The Journal of the American Medical Association (JAMA) did something very unusual with its June 27, 2007 issue - the entire issue is devoted to children’s illnesses.
It’s no secret childhood obesity is epidemic in the United States. The number of children who are overweight has doubled in the last two to three decades; currently one child in five is overweight. The increase is in both children and adolescents, and in all age, race and gender groups. No other chronic disease has spread so rapidly.
How did this happen? If you look closely, the JAMA issue tells us. In the article,Improved Use of BMI Needed to Screen Children for Overweight, the author states that:
“…some physicians feel kind of hopeless about obesity. … They say, ‘What can we do, we tell [patients] don’t eat so much and to exercise more. There isn’t a lot more to tell them to help them.'”[1]
The article goes on to basically scold the medical profession for not making better use of the BMI, or Body Mass Index, a reliable gauge of body fatness:
“…new research shows that despite recommendations from prominent health groups, pediatricians have not widely adopted the practice. At best, roughly half of pediatricians use BMI percentile measurements to assess overweight, but the figure dips to as few as 6% in some areas. The result is missed diagnoses of overweight and lost opportunities to help pediatric patients maintain a healthful weight and prevent comorbidities.”
If we look to “the experts” to keep us out of trouble, we are looking in the wrong place. The American medical profession is more geared to treating disease than preventing it. Thus, doctors get perhaps a mere 6 hours of nutrition in medical school, but entire semesters on drug therapies and surgical procedures. I think it is telling that the advertisement on the inside of the front cover of this issue of JAMA is for Levemir®, a long-acting insulin sold in a handy easy-to-use injection pen.
For the most part, doctors today work in an environment that allows them about 10 minutes for each patient appointment. You can write a prescription in that time, but you can’t do much to help overweight kids – and their parents – understand what is happening and change dietary habits.
The “health” insurance industry does not speak much about prevention either.
And then well-meaning groups pile on, like former President William Clinton, who advocates diet sodas in schools. Diet foods often trigger cravings that simply cause you to eat more.
It doesn’t take a rocket scientist to figure out what caused the epidemic obesity in children:
- television and computer use; almost half of children aged 8-16 years watch three to five hours of television a day
- mass marketing of junk food through television ads and movies
- proliferation of fast-food restaurants with food high in trans fats, sugars and processed white flour
- processed food displayed at children’s eye level in supermarkets
- the addition of sugar and its addictive chemical substitutes to all manner of food “products”
- school-sponsored sales of junk food and soda at the same time physical education classes and recess were cut
- working parents made home cooked meals a low priority
- fear of child kidnappings which kept children away from outdoor activities
Carrying excessive weight early in life may trigger irreversible changes in hormonal pathways, fat cells, and the brain that increase hunger and adversely affect metabolism.[2]
Education alone will not stop this epidemic. There are too many factors at work. In nature, animals know what to eat and what to avoid. Mankind either never did or lost that basic instinct. What we do know is never before have we had such much affluence - the ability to have food - combined with such little need to do physical labor - the couch potato syndrome. Our genetic makeup is hardwired to protect us from starvation. In olden times, the king and the elite members of society may have had expanding waistlines, but not the rank and file citizen. Today, we are all at risk for that expanding waistline and the multitude of health problems that go with it.
1 in 3 Americans is Obese
In 2010, the CDC made a dire prediction that 1 in 3 people will have diabetes by the year 2050 unless something is done to curb unhealthy lifestyle trends in the United States. The current number is that 1 in 10 have diabetes. The rise in number of obese Americans is the largest contributor to the CDC’s projection. Obesity is the largest risk factor that can be changed - you can't change getting old or your family history - but you can change how you eat and whether you exercise.
Obese children now have diseases like type 2 diabetes that used to only occur in adults. And overweight kids tend to become overweight adults, continuing to put them at greater risk for heart disease, high blood pressure and stroke.
Living with type 2 diabetes beginning around age fifty is one thing; living with it from age sixteen is quite another.
I like the way a group of experts writing for The Future of Our Children put it:
“Most agree that the nation has seen dramatic changes in the past thirty years in the ways Americans work, live, and eat. Broad societal and environmental trends have engineered routine physical activity out of everyday life for most Americans and made low-nutrition, energy-dense foods and beverages more accessible, affordable, and appealing than more healthful foods. Although reducing obesity requires changes in behaviors surrounding eating and physical activity, strategies that rely only on individual “self-control” are unlikely to be effective in environments that are conducive to poor eating habits and sedentary activity. This is especially true for children, who don’t control the environments in which they live, learn, and play. In addition, children have a more limited capacity to make informed choices about what is healthful and what is not. For this reason, there is a clear rationale for modifying children’s environments to make it easier for them to be physically active and to make healthful food choices, thus reducing their chances of becoming obese.”[3]
Children can’t change their exercise and eating habits by themselves. They need the help and support of their families. Same goes for adults.
Grown-ups have been bombarded with decades of bad dietary advice – eat margarine, eat a high carbohydrate diet, eating fat will make you fat. Grown-ups have also been living in a toxic world for decades, and their bodies have stored many of those toxins in fat which the body hesitates now to shed because too many toxins in the bloodstream can be fatal.
The Chemistry of Overeating
Extra fat produces more of the leptin hormone which is supposed to tell the hypothalamus there is too much fat stored, so don’t store any more and burn off the excess. But overexposure to high levels of leptin is thought to work like overexposure to insulin – the cells to become “insulin-resistant” and “leptin-resistant” which feeds the diabetes problem. With leptin-resistance, after a while you don’t get strong signals to stop eating, to stop storing fat, and to start burning off extra fat.
Low levels of dopamine can drive over-eating. Brain-imaging studies conducted by the Brookhaven National Laboratory suggest that many overweight people, like drug addicts, have fewer brain receptors for dopamine – the neurotransmitter that signals feelings of satisfaction and pleasure. The more you eat, the more dopamine you release.[4] The science suggests that obese people may be overeating to get a feel-good feeling, much like a drug addict does with drugs. The good news here is that exercise - when people do it - also triggers the release of dopamine.
Since the early 1990s, we've been learning about the genetic component that food and drug addictions share. Most recently, a study of 31,000 people of European origin, ages 45 to 76, found that the NRXN3 gene variant – previously associated with alcohol dependence, cocaine addiction, and illegal substance abuse – also predicts the tendency to become obese. People who inherited the gene variant NRXN3 have a 10-15 percent increased risk of being obese compared with people who do not have the variant. About 20 percent of the people studied had the gene variant. NRXN3 is the third obesity-associated gene to be identified; all three are highly active in encoding brain proteins.[5]
The biggest contributor to the growing obesity epidemic, however, may be that we alter our brain chemistry by what we eat. Doing drugs such as cocaine and eating too much junk food both gradually overload the so-called pleasure centers in the brain, according to Paul J. Kenny, an associate professor of molecular therapeutics at the Scripps Research Institute. Eventually it takes increasing amounts of the drug or food to get the same pleasurable feelings. Kenny found that rats that gorge themselves on the human food quickly became obese. But their brains also changed. By monitoring implanted brain electrodes, the researchers found that the rats gradually developed a tolerance to the pleasure the food gave them and had to eat more to experience a high. They began to eat compulsively, to the point where they continued to do so in the face of pain.[6]
What Else?
Mayo Clinic research found that obese adults don't burn as many calories during everyday activities - walking, fidgeting, or even just standing - as non-obese people. The study’s lead author, James Levine, a Mayo Clinic endocrinologist, said, “Our patients have told us for years that they have low metabolisms. We have never quite understood what that means. The answer is they have low NEAT [non-exercise activity thermogenesis].”[7]
Adenoviruses, which typically cause respiratory infections, have been implicated in obesity. Researchers at the University of Wisconsin, Madison. found that the virus goes to the lungs and then, after the cold is gone, spreads through the body. When this virus goes to fat tissue, it replicates and increases the number of new fat cells. Human studies show that almost a third of obese adults carry the virus compared with 11 per cent of lean men and women.[8]
Obesity has also been linked with relative abundance of two particular species of bacteria in the gut. Some bacteria are associated with increased ability to extract nutrients from the diet and build fat, as has been shown by studies where lean mice are colonized with “obese-associated bacteria” and develop more body fat than mice colonized with “lean-associated bacteria”.[9]
Society norms and the convenience of fast food play an important role. Note the experience of the country of Qatar: it ranks sixth globally for prevalence of obesity and has the highest rate of obesity among boys in the Middle East and North African region. It is predicted that by 2016, 73 percent of Qatari women and 69 percent of the men will qualify as obese. Social occasions center around eating large platters of food. Walking is not popular; summer temperatures are a humid 106 degrees. As the New York Times said, "Like other oil-rich nations, Qatar has leaped across decades of development in a short time, leaving behind the physically demanding life of the desert for air-conditioned comfort, servants and fast food."[10]
A 2009 report from the American Institute for Cancer Research (AIRC) revealed that more than 100,000 cases of cancer each year are caused by excess body fat. Excess body fat appears to increase the amount of hormones like estrogen circulating in the body, and it can also disrupt how the body processes insulin. Both of those factors have been linked to an increased cancer risk. Also, obesity creates low-grade inflammation in the body, and much current research links chronic inflammation to cancer.[11]
Studies have shown that increased body fat can lead to increased levels of oxidative stress and inflammatory compounds in the blood, which are linked to DNA mutation and diseased cell growth, as is seen in many cancers.
Born to Be Big? Epigenetics and Chemicals
If you are an obese woman and you start a family, your children and their children down the line may struggle with the “imprint” of your obesity. Adult obesity appears to increase the risk of obesity in offspring through non-genetic influences, a phenomenon termed perinatal programming.[12] A 2007 study found that maternal hyperglycemia during pregnancy strongly predicted high BMI in offspring at 5 to 7 years of age.[13] By age 10-16 years, offspring of a diabetic pregnancy have an almost 1 in 5 rate of impaired glucose intolerance.[14]
How might that happen, that an obese mother can create future generations of obese children? Because the baby is born programmed to be obese:[15]
- Each time a pregnant woman eats, her hormones launch a flurry of activity, including a rise in blood glucose with a resultant rise in insulin secreted by the pancreas. This makes sure that an ample supply of glucose is available to both her and her fetus.
- Throughout the 2nd and 3rd trimesters, hormone levels rise, the pancreas works harder, and mom's amount of insulin resistance rises, because her muscles do not like being bathed in insulin and drowned in glucose.
- When the mother's pancreas doesn't secret enough insulin to keep the blood sugar level low, the mother and the fetus experience hyperglycemia. The fetus is exposed to bouts of hyperglycemia which promotes excess nutrient storage. The result is excessive birth weight (macrosomia).
- Excessive body fat stores, stimulated by excessive glucose delivery during diabetic pregnancy, often extends into childhood and adult life.
Exposure in the womb seems to permanently disrupt or dysregulate appetite control and hormones and impair energy metabolism. “Fetal metabolic programming” may lead to obesity in adolescence and young adulthood, spawning a potential vicious cycle of transgenerational transmission of the obesity epidemic from parents to offspring, regardless of offspring genetics or childhood environment.[16]
Chemicals also play a big role in obesity. Ever since Rachel Carson wrote Silent Spring back in the 1960s, the book that rang the first big warning about the dangers of pesticides, we have been slowly waking up to the dangers of the 80,000 or so chemicals in our midst.
Sharon Begley reported in Newsweek in 2009 that early exposure to common chemicals may be programming kids to be fat:
“Certain hormone-mimicking pollutants, ubiquitous in the food chain, have two previously unsuspected effects. They act on genes in the developing fetus and newborn to turn more precursor cells into fat cells, which stay with you for life. And they may alter metabolic rate, so that the body hoards calories rather than burning them, like a physiological Scrooge. 'The evidence now emerging says that being overweight is not just the result of personal choices about what you eat, combined with inactivity,' says Retha Newbold of the National Institute of Environmental Health Sciences (NIEHS) in North Carolina, part of the National Institutes of Health (NIH). 'Exposure to environmental chemicals during development may be contributing to the obesity epidemic.' They are not the cause of extra pounds in every person who is overweight-for older adults, who were less likely to be exposed to so many of the compounds before birth, the standard explanations of genetics and lifestyle probably suffice-but environmental chemicals may well account for a good part of the current epidemic, especially in those under 50. And at the individual level, exposure to the compounds during a critical period of development may explain one of the most frustrating aspects of weight gain: you eat no more than your slim friends, and exercise no less, yet are still unable to shed pounds.”[17]
Dr. David Ludwig is the director of the Optimal Weight for Life Program in the Division of Endocrinology, Children's Hospital Boston. He is also an associate professor of pediatrics at Harvard Medical School. He wrote in the New England Journal of Medicine about a family who came to his clinic:
“One of the parents was overweight, and the other was obese. The five children were more severely obese and had numerous weight-related complications - one had evidence of fatty liver, one had high blood pressure, two had gastroesophageal reflux, two had orthopedic problems, three had marked insulin resistance, four had dyslipidemia, and all had emotional problems related to their weight.
“Unfortunately, the U.S. government has thus far invested only a fraction of a cent in research for every dollar that obesity costs society. And although broad consensus exists regarding the dietary and lifestyle habits needed to prevent and treat childhood obesity, we lack anything resembling a comprehensive strategy for encouraging children to eat a healthful diet and engage in physical activity. Such a strategy would include legislation that regulates junk-food advertising, provides adequate funding for decent lunches and regular physical activities at school, restructures the farm-subsidies program to favor nutrient-dense rather than calorie-dense produce, and mandates insurance coverage for preventing and treating pediatric obesity.”[18]
Nutrient-dense versus Calorie-dense
Nutrient-dense means that each bite of food has a lot of nutrition - vitamins, minerals, enzymes, maybe antioxidants and more. Calorie-dense is something like soda - no nutrition, but packing the calories. Most of us need help learning how to make the switch to nutrient-dense food, and organic food that has less chemicals.
Losing weight safely sometimes requires a safe detox program along with dietary changes. At the Arizona Center for Advanced Medicine, we have such a program for change. It is called FirstLine Therapy™. We measure the BMI routinely on all our patients. During the course of the program we measure the BMI twice a month to determine whether muscle mass is being maintained while fat mass is lost. We take time to do lots of hand-holding and education. The program works for children, adolescents and adults. We show you how to choose nutrient-dense foods over calorie-dense foods. We help you plan a do-able nutritional program which will allow both children and adults to lose weight (fat), while maintaining muscle mass. And we hold your hand as you tackle that tough one, exercise - how much, what type, how to do it, and how often. We show you for example what you can do while sitting at your desk during a phone call. We also offer colonics which can flush out the colon and rebalance the intestinal flora. The 12-week program gives you the tools to enable you and your children to choose a healthy lifestyle for the rest of your lives.
[1] Rebecca Voelker, Improved Use of BMI Needed to Screen Children for Overweight, JAMA, 2007;297:2684-2685.[2] David S. Ludwig, M.D., Ph.D. Childhood Obesity - The Shape of Things to Come, NEJM, December 6, 2007[3] Christina Paxson, Elisabeth Donahue, C. Tracy Orleans, and Jeanne Ann Grisso, Childhood Obesity-Introducing the Issue, Childhood Obesity, The Future of Children, a publication of the Woodrow Wilson School of Public and International Affairs at Princeton University and the Brookings Institution, Volume 16, Number 1 Spring 2006.[4] News Release: Scientists Find Link Between Dopamine and Obesity. Brookhaven National Laboratory. February 1, 2001[5] News Release: New gene discovery links obesity to the brain. Albert Einstein College of Medicine. June 25, 2009 [6] Johnson, Paul M; Kenny, Paul J. Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats. Nature Neuroscience. March 28, 2010; DOI: 10.1038/nn.2519 [7]James Owen, Some Couch Potatoes Born That Way, Fat Study Says, National Geographic News, January 27, 2007 [8] Contagious Obesity? Identifying The Human Adenoviruses That May Make Us Fat. ScienceDaily, January 30, 2006 [9] Turnbaugh PJ, Ley RE et al. An obesity-associated gut microbiome with increased capacity for energy harvest. Nature 444, 1027-131 (21 December 2006) [7] http://www.cancer.org/…Over_100000_Cancers_Linked_to_Excess_Body_Fat.asp [8] Plagemann A. Perinatal programming and functional teratogenesis: impact on body weight regulation and obesity. Physiol Behav. Dec 15 2005;86(5):661-8 [9] Hillier TA, Pedula KL, et al. Childhood obesity and metabolic imprinting: the ongoing effects of maternal hyperglycemia. Diabetes Care 2007;30:2287-92. [10] Slackman, Michael. Privilege Pulls Qatar Toward Unhealthy Choices. New York Times. April 26, 2010 [11] http://www.cancer.org…NWS_1_1x_Report_Over_100000_Cancers_Linked_to_Excess_Body_Fat.asp [12] Plagemann A. Perinatal programming and functional teratogenesis: impact on body weight regulation and obesity. Physiol Behav. Dec 15 2005;86(5):661-8 [13] Hillier TA, Pedula KL, et al. Childhood obesity and metabolic imprinting: the ongoing effects of maternal hyperglycemia. Diabetes Care 2007;30:2287-92. [14] McKinney PA, Parslow R, Gurney KA, Law GR, Bodansky HJ, Williams R. Perinatal and neonatal determinants of childhood type 1 diabetes. A case-control study in Yorkshire, U.K. Diabetes Care. Jun 1999;22(6):928-32 [15] http://emedicine.medscape.com/article/127547-overview [16] Eric L Ding and Frank B Hu. Determining Origins and Causes of Childhood Obesity via Mendelian Randomization Analysis. PLoS Med. 2008 March; 5(3): e65. [17] Sharon Begley, Born to be Big - Early exposure to common chemicals may be programming kids to be fat. Newsweek, September 11, 2009 [18] David S. Ludwig, M.D., Ph.D. Childhood Obesity - The Shape of Things to Come, NEJM, December 6, 2007Obesity
The article goes on to basically scold the medical profession for not making better use of the BMI, or Body Mass Index, a reliable gauge of body fatness:
“…new research shows that despite recommendations from prominent health groups, pediatricians have not widely adopted the practice. At best, roughly half of pediatricians use BMI percentile measurements to assess overweight, but the figure dips to as few as 6% in some areas. The result is missed diagnoses of overweight and lost opportunities to help pediatric patients maintain a healthful weight and prevent comorbidities.”
If we look to “the experts” to keep us out of trouble, we are looking in the wrong place. The American medical profession is more geared to treating disease than preventing it. Thus, doctors get perhaps a mere 6 hours of nutrition in medical school, but entire semesters on drug therapies and surgical procedures. I think it is telling that the advertisement on the inside of the front cover of this issue of JAMA is for Levemir®, a long-acting insulin sold in a handy easy-to-use injection pen.
For the most part, doctors today work in an environment that allows them about 10 minutes for each patient appointment. You can write a prescription in that time, but you can’t do much to help overweight kids – and their parents – understand what is happening and change dietary habits.
The “health” insurance industry does not speak much about prevention either.
And then well-meaning groups pile on, like former President William Clinton, who advocates diet sodas in schools. Diet foods often trigger cravings that simply cause you to eat more.
It doesn’t take a rocket scientist to figure out what caused the epidemic obesity in children:
Carrying excessive weight early in life may trigger irreversible changes in hormonal pathways, fat cells, and the brain that increase hunger and adversely affect metabolism.[2]
Education alone will not stop this epidemic. There are too many factors at work. In nature, animals know what to eat and what to avoid. Mankind either never did or lost that basic instinct. What we do know is never before have we had such much affluence - the ability to have food - combined with such little need to do physical labor - the couch potato syndrome. Our genetic makeup is hardwired to protect us from starvation. In olden times, the king and the elite members of society may have had expanding waistlines, but not the rank and file citizen. Today, we are all at risk for that expanding waistline and the multitude of health problems that go with it.
1 in 3 Americans is Obese
In 2010, the CDC made a dire prediction that 1 in 3 people will have diabetes by the year 2050 unless something is done to curb unhealthy lifestyle trends in the United States. The current number is that 1 in 10 have diabetes. The rise in number of obese Americans is the largest contributor to the CDC’s projection. Obesity is the largest risk factor that can be changed - you can't change getting old or your family history - but you can change how you eat and whether you exercise.
Obese children now have diseases like type 2 diabetes that used to only occur in adults. And overweight kids tend to become overweight adults, continuing to put them at greater risk for heart disease, high blood pressure and stroke.
Living with type 2 diabetes beginning around age fifty is one thing; living with it from age sixteen is quite another.
I like the way a group of experts writing for The Future of Our Children put it:
“Most agree that the nation has seen dramatic changes in the past thirty years in the ways Americans work, live, and eat. Broad societal and environmental trends have engineered routine physical activity out of everyday life for most Americans and made low-nutrition, energy-dense foods and beverages more accessible, affordable, and appealing than more healthful foods. Although reducing obesity requires changes in behaviors surrounding eating and physical activity, strategies that rely only on individual “self-control” are unlikely to be effective in environments that are conducive to poor eating habits and sedentary activity. This is especially true for children, who don’t control the environments in which they live, learn, and play. In addition, children have a more limited capacity to make informed choices about what is healthful and what is not. For this reason, there is a clear rationale for modifying children’s environments to make it easier for them to be physically active and to make healthful food choices, thus reducing their chances of becoming obese.”[3]
Children can’t change their exercise and eating habits by themselves. They need the help and support of their families. Same goes for adults.
Grown-ups have been bombarded with decades of bad dietary advice – eat margarine, eat a high carbohydrate diet, eating fat will make you fat. Grown-ups have also been living in a toxic world for decades, and their bodies have stored many of those toxins in fat which the body hesitates now to shed because too many toxins in the bloodstream can be fatal.
The Chemistry of Overeating
Extra fat produces more of the leptin hormone which is supposed to tell the hypothalamus there is too much fat stored, so don’t store any more and burn off the excess. But overexposure to high levels of leptin is thought to work like overexposure to insulin – the cells to become “insulin-resistant” and “leptin-resistant” which feeds the diabetes problem. With leptin-resistance, after a while you don’t get strong signals to stop eating, to stop storing fat, and to start burning off extra fat.
Low levels of dopamine can drive over-eating. Brain-imaging studies conducted by the Brookhaven National Laboratory suggest that many overweight people, like drug addicts, have fewer brain receptors for dopamine – the neurotransmitter that signals feelings of satisfaction and pleasure. The more you eat, the more dopamine you release.[4] The science suggests that obese people may be overeating to get a feel-good feeling, much like a drug addict does with drugs. The good news here is that exercise - when people do it - also triggers the release of dopamine.
Since the early 1990s, we've been learning about the genetic component that food and drug addictions share. Most recently, a study of 31,000 people of European origin, ages 45 to 76, found that the NRXN3 gene variant – previously associated with alcohol dependence, cocaine addiction, and illegal substance abuse – also predicts the tendency to become obese. People who inherited the gene variant NRXN3 have a 10-15 percent increased risk of being obese compared with people who do not have the variant. About 20 percent of the people studied had the gene variant. NRXN3 is the third obesity-associated gene to be identified; all three are highly active in encoding brain proteins.[5]
The biggest contributor to the growing obesity epidemic, however, may be that we alter our brain chemistry by what we eat. Doing drugs such as cocaine and eating too much junk food both gradually overload the so-called pleasure centers in the brain, according to Paul J. Kenny, an associate professor of molecular therapeutics at the Scripps Research Institute. Eventually it takes increasing amounts of the drug or food to get the same pleasurable feelings. Kenny found that rats that gorge themselves on the human food quickly became obese. But their brains also changed. By monitoring implanted brain electrodes, the researchers found that the rats gradually developed a tolerance to the pleasure the food gave them and had to eat more to experience a high. They began to eat compulsively, to the point where they continued to do so in the face of pain.[6]
What Else?
Mayo Clinic research found that obese adults don't burn as many calories during everyday activities - walking, fidgeting, or even just standing - as non-obese people. The study’s lead author, James Levine, a Mayo Clinic endocrinologist, said, “Our patients have told us for years that they have low metabolisms. We have never quite understood what that means. The answer is they have low NEAT [non-exercise activity thermogenesis].”[7]
Adenoviruses, which typically cause respiratory infections, have been implicated in obesity. Researchers at the University of Wisconsin, Madison. found that the virus goes to the lungs and then, after the cold is gone, spreads through the body. When this virus goes to fat tissue, it replicates and increases the number of new fat cells. Human studies show that almost a third of obese adults carry the virus compared with 11 per cent of lean men and women.[8]
Obesity has also been linked with relative abundance of two particular species of bacteria in the gut. Some bacteria are associated with increased ability to extract nutrients from the diet and build fat, as has been shown by studies where lean mice are colonized with “obese-associated bacteria” and develop more body fat than mice colonized with “lean-associated bacteria”.[9]
Society norms and the convenience of fast food play an important role. Note the experience of the country of Qatar: it ranks sixth globally for prevalence of obesity and has the highest rate of obesity among boys in the Middle East and North African region. It is predicted that by 2016, 73 percent of Qatari women and 69 percent of the men will qualify as obese. Social occasions center around eating large platters of food. Walking is not popular; summer temperatures are a humid 106 degrees. As the New York Times said, "Like other oil-rich nations, Qatar has leaped across decades of development in a short time, leaving behind the physically demanding life of the desert for air-conditioned comfort, servants and fast food."[10]
A 2009 report from the American Institute for Cancer Research (AIRC) revealed that more than 100,000 cases of cancer each year are caused by excess body fat. Excess body fat appears to increase the amount of hormones like estrogen circulating in the body, and it can also disrupt how the body processes insulin. Both of those factors have been linked to an increased cancer risk. Also, obesity creates low-grade inflammation in the body, and much current research links chronic inflammation to cancer.[11]
Studies have shown that increased body fat can lead to increased levels of oxidative stress and inflammatory compounds in the blood, which are linked to DNA mutation and diseased cell growth, as is seen in many cancers.
Born to Be Big? Epigenetics and Chemicals
If you are an obese woman and you start a family, your children and their children down the line may struggle with the “imprint” of your obesity. Adult obesity appears to increase the risk of obesity in offspring through non-genetic influences, a phenomenon termed perinatal programming.[12] A 2007 study found that maternal hyperglycemia during pregnancy strongly predicted high BMI in offspring at 5 to 7 years of age.[13] By age 10-16 years, offspring of a diabetic pregnancy have an almost 1 in 5 rate of impaired glucose intolerance.[14]
How might that happen, that an obese mother can create future generations of obese children? Because the baby is born programmed to be obese:[15]
- Each time a pregnant woman eats, her hormones launch a flurry of activity, including a rise in blood glucose with a resultant rise in insulin secreted by the pancreas. This makes sure that an ample supply of glucose is available to both her and her fetus.
- Throughout the 2nd and 3rd trimesters, hormone levels rise, the pancreas works harder, and mom's amount of insulin resistance rises, because her muscles do not like being bathed in insulin and drowned in glucose.
- When the mother's pancreas doesn't secret enough insulin to keep the blood sugar level low, the mother and the fetus experience hyperglycemia. The fetus is exposed to bouts of hyperglycemia which promotes excess nutrient storage. The result is excessive birth weight (macrosomia).
- Excessive body fat stores, stimulated by excessive glucose delivery during diabetic pregnancy, often extends into childhood and adult life.
Exposure in the womb seems to permanently disrupt or dysregulate appetite control and hormones and impair energy metabolism. “Fetal metabolic programming” may lead to obesity in adolescence and young adulthood, spawning a potential vicious cycle of transgenerational transmission of the obesity epidemic from parents to offspring, regardless of offspring genetics or childhood environment.[16]
Chemicals also play a big role in obesity. Ever since Rachel Carson wrote Silent Spring back in the 1960s, the book that rang the first big warning about the dangers of pesticides, we have been slowly waking up to the dangers of the 80,000 or so chemicals in our midst.
Sharon Begley reported in Newsweek in 2009 that early exposure to common chemicals may be programming kids to be fat:
“Certain hormone-mimicking pollutants, ubiquitous in the food chain, have two previously unsuspected effects. They act on genes in the developing fetus and newborn to turn more precursor cells into fat cells, which stay with you for life. And they may alter metabolic rate, so that the body hoards calories rather than burning them, like a physiological Scrooge. 'The evidence now emerging says that being overweight is not just the result of personal choices about what you eat, combined with inactivity,' says Retha Newbold of the National Institute of Environmental Health Sciences (NIEHS) in North Carolina, part of the National Institutes of Health (NIH). 'Exposure to environmental chemicals during development may be contributing to the obesity epidemic.' They are not the cause of extra pounds in every person who is overweight-for older adults, who were less likely to be exposed to so many of the compounds before birth, the standard explanations of genetics and lifestyle probably suffice-but environmental chemicals may well account for a good part of the current epidemic, especially in those under 50. And at the individual level, exposure to the compounds during a critical period of development may explain one of the most frustrating aspects of weight gain: you eat no more than your slim friends, and exercise no less, yet are still unable to shed pounds.”[17]
Dr. David Ludwig is the director of the Optimal Weight for Life Program in the Division of Endocrinology, Children's Hospital Boston. He is also an associate professor of pediatrics at Harvard Medical School. He wrote in the New England Journal of Medicine about a family who came to his clinic:
“One of the parents was overweight, and the other was obese. The five children were more severely obese and had numerous weight-related complications - one had evidence of fatty liver, one had high blood pressure, two had gastroesophageal reflux, two had orthopedic problems, three had marked insulin resistance, four had dyslipidemia, and all had emotional problems related to their weight.
“Unfortunately, the U.S. government has thus far invested only a fraction of a cent in research for every dollar that obesity costs society. And although broad consensus exists regarding the dietary and lifestyle habits needed to prevent and treat childhood obesity, we lack anything resembling a comprehensive strategy for encouraging children to eat a healthful diet and engage in physical activity. Such a strategy would include legislation that regulates junk-food advertising, provides adequate funding for decent lunches and regular physical activities at school, restructures the farm-subsidies program to favor nutrient-dense rather than calorie-dense produce, and mandates insurance coverage for preventing and treating pediatric obesity.”[18]
Nutrient-dense versus Calorie-dense
Nutrient-dense means that each bite of food has a lot of nutrition - vitamins, minerals, enzymes, maybe antioxidants and more. Calorie-dense is something like soda - no nutrition, but packing the calories. Most of us need help learning how to make the switch to nutrient-dense food, and organic food that has less chemicals.
Losing weight safely sometimes requires a safe detox program along with dietary changes. At the Arizona Center for Advanced Medicine, we have such a program for change. It is called FirstLine Therapy™. We measure the BMI routinely on all our patients. During the course of the program we measure the BMI twice a month to determine whether muscle mass is being maintained while fat mass is lost. We take time to do lots of hand-holding and education. The program works for children, adolescents and adults. We show you how to choose nutrient-dense foods over calorie-dense foods. We help you plan a do-able nutritional program which will allow both children and adults to lose weight (fat), while maintaining muscle mass. And we hold your hand as you tackle that tough one, exercise - how much, what type, how to do it, and how often. We show you for example what you can do while sitting at your desk during a phone call. We also offer colonics which can flush out the colon and rebalance the intestinal flora. The 12-week program gives you the tools to enable you and your children to choose a healthy lifestyle for the rest of your lives.
[1] Rebecca Voelker, Improved Use of BMI Needed to Screen Children for Overweight, JAMA, 2007;297:2684-2685.[2] David S. Ludwig, M.D., Ph.D. Childhood Obesity - The Shape of Things to Come, NEJM, December 6, 2007[3] Christina Paxson, Elisabeth Donahue, C. Tracy Orleans, and Jeanne Ann Grisso, Childhood Obesity-Introducing the Issue, Childhood Obesity, The Future of Children, a publication of the Woodrow Wilson School of Public and International Affairs at Princeton University and the Brookings Institution, Volume 16, Number 1 Spring 2006.[4] News Release: Scientists Find Link Between Dopamine and Obesity. Brookhaven National Laboratory. February 1, 2001[5] News Release: New gene discovery links obesity to the brain. Albert Einstein College of Medicine. June 25, 2009 [6] Johnson, Paul M; Kenny, Paul J. Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats. Nature Neuroscience. March 28, 2010; DOI: 10.1038/nn.2519 [7]James Owen, Some Couch Potatoes Born That Way, Fat Study Says, National Geographic News, January 27, 2007 [8] Contagious Obesity? Identifying The Human Adenoviruses That May Make Us Fat. ScienceDaily, January 30, 2006 [9] Turnbaugh PJ, Ley RE et al. An obesity-associated gut microbiome with increased capacity for energy harvest. Nature 444, 1027-131 (21 December 2006) [7] http://www.cancer.org/…Over_100000_Cancers_Linked_to_Excess_Body_Fat.asp [8] Plagemann A. Perinatal programming and functional teratogenesis: impact on body weight regulation and obesity. Physiol Behav. Dec 15 2005;86(5):661-8 [9] Hillier TA, Pedula KL, et al. Childhood obesity and metabolic imprinting: the ongoing effects of maternal hyperglycemia. Diabetes Care 2007;30:2287-92. [10] Slackman, Michael. Privilege Pulls Qatar Toward Unhealthy Choices. New York Times. April 26, 2010 [11] http://www.cancer.org…NWS_1_1x_Report_Over_100000_Cancers_Linked_to_Excess_Body_Fat.asp [12] Plagemann A. Perinatal programming and functional teratogenesis: impact on body weight regulation and obesity. Physiol Behav. Dec 15 2005;86(5):661-8 [13] Hillier TA, Pedula KL, et al. Childhood obesity and metabolic imprinting: the ongoing effects of maternal hyperglycemia. Diabetes Care 2007;30:2287-92. [14] McKinney PA, Parslow R, Gurney KA, Law GR, Bodansky HJ, Williams R. Perinatal and neonatal determinants of childhood type 1 diabetes. A case-control study in Yorkshire, U.K. Diabetes Care. Jun 1999;22(6):928-32 [15] http://emedicine.medscape.com/article/127547-overview [16] Eric L Ding and Frank B Hu. Determining Origins and Causes of Childhood Obesity via Mendelian Randomization Analysis. PLoS Med. 2008 March; 5(3): e65. [17] Sharon Begley, Born to be Big - Early exposure to common chemicals may be programming kids to be fat. Newsweek, September 11, 2009 [18] David S. Ludwig, M.D., Ph.D. Childhood Obesity - The Shape of Things to Come, NEJM, December 6, 2007Obesity
Education alone will not stop this epidemic. There are too many factors at work. In nature, animals know what to eat and what to avoid. Mankind either never did or lost that basic instinct. What we do know is never before have we had such much affluence - the ability to have food - combined with such little need to do physical labor - the couch potato syndrome. Our genetic makeup is hardwired to protect us from starvation. In olden times, the king and the elite members of society may have had expanding waistlines, but not the rank and file citizen. Today, we are all at risk for that expanding waistline and the multitude of health problems that go with it.
In 2010, the CDC made a dire prediction that 1 in 3 people will have diabetes by the year 2050 unless something is done to curb unhealthy lifestyle trends in the United States. The current number is that 1 in 10 have diabetes. The rise in number of obese Americans is the largest contributor to the CDC’s projection. Obesity is the largest risk factor that can be changed - you can't change getting old or your family history - but you can change how you eat and whether you exercise.
Obese children now have diseases like type 2 diabetes that used to only occur in adults. And overweight kids tend to become overweight adults, continuing to put them at greater risk for heart disease, high blood pressure and stroke.
Living with type 2 diabetes beginning around age fifty is one thing; living with it from age sixteen is quite another.
I like the way a group of experts writing for The Future of Our Children put it:
“Most agree that the nation has seen dramatic changes in the past thirty years in the ways Americans work, live, and eat. Broad societal and environmental trends have engineered routine physical activity out of everyday life for most Americans and made low-nutrition, energy-dense foods and beverages more accessible, affordable, and appealing than more healthful foods. Although reducing obesity requires changes in behaviors surrounding eating and physical activity, strategies that rely only on individual “self-control” are unlikely to be effective in environments that are conducive to poor eating habits and sedentary activity. This is especially true for children, who don’t control the environments in which they live, learn, and play. In addition, children have a more limited capacity to make informed choices about what is healthful and what is not. For this reason, there is a clear rationale for modifying children’s environments to make it easier for them to be physically active and to make healthful food choices, thus reducing their chances of becoming obese.”[3]
Children can’t change their exercise and eating habits by themselves. They need the help and support of their families. Same goes for adults.
Grown-ups have been bombarded with decades of bad dietary advice – eat margarine, eat a high carbohydrate diet, eating fat will make you fat. Grown-ups have also been living in a toxic world for decades, and their bodies have stored many of those toxins in fat which the body hesitates now to shed because too many toxins in the bloodstream can be fatal.
The Chemistry of Overeating
Extra fat produces more of the leptin hormone which is supposed to tell the hypothalamus there is too much fat stored, so don’t store any more and burn off the excess. But overexposure to high levels of leptin is thought to work like overexposure to insulin – the cells to become “insulin-resistant” and “leptin-resistant” which feeds the diabetes problem. With leptin-resistance, after a while you don’t get strong signals to stop eating, to stop storing fat, and to start burning off extra fat.
Low levels of dopamine can drive over-eating. Brain-imaging studies conducted by the Brookhaven National Laboratory suggest that many overweight people, like drug addicts, have fewer brain receptors for dopamine – the neurotransmitter that signals feelings of satisfaction and pleasure. The more you eat, the more dopamine you release.[4] The science suggests that obese people may be overeating to get a feel-good feeling, much like a drug addict does with drugs. The good news here is that exercise - when people do it - also triggers the release of dopamine.
Since the early 1990s, we've been learning about the genetic component that food and drug addictions share. Most recently, a study of 31,000 people of European origin, ages 45 to 76, found that the NRXN3 gene variant – previously associated with alcohol dependence, cocaine addiction, and illegal substance abuse – also predicts the tendency to become obese. People who inherited the gene variant NRXN3 have a 10-15 percent increased risk of being obese compared with people who do not have the variant. About 20 percent of the people studied had the gene variant. NRXN3 is the third obesity-associated gene to be identified; all three are highly active in encoding brain proteins.[5]
The biggest contributor to the growing obesity epidemic, however, may be that we alter our brain chemistry by what we eat. Doing drugs such as cocaine and eating too much junk food both gradually overload the so-called pleasure centers in the brain, according to Paul J. Kenny, an associate professor of molecular therapeutics at the Scripps Research Institute. Eventually it takes increasing amounts of the drug or food to get the same pleasurable feelings. Kenny found that rats that gorge themselves on the human food quickly became obese. But their brains also changed. By monitoring implanted brain electrodes, the researchers found that the rats gradually developed a tolerance to the pleasure the food gave them and had to eat more to experience a high. They began to eat compulsively, to the point where they continued to do so in the face of pain.[6]
What Else?
Mayo Clinic research found that obese adults don't burn as many calories during everyday activities - walking, fidgeting, or even just standing - as non-obese people. The study’s lead author, James Levine, a Mayo Clinic endocrinologist, said, “Our patients have told us for years that they have low metabolisms. We have never quite understood what that means. The answer is they have low NEAT [non-exercise activity thermogenesis].”[7]
Adenoviruses, which typically cause respiratory infections, have been implicated in obesity. Researchers at the University of Wisconsin, Madison. found that the virus goes to the lungs and then, after the cold is gone, spreads through the body. When this virus goes to fat tissue, it replicates and increases the number of new fat cells. Human studies show that almost a third of obese adults carry the virus compared with 11 per cent of lean men and women.[8]
Obesity has also been linked with relative abundance of two particular species of bacteria in the gut. Some bacteria are associated with increased ability to extract nutrients from the diet and build fat, as has been shown by studies where lean mice are colonized with “obese-associated bacteria” and develop more body fat than mice colonized with “lean-associated bacteria”.[9]
Society norms and the convenience of fast food play an important role. Note the experience of the country of Qatar: it ranks sixth globally for prevalence of obesity and has the highest rate of obesity among boys in the Middle East and North African region. It is predicted that by 2016, 73 percent of Qatari women and 69 percent of the men will qualify as obese. Social occasions center around eating large platters of food. Walking is not popular; summer temperatures are a humid 106 degrees. As the New York Times said, "Like other oil-rich nations, Qatar has leaped across decades of development in a short time, leaving behind the physically demanding life of the desert for air-conditioned comfort, servants and fast food."[10]
A 2009 report from the American Institute for Cancer Research (AIRC) revealed that more than 100,000 cases of cancer each year are caused by excess body fat. Excess body fat appears to increase the amount of hormones like estrogen circulating in the body, and it can also disrupt how the body processes insulin. Both of those factors have been linked to an increased cancer risk. Also, obesity creates low-grade inflammation in the body, and much current research links chronic inflammation to cancer.[11]
Studies have shown that increased body fat can lead to increased levels of oxidative stress and inflammatory compounds in the blood, which are linked to DNA mutation and diseased cell growth, as is seen in many cancers.
Born to Be Big? Epigenetics and Chemicals
If you are an obese woman and you start a family, your children and their children down the line may struggle with the “imprint” of your obesity. Adult obesity appears to increase the risk of obesity in offspring through non-genetic influences, a phenomenon termed perinatal programming.[12] A 2007 study found that maternal hyperglycemia during pregnancy strongly predicted high BMI in offspring at 5 to 7 years of age.[13] By age 10-16 years, offspring of a diabetic pregnancy have an almost 1 in 5 rate of impaired glucose intolerance.[14]
How might that happen, that an obese mother can create future generations of obese children? Because the baby is born programmed to be obese:[15]
- Each time a pregnant woman eats, her hormones launch a flurry of activity, including a rise in blood glucose with a resultant rise in insulin secreted by the pancreas. This makes sure that an ample supply of glucose is available to both her and her fetus.
- Throughout the 2nd and 3rd trimesters, hormone levels rise, the pancreas works harder, and mom's amount of insulin resistance rises, because her muscles do not like being bathed in insulin and drowned in glucose.
- When the mother's pancreas doesn't secret enough insulin to keep the blood sugar level low, the mother and the fetus experience hyperglycemia. The fetus is exposed to bouts of hyperglycemia which promotes excess nutrient storage. The result is excessive birth weight (macrosomia).
- Excessive body fat stores, stimulated by excessive glucose delivery during diabetic pregnancy, often extends into childhood and adult life.
Exposure in the womb seems to permanently disrupt or dysregulate appetite control and hormones and impair energy metabolism. “Fetal metabolic programming” may lead to obesity in adolescence and young adulthood, spawning a potential vicious cycle of transgenerational transmission of the obesity epidemic from parents to offspring, regardless of offspring genetics or childhood environment.[16]
Chemicals also play a big role in obesity. Ever since Rachel Carson wrote Silent Spring back in the 1960s, the book that rang the first big warning about the dangers of pesticides, we have been slowly waking up to the dangers of the 80,000 or so chemicals in our midst.
Sharon Begley reported in Newsweek in 2009 that early exposure to common chemicals may be programming kids to be fat:
“Certain hormone-mimicking pollutants, ubiquitous in the food chain, have two previously unsuspected effects. They act on genes in the developing fetus and newborn to turn more precursor cells into fat cells, which stay with you for life. And they may alter metabolic rate, so that the body hoards calories rather than burning them, like a physiological Scrooge. 'The evidence now emerging says that being overweight is not just the result of personal choices about what you eat, combined with inactivity,' says Retha Newbold of the National Institute of Environmental Health Sciences (NIEHS) in North Carolina, part of the National Institutes of Health (NIH). 'Exposure to environmental chemicals during development may be contributing to the obesity epidemic.' They are not the cause of extra pounds in every person who is overweight-for older adults, who were less likely to be exposed to so many of the compounds before birth, the standard explanations of genetics and lifestyle probably suffice-but environmental chemicals may well account for a good part of the current epidemic, especially in those under 50. And at the individual level, exposure to the compounds during a critical period of development may explain one of the most frustrating aspects of weight gain: you eat no more than your slim friends, and exercise no less, yet are still unable to shed pounds.”[17]
Dr. David Ludwig is the director of the Optimal Weight for Life Program in the Division of Endocrinology, Children's Hospital Boston. He is also an associate professor of pediatrics at Harvard Medical School. He wrote in the New England Journal of Medicine about a family who came to his clinic:
“One of the parents was overweight, and the other was obese. The five children were more severely obese and had numerous weight-related complications - one had evidence of fatty liver, one had high blood pressure, two had gastroesophageal reflux, two had orthopedic problems, three had marked insulin resistance, four had dyslipidemia, and all had emotional problems related to their weight.
“Unfortunately, the U.S. government has thus far invested only a fraction of a cent in research for every dollar that obesity costs society. And although broad consensus exists regarding the dietary and lifestyle habits needed to prevent and treat childhood obesity, we lack anything resembling a comprehensive strategy for encouraging children to eat a healthful diet and engage in physical activity. Such a strategy would include legislation that regulates junk-food advertising, provides adequate funding for decent lunches and regular physical activities at school, restructures the farm-subsidies program to favor nutrient-dense rather than calorie-dense produce, and mandates insurance coverage for preventing and treating pediatric obesity.”[18]
Nutrient-dense versus Calorie-dense
Nutrient-dense means that each bite of food has a lot of nutrition - vitamins, minerals, enzymes, maybe antioxidants and more. Calorie-dense is something like soda - no nutrition, but packing the calories. Most of us need help learning how to make the switch to nutrient-dense food, and organic food that has less chemicals.
Losing weight safely sometimes requires a safe detox program along with dietary changes. At the Arizona Center for Advanced Medicine, we have such a program for change. It is called FirstLine Therapy™. We measure the BMI routinely on all our patients. During the course of the program we measure the BMI twice a month to determine whether muscle mass is being maintained while fat mass is lost. We take time to do lots of hand-holding and education. The program works for children, adolescents and adults. We show you how to choose nutrient-dense foods over calorie-dense foods. We help you plan a do-able nutritional program which will allow both children and adults to lose weight (fat), while maintaining muscle mass. And we hold your hand as you tackle that tough one, exercise - how much, what type, how to do it, and how often. We show you for example what you can do while sitting at your desk during a phone call. We also offer colonics which can flush out the colon and rebalance the intestinal flora. The 12-week program gives you the tools to enable you and your children to choose a healthy lifestyle for the rest of your lives.
[1] Rebecca Voelker, Improved Use of BMI Needed to Screen Children for Overweight, JAMA, 2007;297:2684-2685.[2] David S. Ludwig, M.D., Ph.D. Childhood Obesity - The Shape of Things to Come, NEJM, December 6, 2007[3] Christina Paxson, Elisabeth Donahue, C. Tracy Orleans, and Jeanne Ann Grisso, Childhood Obesity-Introducing the Issue, Childhood Obesity, The Future of Children, a publication of the Woodrow Wilson School of Public and International Affairs at Princeton University and the Brookings Institution, Volume 16, Number 1 Spring 2006.[4] News Release: Scientists Find Link Between Dopamine and Obesity. Brookhaven National Laboratory. February 1, 2001[5] News Release: New gene discovery links obesity to the brain. Albert Einstein College of Medicine. June 25, 2009 [6] Johnson, Paul M; Kenny, Paul J. Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats. Nature Neuroscience. March 28, 2010; DOI: 10.1038/nn.2519 [7]James Owen, Some Couch Potatoes Born That Way, Fat Study Says, National Geographic News, January 27, 2007 [8] Contagious Obesity? Identifying The Human Adenoviruses That May Make Us Fat. ScienceDaily, January 30, 2006 [9] Turnbaugh PJ, Ley RE et al. An obesity-associated gut microbiome with increased capacity for energy harvest. Nature 444, 1027-131 (21 December 2006) [7] http://www.cancer.org/…Over_100000_Cancers_Linked_to_Excess_Body_Fat.asp [8] Plagemann A. Perinatal programming and functional teratogenesis: impact on body weight regulation and obesity. Physiol Behav. Dec 15 2005;86(5):661-8 [9] Hillier TA, Pedula KL, et al. Childhood obesity and metabolic imprinting: the ongoing effects of maternal hyperglycemia. Diabetes Care 2007;30:2287-92. [10] Slackman, Michael. Privilege Pulls Qatar Toward Unhealthy Choices. New York Times. April 26, 2010 [11] http://www.cancer.org…NWS_1_1x_Report_Over_100000_Cancers_Linked_to_Excess_Body_Fat.asp [12] Plagemann A. Perinatal programming and functional teratogenesis: impact on body weight regulation and obesity. Physiol Behav. Dec 15 2005;86(5):661-8 [13] Hillier TA, Pedula KL, et al. Childhood obesity and metabolic imprinting: the ongoing effects of maternal hyperglycemia. Diabetes Care 2007;30:2287-92. [14] McKinney PA, Parslow R, Gurney KA, Law GR, Bodansky HJ, Williams R. Perinatal and neonatal determinants of childhood type 1 diabetes. A case-control study in Yorkshire, U.K. Diabetes Care. Jun 1999;22(6):928-32 [15] http://emedicine.medscape.com/article/127547-overview [16] Eric L Ding and Frank B Hu. Determining Origins and Causes of Childhood Obesity via Mendelian Randomization Analysis. PLoS Med. 2008 March; 5(3): e65. [17] Sharon Begley, Born to be Big - Early exposure to common chemicals may be programming kids to be fat. Newsweek, September 11, 2009 [18] David S. Ludwig, M.D., Ph.D. Childhood Obesity - The Shape of Things to Come, NEJM, December 6, 2007Obesity
Children can’t change their exercise and eating habits by themselves. They need the help and support of their families. Same goes for adults.
Grown-ups have been bombarded with decades of bad dietary advice – eat margarine, eat a high carbohydrate diet, eating fat will make you fat. Grown-ups have also been living in a toxic world for decades, and their bodies have stored many of those toxins in fat which the body hesitates now to shed because too many toxins in the bloodstream can be fatal.
Extra fat produces more of the leptin hormone which is supposed to tell the hypothalamus there is too much fat stored, so don’t store any more and burn off the excess. But overexposure to high levels of leptin is thought to work like overexposure to insulin – the cells to become “insulin-resistant” and “leptin-resistant” which feeds the diabetes problem. With leptin-resistance, after a while you don’t get strong signals to stop eating, to stop storing fat, and to start burning off extra fat.
Low levels of dopamine can drive over-eating. Brain-imaging studies conducted by the Brookhaven National Laboratory suggest that many overweight people, like drug addicts, have fewer brain receptors for dopamine – the neurotransmitter that signals feelings of satisfaction and pleasure. The more you eat, the more dopamine you release.[4] The science suggests that obese people may be overeating to get a feel-good feeling, much like a drug addict does with drugs. The good news here is that exercise - when people do it - also triggers the release of dopamine.
Since the early 1990s, we've been learning about the genetic component that food and drug addictions share. Most recently, a study of 31,000 people of European origin, ages 45 to 76, found that the NRXN3 gene variant – previously associated with alcohol dependence, cocaine addiction, and illegal substance abuse – also predicts the tendency to become obese. People who inherited the gene variant NRXN3 have a 10-15 percent increased risk of being obese compared with people who do not have the variant. About 20 percent of the people studied had the gene variant. NRXN3 is the third obesity-associated gene to be identified; all three are highly active in encoding brain proteins.[5]
The biggest contributor to the growing obesity epidemic, however, may be that we alter our brain chemistry by what we eat. Doing drugs such as cocaine and eating too much junk food both gradually overload the so-called pleasure centers in the brain, according to Paul J. Kenny, an associate professor of molecular therapeutics at the Scripps Research Institute. Eventually it takes increasing amounts of the drug or food to get the same pleasurable feelings. Kenny found that rats that gorge themselves on the human food quickly became obese. But their brains also changed. By monitoring implanted brain electrodes, the researchers found that the rats gradually developed a tolerance to the pleasure the food gave them and had to eat more to experience a high. They began to eat compulsively, to the point where they continued to do so in the face of pain.[6]
What Else?
Mayo Clinic research found that obese adults don't burn as many calories during everyday activities - walking, fidgeting, or even just standing - as non-obese people. The study’s lead author, James Levine, a Mayo Clinic endocrinologist, said, “Our patients have told us for years that they have low metabolisms. We have never quite understood what that means. The answer is they have low NEAT [non-exercise activity thermogenesis].”[7]
Adenoviruses, which typically cause respiratory infections, have been implicated in obesity. Researchers at the University of Wisconsin, Madison. found that the virus goes to the lungs and then, after the cold is gone, spreads through the body. When this virus goes to fat tissue, it replicates and increases the number of new fat cells. Human studies show that almost a third of obese adults carry the virus compared with 11 per cent of lean men and women.[8]
Obesity has also been linked with relative abundance of two particular species of bacteria in the gut. Some bacteria are associated with increased ability to extract nutrients from the diet and build fat, as has been shown by studies where lean mice are colonized with “obese-associated bacteria” and develop more body fat than mice colonized with “lean-associated bacteria”.[9]
Society norms and the convenience of fast food play an important role. Note the experience of the country of Qatar: it ranks sixth globally for prevalence of obesity and has the highest rate of obesity among boys in the Middle East and North African region. It is predicted that by 2016, 73 percent of Qatari women and 69 percent of the men will qualify as obese. Social occasions center around eating large platters of food. Walking is not popular; summer temperatures are a humid 106 degrees. As the New York Times said, "Like other oil-rich nations, Qatar has leaped across decades of development in a short time, leaving behind the physically demanding life of the desert for air-conditioned comfort, servants and fast food."[10]
A 2009 report from the American Institute for Cancer Research (AIRC) revealed that more than 100,000 cases of cancer each year are caused by excess body fat. Excess body fat appears to increase the amount of hormones like estrogen circulating in the body, and it can also disrupt how the body processes insulin. Both of those factors have been linked to an increased cancer risk. Also, obesity creates low-grade inflammation in the body, and much current research links chronic inflammation to cancer.[11]
Studies have shown that increased body fat can lead to increased levels of oxidative stress and inflammatory compounds in the blood, which are linked to DNA mutation and diseased cell growth, as is seen in many cancers.
Born to Be Big? Epigenetics and Chemicals
If you are an obese woman and you start a family, your children and their children down the line may struggle with the “imprint” of your obesity. Adult obesity appears to increase the risk of obesity in offspring through non-genetic influences, a phenomenon termed perinatal programming.[12] A 2007 study found that maternal hyperglycemia during pregnancy strongly predicted high BMI in offspring at 5 to 7 years of age.[13] By age 10-16 years, offspring of a diabetic pregnancy have an almost 1 in 5 rate of impaired glucose intolerance.[14]
How might that happen, that an obese mother can create future generations of obese children? Because the baby is born programmed to be obese:[15]
- Each time a pregnant woman eats, her hormones launch a flurry of activity, including a rise in blood glucose with a resultant rise in insulin secreted by the pancreas. This makes sure that an ample supply of glucose is available to both her and her fetus.
- Throughout the 2nd and 3rd trimesters, hormone levels rise, the pancreas works harder, and mom's amount of insulin resistance rises, because her muscles do not like being bathed in insulin and drowned in glucose.
- When the mother's pancreas doesn't secret enough insulin to keep the blood sugar level low, the mother and the fetus experience hyperglycemia. The fetus is exposed to bouts of hyperglycemia which promotes excess nutrient storage. The result is excessive birth weight (macrosomia).
- Excessive body fat stores, stimulated by excessive glucose delivery during diabetic pregnancy, often extends into childhood and adult life.
Exposure in the womb seems to permanently disrupt or dysregulate appetite control and hormones and impair energy metabolism. “Fetal metabolic programming” may lead to obesity in adolescence and young adulthood, spawning a potential vicious cycle of transgenerational transmission of the obesity epidemic from parents to offspring, regardless of offspring genetics or childhood environment.[16]
Chemicals also play a big role in obesity. Ever since Rachel Carson wrote Silent Spring back in the 1960s, the book that rang the first big warning about the dangers of pesticides, we have been slowly waking up to the dangers of the 80,000 or so chemicals in our midst.
Sharon Begley reported in Newsweek in 2009 that early exposure to common chemicals may be programming kids to be fat:
“Certain hormone-mimicking pollutants, ubiquitous in the food chain, have two previously unsuspected effects. They act on genes in the developing fetus and newborn to turn more precursor cells into fat cells, which stay with you for life. And they may alter metabolic rate, so that the body hoards calories rather than burning them, like a physiological Scrooge. 'The evidence now emerging says that being overweight is not just the result of personal choices about what you eat, combined with inactivity,' says Retha Newbold of the National Institute of Environmental Health Sciences (NIEHS) in North Carolina, part of the National Institutes of Health (NIH). 'Exposure to environmental chemicals during development may be contributing to the obesity epidemic.' They are not the cause of extra pounds in every person who is overweight-for older adults, who were less likely to be exposed to so many of the compounds before birth, the standard explanations of genetics and lifestyle probably suffice-but environmental chemicals may well account for a good part of the current epidemic, especially in those under 50. And at the individual level, exposure to the compounds during a critical period of development may explain one of the most frustrating aspects of weight gain: you eat no more than your slim friends, and exercise no less, yet are still unable to shed pounds.”[17]
Dr. David Ludwig is the director of the Optimal Weight for Life Program in the Division of Endocrinology, Children's Hospital Boston. He is also an associate professor of pediatrics at Harvard Medical School. He wrote in the New England Journal of Medicine about a family who came to his clinic:
“One of the parents was overweight, and the other was obese. The five children were more severely obese and had numerous weight-related complications - one had evidence of fatty liver, one had high blood pressure, two had gastroesophageal reflux, two had orthopedic problems, three had marked insulin resistance, four had dyslipidemia, and all had emotional problems related to their weight.
“Unfortunately, the U.S. government has thus far invested only a fraction of a cent in research for every dollar that obesity costs society. And although broad consensus exists regarding the dietary and lifestyle habits needed to prevent and treat childhood obesity, we lack anything resembling a comprehensive strategy for encouraging children to eat a healthful diet and engage in physical activity. Such a strategy would include legislation that regulates junk-food advertising, provides adequate funding for decent lunches and regular physical activities at school, restructures the farm-subsidies program to favor nutrient-dense rather than calorie-dense produce, and mandates insurance coverage for preventing and treating pediatric obesity.”[18]
Nutrient-dense versus Calorie-dense
Nutrient-dense means that each bite of food has a lot of nutrition - vitamins, minerals, enzymes, maybe antioxidants and more. Calorie-dense is something like soda - no nutrition, but packing the calories. Most of us need help learning how to make the switch to nutrient-dense food, and organic food that has less chemicals.
Losing weight safely sometimes requires a safe detox program along with dietary changes. At the Arizona Center for Advanced Medicine, we have such a program for change. It is called FirstLine Therapy™. We measure the BMI routinely on all our patients. During the course of the program we measure the BMI twice a month to determine whether muscle mass is being maintained while fat mass is lost. We take time to do lots of hand-holding and education. The program works for children, adolescents and adults. We show you how to choose nutrient-dense foods over calorie-dense foods. We help you plan a do-able nutritional program which will allow both children and adults to lose weight (fat), while maintaining muscle mass. And we hold your hand as you tackle that tough one, exercise - how much, what type, how to do it, and how often. We show you for example what you can do while sitting at your desk during a phone call. We also offer colonics which can flush out the colon and rebalance the intestinal flora. The 12-week program gives you the tools to enable you and your children to choose a healthy lifestyle for the rest of your lives.
[1] Rebecca Voelker, Improved Use of BMI Needed to Screen Children for Overweight, JAMA, 2007;297:2684-2685.[2] David S. Ludwig, M.D., Ph.D. Childhood Obesity - The Shape of Things to Come, NEJM, December 6, 2007[3] Christina Paxson, Elisabeth Donahue, C. Tracy Orleans, and Jeanne Ann Grisso, Childhood Obesity-Introducing the Issue, Childhood Obesity, The Future of Children, a publication of the Woodrow Wilson School of Public and International Affairs at Princeton University and the Brookings Institution, Volume 16, Number 1 Spring 2006.[4] News Release: Scientists Find Link Between Dopamine and Obesity. Brookhaven National Laboratory. February 1, 2001[5] News Release: New gene discovery links obesity to the brain. Albert Einstein College of Medicine. June 25, 2009 [6] Johnson, Paul M; Kenny, Paul J. Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats. Nature Neuroscience. March 28, 2010; DOI: 10.1038/nn.2519 [7]James Owen, Some Couch Potatoes Born That Way, Fat Study Says, National Geographic News, January 27, 2007 [8] Contagious Obesity? Identifying The Human Adenoviruses That May Make Us Fat. ScienceDaily, January 30, 2006 [9] Turnbaugh PJ, Ley RE et al. An obesity-associated gut microbiome with increased capacity for energy harvest. Nature 444, 1027-131 (21 December 2006) [7] http://www.cancer.org/…Over_100000_Cancers_Linked_to_Excess_Body_Fat.asp [8] Plagemann A. Perinatal programming and functional teratogenesis: impact on body weight regulation and obesity. Physiol Behav. Dec 15 2005;86(5):661-8 [9] Hillier TA, Pedula KL, et al. Childhood obesity and metabolic imprinting: the ongoing effects of maternal hyperglycemia. Diabetes Care 2007;30:2287-92. [10] Slackman, Michael. Privilege Pulls Qatar Toward Unhealthy Choices. New York Times. April 26, 2010 [11] http://www.cancer.org…NWS_1_1x_Report_Over_100000_Cancers_Linked_to_Excess_Body_Fat.asp [12] Plagemann A. Perinatal programming and functional teratogenesis: impact on body weight regulation and obesity. Physiol Behav. Dec 15 2005;86(5):661-8 [13] Hillier TA, Pedula KL, et al. Childhood obesity and metabolic imprinting: the ongoing effects of maternal hyperglycemia. Diabetes Care 2007;30:2287-92. [14] McKinney PA, Parslow R, Gurney KA, Law GR, Bodansky HJ, Williams R. Perinatal and neonatal determinants of childhood type 1 diabetes. A case-control study in Yorkshire, U.K. Diabetes Care. Jun 1999;22(6):928-32 [15] http://emedicine.medscape.com/article/127547-overview [16] Eric L Ding and Frank B Hu. Determining Origins and Causes of Childhood Obesity via Mendelian Randomization Analysis. PLoS Med. 2008 March; 5(3): e65. [17] Sharon Begley, Born to be Big - Early exposure to common chemicals may be programming kids to be fat. Newsweek, September 11, 2009 [18] David S. Ludwig, M.D., Ph.D. Childhood Obesity - The Shape of Things to Come, NEJM, December 6, 2007Obesity
The biggest contributor to the growing obesity epidemic, however, may be that we alter our brain chemistry by what we eat. Doing drugs such as cocaine and eating too much junk food both gradually overload the so-called pleasure centers in the brain, according to Paul J. Kenny, an associate professor of molecular therapeutics at the Scripps Research Institute. Eventually it takes increasing amounts of the drug or food to get the same pleasurable feelings. Kenny found that rats that gorge themselves on the human food quickly became obese. But their brains also changed. By monitoring implanted brain electrodes, the researchers found that the rats gradually developed a tolerance to the pleasure the food gave them and had to eat more to experience a high. They began to eat compulsively, to the point where they continued to do so in the face of pain.[6]
What Else?
Mayo Clinic research found that obese adults don't burn as many calories during everyday activities - walking, fidgeting, or even just standing - as non-obese people. The study’s lead author, James Levine, a Mayo Clinic endocrinologist, said, “Our patients have told us for years that they have low metabolisms. We have never quite understood what that means. The answer is they have low NEAT [non-exercise activity thermogenesis].”[7]
Adenoviruses, which typically cause respiratory infections, have been implicated in obesity. Researchers at the University of Wisconsin, Madison. found that the virus goes to the lungs and then, after the cold is gone, spreads through the body. When this virus goes to fat tissue, it replicates and increases the number of new fat cells. Human studies show that almost a third of obese adults carry the virus compared with 11 per cent of lean men and women.[8]
Obesity has also been linked with relative abundance of two particular species of bacteria in the gut. Some bacteria are associated with increased ability to extract nutrients from the diet and build fat, as has been shown by studies where lean mice are colonized with “obese-associated bacteria” and develop more body fat than mice colonized with “lean-associated bacteria”.[9]
Society norms and the convenience of fast food play an important role. Note the experience of the country of Qatar: it ranks sixth globally for prevalence of obesity and has the highest rate of obesity among boys in the Middle East and North African region. It is predicted that by 2016, 73 percent of Qatari women and 69 percent of the men will qualify as obese. Social occasions center around eating large platters of food. Walking is not popular; summer temperatures are a humid 106 degrees. As the New York Times said, "Like other oil-rich nations, Qatar has leaped across decades of development in a short time, leaving behind the physically demanding life of the desert for air-conditioned comfort, servants and fast food."[10]
A 2009 report from the American Institute for Cancer Research (AIRC) revealed that more than 100,000 cases of cancer each year are caused by excess body fat. Excess body fat appears to increase the amount of hormones like estrogen circulating in the body, and it can also disrupt how the body processes insulin. Both of those factors have been linked to an increased cancer risk. Also, obesity creates low-grade inflammation in the body, and much current research links chronic inflammation to cancer.[11]
Studies have shown that increased body fat can lead to increased levels of oxidative stress and inflammatory compounds in the blood, which are linked to DNA mutation and diseased cell growth, as is seen in many cancers.
Born to Be Big? Epigenetics and Chemicals
If you are an obese woman and you start a family, your children and their children down the line may struggle with the “imprint” of your obesity. Adult obesity appears to increase the risk of obesity in offspring through non-genetic influences, a phenomenon termed perinatal programming.[12] A 2007 study found that maternal hyperglycemia during pregnancy strongly predicted high BMI in offspring at 5 to 7 years of age.[13] By age 10-16 years, offspring of a diabetic pregnancy have an almost 1 in 5 rate of impaired glucose intolerance.[14]
How might that happen, that an obese mother can create future generations of obese children? Because the baby is born programmed to be obese:[15]
- Each time a pregnant woman eats, her hormones launch a flurry of activity, including a rise in blood glucose with a resultant rise in insulin secreted by the pancreas. This makes sure that an ample supply of glucose is available to both her and her fetus.
- Throughout the 2nd and 3rd trimesters, hormone levels rise, the pancreas works harder, and mom's amount of insulin resistance rises, because her muscles do not like being bathed in insulin and drowned in glucose.
- When the mother's pancreas doesn't secret enough insulin to keep the blood sugar level low, the mother and the fetus experience hyperglycemia. The fetus is exposed to bouts of hyperglycemia which promotes excess nutrient storage. The result is excessive birth weight (macrosomia).
- Excessive body fat stores, stimulated by excessive glucose delivery during diabetic pregnancy, often extends into childhood and adult life.
Exposure in the womb seems to permanently disrupt or dysregulate appetite control and hormones and impair energy metabolism. “Fetal metabolic programming” may lead to obesity in adolescence and young adulthood, spawning a potential vicious cycle of transgenerational transmission of the obesity epidemic from parents to offspring, regardless of offspring genetics or childhood environment.[16]
Chemicals also play a big role in obesity. Ever since Rachel Carson wrote Silent Spring back in the 1960s, the book that rang the first big warning about the dangers of pesticides, we have been slowly waking up to the dangers of the 80,000 or so chemicals in our midst.
Sharon Begley reported in Newsweek in 2009 that early exposure to common chemicals may be programming kids to be fat:
“Certain hormone-mimicking pollutants, ubiquitous in the food chain, have two previously unsuspected effects. They act on genes in the developing fetus and newborn to turn more precursor cells into fat cells, which stay with you for life. And they may alter metabolic rate, so that the body hoards calories rather than burning them, like a physiological Scrooge. 'The evidence now emerging says that being overweight is not just the result of personal choices about what you eat, combined with inactivity,' says Retha Newbold of the National Institute of Environmental Health Sciences (NIEHS) in North Carolina, part of the National Institutes of Health (NIH). 'Exposure to environmental chemicals during development may be contributing to the obesity epidemic.' They are not the cause of extra pounds in every person who is overweight-for older adults, who were less likely to be exposed to so many of the compounds before birth, the standard explanations of genetics and lifestyle probably suffice-but environmental chemicals may well account for a good part of the current epidemic, especially in those under 50. And at the individual level, exposure to the compounds during a critical period of development may explain one of the most frustrating aspects of weight gain: you eat no more than your slim friends, and exercise no less, yet are still unable to shed pounds.”[17]
Dr. David Ludwig is the director of the Optimal Weight for Life Program in the Division of Endocrinology, Children's Hospital Boston. He is also an associate professor of pediatrics at Harvard Medical School. He wrote in the New England Journal of Medicine about a family who came to his clinic:
“One of the parents was overweight, and the other was obese. The five children were more severely obese and had numerous weight-related complications - one had evidence of fatty liver, one had high blood pressure, two had gastroesophageal reflux, two had orthopedic problems, three had marked insulin resistance, four had dyslipidemia, and all had emotional problems related to their weight.
“Unfortunately, the U.S. government has thus far invested only a fraction of a cent in research for every dollar that obesity costs society. And although broad consensus exists regarding the dietary and lifestyle habits needed to prevent and treat childhood obesity, we lack anything resembling a comprehensive strategy for encouraging children to eat a healthful diet and engage in physical activity. Such a strategy would include legislation that regulates junk-food advertising, provides adequate funding for decent lunches and regular physical activities at school, restructures the farm-subsidies program to favor nutrient-dense rather than calorie-dense produce, and mandates insurance coverage for preventing and treating pediatric obesity.”[18]
Nutrient-dense versus Calorie-dense
Nutrient-dense means that each bite of food has a lot of nutrition - vitamins, minerals, enzymes, maybe antioxidants and more. Calorie-dense is something like soda - no nutrition, but packing the calories. Most of us need help learning how to make the switch to nutrient-dense food, and organic food that has less chemicals.
Losing weight safely sometimes requires a safe detox program along with dietary changes. At the Arizona Center for Advanced Medicine, we have such a program for change. It is called FirstLine Therapy™. We measure the BMI routinely on all our patients. During the course of the program we measure the BMI twice a month to determine whether muscle mass is being maintained while fat mass is lost. We take time to do lots of hand-holding and education. The program works for children, adolescents and adults. We show you how to choose nutrient-dense foods over calorie-dense foods. We help you plan a do-able nutritional program which will allow both children and adults to lose weight (fat), while maintaining muscle mass. And we hold your hand as you tackle that tough one, exercise - how much, what type, how to do it, and how often. We show you for example what you can do while sitting at your desk during a phone call. We also offer colonics which can flush out the colon and rebalance the intestinal flora. The 12-week program gives you the tools to enable you and your children to choose a healthy lifestyle for the rest of your lives.
[1] Rebecca Voelker, Improved Use of BMI Needed to Screen Children for Overweight, JAMA, 2007;297:2684-2685.[2] David S. Ludwig, M.D., Ph.D. Childhood Obesity - The Shape of Things to Come, NEJM, December 6, 2007[3] Christina Paxson, Elisabeth Donahue, C. Tracy Orleans, and Jeanne Ann Grisso, Childhood Obesity-Introducing the Issue, Childhood Obesity, The Future of Children, a publication of the Woodrow Wilson School of Public and International Affairs at Princeton University and the Brookings Institution, Volume 16, Number 1 Spring 2006.[4] News Release: Scientists Find Link Between Dopamine and Obesity. Brookhaven National Laboratory. February 1, 2001[5] News Release: New gene discovery links obesity to the brain. Albert Einstein College of Medicine. June 25, 2009 [6] Johnson, Paul M; Kenny, Paul J. Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats. Nature Neuroscience. March 28, 2010; DOI: 10.1038/nn.2519 [7]James Owen, Some Couch Potatoes Born That Way, Fat Study Says, National Geographic News, January 27, 2007 [8] Contagious Obesity? Identifying The Human Adenoviruses That May Make Us Fat. ScienceDaily, January 30, 2006 [9] Turnbaugh PJ, Ley RE et al. An obesity-associated gut microbiome with increased capacity for energy harvest. Nature 444, 1027-131 (21 December 2006) [7] http://www.cancer.org/…Over_100000_Cancers_Linked_to_Excess_Body_Fat.asp [8] Plagemann A. Perinatal programming and functional teratogenesis: impact on body weight regulation and obesity. Physiol Behav. Dec 15 2005;86(5):661-8 [9] Hillier TA, Pedula KL, et al. Childhood obesity and metabolic imprinting: the ongoing effects of maternal hyperglycemia. Diabetes Care 2007;30:2287-92. [10] Slackman, Michael. Privilege Pulls Qatar Toward Unhealthy Choices. New York Times. April 26, 2010 [11] http://www.cancer.org…NWS_1_1x_Report_Over_100000_Cancers_Linked_to_Excess_Body_Fat.asp [12] Plagemann A. Perinatal programming and functional teratogenesis: impact on body weight regulation and obesity. Physiol Behav. Dec 15 2005;86(5):661-8 [13] Hillier TA, Pedula KL, et al. Childhood obesity and metabolic imprinting: the ongoing effects of maternal hyperglycemia. Diabetes Care 2007;30:2287-92. [14] McKinney PA, Parslow R, Gurney KA, Law GR, Bodansky HJ, Williams R. Perinatal and neonatal determinants of childhood type 1 diabetes. A case-control study in Yorkshire, U.K. Diabetes Care. Jun 1999;22(6):928-32 [15] http://emedicine.medscape.com/article/127547-overview [16] Eric L Ding and Frank B Hu. Determining Origins and Causes of Childhood Obesity via Mendelian Randomization Analysis. PLoS Med. 2008 March; 5(3): e65. [17] Sharon Begley, Born to be Big - Early exposure to common chemicals may be programming kids to be fat. Newsweek, September 11, 2009 [18] David S. Ludwig, M.D., Ph.D. Childhood Obesity - The Shape of Things to Come, NEJM, December 6, 2007Obesity
Mayo Clinic research found that obese adults don't burn as many calories during everyday activities - walking, fidgeting, or even just standing - as non-obese people. The study’s lead author, James Levine, a Mayo Clinic endocrinologist, said, “Our patients have told us for years that they have low metabolisms. We have never quite understood what that means. The answer is they have low NEAT [non-exercise activity thermogenesis].”[7]
Adenoviruses, which typically cause respiratory infections, have been implicated in obesity. Researchers at the University of Wisconsin, Madison. found that the virus goes to the lungs and then, after the cold is gone, spreads through the body. When this virus goes to fat tissue, it replicates and increases the number of new fat cells. Human studies show that almost a third of obese adults carry the virus compared with 11 per cent of lean men and women.[8]
Obesity has also been linked with relative abundance of two particular species of bacteria in the gut. Some bacteria are associated with increased ability to extract nutrients from the diet and build fat, as has been shown by studies where lean mice are colonized with “obese-associated bacteria” and develop more body fat than mice colonized with “lean-associated bacteria”.[9]
Society norms and the convenience of fast food play an important role. Note the experience of the country of Qatar: it ranks sixth globally for prevalence of obesity and has the highest rate of obesity among boys in the Middle East and North African region. It is predicted that by 2016, 73 percent of Qatari women and 69 percent of the men will qualify as obese. Social occasions center around eating large platters of food. Walking is not popular; summer temperatures are a humid 106 degrees. As the New York Times said, "Like other oil-rich nations, Qatar has leaped across decades of development in a short time, leaving behind the physically demanding life of the desert for air-conditioned comfort, servants and fast food."[10]
A 2009 report from the American Institute for Cancer Research (AIRC) revealed that more than 100,000 cases of cancer each year are caused by excess body fat. Excess body fat appears to increase the amount of hormones like estrogen circulating in the body, and it can also disrupt how the body processes insulin. Both of those factors have been linked to an increased cancer risk. Also, obesity creates low-grade inflammation in the body, and much current research links chronic inflammation to cancer.[11]
Studies have shown that increased body fat can lead to increased levels of oxidative stress and inflammatory compounds in the blood, which are linked to DNA mutation and diseased cell growth, as is seen in many cancers.
Born to Be Big? Epigenetics and Chemicals
If you are an obese woman and you start a family, your children and their children down the line may struggle with the “imprint” of your obesity. Adult obesity appears to increase the risk of obesity in offspring through non-genetic influences, a phenomenon termed perinatal programming.[12] A 2007 study found that maternal hyperglycemia during pregnancy strongly predicted high BMI in offspring at 5 to 7 years of age.[13] By age 10-16 years, offspring of a diabetic pregnancy have an almost 1 in 5 rate of impaired glucose intolerance.[14]
How might that happen, that an obese mother can create future generations of obese children? Because the baby is born programmed to be obese:[15]
- Each time a pregnant woman eats, her hormones launch a flurry of activity, including a rise in blood glucose with a resultant rise in insulin secreted by the pancreas. This makes sure that an ample supply of glucose is available to both her and her fetus.
- Throughout the 2nd and 3rd trimesters, hormone levels rise, the pancreas works harder, and mom's amount of insulin resistance rises, because her muscles do not like being bathed in insulin and drowned in glucose.
- When the mother's pancreas doesn't secret enough insulin to keep the blood sugar level low, the mother and the fetus experience hyperglycemia. The fetus is exposed to bouts of hyperglycemia which promotes excess nutrient storage. The result is excessive birth weight (macrosomia).
- Excessive body fat stores, stimulated by excessive glucose delivery during diabetic pregnancy, often extends into childhood and adult life.
Exposure in the womb seems to permanently disrupt or dysregulate appetite control and hormones and impair energy metabolism. “Fetal metabolic programming” may lead to obesity in adolescence and young adulthood, spawning a potential vicious cycle of transgenerational transmission of the obesity epidemic from parents to offspring, regardless of offspring genetics or childhood environment.[16]
Chemicals also play a big role in obesity. Ever since Rachel Carson wrote Silent Spring back in the 1960s, the book that rang the first big warning about the dangers of pesticides, we have been slowly waking up to the dangers of the 80,000 or so chemicals in our midst.
Sharon Begley reported in Newsweek in 2009 that early exposure to common chemicals may be programming kids to be fat:
“Certain hormone-mimicking pollutants, ubiquitous in the food chain, have two previously unsuspected effects. They act on genes in the developing fetus and newborn to turn more precursor cells into fat cells, which stay with you for life. And they may alter metabolic rate, so that the body hoards calories rather than burning them, like a physiological Scrooge. 'The evidence now emerging says that being overweight is not just the result of personal choices about what you eat, combined with inactivity,' says Retha Newbold of the National Institute of Environmental Health Sciences (NIEHS) in North Carolina, part of the National Institutes of Health (NIH). 'Exposure to environmental chemicals during development may be contributing to the obesity epidemic.' They are not the cause of extra pounds in every person who is overweight-for older adults, who were less likely to be exposed to so many of the compounds before birth, the standard explanations of genetics and lifestyle probably suffice-but environmental chemicals may well account for a good part of the current epidemic, especially in those under 50. And at the individual level, exposure to the compounds during a critical period of development may explain one of the most frustrating aspects of weight gain: you eat no more than your slim friends, and exercise no less, yet are still unable to shed pounds.”[17]
Dr. David Ludwig is the director of the Optimal Weight for Life Program in the Division of Endocrinology, Children's Hospital Boston. He is also an associate professor of pediatrics at Harvard Medical School. He wrote in the New England Journal of Medicine about a family who came to his clinic:
“One of the parents was overweight, and the other was obese. The five children were more severely obese and had numerous weight-related complications - one had evidence of fatty liver, one had high blood pressure, two had gastroesophageal reflux, two had orthopedic problems, three had marked insulin resistance, four had dyslipidemia, and all had emotional problems related to their weight.
“Unfortunately, the U.S. government has thus far invested only a fraction of a cent in research for every dollar that obesity costs society. And although broad consensus exists regarding the dietary and lifestyle habits needed to prevent and treat childhood obesity, we lack anything resembling a comprehensive strategy for encouraging children to eat a healthful diet and engage in physical activity. Such a strategy would include legislation that regulates junk-food advertising, provides adequate funding for decent lunches and regular physical activities at school, restructures the farm-subsidies program to favor nutrient-dense rather than calorie-dense produce, and mandates insurance coverage for preventing and treating pediatric obesity.”[18]
Nutrient-dense versus Calorie-dense
Nutrient-dense means that each bite of food has a lot of nutrition - vitamins, minerals, enzymes, maybe antioxidants and more. Calorie-dense is something like soda - no nutrition, but packing the calories. Most of us need help learning how to make the switch to nutrient-dense food, and organic food that has less chemicals.
Losing weight safely sometimes requires a safe detox program along with dietary changes. At the Arizona Center for Advanced Medicine, we have such a program for change. It is called FirstLine Therapy™. We measure the BMI routinely on all our patients. During the course of the program we measure the BMI twice a month to determine whether muscle mass is being maintained while fat mass is lost. We take time to do lots of hand-holding and education. The program works for children, adolescents and adults. We show you how to choose nutrient-dense foods over calorie-dense foods. We help you plan a do-able nutritional program which will allow both children and adults to lose weight (fat), while maintaining muscle mass. And we hold your hand as you tackle that tough one, exercise - how much, what type, how to do it, and how often. We show you for example what you can do while sitting at your desk during a phone call. We also offer colonics which can flush out the colon and rebalance the intestinal flora. The 12-week program gives you the tools to enable you and your children to choose a healthy lifestyle for the rest of your lives.
[1] Rebecca Voelker, Improved Use of BMI Needed to Screen Children for Overweight, JAMA, 2007;297:2684-2685.[2] David S. Ludwig, M.D., Ph.D. Childhood Obesity - The Shape of Things to Come, NEJM, December 6, 2007[3] Christina Paxson, Elisabeth Donahue, C. Tracy Orleans, and Jeanne Ann Grisso, Childhood Obesity-Introducing the Issue, Childhood Obesity, The Future of Children, a publication of the Woodrow Wilson School of Public and International Affairs at Princeton University and the Brookings Institution, Volume 16, Number 1 Spring 2006.[4] News Release: Scientists Find Link Between Dopamine and Obesity. Brookhaven National Laboratory. February 1, 2001[5] News Release: New gene discovery links obesity to the brain. Albert Einstein College of Medicine. June 25, 2009 [6] Johnson, Paul M; Kenny, Paul J. Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats. Nature Neuroscience. March 28, 2010; DOI: 10.1038/nn.2519 [7]James Owen, Some Couch Potatoes Born That Way, Fat Study Says, National Geographic News, January 27, 2007 [8] Contagious Obesity? Identifying The Human Adenoviruses That May Make Us Fat. ScienceDaily, January 30, 2006 [9] Turnbaugh PJ, Ley RE et al. An obesity-associated gut microbiome with increased capacity for energy harvest. Nature 444, 1027-131 (21 December 2006) [7] http://www.cancer.org/…Over_100000_Cancers_Linked_to_Excess_Body_Fat.asp [8] Plagemann A. Perinatal programming and functional teratogenesis: impact on body weight regulation and obesity. Physiol Behav. Dec 15 2005;86(5):661-8 [9] Hillier TA, Pedula KL, et al. Childhood obesity and metabolic imprinting: the ongoing effects of maternal hyperglycemia. Diabetes Care 2007;30:2287-92. [10] Slackman, Michael. Privilege Pulls Qatar Toward Unhealthy Choices. New York Times. April 26, 2010 [11] http://www.cancer.org…NWS_1_1x_Report_Over_100000_Cancers_Linked_to_Excess_Body_Fat.asp [12] Plagemann A. Perinatal programming and functional teratogenesis: impact on body weight regulation and obesity. Physiol Behav. Dec 15 2005;86(5):661-8 [13] Hillier TA, Pedula KL, et al. Childhood obesity and metabolic imprinting: the ongoing effects of maternal hyperglycemia. Diabetes Care 2007;30:2287-92. [14] McKinney PA, Parslow R, Gurney KA, Law GR, Bodansky HJ, Williams R. Perinatal and neonatal determinants of childhood type 1 diabetes. A case-control study in Yorkshire, U.K. Diabetes Care. Jun 1999;22(6):928-32 [15] http://emedicine.medscape.com/article/127547-overview [16] Eric L Ding and Frank B Hu. Determining Origins and Causes of Childhood Obesity via Mendelian Randomization Analysis. PLoS Med. 2008 March; 5(3): e65. [17] Sharon Begley, Born to be Big - Early exposure to common chemicals may be programming kids to be fat. Newsweek, September 11, 2009 [18] David S. Ludwig, M.D., Ph.D. Childhood Obesity - The Shape of Things to Come, NEJM, December 6, 2007Obesity
Adenoviruses, which typically cause respiratory infections, have been implicated in obesity. Researchers at the University of Wisconsin, Madison. found that the virus goes to the lungs and then, after the cold is gone, spreads through the body. When this virus goes to fat tissue, it replicates and increases the number of new fat cells. Human studies show that almost a third of obese adults carry the virus compared with 11 per cent of lean men and women.[8]
Obesity has also been linked with relative abundance of two particular species of bacteria in the gut. Some bacteria are associated with increased ability to extract nutrients from the diet and build fat, as has been shown by studies where lean mice are colonized with “obese-associated bacteria” and develop more body fat than mice colonized with “lean-associated bacteria”.[9]
Society norms and the convenience of fast food play an important role. Note the experience of the country of Qatar: it ranks sixth globally for prevalence of obesity and has the highest rate of obesity among boys in the Middle East and North African region. It is predicted that by 2016, 73 percent of Qatari women and 69 percent of the men will qualify as obese. Social occasions center around eating large platters of food. Walking is not popular; summer temperatures are a humid 106 degrees. As the New York Times said, "Like other oil-rich nations, Qatar has leaped across decades of development in a short time, leaving behind the physically demanding life of the desert for air-conditioned comfort, servants and fast food."[10]
A 2009 report from the American Institute for Cancer Research (AIRC) revealed that more than 100,000 cases of cancer each year are caused by excess body fat. Excess body fat appears to increase the amount of hormones like estrogen circulating in the body, and it can also disrupt how the body processes insulin. Both of those factors have been linked to an increased cancer risk. Also, obesity creates low-grade inflammation in the body, and much current research links chronic inflammation to cancer.[11]
Studies have shown that increased body fat can lead to increased levels of oxidative stress and inflammatory compounds in the blood, which are linked to DNA mutation and diseased cell growth, as is seen in many cancers.
Born to Be Big? Epigenetics and Chemicals
If you are an obese woman and you start a family, your children and their children down the line may struggle with the “imprint” of your obesity. Adult obesity appears to increase the risk of obesity in offspring through non-genetic influences, a phenomenon termed perinatal programming.[12] A 2007 study found that maternal hyperglycemia during pregnancy strongly predicted high BMI in offspring at 5 to 7 years of age.[13] By age 10-16 years, offspring of a diabetic pregnancy have an almost 1 in 5 rate of impaired glucose intolerance.[14]
How might that happen, that an obese mother can create future generations of obese children? Because the baby is born programmed to be obese:[15]
- Each time a pregnant woman eats, her hormones launch a flurry of activity, including a rise in blood glucose with a resultant rise in insulin secreted by the pancreas. This makes sure that an ample supply of glucose is available to both her and her fetus.
- Throughout the 2nd and 3rd trimesters, hormone levels rise, the pancreas works harder, and mom's amount of insulin resistance rises, because her muscles do not like being bathed in insulin and drowned in glucose.
- When the mother's pancreas doesn't secret enough insulin to keep the blood sugar level low, the mother and the fetus experience hyperglycemia. The fetus is exposed to bouts of hyperglycemia which promotes excess nutrient storage. The result is excessive birth weight (macrosomia).
- Excessive body fat stores, stimulated by excessive glucose delivery during diabetic pregnancy, often extends into childhood and adult life.
Exposure in the womb seems to permanently disrupt or dysregulate appetite control and hormones and impair energy metabolism. “Fetal metabolic programming” may lead to obesity in adolescence and young adulthood, spawning a potential vicious cycle of transgenerational transmission of the obesity epidemic from parents to offspring, regardless of offspring genetics or childhood environment.[16]
Chemicals also play a big role in obesity. Ever since Rachel Carson wrote Silent Spring back in the 1960s, the book that rang the first big warning about the dangers of pesticides, we have been slowly waking up to the dangers of the 80,000 or so chemicals in our midst.
Sharon Begley reported in Newsweek in 2009 that early exposure to common chemicals may be programming kids to be fat:
“Certain hormone-mimicking pollutants, ubiquitous in the food chain, have two previously unsuspected effects. They act on genes in the developing fetus and newborn to turn more precursor cells into fat cells, which stay with you for life. And they may alter metabolic rate, so that the body hoards calories rather than burning them, like a physiological Scrooge. 'The evidence now emerging says that being overweight is not just the result of personal choices about what you eat, combined with inactivity,' says Retha Newbold of the National Institute of Environmental Health Sciences (NIEHS) in North Carolina, part of the National Institutes of Health (NIH). 'Exposure to environmental chemicals during development may be contributing to the obesity epidemic.' They are not the cause of extra pounds in every person who is overweight-for older adults, who were less likely to be exposed to so many of the compounds before birth, the standard explanations of genetics and lifestyle probably suffice-but environmental chemicals may well account for a good part of the current epidemic, especially in those under 50. And at the individual level, exposure to the compounds during a critical period of development may explain one of the most frustrating aspects of weight gain: you eat no more than your slim friends, and exercise no less, yet are still unable to shed pounds.”[17]
Dr. David Ludwig is the director of the Optimal Weight for Life Program in the Division of Endocrinology, Children's Hospital Boston. He is also an associate professor of pediatrics at Harvard Medical School. He wrote in the New England Journal of Medicine about a family who came to his clinic:
“One of the parents was overweight, and the other was obese. The five children were more severely obese and had numerous weight-related complications - one had evidence of fatty liver, one had high blood pressure, two had gastroesophageal reflux, two had orthopedic problems, three had marked insulin resistance, four had dyslipidemia, and all had emotional problems related to their weight.
“Unfortunately, the U.S. government has thus far invested only a fraction of a cent in research for every dollar that obesity costs society. And although broad consensus exists regarding the dietary and lifestyle habits needed to prevent and treat childhood obesity, we lack anything resembling a comprehensive strategy for encouraging children to eat a healthful diet and engage in physical activity. Such a strategy would include legislation that regulates junk-food advertising, provides adequate funding for decent lunches and regular physical activities at school, restructures the farm-subsidies program to favor nutrient-dense rather than calorie-dense produce, and mandates insurance coverage for preventing and treating pediatric obesity.”[18]
Nutrient-dense versus Calorie-dense
Nutrient-dense means that each bite of food has a lot of nutrition - vitamins, minerals, enzymes, maybe antioxidants and more. Calorie-dense is something like soda - no nutrition, but packing the calories. Most of us need help learning how to make the switch to nutrient-dense food, and organic food that has less chemicals.
Losing weight safely sometimes requires a safe detox program along with dietary changes. At the Arizona Center for Advanced Medicine, we have such a program for change. It is called FirstLine Therapy™. We measure the BMI routinely on all our patients. During the course of the program we measure the BMI twice a month to determine whether muscle mass is being maintained while fat mass is lost. We take time to do lots of hand-holding and education. The program works for children, adolescents and adults. We show you how to choose nutrient-dense foods over calorie-dense foods. We help you plan a do-able nutritional program which will allow both children and adults to lose weight (fat), while maintaining muscle mass. And we hold your hand as you tackle that tough one, exercise - how much, what type, how to do it, and how often. We show you for example what you can do while sitting at your desk during a phone call. We also offer colonics which can flush out the colon and rebalance the intestinal flora. The 12-week program gives you the tools to enable you and your children to choose a healthy lifestyle for the rest of your lives.
[1] Rebecca Voelker, Improved Use of BMI Needed to Screen Children for Overweight, JAMA, 2007;297:2684-2685.[2] David S. Ludwig, M.D., Ph.D. Childhood Obesity - The Shape of Things to Come, NEJM, December 6, 2007[3] Christina Paxson, Elisabeth Donahue, C. Tracy Orleans, and Jeanne Ann Grisso, Childhood Obesity-Introducing the Issue, Childhood Obesity, The Future of Children, a publication of the Woodrow Wilson School of Public and International Affairs at Princeton University and the Brookings Institution, Volume 16, Number 1 Spring 2006.[4] News Release: Scientists Find Link Between Dopamine and Obesity. Brookhaven National Laboratory. February 1, 2001[5] News Release: New gene discovery links obesity to the brain. Albert Einstein College of Medicine. June 25, 2009 [6] Johnson, Paul M; Kenny, Paul J. Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats. Nature Neuroscience. March 28, 2010; DOI: 10.1038/nn.2519 [7]James Owen, Some Couch Potatoes Born That Way, Fat Study Says, National Geographic News, January 27, 2007 [8] Contagious Obesity? Identifying The Human Adenoviruses That May Make Us Fat. ScienceDaily, January 30, 2006 [9] Turnbaugh PJ, Ley RE et al. An obesity-associated gut microbiome with increased capacity for energy harvest. Nature 444, 1027-131 (21 December 2006) [7] http://www.cancer.org/…Over_100000_Cancers_Linked_to_Excess_Body_Fat.asp [8] Plagemann A. Perinatal programming and functional teratogenesis: impact on body weight regulation and obesity. Physiol Behav. Dec 15 2005;86(5):661-8 [9] Hillier TA, Pedula KL, et al. Childhood obesity and metabolic imprinting: the ongoing effects of maternal hyperglycemia. Diabetes Care 2007;30:2287-92. [10] Slackman, Michael. Privilege Pulls Qatar Toward Unhealthy Choices. New York Times. April 26, 2010 [11] http://www.cancer.org…NWS_1_1x_Report_Over_100000_Cancers_Linked_to_Excess_Body_Fat.asp [12] Plagemann A. Perinatal programming and functional teratogenesis: impact on body weight regulation and obesity. Physiol Behav. Dec 15 2005;86(5):661-8 [13] Hillier TA, Pedula KL, et al. Childhood obesity and metabolic imprinting: the ongoing effects of maternal hyperglycemia. Diabetes Care 2007;30:2287-92. [14] McKinney PA, Parslow R, Gurney KA, Law GR, Bodansky HJ, Williams R. Perinatal and neonatal determinants of childhood type 1 diabetes. A case-control study in Yorkshire, U.K. Diabetes Care. Jun 1999;22(6):928-32 [15] http://emedicine.medscape.com/article/127547-overview [16] Eric L Ding and Frank B Hu. Determining Origins and Causes of Childhood Obesity via Mendelian Randomization Analysis. PLoS Med. 2008 March; 5(3): e65. [17] Sharon Begley, Born to be Big - Early exposure to common chemicals may be programming kids to be fat. Newsweek, September 11, 2009 [18] David S. Ludwig, M.D., Ph.D. Childhood Obesity - The Shape of Things to Come, NEJM, December 6, 2007Obesity
Obesity has also been linked with relative abundance of two particular species of bacteria in the gut. Some bacteria are associated with increased ability to extract nutrients from the diet and build fat, as has been shown by studies where lean mice are colonized with “obese-associated bacteria” and develop more body fat than mice colonized with “lean-associated bacteria”.[9]
Society norms and the convenience of fast food play an important role. Note the experience of the country of Qatar: it ranks sixth globally for prevalence of obesity and has the highest rate of obesity among boys in the Middle East and North African region. It is predicted that by 2016, 73 percent of Qatari women and 69 percent of the men will qualify as obese. Social occasions center around eating large platters of food. Walking is not popular; summer temperatures are a humid 106 degrees. As the New York Times said, "Like other oil-rich nations, Qatar has leaped across decades of development in a short time, leaving behind the physically demanding life of the desert for air-conditioned comfort, servants and fast food."[10]
A 2009 report from the American Institute for Cancer Research (AIRC) revealed that more than 100,000 cases of cancer each year are caused by excess body fat. Excess body fat appears to increase the amount of hormones like estrogen circulating in the body, and it can also disrupt how the body processes insulin. Both of those factors have been linked to an increased cancer risk. Also, obesity creates low-grade inflammation in the body, and much current research links chronic inflammation to cancer.[11]
Studies have shown that increased body fat can lead to increased levels of oxidative stress and inflammatory compounds in the blood, which are linked to DNA mutation and diseased cell growth, as is seen in many cancers.
Born to Be Big? Epigenetics and Chemicals
If you are an obese woman and you start a family, your children and their children down the line may struggle with the “imprint” of your obesity. Adult obesity appears to increase the risk of obesity in offspring through non-genetic influences, a phenomenon termed perinatal programming.[12] A 2007 study found that maternal hyperglycemia during pregnancy strongly predicted high BMI in offspring at 5 to 7 years of age.[13] By age 10-16 years, offspring of a diabetic pregnancy have an almost 1 in 5 rate of impaired glucose intolerance.[14]
How might that happen, that an obese mother can create future generations of obese children? Because the baby is born programmed to be obese:[15]
- Each time a pregnant woman eats, her hormones launch a flurry of activity, including a rise in blood glucose with a resultant rise in insulin secreted by the pancreas. This makes sure that an ample supply of glucose is available to both her and her fetus.
- Throughout the 2nd and 3rd trimesters, hormone levels rise, the pancreas works harder, and mom's amount of insulin resistance rises, because her muscles do not like being bathed in insulin and drowned in glucose.
- When the mother's pancreas doesn't secret enough insulin to keep the blood sugar level low, the mother and the fetus experience hyperglycemia. The fetus is exposed to bouts of hyperglycemia which promotes excess nutrient storage. The result is excessive birth weight (macrosomia).
- Excessive body fat stores, stimulated by excessive glucose delivery during diabetic pregnancy, often extends into childhood and adult life.
Exposure in the womb seems to permanently disrupt or dysregulate appetite control and hormones and impair energy metabolism. “Fetal metabolic programming” may lead to obesity in adolescence and young adulthood, spawning a potential vicious cycle of transgenerational transmission of the obesity epidemic from parents to offspring, regardless of offspring genetics or childhood environment.[16]
Chemicals also play a big role in obesity. Ever since Rachel Carson wrote Silent Spring back in the 1960s, the book that rang the first big warning about the dangers of pesticides, we have been slowly waking up to the dangers of the 80,000 or so chemicals in our midst.
Sharon Begley reported in Newsweek in 2009 that early exposure to common chemicals may be programming kids to be fat:
“Certain hormone-mimicking pollutants, ubiquitous in the food chain, have two previously unsuspected effects. They act on genes in the developing fetus and newborn to turn more precursor cells into fat cells, which stay with you for life. And they may alter metabolic rate, so that the body hoards calories rather than burning them, like a physiological Scrooge. 'The evidence now emerging says that being overweight is not just the result of personal choices about what you eat, combined with inactivity,' says Retha Newbold of the National Institute of Environmental Health Sciences (NIEHS) in North Carolina, part of the National Institutes of Health (NIH). 'Exposure to environmental chemicals during development may be contributing to the obesity epidemic.' They are not the cause of extra pounds in every person who is overweight-for older adults, who were less likely to be exposed to so many of the compounds before birth, the standard explanations of genetics and lifestyle probably suffice-but environmental chemicals may well account for a good part of the current epidemic, especially in those under 50. And at the individual level, exposure to the compounds during a critical period of development may explain one of the most frustrating aspects of weight gain: you eat no more than your slim friends, and exercise no less, yet are still unable to shed pounds.”[17]
Dr. David Ludwig is the director of the Optimal Weight for Life Program in the Division of Endocrinology, Children's Hospital Boston. He is also an associate professor of pediatrics at Harvard Medical School. He wrote in the New England Journal of Medicine about a family who came to his clinic:
“One of the parents was overweight, and the other was obese. The five children were more severely obese and had numerous weight-related complications - one had evidence of fatty liver, one had high blood pressure, two had gastroesophageal reflux, two had orthopedic problems, three had marked insulin resistance, four had dyslipidemia, and all had emotional problems related to their weight.
“Unfortunately, the U.S. government has thus far invested only a fraction of a cent in research for every dollar that obesity costs society. And although broad consensus exists regarding the dietary and lifestyle habits needed to prevent and treat childhood obesity, we lack anything resembling a comprehensive strategy for encouraging children to eat a healthful diet and engage in physical activity. Such a strategy would include legislation that regulates junk-food advertising, provides adequate funding for decent lunches and regular physical activities at school, restructures the farm-subsidies program to favor nutrient-dense rather than calorie-dense produce, and mandates insurance coverage for preventing and treating pediatric obesity.”[18]
Nutrient-dense versus Calorie-dense
Nutrient-dense means that each bite of food has a lot of nutrition - vitamins, minerals, enzymes, maybe antioxidants and more. Calorie-dense is something like soda - no nutrition, but packing the calories. Most of us need help learning how to make the switch to nutrient-dense food, and organic food that has less chemicals.
Losing weight safely sometimes requires a safe detox program along with dietary changes. At the Arizona Center for Advanced Medicine, we have such a program for change. It is called FirstLine Therapy™. We measure the BMI routinely on all our patients. During the course of the program we measure the BMI twice a month to determine whether muscle mass is being maintained while fat mass is lost. We take time to do lots of hand-holding and education. The program works for children, adolescents and adults. We show you how to choose nutrient-dense foods over calorie-dense foods. We help you plan a do-able nutritional program which will allow both children and adults to lose weight (fat), while maintaining muscle mass. And we hold your hand as you tackle that tough one, exercise - how much, what type, how to do it, and how often. We show you for example what you can do while sitting at your desk during a phone call. We also offer colonics which can flush out the colon and rebalance the intestinal flora. The 12-week program gives you the tools to enable you and your children to choose a healthy lifestyle for the rest of your lives.
[1] Rebecca Voelker, Improved Use of BMI Needed to Screen Children for Overweight, JAMA, 2007;297:2684-2685.[2] David S. Ludwig, M.D., Ph.D. Childhood Obesity - The Shape of Things to Come, NEJM, December 6, 2007[3] Christina Paxson, Elisabeth Donahue, C. Tracy Orleans, and Jeanne Ann Grisso, Childhood Obesity-Introducing the Issue, Childhood Obesity, The Future of Children, a publication of the Woodrow Wilson School of Public and International Affairs at Princeton University and the Brookings Institution, Volume 16, Number 1 Spring 2006.[4] News Release: Scientists Find Link Between Dopamine and Obesity. Brookhaven National Laboratory. February 1, 2001[5] News Release: New gene discovery links obesity to the brain. Albert Einstein College of Medicine. June 25, 2009 [6] Johnson, Paul M; Kenny, Paul J. Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats. Nature Neuroscience. March 28, 2010; DOI: 10.1038/nn.2519 [7]James Owen, Some Couch Potatoes Born That Way, Fat Study Says, National Geographic News, January 27, 2007 [8] Contagious Obesity? Identifying The Human Adenoviruses That May Make Us Fat. ScienceDaily, January 30, 2006 [9] Turnbaugh PJ, Ley RE et al. An obesity-associated gut microbiome with increased capacity for energy harvest. Nature 444, 1027-131 (21 December 2006) [7] http://www.cancer.org/…Over_100000_Cancers_Linked_to_Excess_Body_Fat.asp [8] Plagemann A. Perinatal programming and functional teratogenesis: impact on body weight regulation and obesity. Physiol Behav. Dec 15 2005;86(5):661-8 [9] Hillier TA, Pedula KL, et al. Childhood obesity and metabolic imprinting: the ongoing effects of maternal hyperglycemia. Diabetes Care 2007;30:2287-92. [10] Slackman, Michael. Privilege Pulls Qatar Toward Unhealthy Choices. New York Times. April 26, 2010 [11] http://www.cancer.org…NWS_1_1x_Report_Over_100000_Cancers_Linked_to_Excess_Body_Fat.asp [12] Plagemann A. Perinatal programming and functional teratogenesis: impact on body weight regulation and obesity. Physiol Behav. Dec 15 2005;86(5):661-8 [13] Hillier TA, Pedula KL, et al. Childhood obesity and metabolic imprinting: the ongoing effects of maternal hyperglycemia. Diabetes Care 2007;30:2287-92. [14] McKinney PA, Parslow R, Gurney KA, Law GR, Bodansky HJ, Williams R. Perinatal and neonatal determinants of childhood type 1 diabetes. A case-control study in Yorkshire, U.K. Diabetes Care. Jun 1999;22(6):928-32 [15] http://emedicine.medscape.com/article/127547-overview [16] Eric L Ding and Frank B Hu. Determining Origins and Causes of Childhood Obesity via Mendelian Randomization Analysis. PLoS Med. 2008 March; 5(3): e65. [17] Sharon Begley, Born to be Big - Early exposure to common chemicals may be programming kids to be fat. Newsweek, September 11, 2009 [18] David S. Ludwig, M.D., Ph.D. Childhood Obesity - The Shape of Things to Come, NEJM, December 6, 2007Obesity
Society norms and the convenience of fast food play an important role. Note the experience of the country of Qatar: it ranks sixth globally for prevalence of obesity and has the highest rate of obesity among boys in the Middle East and North African region. It is predicted that by 2016, 73 percent of Qatari women and 69 percent of the men will qualify as obese. Social occasions center around eating large platters of food. Walking is not popular; summer temperatures are a humid 106 degrees. As the New York Times said, "Like other oil-rich nations, Qatar has leaped across decades of development in a short time, leaving behind the physically demanding life of the desert for air-conditioned comfort, servants and fast food."[10]
A 2009 report from the American Institute for Cancer Research (AIRC) revealed that more than 100,000 cases of cancer each year are caused by excess body fat. Excess body fat appears to increase the amount of hormones like estrogen circulating in the body, and it can also disrupt how the body processes insulin. Both of those factors have been linked to an increased cancer risk. Also, obesity creates low-grade inflammation in the body, and much current research links chronic inflammation to cancer.[11]
Studies have shown that increased body fat can lead to increased levels of oxidative stress and inflammatory compounds in the blood, which are linked to DNA mutation and diseased cell growth, as is seen in many cancers.
Born to Be Big? Epigenetics and Chemicals
If you are an obese woman and you start a family, your children and their children down the line may struggle with the “imprint” of your obesity. Adult obesity appears to increase the risk of obesity in offspring through non-genetic influences, a phenomenon termed perinatal programming.[12] A 2007 study found that maternal hyperglycemia during pregnancy strongly predicted high BMI in offspring at 5 to 7 years of age.[13] By age 10-16 years, offspring of a diabetic pregnancy have an almost 1 in 5 rate of impaired glucose intolerance.[14]
How might that happen, that an obese mother can create future generations of obese children? Because the baby is born programmed to be obese:[15]
- Each time a pregnant woman eats, her hormones launch a flurry of activity, including a rise in blood glucose with a resultant rise in insulin secreted by the pancreas. This makes sure that an ample supply of glucose is available to both her and her fetus.
- Throughout the 2nd and 3rd trimesters, hormone levels rise, the pancreas works harder, and mom's amount of insulin resistance rises, because her muscles do not like being bathed in insulin and drowned in glucose.
- When the mother's pancreas doesn't secret enough insulin to keep the blood sugar level low, the mother and the fetus experience hyperglycemia. The fetus is exposed to bouts of hyperglycemia which promotes excess nutrient storage. The result is excessive birth weight (macrosomia).
- Excessive body fat stores, stimulated by excessive glucose delivery during diabetic pregnancy, often extends into childhood and adult life.
Exposure in the womb seems to permanently disrupt or dysregulate appetite control and hormones and impair energy metabolism. “Fetal metabolic programming” may lead to obesity in adolescence and young adulthood, spawning a potential vicious cycle of transgenerational transmission of the obesity epidemic from parents to offspring, regardless of offspring genetics or childhood environment.[16]
Chemicals also play a big role in obesity. Ever since Rachel Carson wrote Silent Spring back in the 1960s, the book that rang the first big warning about the dangers of pesticides, we have been slowly waking up to the dangers of the 80,000 or so chemicals in our midst.
Sharon Begley reported in Newsweek in 2009 that early exposure to common chemicals may be programming kids to be fat:
“Certain hormone-mimicking pollutants, ubiquitous in the food chain, have two previously unsuspected effects. They act on genes in the developing fetus and newborn to turn more precursor cells into fat cells, which stay with you for life. And they may alter metabolic rate, so that the body hoards calories rather than burning them, like a physiological Scrooge. 'The evidence now emerging says that being overweight is not just the result of personal choices about what you eat, combined with inactivity,' says Retha Newbold of the National Institute of Environmental Health Sciences (NIEHS) in North Carolina, part of the National Institutes of Health (NIH). 'Exposure to environmental chemicals during development may be contributing to the obesity epidemic.' They are not the cause of extra pounds in every person who is overweight-for older adults, who were less likely to be exposed to so many of the compounds before birth, the standard explanations of genetics and lifestyle probably suffice-but environmental chemicals may well account for a good part of the current epidemic, especially in those under 50. And at the individual level, exposure to the compounds during a critical period of development may explain one of the most frustrating aspects of weight gain: you eat no more than your slim friends, and exercise no less, yet are still unable to shed pounds.”[17]
Dr. David Ludwig is the director of the Optimal Weight for Life Program in the Division of Endocrinology, Children's Hospital Boston. He is also an associate professor of pediatrics at Harvard Medical School. He wrote in the New England Journal of Medicine about a family who came to his clinic:
“One of the parents was overweight, and the other was obese. The five children were more severely obese and had numerous weight-related complications - one had evidence of fatty liver, one had high blood pressure, two had gastroesophageal reflux, two had orthopedic problems, three had marked insulin resistance, four had dyslipidemia, and all had emotional problems related to their weight.
“Unfortunately, the U.S. government has thus far invested only a fraction of a cent in research for every dollar that obesity costs society. And although broad consensus exists regarding the dietary and lifestyle habits needed to prevent and treat childhood obesity, we lack anything resembling a comprehensive strategy for encouraging children to eat a healthful diet and engage in physical activity. Such a strategy would include legislation that regulates junk-food advertising, provides adequate funding for decent lunches and regular physical activities at school, restructures the farm-subsidies program to favor nutrient-dense rather than calorie-dense produce, and mandates insurance coverage for preventing and treating pediatric obesity.”[18]
Nutrient-dense versus Calorie-dense
Nutrient-dense means that each bite of food has a lot of nutrition - vitamins, minerals, enzymes, maybe antioxidants and more. Calorie-dense is something like soda - no nutrition, but packing the calories. Most of us need help learning how to make the switch to nutrient-dense food, and organic food that has less chemicals.
Losing weight safely sometimes requires a safe detox program along with dietary changes. At the Arizona Center for Advanced Medicine, we have such a program for change. It is called FirstLine Therapy™. We measure the BMI routinely on all our patients. During the course of the program we measure the BMI twice a month to determine whether muscle mass is being maintained while fat mass is lost. We take time to do lots of hand-holding and education. The program works for children, adolescents and adults. We show you how to choose nutrient-dense foods over calorie-dense foods. We help you plan a do-able nutritional program which will allow both children and adults to lose weight (fat), while maintaining muscle mass. And we hold your hand as you tackle that tough one, exercise - how much, what type, how to do it, and how often. We show you for example what you can do while sitting at your desk during a phone call. We also offer colonics which can flush out the colon and rebalance the intestinal flora. The 12-week program gives you the tools to enable you and your children to choose a healthy lifestyle for the rest of your lives.
[1] Rebecca Voelker, Improved Use of BMI Needed to Screen Children for Overweight, JAMA, 2007;297:2684-2685.[2] David S. Ludwig, M.D., Ph.D. Childhood Obesity - The Shape of Things to Come, NEJM, December 6, 2007[3] Christina Paxson, Elisabeth Donahue, C. Tracy Orleans, and Jeanne Ann Grisso, Childhood Obesity-Introducing the Issue, Childhood Obesity, The Future of Children, a publication of the Woodrow Wilson School of Public and International Affairs at Princeton University and the Brookings Institution, Volume 16, Number 1 Spring 2006.[4] News Release: Scientists Find Link Between Dopamine and Obesity. Brookhaven National Laboratory. February 1, 2001[5] News Release: New gene discovery links obesity to the brain. Albert Einstein College of Medicine. June 25, 2009 [6] Johnson, Paul M; Kenny, Paul J. Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats. Nature Neuroscience. March 28, 2010; DOI: 10.1038/nn.2519 [7]James Owen, Some Couch Potatoes Born That Way, Fat Study Says, National Geographic News, January 27, 2007 [8] Contagious Obesity? Identifying The Human Adenoviruses That May Make Us Fat. ScienceDaily, January 30, 2006 [9] Turnbaugh PJ, Ley RE et al. An obesity-associated gut microbiome with increased capacity for energy harvest. Nature 444, 1027-131 (21 December 2006) [7] http://www.cancer.org/…Over_100000_Cancers_Linked_to_Excess_Body_Fat.asp [8] Plagemann A. Perinatal programming and functional teratogenesis: impact on body weight regulation and obesity. Physiol Behav. Dec 15 2005;86(5):661-8 [9] Hillier TA, Pedula KL, et al. Childhood obesity and metabolic imprinting: the ongoing effects of maternal hyperglycemia. Diabetes Care 2007;30:2287-92. [10] Slackman, Michael. Privilege Pulls Qatar Toward Unhealthy Choices. New York Times. April 26, 2010 [11] http://www.cancer.org…NWS_1_1x_Report_Over_100000_Cancers_Linked_to_Excess_Body_Fat.asp [12] Plagemann A. Perinatal programming and functional teratogenesis: impact on body weight regulation and obesity. Physiol Behav. Dec 15 2005;86(5):661-8 [13] Hillier TA, Pedula KL, et al. Childhood obesity and metabolic imprinting: the ongoing effects of maternal hyperglycemia. Diabetes Care 2007;30:2287-92. [14] McKinney PA, Parslow R, Gurney KA, Law GR, Bodansky HJ, Williams R. Perinatal and neonatal determinants of childhood type 1 diabetes. A case-control study in Yorkshire, U.K. Diabetes Care. Jun 1999;22(6):928-32 [15] http://emedicine.medscape.com/article/127547-overview [16] Eric L Ding and Frank B Hu. Determining Origins and Causes of Childhood Obesity via Mendelian Randomization Analysis. PLoS Med. 2008 March; 5(3): e65. [17] Sharon Begley, Born to be Big - Early exposure to common chemicals may be programming kids to be fat. Newsweek, September 11, 2009 [18] David S. Ludwig, M.D., Ph.D. Childhood Obesity - The Shape of Things to Come, NEJM, December 6, 2007Obesity
A 2009 report from the American Institute for Cancer Research (AIRC) revealed that more than 100,000 cases of cancer each year are caused by excess body fat. Excess body fat appears to increase the amount of hormones like estrogen circulating in the body, and it can also disrupt how the body processes insulin. Both of those factors have been linked to an increased cancer risk. Also, obesity creates low-grade inflammation in the body, and much current research links chronic inflammation to cancer.[11]
Studies have shown that increased body fat can lead to increased levels of oxidative stress and inflammatory compounds in the blood, which are linked to DNA mutation and diseased cell growth, as is seen in many cancers.
Born to Be Big? Epigenetics and Chemicals
If you are an obese woman and you start a family, your children and their children down the line may struggle with the “imprint” of your obesity. Adult obesity appears to increase the risk of obesity in offspring through non-genetic influences, a phenomenon termed perinatal programming.[12] A 2007 study found that maternal hyperglycemia during pregnancy strongly predicted high BMI in offspring at 5 to 7 years of age.[13] By age 10-16 years, offspring of a diabetic pregnancy have an almost 1 in 5 rate of impaired glucose intolerance.[14]
How might that happen, that an obese mother can create future generations of obese children? Because the baby is born programmed to be obese:[15]
- Each time a pregnant woman eats, her hormones launch a flurry of activity, including a rise in blood glucose with a resultant rise in insulin secreted by the pancreas. This makes sure that an ample supply of glucose is available to both her and her fetus.
- Throughout the 2nd and 3rd trimesters, hormone levels rise, the pancreas works harder, and mom's amount of insulin resistance rises, because her muscles do not like being bathed in insulin and drowned in glucose.
- When the mother's pancreas doesn't secret enough insulin to keep the blood sugar level low, the mother and the fetus experience hyperglycemia. The fetus is exposed to bouts of hyperglycemia which promotes excess nutrient storage. The result is excessive birth weight (macrosomia).
- Excessive body fat stores, stimulated by excessive glucose delivery during diabetic pregnancy, often extends into childhood and adult life.
Exposure in the womb seems to permanently disrupt or dysregulate appetite control and hormones and impair energy metabolism. “Fetal metabolic programming” may lead to obesity in adolescence and young adulthood, spawning a potential vicious cycle of transgenerational transmission of the obesity epidemic from parents to offspring, regardless of offspring genetics or childhood environment.[16]
Chemicals also play a big role in obesity. Ever since Rachel Carson wrote Silent Spring back in the 1960s, the book that rang the first big warning about the dangers of pesticides, we have been slowly waking up to the dangers of the 80,000 or so chemicals in our midst.
Sharon Begley reported in Newsweek in 2009 that early exposure to common chemicals may be programming kids to be fat:
“Certain hormone-mimicking pollutants, ubiquitous in the food chain, have two previously unsuspected effects. They act on genes in the developing fetus and newborn to turn more precursor cells into fat cells, which stay with you for life. And they may alter metabolic rate, so that the body hoards calories rather than burning them, like a physiological Scrooge. 'The evidence now emerging says that being overweight is not just the result of personal choices about what you eat, combined with inactivity,' says Retha Newbold of the National Institute of Environmental Health Sciences (NIEHS) in North Carolina, part of the National Institutes of Health (NIH). 'Exposure to environmental chemicals during development may be contributing to the obesity epidemic.' They are not the cause of extra pounds in every person who is overweight-for older adults, who were less likely to be exposed to so many of the compounds before birth, the standard explanations of genetics and lifestyle probably suffice-but environmental chemicals may well account for a good part of the current epidemic, especially in those under 50. And at the individual level, exposure to the compounds during a critical period of development may explain one of the most frustrating aspects of weight gain: you eat no more than your slim friends, and exercise no less, yet are still unable to shed pounds.”[17]
Dr. David Ludwig is the director of the Optimal Weight for Life Program in the Division of Endocrinology, Children's Hospital Boston. He is also an associate professor of pediatrics at Harvard Medical School. He wrote in the New England Journal of Medicine about a family who came to his clinic:
“One of the parents was overweight, and the other was obese. The five children were more severely obese and had numerous weight-related complications - one had evidence of fatty liver, one had high blood pressure, two had gastroesophageal reflux, two had orthopedic problems, three had marked insulin resistance, four had dyslipidemia, and all had emotional problems related to their weight.
“Unfortunately, the U.S. government has thus far invested only a fraction of a cent in research for every dollar that obesity costs society. And although broad consensus exists regarding the dietary and lifestyle habits needed to prevent and treat childhood obesity, we lack anything resembling a comprehensive strategy for encouraging children to eat a healthful diet and engage in physical activity. Such a strategy would include legislation that regulates junk-food advertising, provides adequate funding for decent lunches and regular physical activities at school, restructures the farm-subsidies program to favor nutrient-dense rather than calorie-dense produce, and mandates insurance coverage for preventing and treating pediatric obesity.”[18]
Nutrient-dense versus Calorie-dense
Nutrient-dense means that each bite of food has a lot of nutrition - vitamins, minerals, enzymes, maybe antioxidants and more. Calorie-dense is something like soda - no nutrition, but packing the calories. Most of us need help learning how to make the switch to nutrient-dense food, and organic food that has less chemicals.
Losing weight safely sometimes requires a safe detox program along with dietary changes. At the Arizona Center for Advanced Medicine, we have such a program for change. It is called FirstLine Therapy™. We measure the BMI routinely on all our patients. During the course of the program we measure the BMI twice a month to determine whether muscle mass is being maintained while fat mass is lost. We take time to do lots of hand-holding and education. The program works for children, adolescents and adults. We show you how to choose nutrient-dense foods over calorie-dense foods. We help you plan a do-able nutritional program which will allow both children and adults to lose weight (fat), while maintaining muscle mass. And we hold your hand as you tackle that tough one, exercise - how much, what type, how to do it, and how often. We show you for example what you can do while sitting at your desk during a phone call. We also offer colonics which can flush out the colon and rebalance the intestinal flora. The 12-week program gives you the tools to enable you and your children to choose a healthy lifestyle for the rest of your lives.
[1] Rebecca Voelker, Improved Use of BMI Needed to Screen Children for Overweight, JAMA, 2007;297:2684-2685.[2] David S. Ludwig, M.D., Ph.D. Childhood Obesity - The Shape of Things to Come, NEJM, December 6, 2007[3] Christina Paxson, Elisabeth Donahue, C. Tracy Orleans, and Jeanne Ann Grisso, Childhood Obesity-Introducing the Issue, Childhood Obesity, The Future of Children, a publication of the Woodrow Wilson School of Public and International Affairs at Princeton University and the Brookings Institution, Volume 16, Number 1 Spring 2006.[4] News Release: Scientists Find Link Between Dopamine and Obesity. Brookhaven National Laboratory. February 1, 2001[5] News Release: New gene discovery links obesity to the brain. Albert Einstein College of Medicine. June 25, 2009 [6] Johnson, Paul M; Kenny, Paul J. Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats. Nature Neuroscience. March 28, 2010; DOI: 10.1038/nn.2519 [7]James Owen, Some Couch Potatoes Born That Way, Fat Study Says, National Geographic News, January 27, 2007 [8] Contagious Obesity? Identifying The Human Adenoviruses That May Make Us Fat. ScienceDaily, January 30, 2006 [9] Turnbaugh PJ, Ley RE et al. An obesity-associated gut microbiome with increased capacity for energy harvest. Nature 444, 1027-131 (21 December 2006) [7] http://www.cancer.org/…Over_100000_Cancers_Linked_to_Excess_Body_Fat.asp [8] Plagemann A. Perinatal programming and functional teratogenesis: impact on body weight regulation and obesity. Physiol Behav. Dec 15 2005;86(5):661-8 [9] Hillier TA, Pedula KL, et al. Childhood obesity and metabolic imprinting: the ongoing effects of maternal hyperglycemia. Diabetes Care 2007;30:2287-92. [10] Slackman, Michael. Privilege Pulls Qatar Toward Unhealthy Choices. New York Times. April 26, 2010 [11] http://www.cancer.org…NWS_1_1x_Report_Over_100000_Cancers_Linked_to_Excess_Body_Fat.asp [12] Plagemann A. Perinatal programming and functional teratogenesis: impact on body weight regulation and obesity. Physiol Behav. Dec 15 2005;86(5):661-8 [13] Hillier TA, Pedula KL, et al. Childhood obesity and metabolic imprinting: the ongoing effects of maternal hyperglycemia. Diabetes Care 2007;30:2287-92. [14] McKinney PA, Parslow R, Gurney KA, Law GR, Bodansky HJ, Williams R. Perinatal and neonatal determinants of childhood type 1 diabetes. A case-control study in Yorkshire, U.K. Diabetes Care. Jun 1999;22(6):928-32 [15] http://emedicine.medscape.com/article/127547-overview [16] Eric L Ding and Frank B Hu. Determining Origins and Causes of Childhood Obesity via Mendelian Randomization Analysis. PLoS Med. 2008 March; 5(3): e65. [17] Sharon Begley, Born to be Big - Early exposure to common chemicals may be programming kids to be fat. Newsweek, September 11, 2009 [18] David S. Ludwig, M.D., Ph.D. Childhood Obesity - The Shape of Things to Come, NEJM, December 6, 2007Obesity
Studies have shown that increased body fat can lead to increased levels of oxidative stress and inflammatory compounds in the blood, which are linked to DNA mutation and diseased cell growth, as is seen in many cancers.
If you are an obese woman and you start a family, your children and their children down the line may struggle with the “imprint” of your obesity. Adult obesity appears to increase the risk of obesity in offspring through non-genetic influences, a phenomenon termed perinatal programming.[12] A 2007 study found that maternal hyperglycemia during pregnancy strongly predicted high BMI in offspring at 5 to 7 years of age.[13] By age 10-16 years, offspring of a diabetic pregnancy have an almost 1 in 5 rate of impaired glucose intolerance.[14]
How might that happen, that an obese mother can create future generations of obese children? Because the baby is born programmed to be obese:[15]
- Each time a pregnant woman eats, her hormones launch a flurry of activity, including a rise in blood glucose with a resultant rise in insulin secreted by the pancreas. This makes sure that an ample supply of glucose is available to both her and her fetus.
- Throughout the 2nd and 3rd trimesters, hormone levels rise, the pancreas works harder, and mom's amount of insulin resistance rises, because her muscles do not like being bathed in insulin and drowned in glucose.
- When the mother's pancreas doesn't secret enough insulin to keep the blood sugar level low, the mother and the fetus experience hyperglycemia. The fetus is exposed to bouts of hyperglycemia which promotes excess nutrient storage. The result is excessive birth weight (macrosomia).
- Excessive body fat stores, stimulated by excessive glucose delivery during diabetic pregnancy, often extends into childhood and adult life.
Exposure in the womb seems to permanently disrupt or dysregulate appetite control and hormones and impair energy metabolism. “Fetal metabolic programming” may lead to obesity in adolescence and young adulthood, spawning a potential vicious cycle of transgenerational transmission of the obesity epidemic from parents to offspring, regardless of offspring genetics or childhood environment.[16]
Chemicals also play a big role in obesity. Ever since Rachel Carson wrote Silent Spring back in the 1960s, the book that rang the first big warning about the dangers of pesticides, we have been slowly waking up to the dangers of the 80,000 or so chemicals in our midst.
Sharon Begley reported in Newsweek in 2009 that early exposure to common chemicals may be programming kids to be fat:
“Certain hormone-mimicking pollutants, ubiquitous in the food chain, have two previously unsuspected effects. They act on genes in the developing fetus and newborn to turn more precursor cells into fat cells, which stay with you for life. And they may alter metabolic rate, so that the body hoards calories rather than burning them, like a physiological Scrooge. 'The evidence now emerging says that being overweight is not just the result of personal choices about what you eat, combined with inactivity,' says Retha Newbold of the National Institute of Environmental Health Sciences (NIEHS) in North Carolina, part of the National Institutes of Health (NIH). 'Exposure to environmental chemicals during development may be contributing to the obesity epidemic.' They are not the cause of extra pounds in every person who is overweight-for older adults, who were less likely to be exposed to so many of the compounds before birth, the standard explanations of genetics and lifestyle probably suffice-but environmental chemicals may well account for a good part of the current epidemic, especially in those under 50. And at the individual level, exposure to the compounds during a critical period of development may explain one of the most frustrating aspects of weight gain: you eat no more than your slim friends, and exercise no less, yet are still unable to shed pounds.”[17]
Dr. David Ludwig is the director of the Optimal Weight for Life Program in the Division of Endocrinology, Children's Hospital Boston. He is also an associate professor of pediatrics at Harvard Medical School. He wrote in the New England Journal of Medicine about a family who came to his clinic:
“One of the parents was overweight, and the other was obese. The five children were more severely obese and had numerous weight-related complications - one had evidence of fatty liver, one had high blood pressure, two had gastroesophageal reflux, two had orthopedic problems, three had marked insulin resistance, four had dyslipidemia, and all had emotional problems related to their weight.
“Unfortunately, the U.S. government has thus far invested only a fraction of a cent in research for every dollar that obesity costs society. And although broad consensus exists regarding the dietary and lifestyle habits needed to prevent and treat childhood obesity, we lack anything resembling a comprehensive strategy for encouraging children to eat a healthful diet and engage in physical activity. Such a strategy would include legislation that regulates junk-food advertising, provides adequate funding for decent lunches and regular physical activities at school, restructures the farm-subsidies program to favor nutrient-dense rather than calorie-dense produce, and mandates insurance coverage for preventing and treating pediatric obesity.”[18]
Nutrient-dense versus Calorie-dense
Nutrient-dense means that each bite of food has a lot of nutrition - vitamins, minerals, enzymes, maybe antioxidants and more. Calorie-dense is something like soda - no nutrition, but packing the calories. Most of us need help learning how to make the switch to nutrient-dense food, and organic food that has less chemicals.
Losing weight safely sometimes requires a safe detox program along with dietary changes. At the Arizona Center for Advanced Medicine, we have such a program for change. It is called FirstLine Therapy™. We measure the BMI routinely on all our patients. During the course of the program we measure the BMI twice a month to determine whether muscle mass is being maintained while fat mass is lost. We take time to do lots of hand-holding and education. The program works for children, adolescents and adults. We show you how to choose nutrient-dense foods over calorie-dense foods. We help you plan a do-able nutritional program which will allow both children and adults to lose weight (fat), while maintaining muscle mass. And we hold your hand as you tackle that tough one, exercise - how much, what type, how to do it, and how often. We show you for example what you can do while sitting at your desk during a phone call. We also offer colonics which can flush out the colon and rebalance the intestinal flora. The 12-week program gives you the tools to enable you and your children to choose a healthy lifestyle for the rest of your lives.
[1] Rebecca Voelker, Improved Use of BMI Needed to Screen Children for Overweight, JAMA, 2007;297:2684-2685.[2] David S. Ludwig, M.D., Ph.D. Childhood Obesity - The Shape of Things to Come, NEJM, December 6, 2007[3] Christina Paxson, Elisabeth Donahue, C. Tracy Orleans, and Jeanne Ann Grisso, Childhood Obesity-Introducing the Issue, Childhood Obesity, The Future of Children, a publication of the Woodrow Wilson School of Public and International Affairs at Princeton University and the Brookings Institution, Volume 16, Number 1 Spring 2006.[4] News Release: Scientists Find Link Between Dopamine and Obesity. Brookhaven National Laboratory. February 1, 2001[5] News Release: New gene discovery links obesity to the brain. Albert Einstein College of Medicine. June 25, 2009 [6] Johnson, Paul M; Kenny, Paul J. Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats. Nature Neuroscience. March 28, 2010; DOI: 10.1038/nn.2519 [7]James Owen, Some Couch Potatoes Born That Way, Fat Study Says, National Geographic News, January 27, 2007 [8] Contagious Obesity? Identifying The Human Adenoviruses That May Make Us Fat. ScienceDaily, January 30, 2006 [9] Turnbaugh PJ, Ley RE et al. An obesity-associated gut microbiome with increased capacity for energy harvest. Nature 444, 1027-131 (21 December 2006) [7] http://www.cancer.org/…Over_100000_Cancers_Linked_to_Excess_Body_Fat.asp [8] Plagemann A. Perinatal programming and functional teratogenesis: impact on body weight regulation and obesity. Physiol Behav. Dec 15 2005;86(5):661-8 [9] Hillier TA, Pedula KL, et al. Childhood obesity and metabolic imprinting: the ongoing effects of maternal hyperglycemia. Diabetes Care 2007;30:2287-92. [10] Slackman, Michael. Privilege Pulls Qatar Toward Unhealthy Choices. New York Times. April 26, 2010 [11] http://www.cancer.org…NWS_1_1x_Report_Over_100000_Cancers_Linked_to_Excess_Body_Fat.asp [12] Plagemann A. Perinatal programming and functional teratogenesis: impact on body weight regulation and obesity. Physiol Behav. Dec 15 2005;86(5):661-8 [13] Hillier TA, Pedula KL, et al. Childhood obesity and metabolic imprinting: the ongoing effects of maternal hyperglycemia. Diabetes Care 2007;30:2287-92. [14] McKinney PA, Parslow R, Gurney KA, Law GR, Bodansky HJ, Williams R. Perinatal and neonatal determinants of childhood type 1 diabetes. A case-control study in Yorkshire, U.K. Diabetes Care. Jun 1999;22(6):928-32 [15] http://emedicine.medscape.com/article/127547-overview [16] Eric L Ding and Frank B Hu. Determining Origins and Causes of Childhood Obesity via Mendelian Randomization Analysis. PLoS Med. 2008 March; 5(3): e65. [17] Sharon Begley, Born to be Big - Early exposure to common chemicals may be programming kids to be fat. Newsweek, September 11, 2009 [18] David S. Ludwig, M.D., Ph.D. Childhood Obesity - The Shape of Things to Come, NEJM, December 6, 2007Obesity
How might that happen, that an obese mother can create future generations of obese children? Because the baby is born programmed to be obese:[15]
- Each time a pregnant woman eats, her hormones launch a flurry of activity, including a rise in blood glucose with a resultant rise in insulin secreted by the pancreas. This makes sure that an ample supply of glucose is available to both her and her fetus.
- Throughout the 2nd and 3rd trimesters, hormone levels rise, the pancreas works harder, and mom's amount of insulin resistance rises, because her muscles do not like being bathed in insulin and drowned in glucose.
- When the mother's pancreas doesn't secret enough insulin to keep the blood sugar level low, the mother and the fetus experience hyperglycemia. The fetus is exposed to bouts of hyperglycemia which promotes excess nutrient storage. The result is excessive birth weight (macrosomia).
- Excessive body fat stores, stimulated by excessive glucose delivery during diabetic pregnancy, often extends into childhood and adult life.
Exposure in the womb seems to permanently disrupt or dysregulate appetite control and hormones and impair energy metabolism. “Fetal metabolic programming” may lead to obesity in adolescence and young adulthood, spawning a potential vicious cycle of transgenerational transmission of the obesity epidemic from parents to offspring, regardless of offspring genetics or childhood environment.[16]
Chemicals also play a big role in obesity. Ever since Rachel Carson wrote Silent Spring back in the 1960s, the book that rang the first big warning about the dangers of pesticides, we have been slowly waking up to the dangers of the 80,000 or so chemicals in our midst.
Sharon Begley reported in Newsweek in 2009 that early exposure to common chemicals may be programming kids to be fat:
“Certain hormone-mimicking pollutants, ubiquitous in the food chain, have two previously unsuspected effects. They act on genes in the developing fetus and newborn to turn more precursor cells into fat cells, which stay with you for life. And they may alter metabolic rate, so that the body hoards calories rather than burning them, like a physiological Scrooge. 'The evidence now emerging says that being overweight is not just the result of personal choices about what you eat, combined with inactivity,' says Retha Newbold of the National Institute of Environmental Health Sciences (NIEHS) in North Carolina, part of the National Institutes of Health (NIH). 'Exposure to environmental chemicals during development may be contributing to the obesity epidemic.' They are not the cause of extra pounds in every person who is overweight-for older adults, who were less likely to be exposed to so many of the compounds before birth, the standard explanations of genetics and lifestyle probably suffice-but environmental chemicals may well account for a good part of the current epidemic, especially in those under 50. And at the individual level, exposure to the compounds during a critical period of development may explain one of the most frustrating aspects of weight gain: you eat no more than your slim friends, and exercise no less, yet are still unable to shed pounds.”[17]
Dr. David Ludwig is the director of the Optimal Weight for Life Program in the Division of Endocrinology, Children's Hospital Boston. He is also an associate professor of pediatrics at Harvard Medical School. He wrote in the New England Journal of Medicine about a family who came to his clinic:
“One of the parents was overweight, and the other was obese. The five children were more severely obese and had numerous weight-related complications - one had evidence of fatty liver, one had high blood pressure, two had gastroesophageal reflux, two had orthopedic problems, three had marked insulin resistance, four had dyslipidemia, and all had emotional problems related to their weight.
“Unfortunately, the U.S. government has thus far invested only a fraction of a cent in research for every dollar that obesity costs society. And although broad consensus exists regarding the dietary and lifestyle habits needed to prevent and treat childhood obesity, we lack anything resembling a comprehensive strategy for encouraging children to eat a healthful diet and engage in physical activity. Such a strategy would include legislation that regulates junk-food advertising, provides adequate funding for decent lunches and regular physical activities at school, restructures the farm-subsidies program to favor nutrient-dense rather than calorie-dense produce, and mandates insurance coverage for preventing and treating pediatric obesity.”[18]
Nutrient-dense versus Calorie-dense
Nutrient-dense means that each bite of food has a lot of nutrition - vitamins, minerals, enzymes, maybe antioxidants and more. Calorie-dense is something like soda - no nutrition, but packing the calories. Most of us need help learning how to make the switch to nutrient-dense food, and organic food that has less chemicals.
Losing weight safely sometimes requires a safe detox program along with dietary changes. At the Arizona Center for Advanced Medicine, we have such a program for change. It is called FirstLine Therapy™. We measure the BMI routinely on all our patients. During the course of the program we measure the BMI twice a month to determine whether muscle mass is being maintained while fat mass is lost. We take time to do lots of hand-holding and education. The program works for children, adolescents and adults. We show you how to choose nutrient-dense foods over calorie-dense foods. We help you plan a do-able nutritional program which will allow both children and adults to lose weight (fat), while maintaining muscle mass. And we hold your hand as you tackle that tough one, exercise - how much, what type, how to do it, and how often. We show you for example what you can do while sitting at your desk during a phone call. We also offer colonics which can flush out the colon and rebalance the intestinal flora. The 12-week program gives you the tools to enable you and your children to choose a healthy lifestyle for the rest of your lives.
[1] Rebecca Voelker, Improved Use of BMI Needed to Screen Children for Overweight, JAMA, 2007;297:2684-2685.[2] David S. Ludwig, M.D., Ph.D. Childhood Obesity - The Shape of Things to Come, NEJM, December 6, 2007[3] Christina Paxson, Elisabeth Donahue, C. Tracy Orleans, and Jeanne Ann Grisso, Childhood Obesity-Introducing the Issue, Childhood Obesity, The Future of Children, a publication of the Woodrow Wilson School of Public and International Affairs at Princeton University and the Brookings Institution, Volume 16, Number 1 Spring 2006.[4] News Release: Scientists Find Link Between Dopamine and Obesity. Brookhaven National Laboratory. February 1, 2001[5] News Release: New gene discovery links obesity to the brain. Albert Einstein College of Medicine. June 25, 2009 [6] Johnson, Paul M; Kenny, Paul J. Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats. Nature Neuroscience. March 28, 2010; DOI: 10.1038/nn.2519 [7]James Owen, Some Couch Potatoes Born That Way, Fat Study Says, National Geographic News, January 27, 2007 [8] Contagious Obesity? Identifying The Human Adenoviruses That May Make Us Fat. ScienceDaily, January 30, 2006 [9] Turnbaugh PJ, Ley RE et al. An obesity-associated gut microbiome with increased capacity for energy harvest. Nature 444, 1027-131 (21 December 2006) [7] http://www.cancer.org/…Over_100000_Cancers_Linked_to_Excess_Body_Fat.asp [8] Plagemann A. Perinatal programming and functional teratogenesis: impact on body weight regulation and obesity. Physiol Behav. Dec 15 2005;86(5):661-8 [9] Hillier TA, Pedula KL, et al. Childhood obesity and metabolic imprinting: the ongoing effects of maternal hyperglycemia. Diabetes Care 2007;30:2287-92. [10] Slackman, Michael. Privilege Pulls Qatar Toward Unhealthy Choices. New York Times. April 26, 2010 [11] http://www.cancer.org…NWS_1_1x_Report_Over_100000_Cancers_Linked_to_Excess_Body_Fat.asp [12] Plagemann A. Perinatal programming and functional teratogenesis: impact on body weight regulation and obesity. Physiol Behav. Dec 15 2005;86(5):661-8 [13] Hillier TA, Pedula KL, et al. Childhood obesity and metabolic imprinting: the ongoing effects of maternal hyperglycemia. Diabetes Care 2007;30:2287-92. [14] McKinney PA, Parslow R, Gurney KA, Law GR, Bodansky HJ, Williams R. Perinatal and neonatal determinants of childhood type 1 diabetes. A case-control study in Yorkshire, U.K. Diabetes Care. Jun 1999;22(6):928-32 [15] http://emedicine.medscape.com/article/127547-overview [16] Eric L Ding and Frank B Hu. Determining Origins and Causes of Childhood Obesity via Mendelian Randomization Analysis. PLoS Med. 2008 March; 5(3): e65. [17] Sharon Begley, Born to be Big - Early exposure to common chemicals may be programming kids to be fat. Newsweek, September 11, 2009 [18] David S. Ludwig, M.D., Ph.D. Childhood Obesity - The Shape of Things to Come, NEJM, December 6, 2007Obesity
Exposure in the womb seems to permanently disrupt or dysregulate appetite control and hormones and impair energy metabolism. “Fetal metabolic programming” may lead to obesity in adolescence and young adulthood, spawning a potential vicious cycle of transgenerational transmission of the obesity epidemic from parents to offspring, regardless of offspring genetics or childhood environment.[16]
Chemicals also play a big role in obesity. Ever since Rachel Carson wrote Silent Spring back in the 1960s, the book that rang the first big warning about the dangers of pesticides, we have been slowly waking up to the dangers of the 80,000 or so chemicals in our midst.
Sharon Begley reported in Newsweek in 2009 that early exposure to common chemicals may be programming kids to be fat:
“Certain hormone-mimicking pollutants, ubiquitous in the food chain, have two previously unsuspected effects. They act on genes in the developing fetus and newborn to turn more precursor cells into fat cells, which stay with you for life. And they may alter metabolic rate, so that the body hoards calories rather than burning them, like a physiological Scrooge. 'The evidence now emerging says that being overweight is not just the result of personal choices about what you eat, combined with inactivity,' says Retha Newbold of the National Institute of Environmental Health Sciences (NIEHS) in North Carolina, part of the National Institutes of Health (NIH). 'Exposure to environmental chemicals during development may be contributing to the obesity epidemic.' They are not the cause of extra pounds in every person who is overweight-for older adults, who were less likely to be exposed to so many of the compounds before birth, the standard explanations of genetics and lifestyle probably suffice-but environmental chemicals may well account for a good part of the current epidemic, especially in those under 50. And at the individual level, exposure to the compounds during a critical period of development may explain one of the most frustrating aspects of weight gain: you eat no more than your slim friends, and exercise no less, yet are still unable to shed pounds.”[17]
Dr. David Ludwig is the director of the Optimal Weight for Life Program in the Division of Endocrinology, Children's Hospital Boston. He is also an associate professor of pediatrics at Harvard Medical School. He wrote in the New England Journal of Medicine about a family who came to his clinic:
“One of the parents was overweight, and the other was obese. The five children were more severely obese and had numerous weight-related complications - one had evidence of fatty liver, one had high blood pressure, two had gastroesophageal reflux, two had orthopedic problems, three had marked insulin resistance, four had dyslipidemia, and all had emotional problems related to their weight.
“Unfortunately, the U.S. government has thus far invested only a fraction of a cent in research for every dollar that obesity costs society. And although broad consensus exists regarding the dietary and lifestyle habits needed to prevent and treat childhood obesity, we lack anything resembling a comprehensive strategy for encouraging children to eat a healthful diet and engage in physical activity. Such a strategy would include legislation that regulates junk-food advertising, provides adequate funding for decent lunches and regular physical activities at school, restructures the farm-subsidies program to favor nutrient-dense rather than calorie-dense produce, and mandates insurance coverage for preventing and treating pediatric obesity.”[18]
Nutrient-dense versus Calorie-dense
Nutrient-dense means that each bite of food has a lot of nutrition - vitamins, minerals, enzymes, maybe antioxidants and more. Calorie-dense is something like soda - no nutrition, but packing the calories. Most of us need help learning how to make the switch to nutrient-dense food, and organic food that has less chemicals.
Losing weight safely sometimes requires a safe detox program along with dietary changes. At the Arizona Center for Advanced Medicine, we have such a program for change. It is called FirstLine Therapy™. We measure the BMI routinely on all our patients. During the course of the program we measure the BMI twice a month to determine whether muscle mass is being maintained while fat mass is lost. We take time to do lots of hand-holding and education. The program works for children, adolescents and adults. We show you how to choose nutrient-dense foods over calorie-dense foods. We help you plan a do-able nutritional program which will allow both children and adults to lose weight (fat), while maintaining muscle mass. And we hold your hand as you tackle that tough one, exercise - how much, what type, how to do it, and how often. We show you for example what you can do while sitting at your desk during a phone call. We also offer colonics which can flush out the colon and rebalance the intestinal flora. The 12-week program gives you the tools to enable you and your children to choose a healthy lifestyle for the rest of your lives.
[1] Rebecca Voelker, Improved Use of BMI Needed to Screen Children for Overweight, JAMA, 2007;297:2684-2685.[2] David S. Ludwig, M.D., Ph.D. Childhood Obesity - The Shape of Things to Come, NEJM, December 6, 2007[3] Christina Paxson, Elisabeth Donahue, C. Tracy Orleans, and Jeanne Ann Grisso, Childhood Obesity-Introducing the Issue, Childhood Obesity, The Future of Children, a publication of the Woodrow Wilson School of Public and International Affairs at Princeton University and the Brookings Institution, Volume 16, Number 1 Spring 2006.[4] News Release: Scientists Find Link Between Dopamine and Obesity. Brookhaven National Laboratory. February 1, 2001[5] News Release: New gene discovery links obesity to the brain. Albert Einstein College of Medicine. June 25, 2009 [6] Johnson, Paul M; Kenny, Paul J. Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats. Nature Neuroscience. March 28, 2010; DOI: 10.1038/nn.2519 [7]James Owen, Some Couch Potatoes Born That Way, Fat Study Says, National Geographic News, January 27, 2007 [8] Contagious Obesity? Identifying The Human Adenoviruses That May Make Us Fat. ScienceDaily, January 30, 2006 [9] Turnbaugh PJ, Ley RE et al. An obesity-associated gut microbiome with increased capacity for energy harvest. Nature 444, 1027-131 (21 December 2006) [7] http://www.cancer.org/…Over_100000_Cancers_Linked_to_Excess_Body_Fat.asp [8] Plagemann A. Perinatal programming and functional teratogenesis: impact on body weight regulation and obesity. Physiol Behav. Dec 15 2005;86(5):661-8 [9] Hillier TA, Pedula KL, et al. Childhood obesity and metabolic imprinting: the ongoing effects of maternal hyperglycemia. Diabetes Care 2007;30:2287-92. [10] Slackman, Michael. Privilege Pulls Qatar Toward Unhealthy Choices. New York Times. April 26, 2010 [11] http://www.cancer.org…NWS_1_1x_Report_Over_100000_Cancers_Linked_to_Excess_Body_Fat.asp [12] Plagemann A. Perinatal programming and functional teratogenesis: impact on body weight regulation and obesity. Physiol Behav. Dec 15 2005;86(5):661-8 [13] Hillier TA, Pedula KL, et al. Childhood obesity and metabolic imprinting: the ongoing effects of maternal hyperglycemia. Diabetes Care 2007;30:2287-92. [14] McKinney PA, Parslow R, Gurney KA, Law GR, Bodansky HJ, Williams R. Perinatal and neonatal determinants of childhood type 1 diabetes. A case-control study in Yorkshire, U.K. Diabetes Care. Jun 1999;22(6):928-32 [15] http://emedicine.medscape.com/article/127547-overview [16] Eric L Ding and Frank B Hu. Determining Origins and Causes of Childhood Obesity via Mendelian Randomization Analysis. PLoS Med. 2008 March; 5(3): e65. [17] Sharon Begley, Born to be Big - Early exposure to common chemicals may be programming kids to be fat. Newsweek, September 11, 2009 [18] David S. Ludwig, M.D., Ph.D. Childhood Obesity - The Shape of Things to Come, NEJM, December 6, 2007Obesity
Chemicals also play a big role in obesity. Ever since Rachel Carson wrote Silent Spring back in the 1960s, the book that rang the first big warning about the dangers of pesticides, we have been slowly waking up to the dangers of the 80,000 or so chemicals in our midst.
Sharon Begley reported in Newsweek in 2009 that early exposure to common chemicals may be programming kids to be fat:
“Certain hormone-mimicking pollutants, ubiquitous in the food chain, have two previously unsuspected effects. They act on genes in the developing fetus and newborn to turn more precursor cells into fat cells, which stay with you for life. And they may alter metabolic rate, so that the body hoards calories rather than burning them, like a physiological Scrooge. 'The evidence now emerging says that being overweight is not just the result of personal choices about what you eat, combined with inactivity,' says Retha Newbold of the National Institute of Environmental Health Sciences (NIEHS) in North Carolina, part of the National Institutes of Health (NIH). 'Exposure to environmental chemicals during development may be contributing to the obesity epidemic.' They are not the cause of extra pounds in every person who is overweight-for older adults, who were less likely to be exposed to so many of the compounds before birth, the standard explanations of genetics and lifestyle probably suffice-but environmental chemicals may well account for a good part of the current epidemic, especially in those under 50. And at the individual level, exposure to the compounds during a critical period of development may explain one of the most frustrating aspects of weight gain: you eat no more than your slim friends, and exercise no less, yet are still unable to shed pounds.”[17]
Dr. David Ludwig is the director of the Optimal Weight for Life Program in the Division of Endocrinology, Children's Hospital Boston. He is also an associate professor of pediatrics at Harvard Medical School. He wrote in the New England Journal of Medicine about a family who came to his clinic:
“One of the parents was overweight, and the other was obese. The five children were more severely obese and had numerous weight-related complications - one had evidence of fatty liver, one had high blood pressure, two had gastroesophageal reflux, two had orthopedic problems, three had marked insulin resistance, four had dyslipidemia, and all had emotional problems related to their weight.
“Unfortunately, the U.S. government has thus far invested only a fraction of a cent in research for every dollar that obesity costs society. And although broad consensus exists regarding the dietary and lifestyle habits needed to prevent and treat childhood obesity, we lack anything resembling a comprehensive strategy for encouraging children to eat a healthful diet and engage in physical activity. Such a strategy would include legislation that regulates junk-food advertising, provides adequate funding for decent lunches and regular physical activities at school, restructures the farm-subsidies program to favor nutrient-dense rather than calorie-dense produce, and mandates insurance coverage for preventing and treating pediatric obesity.”[18]
Nutrient-dense versus Calorie-dense
Nutrient-dense means that each bite of food has a lot of nutrition - vitamins, minerals, enzymes, maybe antioxidants and more. Calorie-dense is something like soda - no nutrition, but packing the calories. Most of us need help learning how to make the switch to nutrient-dense food, and organic food that has less chemicals.
Losing weight safely sometimes requires a safe detox program along with dietary changes. At the Arizona Center for Advanced Medicine, we have such a program for change. It is called FirstLine Therapy™. We measure the BMI routinely on all our patients. During the course of the program we measure the BMI twice a month to determine whether muscle mass is being maintained while fat mass is lost. We take time to do lots of hand-holding and education. The program works for children, adolescents and adults. We show you how to choose nutrient-dense foods over calorie-dense foods. We help you plan a do-able nutritional program which will allow both children and adults to lose weight (fat), while maintaining muscle mass. And we hold your hand as you tackle that tough one, exercise - how much, what type, how to do it, and how often. We show you for example what you can do while sitting at your desk during a phone call. We also offer colonics which can flush out the colon and rebalance the intestinal flora. The 12-week program gives you the tools to enable you and your children to choose a healthy lifestyle for the rest of your lives.
[1] Rebecca Voelker, Improved Use of BMI Needed to Screen Children for Overweight, JAMA, 2007;297:2684-2685.[2] David S. Ludwig, M.D., Ph.D. Childhood Obesity - The Shape of Things to Come, NEJM, December 6, 2007[3] Christina Paxson, Elisabeth Donahue, C. Tracy Orleans, and Jeanne Ann Grisso, Childhood Obesity-Introducing the Issue, Childhood Obesity, The Future of Children, a publication of the Woodrow Wilson School of Public and International Affairs at Princeton University and the Brookings Institution, Volume 16, Number 1 Spring 2006.[4] News Release: Scientists Find Link Between Dopamine and Obesity. Brookhaven National Laboratory. February 1, 2001[5] News Release: New gene discovery links obesity to the brain. Albert Einstein College of Medicine. June 25, 2009 [6] Johnson, Paul M; Kenny, Paul J. Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats. Nature Neuroscience. March 28, 2010; DOI: 10.1038/nn.2519 [7]James Owen, Some Couch Potatoes Born That Way, Fat Study Says, National Geographic News, January 27, 2007 [8] Contagious Obesity? Identifying The Human Adenoviruses That May Make Us Fat. ScienceDaily, January 30, 2006 [9] Turnbaugh PJ, Ley RE et al. An obesity-associated gut microbiome with increased capacity for energy harvest. Nature 444, 1027-131 (21 December 2006) [7] http://www.cancer.org/…Over_100000_Cancers_Linked_to_Excess_Body_Fat.asp [8] Plagemann A. Perinatal programming and functional teratogenesis: impact on body weight regulation and obesity. Physiol Behav. Dec 15 2005;86(5):661-8 [9] Hillier TA, Pedula KL, et al. Childhood obesity and metabolic imprinting: the ongoing effects of maternal hyperglycemia. Diabetes Care 2007;30:2287-92. [10] Slackman, Michael. Privilege Pulls Qatar Toward Unhealthy Choices. New York Times. April 26, 2010 [11] http://www.cancer.org…NWS_1_1x_Report_Over_100000_Cancers_Linked_to_Excess_Body_Fat.asp [12] Plagemann A. Perinatal programming and functional teratogenesis: impact on body weight regulation and obesity. Physiol Behav. Dec 15 2005;86(5):661-8 [13] Hillier TA, Pedula KL, et al. Childhood obesity and metabolic imprinting: the ongoing effects of maternal hyperglycemia. Diabetes Care 2007;30:2287-92. [14] McKinney PA, Parslow R, Gurney KA, Law GR, Bodansky HJ, Williams R. Perinatal and neonatal determinants of childhood type 1 diabetes. A case-control study in Yorkshire, U.K. Diabetes Care. Jun 1999;22(6):928-32 [15] http://emedicine.medscape.com/article/127547-overview [16] Eric L Ding and Frank B Hu. Determining Origins and Causes of Childhood Obesity via Mendelian Randomization Analysis. PLoS Med. 2008 March; 5(3): e65. [17] Sharon Begley, Born to be Big - Early exposure to common chemicals may be programming kids to be fat. Newsweek, September 11, 2009 [18] David S. Ludwig, M.D., Ph.D. Childhood Obesity - The Shape of Things to Come, NEJM, December 6, 2007Obesity
Dr. David Ludwig is the director of the Optimal Weight for Life Program in the Division of Endocrinology, Children's Hospital Boston. He is also an associate professor of pediatrics at Harvard Medical School. He wrote in the New England Journal of Medicine about a family who came to his clinic:
“One of the parents was overweight, and the other was obese. The five children were more severely obese and had numerous weight-related complications - one had evidence of fatty liver, one had high blood pressure, two had gastroesophageal reflux, two had orthopedic problems, three had marked insulin resistance, four had dyslipidemia, and all had emotional problems related to their weight.
“Unfortunately, the U.S. government has thus far invested only a fraction of a cent in research for every dollar that obesity costs society. And although broad consensus exists regarding the dietary and lifestyle habits needed to prevent and treat childhood obesity, we lack anything resembling a comprehensive strategy for encouraging children to eat a healthful diet and engage in physical activity. Such a strategy would include legislation that regulates junk-food advertising, provides adequate funding for decent lunches and regular physical activities at school, restructures the farm-subsidies program to favor nutrient-dense rather than calorie-dense produce, and mandates insurance coverage for preventing and treating pediatric obesity.”[18]
Nutrient-dense versus Calorie-dense
Nutrient-dense means that each bite of food has a lot of nutrition - vitamins, minerals, enzymes, maybe antioxidants and more. Calorie-dense is something like soda - no nutrition, but packing the calories. Most of us need help learning how to make the switch to nutrient-dense food, and organic food that has less chemicals.
Losing weight safely sometimes requires a safe detox program along with dietary changes. At the Arizona Center for Advanced Medicine, we have such a program for change. It is called FirstLine Therapy™. We measure the BMI routinely on all our patients. During the course of the program we measure the BMI twice a month to determine whether muscle mass is being maintained while fat mass is lost. We take time to do lots of hand-holding and education. The program works for children, adolescents and adults. We show you how to choose nutrient-dense foods over calorie-dense foods. We help you plan a do-able nutritional program which will allow both children and adults to lose weight (fat), while maintaining muscle mass. And we hold your hand as you tackle that tough one, exercise - how much, what type, how to do it, and how often. We show you for example what you can do while sitting at your desk during a phone call. We also offer colonics which can flush out the colon and rebalance the intestinal flora. The 12-week program gives you the tools to enable you and your children to choose a healthy lifestyle for the rest of your lives.
Nutrient-dense means that each bite of food has a lot of nutrition - vitamins, minerals, enzymes, maybe antioxidants and more. Calorie-dense is something like soda - no nutrition, but packing the calories. Most of us need help learning how to make the switch to nutrient-dense food, and organic food that has less chemicals.
Losing weight safely sometimes requires a safe detox program along with dietary changes. At the Arizona Center for Advanced Medicine, we have such a program for change. It is called FirstLine Therapy™. We measure the BMI routinely on all our patients. During the course of the program we measure the BMI twice a month to determine whether muscle mass is being maintained while fat mass is lost. We take time to do lots of hand-holding and education. The program works for children, adolescents and adults. We show you how to choose nutrient-dense foods over calorie-dense foods. We help you plan a do-able nutritional program which will allow both children and adults to lose weight (fat), while maintaining muscle mass. And we hold your hand as you tackle that tough one, exercise - how much, what type, how to do it, and how often. We show you for example what you can do while sitting at your desk during a phone call. We also offer colonics which can flush out the colon and rebalance the intestinal flora. The 12-week program gives you the tools to enable you and your children to choose a healthy lifestyle for the rest of your lives.