milestone was the discovery of antibiotics in the 1940’s by Fleming.  He received the Nobel prize for the discovery of penicillin.  These were the miracles of the 19th century.   In those days, old people didn’t die of cancer, they died of infections.   They simply did not live long enough to develop cancers  that occur related to aging.

But, you might ask, didn’t our ancestors have an immune response to protect them? Yes, they did. And indeed younger people could survive their infectious disease surprisingly well. But as their immune response started to decline after age 30, they started to succumb.

Does this have any relevance to longevity in the 21^st century? Yes, because when we fail to mount an immune response due to age or disease (a condition called ‘immunodeficiency’), drugs alone are of limited utility.

How can we boost the immune response in the elderly?

The answer to that is still being investigated. But there is research, conducted by Richard Miller and his colleagues at the University of Michigan, showing that mice on caloric restriction suffer less infections and live significantly longer.

But this is mice.  What about men (and women)? To do an experiment on humans will be tough, long and expensive. But researchers at the Oregon National Research Primate Center reported in the Dec.4 issue of the Proceedings of the National Academy of Sciences (http://pnas.org) that in calorie-restricted old monkeys (30% reduction of normal diet) 30-35% of the total T cell pool were naïve T lymphocytes.  Monkeys of the same age on a regular diet had only 20-25% of these lymphocytes. This is a 50% increase in naive lymphocyte in the calorie-restricted group which is very impressive. This experiment unequivocally demonstrates that caloric restriction slows down immunological aging.

Did the boost in immunity result in increased longevity?

We don’t know yet because the monkeys are still alive and kicking -- so the experiment will have to continue for a longer period of time.  However, mouse data from the University of Michigan, that show an increased immune capacity coupled with increased longevity, are very intriguing.

Bottom line-what shall I do?

As far as I am concerned, calorie restriction (CR) to the degree used in these experiments may not be worth the pain for ordinary humans.  CR may boost my immune response,.  I may even live longer- but you call that living? Starving for life??

I’d much rather exercise aerobically on a regular basis for the following reasons:

• It makes me feel better
• It makes my brain work better
• It also might help me live healthier and longer

In addition to a good diet and exercise, I also have a couple of glasses of red wine with dinner.  It tastes great and it makes me  feel great.  It may also  make my life on earth a bit longer, but certainly, it makes my life a lot more pleasant.

Le’chaim (to life)!

Posted by Dov Michaeli, MD, PhD

A new report by experts in fetal medicine has found that being overweight is not good for mother or baby. The report is summarized in an article by Dr. Rajesh Swaminathan that appeared on abcnews.go.com.  It is definitely worth reading.

Here are some of the important points:

• Babies born to overweight mothers have various types of birth defects, such as macrosomia (large body size) and shoulder dystocia (the baby's shoulder is injured when the baby tries to pass through the birth canal).
• Spina bifida, a serious birth defect that can cause paralysis, occurs twice as often in obese women compared to normal weight women. This may be because it is more difficult to detect neural tube defects, the abnormality that leads to spina bifida, by ultrasound because of the lower quality of ultrasound images in obese women.
• Obese moms also have a higher incidence of pregnancy-related high blood pressure, diabetes, and dangerous blood clots. They are more likely to have C-sections, post-operative infections, and spend more time recovering in the hospital after the birth.

The report recommends that women lose weight by dieting and exercise well before trying to get pregnant. Some women may want to consider weight-reduction surgery. Losing weight may help with conception because of improvements in the hormonal profile. Finally, good health habits established by moms before pregnancy may translate into good health habits for her and the whole family for years to come.

This blog was originally posted on the PEERtrainer website (www.peertrainer.com) on Febuary 4, 2006.

The front page of the NY Times Business section has a lead article, written by Damon Darlin, titled “Extra Weight, Higher Costs.” It has the usual information about how obesity is linked to a number of costly diseases, including diabetes, heart disease, stroke and renal failure. But it also contains data that suggests that overweight individuals, particularly obese white women, earn less than their normal weight counterparts. Studies show obese people earn less One study that is described in the Times article was led by John H. Cawley, an associated professor of human ecology at Cornell University. He found that a weight increase of 64 pounds above the average for white women was associated with 9% lower wages. That’s huge! Indeed, in addition to being dangerous to you health, Jay L. Zagorsky, an economist at Ohio State University, is quoted as saying, “Being overweight can be dangerous to your wealth." He has studied the relationship between body mass index (a measure of overweight and obesity) and various economic factors, such as wages and overall accumulation of wealth. He used data from a multiyear sampling survey, the National Longitudinal Survey of Youth, done by the Bureau of Labor Statistics. He found for every one-point increase in BMI, net worth dropped by $1000. According to the the results of his study, the typical middle aged woman earned $313.70 less per year for every one-point increase in BMI; the typical male earned $161.30 less for every one-point increase.

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Another oldie, but goodie -- I am at the American Diabetes Association Leadership meetings in Dallas this week.  I hope you enjoy these reposts until I am able to return to my everyday blogging life .  Here goes: 

Great news today for Hubert, the Beaglebasset.  He had his annual physical today and we learned that he has lost 9 pounds!  He now weighs 52 pounds.  He was 61 pounds a year ago, so this is an almost 15% loss of total body weight.  Yay, Hubert! 

The vet says he still needs to lose 7 more, but he was quite proud of Hubert's accomplishment.  I guess most of his patients never get to their weight loss goals.

How did "we" do this?  No surprise!  Portion control and exercise.  When Hubert was at his maximum weight, he was eating two full bowls of chow with canned "wet stuff" mixed in twice a day.  And, because he was such a good boy, he also got to devour 1 or 2 or 3 Milk Bones as well.  He also was a successful dinner table begger.  He will eat almost anything (even some vegetables). 

 I thought I was being a good dog mother--passing my love to him via food.  Once we (or rather my husband) decided enough was enough, Hubert got put on a diet.  He gets only 1.5  (measured cup) of dry dog food each evening.  He now gets an occasional Milk Bone (I had to give him one to get him to pose for his photos).  And he gets nothing from our plates (he still begs, though).  We also instituted an exercise program with 2 one hour walks per day.  About a week ago, we added running to his regimen.  He is looking sleek.

Twenty-five to forty percent of the 67 million dogs and 77 million cats in the United States are overweight.  Sixty-six percent of American human beings are likewise overweight.  Animals, like humans, suffer from the same types of problems with their health as we do when the fat gets out of control.  So we now have millions of dogs and cats with diabetes, heart problems and weight-related joint problems.  When I was growing up, I didn't know anyone who had a pet on insulin.  Now it seems most of my friends are rushing home from work to inject an affected pet.

Vetrinarian, George Fahey, of the Department of Animal Sciences at the University of Iowa says, "While there have been no studies on this particular question, there appears to be anecdotal evidence that there is a correlation between overweight owners and overweight pets."  He goes on to point out that 50 years ago, most dogs and cats lived outdoors.  They got plenty of exercise.  However, once we moved our pets inside, they have become the "animal equivalent of couch potatoes."

Now. one difference between our pets and ourselves, as my vet pointed out today, is that their food intake and physical activity is not subject to vagaries of will power (at least not their own will power).   For the most part, we, the human owners, control what they eat and when and how much they exercise.   So here's my suggestion, as you are working on eating better and exercising more, include your pet in your diet and exercise plan: control the portions and expand the walks.  It is a prescription that is good for them and good for you as well.

Yay, Hubert Beaglebassett, you are really getting in shape. Yay!

This blog was originally publsihed on the PEERtrainer website (www.peertrainer.com) on May 2, 2006.

Dov Michaeli is at it again. In this post, he describes what we can learn from roundworms about our ability to live long lives. What Can the Lowly Roundworm Teach Us About Longevity? by Dov Michaeli, MD, PhD In this post I’d like to describe very briefly how C. elegans, a tiny roundworm used extensively in biological studies, can teach us lessons of momentous importance to our own longevity and wellness. Daf-2: What can this gene do? The short answer is: a lot! Daf-2 encodes the worm-equivalent of mammalian Insulin/IGF-1 receptor. When insulin or IGF-1 binds to this receptor they activate a sequence of intracellular molecules -- a so called a signal transduction pathway). This pathway eventually determines the worm’s metabolic rate. Insulin receptors in mammals (and we are mammals too) do exactly the same thing. I wrote in an earlier blog, that we already know that increased metabolic rate is associated with a shortened lifespan. So we could expect that a mutation in the Daf-2 gene that reduces its activity would also reduce the metabolic rate of the worm. Indeed, such mutations exist and, as expected, they reduce the metabolic rate of the worm. As a consequence they double the lifespan of the worms. This is a remarkable feat. If we could mimic the actions of Daf-2 mutations in us, we could potentially live to 200 years! But wait, wait--there is more!

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In today's post, Dov Michaeli, MD, PhD explains the relationship between too much food and too little exercise to aging. Exercise and the flow of energy from food to you By Dr. Dov Michaeli Cell death due to oxidative damage is considered to be one of the major causes of aging and chronic degenerative diseases. Oxygen free radicals react with everything in sight inside of cells and wreak havoc with normal cell function. When the mayhem reaches a critical level, the cell literally commits suicide and dies -- this is known in the scientific world as apoptosis (pronounced A POP TOE SIS). When enough cells doing it, whole organs fail, and eventually the grim reaper gets his quarry. So, what are those radicals (chemically speaking, not the political ones)? Where do they come from? What’s their connection to longevity? Let me try to explain.

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Dov Michaeli continues his exploration of factors that affect how long we live in Part 2 of "The Quest for Longevity."   It is fascinating stuff that may one day change the way we eat and drink and how long we live.

The Quest for Longevity (part 2):  The Resveratrol Story

by Dov Michaeli, MD, PhD

There is a lot of buzz in the press about red wine, resveratrol, and longevity.  Here is the real inside story of how resveratrol, the chemical in red wine that impacts longevity, works its wonders.

Yep, I am going to talk to you about cell biochemistry. But, I promise, I will make it as simple as I can. It is a tale about genes. In particular, it is the story of a gene called SIR 2 (or “Silent Information Regulator – sounds kind of creepy, huh?)

First, a bit of history

In 2000, Lenny Guarente and three of his postdoctoral students, discovered that a key chemical in yeast cells-- one that plays a key role in the energy metabolism. This chemical, named NAD (or Nicotine Adenine Dinucleotide) activates a gene in the yeast cells, called SIR2.

When the cell are flush with nutrients, in times of plenty, NAD levels are low and the SIR2 gene is inactive. On the other hand, a whole raft of genes, ones that have to do  ‘normal functioning’ of the organism, like insulin and insulin receptors, as well as reproduction, are active .

When nutrients are scarce, NAD levels go up and SIR2 is activated. It, in turn, inactivates the  “normal functioning” genes. One of the many things that happens as a result of SIR2 activation is insulin levels decline. This makes sense, because in conditions of nutrient scarcity, you don’t need as much insulin…indeed, too much insulin in the face of low nutrient levels could lead to a dangerously low level of blood glucose. In this state of nutrient scarcity, we also find that the gears of the aging process are slowed. This explains, at least in part, the link between caloric restriction and longevity.

Shortly after the discovery of SIR2 in yeast, the equivalent gene in mice was discovered. It was named SIRT1 (which stands for  “SIR Two One”).  Next, scientists discovered the enzyme sirtuin, a protein that carries out the instructions coded in SIR2/SIRT1 genes. So now we have a feedback loop. High nutrient levels lead to low NAD levels and suppression of SIR activity. Low nutrient levels lead to high NAD levels, expression of SIR activity, and production of the enzyme, sirtuin. NAD serves another function in this biochemical pathway, it binds to the sirtuin molecule and causes its activation.

Enter Sinclair and resveratrol

In 1995 David Sinclair, an Aussie, joined Guarente’s lab as a postdoctoral student. In 2003, he discovered that a substance that is present in the skin of red grapes and in red wine, resveratrol, seemed to activate SIR2 in yeast mimicking the low nutrient, low NAD, status of the cell. Yeast cell longevity just about doubled after resveratrol was added to their culture mix.

Moving on to the current report, Sinclair’s research group at MIT and another research group, headed by Rafael Cabo at the National Institute of Aging, reported the results everyone is talking about in the November 1 online publication of Nature.

The researchers fed mice fed a high calorie diet (60% fat) causing them to become obese.
Doug Hansen/National Institute on Aging. From NY Times onlineHalf of the mice on the high calorie diet also received resveratrol. A third group that received a normal diet, served as a control.

Here are the results:

• The fat mice on the high fat diet that received resveratrol ended up living significantly longer than mice on the same bad diet that did not get to eat resveratrol.

• The obese mice that got resveratrol lived as long as the control mice that were fed a normal diet and maintained a normal weight. This is an important finding because it appears that resveratrol prevented the shortening of lifespan that is ordinarily associated with obesity.

• The obese mice that did not receive resveratrol showed all the signs of metabolic syndrome, like high blood sugar, high insulin levels and enlarged livers. The obese group that received resveratrol did not develop this syndrome. Their blood sugars, insulin levels and liver size of obese resveratrol-eating mice was indistinguishable from the normal weight, normal diet mice. Again, it looks like resveratrol prevents these obesity-related pathologies.

• Finally, it is of interest that the obese mice who did not receive reseveratrol were sluggish, lost motor control, and had reduced endurance as measured by running on a treadmill. The ones receiving resveratol were almost twice as fit by the treadmill test and were more vibrant.

Not yet ready for prime time

So, will resveratrol be a simple antidote to our current obesity and diabetes crisis? It is probably too early to tell. Some important questions remain. Here are some:

• Will resveratrol show any benefits in animals on a normal diet? Will it have an equally significant life-extending effect? Evidently, this experiment is already underway.
• Exactly what does resveratrol do inside of the cell? Does it act on the SIR gene directly or does it act on the enzyme sertuin, or does it affect both? And once sertuin is activated, what exactly does it do? Does it act directly to “silence” silence some or all of the genes controlling aging, fertility and other normal functions? The answers to these questions may one day allow scientists to tease out or even separate the control of these functions.
• Will resveratrol have the same effects in humans? Drug developers know through long experience that mice are not men. Many a drug that cured cancer in mice were either too toxic in humans or were just plain ineffective.
• If it does work in humans, what dose level is needed? The mice in the experiment received the equivalent of humans consuming about a thousand bottles of wine per day!
• So this leads to the next concern. Will effective doses of resveratrol be safe in humans? Obviously, if we try to use red wine as the vehicle for consuming resveratrol, out metabolism may be healthier, but our brains will be fried!

So what is a mere mortal to do while we wait for the scientists to sort all of this out?

Here are my suggestions (the doctor is now weighing in):

• Enjoy up to a glass or two of red wine per day. But no more! Several studies have demonstrated that the maximum benefits are obtained at this level. More than that and the negative effects of alcohol consumption, such as cirrhosis of the liver, kick in.
• You can also ingest resveratrol from non-alcoholic sources, like red grapes and grape juice. This seemed have gotten lost in the midst of all the media hoopla about the benefits of red wine.
• There are several companies that market food supplements of resveratrol. But, caveat emptor: supplements may vary from 100% of the stated content to 0%. The food supplement market is an unregulated “Wild West.” Buying a resveratrol supplement that has hardly any resveratrol will be dangerous for your pocketbook, but, more importantly very high amounts of resveratrol (unlikely), or, more likely, some toxic contaminants of the supplement could turn out to be hazardous to your health.

I will be writing more about the intricacies of cell life and death in future posts. I hope you will join me as I explore this vast and fascinating topic.

Oh no! CNNMoney.com reports that Americans are consuming 938 million more gallons of fuel on a yearly basis than we did in 1960. The reason is -- are you ready for this ?-- it is because we are fatter, heavier, weigh more, or are more obese . However you want to frame it, our collective weight gain is costing us more at the pump. The CNNMoney story is based on a study from the University of Illinois at Urbana-Champaign and Virginia Commonwealth University (VCU). Laura McLay a researcher at VCU and author of the report states that: "The amount of fuel consumed as a result of the rising prevalence of obesity is small compared to the increase in the amount of fuel consumed stemming from other factors such as increased car reliance and an increase in the number of drivers." She goes on to say, however, that "it still represents a large amount of fuel, and will become even more significant as the rate of obesity increases." McLay began the study as a doctoral student working under the direction of Sheldon H. Jacobson, a professor of computer science and director of the simulation and optimization laboratory at Illinois. According to CNNMoney, the report's conclusions "are drawn from mathematical computations of weight gain applied to passenger vehicles, including cars and light trucks driven for non-commercial reasons." Evidently, the study determined that increased cargo weight or poor vehicle performance through lowered maintenance of cars were not major contributors to the increased consumption.

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For most of my career in medicine, the emphasis has been on treating disease. New drugs, new diagnostic tests, and new surgical approaches have improved life, delayed death, and created a culture of “if it’s broke, just fix it.” Prevention has not been a very popular nor lucrative way to practice medicine. Until recently, Medicare did not cover many preventive services. And, commercial insurers limited prevention coverage, often at the urging of their employer customers who were footing the bill. Now that our country and, in fact, the entire world is awash in chronic preventable diseases—such as obesity and type 2 diabetes -- health care professionals, policy wonks and politicians are rediscovering the joys of prevention. Better yet, they are realizing we will not be able to turn the tide on these chronic illnesses by health care alone. We need a strong and effective public health approach. Cigarette smoking is a good example. Although we have known about the link between tobacco and many different diseases, such as lung cancer and heart disease, for many years, we learned relatively late that counseling and/or cajoling of smokers by health professionals is not been nearly as effective as passing laws that restrict where smokers can smoke.

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We have known for a number of years that changes in lifestyle, such as diet, weight loss, and increased physical activity, can slow and may prevent the onset of Type 2 diabetes. But we didn’t know which of those lifestyle changes were the most important. A new study published in the September issue of Diabetes Care sheds some light on this question. Richard F. Hamman, MD, DrPH and his colleagues analyzed data from the Diabetes Prevention Program to try to learn more about the relative contributions of weight loss, diet, and physical activity on diabetes prevention. The Diabetes Prevention Program is a landmark study that documented a 58% reduction in the incidence of diabetes