Health Journal Online

Tag: obesity

  • Childhood obesity through a weight-inclusive lens

    Childhood obesity through a weight-inclusive lens


    In this episode, we’re joined by Dr Brooke Harcourt, an experienced paediatric dietitian and researcher, to explore how dietitians can support children living with overweight or obesity using a compassionate, evidence-based approach. Brooke unpacks the evolving landscape of paediatric obesity care, including the impact of weight stigma, the shift toward non-diet, weight-inclusive practice, and how to build trust with families. We also touch on the emerging use of GLP-1 medications in adolescents and when these rare, specialist-led cases may be considered. Tune in for practical strategies, language tips and real-world insights to support families with care.

    Hosted by Bec Sparrowhawk

    Biography

    Dr Brooke Harcourt is an approachable Accredited Practicing Dietitian and nutrition therapist with over a decade of experience in infant and child nutrition and metabolism conditions. She is nationally and internationally recognised for her medical research into endocrine conditions having completed research fellowships at the UQ Translational Research Institute, Baker Heart and Diabetes Institute, the Royal Children’s Hospital and Murdoch Childrens Research Institute. Brooke runs a large private practice, Family Dietetics, and a specialised ‘Therapy Kitchen’, where her and the team take a practical approach to attainable nutrition through feeding therapy and food learning programs in a real kitchen therapy environment. She also offers dietetics services at specialist paediatric centres, eating disorder services and the Victorian Department of Corrections and Youth Justice System. Brooke has a particular passion for helping infants and young people establish healthy growth curves, overcome eating disorders and traumatic feeding histories, and improving nutrition access for young people with disability, developmental and neurodevelopmental conditions.

     

    In this episode, we discuss how to:

    • Actively challenge weight stigma and create a safe space for families.
    • Communicate with confidence using language that empowers, not shames.
    • Prioritise validating families’ experiences and setting achievable, health-focused goals.
    • Understand the clinical context of GLP-1 use in adolescents

     

    DISCLAIMER:  In this episode, we’ll use clinical terms like ‘childhood obesity’ when needed to reflect current guidelines – but our focus is firmly on weight-inclusive, family-centred approaches that support health without stigma. This episode is targeted to dietitians with experience in paediatrics.

    Additional resources

    The content, products and/or services referred to in this podcast are intended for Health Care Professionals only and are not, and are not intended to be, medical advice, which should be tailored to your individual circumstances. The content is for your information only, and we advise that you exercise your own judgement before deciding to use the information provided. Professional medical advice should be obtained before taking action. The reference to particular products and/or services in this episode does not constitute any form of endorsement. Please see  here  for terms and conditions.


    Source link
  • Plant-Based Meats and Puberty, Obesity, and Fracture Risk

    Plant-Based Meats and Puberty, Obesity, and Fracture Risk

    What are the effects of plant-based meats on premature puberty, childhood obesity, and hip fracture risk?

    As noted in an editorial in the Journal of the American Medical Association on plant-based meats, if you look only at the nutrition facts information for a conventional burger versus a Beyond Meat or Impossible Burger, as seen here and at 0:20 in my video Plant-Based Meat Substitutes Put to the Test, you wouldn’t necessarily be able to predict the health consequences without further studies.

    We’ve had plant-based meats in the marketplace for more than a century, though, as you can see in this ad for “good eating” Protose, below and at 0:35 in my video. Dr. John Harvey Kellogg filed a patent for Protose, what he called “the modern vegetable meat,” in 1899.

    Of course, products like tempeh and tofu have been eaten throughout Asia for centuries, but I think of those as separate foods in their own right, as opposed to products intentionally designed to mimic the taste and texture of meat. With such a rich history, harkening back to the days of pass-the-Proteena—another great ad here and at 1:06 in my video—you’d think there’d be some studies of consumers—and indeed, there are. 

    Researchers have found, for example, that girls who eat meat may start their periods six months earlier than girls who don’t. Is the earlier menstruation because the meat-eating girls were eating a lot of protein and fat? No, because vegetarian girls who instead ate meat analogs, like veggie burgers and veggie dogs, were able to delay menstruation by nine months. Of course, it’s hard to tease out how much of that is just from avoiding meat, but compared with girls who ate meat a few times a week, those who ate meat a few times a day had a significantly earlier age of first menstruation. This may help explain why childhood meat consumption is linked to breast cancer later in life, since the earlier you start your period, the higher your lifetime risk. 

    Now, obesity itself may contribute to the early onset of puberty in girls, so that could be another factor. Studies have suggested that “vegetarian children tend to be lighter and leaner than nonvegetarian children,” but veg kids aren’t smaller in general, though. Vegetarian boys and girls may measure to be about an inch taller than their classmates; they just aren’t as wide. So, the fact that girls who eat plant-based meats may be less likely to experience premature puberty may, in part, be because they were leaner.

    Indeed, as shown here and at 2:48 in my video, childhood obesity research found that meat consumption seems to double the odds of schoolchildren becoming overweight, compared to plant-based meat. Now, whole plant food sources of protein, such as beans, do even better and are associated with halving the odds of kids becoming overweight.

    This is why I consider plant-based meats like the Impossible Burger and Beyond Meat more of a useful stepping stone towards a healthier diet, rather than the endgame ideal. The same amount of protein in a bean burrito would be better in nearly every way, as you can see here and at 3:05 in my video. 

    Similarly, in terms of hip fracture risk, in the Adventist Health Study–2, which followed tens of thousands of men and women for years, researchers found that daily intake of plant-based meats appeared to reduce the risk of hip fracture by nearly half, but daily intake of legumes—beans, split peas, chickpeas, and lentils—may drop the risk of hip fracture by even more—by nearly two-thirds.

    This is the fourth in a nine-part series on plant-based meats. If you missed the first three, see the related posts below.

    Stay tuned for: 



    Source link

  • Exploring the Obesity Paradox 

    Exploring the Obesity Paradox 

    How do we explain studies that suggest overweight individuals live longer?

    Martin Luther King Jr. warned that human progress is neither automatic nor inevitable, and the same may be true of the human lifespan. In the 1800s, life expectancy was less than 40 years, but it has been “advancing steadily” over the last two centuries, “increasing at approximately 2 years per decade”—until recently. Longevity gains appear “to be faltering or even being reversed.” Thanks to the obesity epidemic, we may now be raising the first generation to live shorter lives than their parents.

    “This downward trend in longevity will almost certainly accelerate as the current generation of children—with higher body weights from earlier in life than ever before—reaches adulthood.” Current trends “potentially signal a looming social and economic catastrophe” if the obesity epidemic continues unchecked. In the coming decades, some predict we may lose two to five years or more of life expectancy in the United States. To put that into perspective, a miracle cure for all forms of cancer would only add three and a half years to the average U.S. life expectancy. In other words, reversing the obesity epidemic might save more lives than curing cancer.

    The evidence that being overweight increases our risk for debilitating diseases like diabetes is considered “indisputable.” However, surprisingly, there is controversy surrounding body weight and overall mortality. In 2013, scientists with the Centers for Disease Control and Prevention (CDC) published a meta-analysis in the Journal of the American Medical Association suggesting that being overweight was advantageous. Grades 2 and 3 obesity, such as being an average height of 5’6″ and weighing about 216 pounds (98 kg) or more, were associated with living a shorter life, but grade 1 obesity, weighing about 185 to 215 pounds (84 to 97 kg) at that height, was not. Being overweight (about 155 to 185 pounds/70 to 83 kg at 5’6″) appeared to be protective compared to those who were a “normal weight” of 115 to 155 pounds (52 to 69 kg). The overweight individuals, those with a body mass index (BMI) of 25 to 30, appeared to live the longest.

    Headline writers were giddy. “Being overweight can extend your life rather than shorten it,” read one. “Dreading your diet? Don’t worry—plump people live LONGER than their skinnier counterparts…” read another. “Extra pounds mean a lower chance of death.” Not surprisingly, the study ignited a firestorm of controversy in the public health community. The study was called “ludicrous,” “flawed,” and “misleading.” The chair of nutrition at Harvard lost his cool, calling the study “really a pile of rubbish” and fearing the food industry might exploit the study in the same way the petroleum industry misuses “controversy” over climate change. 

    Public health advocates can’t just dismiss data they find inconvenient, though. Science is science. But how could being overweight increase the risk of life-threatening diseases, yet, at the same time, make you live longer? This became known as “The Obesity Paradox,” the subject of my video Is the Obesity Paradox Real or a Myth?.

    The solution to the puzzle appears to lie with two major sources of bias, the first being “confounding by smoking.” The nicotine in tobacco can lead to weight loss. So, if you’re skinnier because you smoke, then no wonder you’d live a shorter life, albeit with a slimmer waist. The failure to control for the effect of smoking in studies purporting to show an “obesity paradox” leads to the dangers of obesity being “grossly underestimated.”

    The second major source of bias is reverse causality. Instead of lower weight leading to life-threatening diseases, isn’t it more likely that life-threatening diseases lead to lower weight? Conditions such as hidden tumors, chronic heart or lung disease, alcoholism, and depression can all cause unintentional weight loss for months or even years before they are even diagnosed. It’s normal to be overweight in the United States, for example. So, people who are “abnormally” thin—in other words, at an ideal weight—may be taking care of themselves, but they may instead be “heavy smokers, frail and elderly, and seriously ill with weight loss due to their disease…” 

    To put the obesity paradox to the test once and for all, The Global BMI Mortality Collaboration was formed, reviewing data from more than 10 million people from hundreds of studies in dozens of countries—the largest evaluation of BMI and mortality in history. To help eliminate bias, the researchers omitted smokers and those with known chronic disease, then excluded the first five years of follow-up to try to remove from the analysis those with undiagnosed conditions who lost weight due to an impending death. And? The results were clear: “This analysis has shown that both overweight and obesity (all grades) were associated with increased all-cause mortality”—a greater risk of dying prematurely. So, “adjusting for these biases leads to eliminating the obesity paradox.” In other words, the so-called obesity paradox appears to be “just a myth.”

    Indeed, when intentional weight loss is put to the test, people live longer. There are bariatric surgery studies like the SOS trial that show that weight loss reduces long-term mortality, and randomizing study participants to weight loss through lifestyle changes shows the same thing. Losing a dozen pounds through diet and exercise was found to be associated with a 15 percent drop in overall mortality. Now, exercise alone may extend lifespan even without weight loss, but there appears to be a similar longevity benefit of weight loss through dietary means alone.

    If you missed the previous blog posts in my series on the ABCs of obesity, see:

    Check out the final two videos in this series: What’s the Ideal BMI? and What’s the Ideal Waist Size?.

    I cover all of this and more at length in my book How Not to Diet, and its companion, The How Not to Diet Cookbook, has more than 100 delicious Green-Light recipes that incorporate some of my 21 Tweaks for the acceleration of body fat loss.

    Why are people obese in the first place? I have a whole series of videos on that topic. Check the videos in the related posts.



    Source link

  • Epigenetics and Obesity 

    Epigenetics and Obesity 

    Identical twins don’t just share DNA; they also share a uterus. Might that help account for some of their metabolic similarities? “Fetal overnutrition, evidenced by large infant birth weight for gestational age, is a strong predictor of obesity in childhood and later life.” Could it be that you are what your mom ate?

    A dramatic illustration from the animal world is the crossbreeding of Shetland ponies with massive draft horses. Either way, the offspring are half pony/half horse, but when carried in the pony uterus, they come out much smaller, as you can see below and at 0:47 in my video The Role of Epigenetics in the Obesity Epidemic. (Thank heavens for the pony mother!) This is presumably the same reason why the mule (horse mom and donkey dad) is larger than the hinny (donkey mom and horse dad). The way you test this in people is to study the size of babies from surrogates after in vitro fertilization. 

    Who do you think most determines the birth weight of a test-tube baby? Is it the donor mom who provided all the DNA or the surrogate who provided the intrauterine environment? When it was put to the test, the womb won. Incredibly, a baby who had a thin biological mother but was born to a surrogate with obesity may harbor a greater risk of becoming obese than a baby with a heavier biological mother but born to a slim surrogate. The researchers “concluded that the environment provided by the human mother is more important than her genetic contribution to birth weight.”

    The most compelling data come from comparing obesity rates in siblings born to the same mother, before and after her bariatric surgery. Compared to their brothers and sisters born before the surgery, those born when mom weighed about 100 pounds less had lower rates of inflammation, metabolic derangements, and, most critically, three times less risk of developing severe obesity—35 percent of those born before the weight loss were affected, compared to 11 percent born after. The researchers concluded that “these data emphasize how critical it is to prevent obesity and treat it effectively to prevent further transmission to future generations.”

    Hold on. Mom had the same DNA before and after surgery. She passed down the same genes. How could her weight during pregnancy affect the weight destiny of her children any differently? Darwin himself admitted, “In my opinion, the greatest error which I have committed, has been not allowing sufficient weight to the direct action of the environment, i.e. food…independently of natural selection.” We finally figured out the mechanism by which this can happen—epigenetics.

    Epigenetics, which means “above genetics,” layers an extra level of information on top of the DNA sequence that can be affected by our surroundings, as well as potentially passed on to our children. This is thought to explain the “developmental programming” that can occur in the womb, depending on the weight of the mother—or even the grandmother. Since all the eggs in your infant daughter’s ovaries are already preformed before birth, a mother’s weight status during pregnancy could potentially affect the obesity risk of her grandchildren, too. Either way, you can imagine how this could result in an intergenerational vicious cycle where obesity begets obesity.

    Is there anything we can do about it? Well, breastfed infants may be at lower risk for later obesity, though the benefits may be confined to those who are exclusively breastfed, as the effect may be due to growth factors triggered by exposure to the excess protein in baby formula, as you can see below and at 3:51 in my video. The breastfeeding data are controversial, though, with charges leveled of a “white hat bias.” That’s the concern that public health researchers might disproportionally shelve research results that don’t fit some goal for the greater good. (In this case, preferably publishing breastfeeding studies showing more positive results.) But, of course, that criticism came from someone who works for an infant formula company. Breast is best, regardless. However, its role in the childhood obesity epidemic remains arguably uncertain.

    Prevention may be the key. Given the epigenetic influence of maternal weight during pregnancy, a symposium of experts on pediatric nutrition concluded that “planning of pregnancy, including prior optimization of maternal weight and metabolic condition, offers a safe means to initiate the prevention rather than treatment of pediatric obesity.” Easier said than done, but overweight moms-to-be may take comfort in the fact that after the weight loss in the surgery study, even the moms who gave birth to kids with three times lower risk were still, on average, obese themselves, suggesting weight loss before pregnancy is not an all-or-nothing proposition.

    What triggered the whole obesity epidemic to begin with? There are a multitude of factors, and I covered many of them in my 11-video series on the epidemic in the related posts below.

    We are what our moms ate in other ways, too. Check out: 



    Source link

  • History Of Eating Disorders, Pre-Pregnancy Obesity Raises Offspring’s Risk Of Mental Health Diagnosis

    History Of Eating Disorders, Pre-Pregnancy Obesity Raises Offspring’s Risk Of Mental Health Diagnosis

    Children whose mothers have a history of eating disorders and obesity before pregnancy are at a greater risk of mental health diagnosis, a recent study revealed.

    The results of the latest study involving a Finnish population of nearly 400,000 mothers and around 650,000 offspring revealed significant links between maternal health and the mental well-being of their children.

    The research suggests associations between a mother’s history of eating disorders and pre-pregnancy body mass index (BMI) higher than the normal weight range to most of the nine psychiatric diagnoses examined in the offspring.

    The psychiatric diagnoses involved in the study include mood and anxiety disorders, sleep disorders, intellectual disabilities, specific developmental disorders, autism spectrum disorder (ASD), ADHD, conduct disorders, social functioning and tic disorders (like selective mutism and Tourette syndrome), as well as feeding disorders in infancy and childhood.

    The results showed that around 53% had pre-pregnancy overweight or obesity, nearly 6% had underweight, and 1.6% had a history of an eating disorder.

    When comparing differences in the impact of maternal eating disorders and higher BMI on children’s mental health diagnoses, the study found generally stronger associations with maternal eating disorders than those linked to maternal BMI.

    “The largest effect sizes were observed for maternal eating disorders not otherwise specified in association with offspring sleep disorders and social functioning and tic disorders, while for maternal severe pre-pregnancy obesity, offspring intellectual disabilities had the largest effect size,” the researchers wrote in the study published in Jama Network.

    Eating disorders not otherwise specified (EDNOS) refer to a category of eating disorders that do not fit the specific criteria for more commonly recognized disorders such as anorexia nervosa, bulimia nervosa, and binge eating disorder. Some examples of EDNOS include behaviors such as pica, which involves cravings for and consumption of non-food items, or night eating syndrome, characterized by binge eating during the evening hours.

    “The study confirms previously published associations between maternal eating disorders and BMI and offspring psychiatric disorder, but also reports new associations,” Ida Nilsson, a study author told MedPage Today.

    “The findings underline the importance of considering maternal eating disorders and BMI in maternity care, aiming to reduce the number of offspring with neurodevelopmental and psychiatric disorders. The findings also strengthen the importance of the nutrition of pregnant women,” Nilsson said.

    Source link

  • Obesity medications | Dietitian Connection

    Obesity medications | Dietitian Connection

    US dietitians: “Obesity medications: What every dietitian needs to know” awards 1.0 CPEU in accordance with the Commission on Dietetic Registration’s CPEU Prior Approval Program. You can claim 1.0 CPEU for watching the webinar recording OR listening to the podcast version.
    You can access your post-test learner assessment here.  
    CPD/CEU hours are applicable for Australia and New Zealand dietitians. Check your local country requirements to see if you can claim for continuing education.
    To obtain your CPEU/CPD certificate or certificate of completion, click here then fill in your name and the date you listened to the podcast.

    With the ongoing development of medications used in the treatment of obesity and weight management, dietitians must stay on top of the latest information and understand how they fit into a comprehensive treatment plan. In this episode of Dietitian to Dietitian, NBC’s Today Show nutrition and health expert Joy Bauer along with Beth Czerwony, MS, RD, CSOWM, LD and Colleen Dawkins, FNP-C, RDN, CSOWM discuss the integration of GLP-1 medications in nutrition therapy: the indications for use, who is most likely to have success, and the potential side effects and how to manage them.  

    Hosted by Joy Bauer 

    Biographies

    Beth Czerwony MS, RD, CSOWM, LD is a Clinical Registered Dietitian with the Cleveland Clinic’s Center for Human Nutrition since 2007. In 2019, Beth earned her Certification in Obesity and Weight Management and serves as a preceptor for dietetic interns and mentors both ASMBS and Weight Management DPG. She is member of the Weight Management DPG for the Academy of Nutrition and Dietetics, American Society of Metabolic and Bariatric Surgery, and The Obesity Society. Outside of the clinical setting, Beth has completed multiple local and national presentations and media interviews.

     

     

    Colleen Dawkins, MSN, ARNP, FNP-C, MS, RDN, CSOWM is a Nurse Practitioner in private practice at Big Sky Medical Wellness. She is board-certified in family medicine, a Registered Dietitian Nutritionist, and a Certified Specialist in Obesity and Weight Management. Colleen serves as treasurer for the Washington Obesity Society, vice chair for the Commission on Dietetic Registration’s Obesity Certificate of Training program advisory board, member of the Obesity Medicine Association’s algorithm committee, associate editor and reviewer for Obesity Pillars journal, and is a doctoral student at the University of Southern Mississippi.

     

    Joy Bauer, MS, RDN, CDN, one of America’s leading health authorities, is the nutrition and healthy lifestyle expert for NBC’s TODAY show. She also hosts her own Amazon Live weekly show, Health, Happiness, Joy, where she cooks up mouthwatering recipes, answers viewers’ questions in real-time, and shares her favorite products and kitchen hacks. In addition, Joy is the official nutritionist for the New York City Ballet, the creator of JoyBauer.com, and a #1 New York Times bestselling author with 14 bestsellers to her credit.

     

    In this episode, we discuss:​

    • How these medications can complement dietary interventions and the vital role of the dietitian in providing patient-centered care
    • What to do when medication isn’t the answer for a patient 
    • Best practices for collaborating effectively with your medical team 

    Additional resources

    You can find a handout with information and additional resources here and the speakers’ references here.  


    The content, products and/or services referred to in this podcast are intended for Health Care Professionals only and are not, and are not intended to be, medical advice, which should be tailored to your individual circumstances. The content is for your information only, and we advise that you exercise your own judgement before deciding to use the information provided. Professional medical advice should be obtained before taking action. The reference to particular products and/or services in this episode does not constitute any form of endorsement. Please see  here  for terms and conditions.

     

     

     

    Source link

  • What Is the Role of Our Genes in the Obesity Epidemic? 

    What Is the Role of Our Genes in the Obesity Epidemic? 

    The “fat gene” accounts for less than 1 percent of the differences in size between people.

    To date, about a hundred genetic markers have been linked to obesity, but when you put them all together, overall, they account for less than 3 percent of the difference in body mass index (BMI) between people. You may have heard about the “fat gene,” called FTO, short for FaT mass and Obesity-associated). It’s the gene most strongly linked to obesity, but it explains less than 1 percent of the difference in BMI between people, a mere 0.34 percent. 

    As I discuss in my video The Role of Genes in the Obesity Epidemic, FTO codes for a brain protein that appears to affect our appetite. Are you one of the billion people who carry the FTO susceptibility genes? It doesn’t matter because it only appears to result in a difference in intake of a few hundred extra calories a year. The energy imbalance that led to the obesity epidemic is on the order of hundreds of calories a day, and that’s the gene known so far to have the most effect. The chances of accurately predicting obesity risk based on FTO status is “only slightly better than tossing a coin.” In other words, no, those genes don’t make you look fat.

    When it comes to obesity, the power of our genes is nothing compared to the power of our fork. Even the small influence the FTO gene does have appears to be weaker among those who are physically active and may be abolished completely in those eating healthier diets. FTO only appears to affect those eating diets higher in saturated fat, which is predominantly found in meat, dairy, and junk food. Those eating more healthfully appear to be at no greater risk of weight gain, even if they inherited the “fat gene” from both of their parents.

    Physiologically, FTO gene status does not appear to affect our ability to lose weight. Psychologically, knowing we’re at increased genetic risk for obesity may motivate some people to eat and live more healthfully, but it may cause others to fatalistically throw their hands up in the air and resign themselves to thinking that it just runs in their family, as you can see in the graph below and at 2:11 in my video. Obesity does tend to run in families, but so do lousy diets. 

    Comparing the weight of biological versus adopted children can help tease out the contributions of lifestyles versus genetics. Children growing up with two overweight biological parents were found to be 27 percent more likely to be overweight themselves, whereas adopted children placed in a home with two overweight parents were 21 percent more likely to be overweight. So, genetics do play a role, but this suggests that it’s more the children’s environment than their DNA.

    One of the most dramatic examples of the power of diet over DNA comes from the Pima Indians of Arizona. As you can see in the graph below and at 3:05 in my video, they not only have among the highest rates of obesity, but they also have the highest rates of diabetes in the world. This has been ascribed to their relatively fuel-efficient genetic makeup. Their propensity to store calories may have served them well in times of scarcity when they were living off of corn, beans, and squash, but when the area became “settled,” their source of water, the Gila River, was diverted upstream. Those who survived the ensuing famine had to abandon their traditional diet to live off of government food programs and chronic disease rates skyrocketed. Same genes, but different diet, different result. 

    In fact, a natural experiment was set up. The Pima living over the border in Mexico come from the same genetic pool but were able to maintain more of their traditional lifestyle, sticking with their main staples of beans, wheat flour tortillas, and potatoes. Same genes, but seven times less obesity and about four times less diabetes. You can see those graphs below and at 3:58 and 4:02 in my video. Genes may load the gun, but diet pulls the trigger.

    Of course, it’s not our genes! Our genes didn’t suddenly change 40 years ago. At the same time, though, in a certain sense, it could be thought of as all in our genes. That’s the topic of my next video The Thrifty Gene Theory: Survival of the Fattest.

    This is the second in an 11-video series on the obesity epidemic. If you missed the first one, check out The Role of Diet vs. Exercise in the Obesity Epidemic. 



    Source link

  • Processed Foods and Obesity 

    Processed Foods and Obesity 

    The rise in the U.S. calorie supply responsible for the obesity epidemic wasn’t just about more food, but a different kind of food.

    The rise in the number of calories provided by the food supply since the 1970s “is more than sufficient to explain the US epidemic of obesity.” Similar spikes in calorie surplus were noted in developed countries around the world in parallel with and presumed to be primarily responsible for, the expanding waistlines of their populations. After taking exports into account, by the year 2000, the United States was producing 3,900 calories for every man, woman, and child—nearly twice as much as many people need. 

    It wasn’t always this way. The number of calories in the food supply actually declined over the first half of the twentieth century and only started its upward climb to unprecedented heights in the 1970s. The drop in the first half of the century was attributed to the reduction in hard manual labor. The population had decreased energy needs, so they ate decreased energy diets. They didn’t need all the extra calories. But then the “energy balance flipping point” occurred, when the “move less, stay lean phase” that existed throughout most of the century turned into the “eat more, gain weight phase” that plagues us to this day. So, what changed?

    As I discuss in my video The Role of Processed Foods in the Obesity Epidemic, what happened in the 1970s was a revolution in the food industry. In the 1960s, most food was prepared and cooked in the home. The typical “married female, not working” spent hours a day cooking and cleaning up after meals. (The “married male, non-working spouse” averaged nine minutes, as you can see below and at 1:34 in my video.) But then a mixed-blessing transformation took place. Technological advances in food preservation and packaging enabled manufacturers to mass prepare and distribute food for ready consumption. The metamorphosis has been compared to what happened a century before with the mass production and supply of manufactured goods during the Industrial Revolution. But this time, they were just mass-producing food. Using new preservatives, artificial flavors, and techniques, such as deep freezing and vacuum packaging, food corporations could take advantage of economies of scale to mass produce “very durable, palatable, and ready-to-consume” edibles that offer “an enormous commercial advantage over fresh and perishable whole or minimally processed foods.” 

    Think ye of the Twinkie. With enough time and effort, “ambitious cooks” could create a cream-filled cake, but now they are available around every corner for less than a dollar. If every time someone wanted a Twinkie, they had to bake it themselves, they’d probably eat a lot fewer Twinkies. The packaged food sector is now a multitrillion-dollar industry.

    Consider the humble potato. We’ve long been a nation of potato eaters, but we usually baked or boiled them. Anyone who’s made fries from scratch knows what a pain it is, with all the peeling, cutting, and splattering of oil. But with sophisticated machinations of mechanization, production became centralized and fries could be shipped at -40°F to any fast-food deep-fat fryer or frozen food section in the country to become “America’s favorite vegetable.” Nearly all the increase in potato consumption in recent decades has been in the form of french fries and potato chips. 

    Cigarette production offers a compelling parallel. Up until automated rolling machines were invented, cigarettes had to be rolled by hand. It took 50 workers to produce the same number of cigarettes a machine could make in a minute. The price plunged and production leapt into the billions. Cigarette smoking went from being “relatively uncommon” to being almost everywhere. In the 20th century, the average per capita cigarette consumption rose from 54 cigarettes a year to 4,345 cigarettes “just before the first landmark Surgeon General’s Report” in 1964. The average American went from smoking about one cigarette a week to half a pack a day.

    Tobacco itself was just as addictive before and after mass marketing. What changed was cheap, easy access. French fries have always been tasty, but they went from being rare, even in restaurants, to being accessible around each and every corner (likely next to the gas station where you can get your Twinkies and cigarettes).

    The first Twinkie dates back to 1930, though, and Ore-Ida started selling frozen french fries in the 1950s. There has to be more to the story than just technological innovation, and we’ll explore that next.

    This explosion of processed junk was aided and abetted by Big Government at the behest of Big Food, which I explore in my video The Role of Taxpayer Subsidies in the Obesity Epidemic.

    This is the fifth video in an 11-part series. Here are the first four: 

    Videos still to come are listed in the related videos below.



    Source link

  • Do Taxpayer Subsidies Play a Role in the Obesity Epidemic? 

    Do Taxpayer Subsidies Play a Role in the Obesity Epidemic? 

    Why are U.S. taxpayers giving billions of dollars to support the likes of the sugar and meat industries?

    The rise in calorie surplus sufficient to explain the obesity epidemic was less a change in food quantity than in food quality. Access to cheap, high-calorie, low-quality convenience foods exploded, and the federal government very much played a role in making this happen. U.S. taxpayers give billions of dollars in subsidies to prop up the likes of the sugar industry, the corn industry and its high-fructose syrup, and the production of soybeans, about half of which is processed into vegetable oil and the other half is used as cheap feed to help make dollar-menu meat. You can see a table of subsidy recipients below and at 0:49 in my video The Role of Taxpayer Subsidies in the Obesity Epidemic. Why do taxpayers give nearly a quarter of a billion dollars a year to the sorghum industry? When was the last time you sat down to some sorghum? It’s almost all fed to cattle and other livestock. “We have created a food price structure that favors relatively animal source foods, sweets, and fats”—animal products, sugars, and oils.

    The Farm Bill started out as an emergency measure during the Great Depression of the 1930s to protect small farmers but was weaponized by Big Ag into a cash cow with pork barrel politics—including said producers of beef and pork. From 1970 to 1994, global beef prices dropped by more than 60 percent. And, if it weren’t for taxpayers “sweetening the pot” with billions of dollars a year, high-fructose corn syrup would cost the soda industry about 12 percent more. Then we hand Big Soda billions more through the Supplemental Nutrition Assistance Program (SNAP), formerly known as the Food Stamps Program, to give sugary drinks to low-income individuals. Why is chicken so cheap? After one Farm Bill, corn and soy were subsidized below the cost of production for cheap animal fodder. We effectively handed the poultry and pork industries about $10 billion each. That’s not chicken feed—or rather, it is! 

    This is changing what we eat. 

    As you can see below and at 2:03 in my video, thanks in part to subsidies, dairy, meats, sweets, eggs, oils, and soda were all getting relatively cheaper compared to the overall consumer food price index as the obesity epidemic took off, whereas the relative cost of fresh fruits and vegetables doubled. This may help explain why, during about the same period, the percentage of Americans getting five servings of fruits and vegetables a day dropped from 42 percent to 26 percent. Why not just subsidize produce instead? Because that’s not where the money is. 

    “To understand what is shaping our foodscape today, it is important to understand the significance of differential profit.” Whole foods or minimally processed foods, such as canned beans or tomato paste, are what the food business refers to as “commodities.” They have such slim profit margins that “some are typically sold at or below cost, as ‘loss leaders,’ to attract customers to the store” in the hopes that they’ll also buy the “value-added” products. Some of the most profitable products for producers and vendors alike are the ultra-processed, fatty, sugary, and salty concoctions of artificially flavored, artificially colored, and artificially cheap ingredients—thanks to taxpayer subsidies. 

    Different foods reap different returns. Measured in “profit per square foot of selling space” in the supermarket, confectionaries like candy bars consistently rank among the most lucrative. The markups are the only healthy thing about them. Fried snacks like potato chips and corn chips are also highly profitable. PepsiCo’s subsidiary Frito-Lay brags that while its products represented only about 1 percent of total supermarket sales, they may account for more than 10 percent of operating profits for supermarkets and 40 percent of profit growth. 

    It’s no surprise, then, that the entire system is geared towards garbage. The rise in the calorie supply wasn’t just more food but a different kind of food. There’s a dumb dichotomy about the drivers of the obesity epidemic: Is it the sugar or the fat? They’re both highly subsidized, and they both took off. As you can see below and at 4:29 and 4:35 in my video, along with a significant rise in refined grain products that is difficult to quantify, the rise in obesity was accompanied by about a 20 percent increase in per capita pounds of added sugars and a 38 percent increase in added fats. 

     

    More than half of all calories consumed by most adults in the United States were found to originate from these subsidized foods, and they appear to be worse off for it. Those eating the most had significantly higher levels of chronic disease risk factors, including elevated cholesterol, inflammation, and body weight. 

    If it really were a government of, by, and for the people, we’d be subsidizing healthy foods, if anything, to make fruits and vegetables cheap or even free. Instead, our tax dollars are shoveled to the likes of the sugar industry or to livestock feed to make cheap, fast-food meat. 

    Speaking of sorghum, I had never had it before and it’s delicious! In fact, I wish I had discovered it before How Not to Diet was published. I now add sorghum and finger millet to my BROL bowl which used to just include purple barley groats, rye groats, oat groats, and black lentils, so the acronym has become an unpronounceable BROLMS. Anyway, sorghum is a great rice substitute for those who saw my rice and arsenic video series and were as convinced as I am that we need to diversify our grains. 

    We now turn to marketing. After all of the taxpayer-subsidized glut of calories in the market, the food industry had to find a way to get it into people’s mouths. So, next: The Role of Marketing in the Obesity Epidemic. 

    We’re about halfway through this series on the obesity epidemic. If you missed any so far, check out the related videos below.



    Source link

  • Marketing Takes Off and Obesity Soars 

    Marketing Takes Off and Obesity Soars 

    The unprecedented rise in the power, scope, and sophistication of food marketing starting around 1980 aligns well with the blastoff slope of the obesity epidemic.

    In the 1970s, the U.S. government went from just subsidizing some of the worst foods to paying companies to make more of them: “Congress passed laws reversing long-standing farm policies aimed at protecting prices by limiting production” and started giving payouts in proportion to output. Extra calories started pouring into the food supply.

    Then Jack Welch gave a speech. In 1981, the CEO of General Electric effectively launched the “shareholder value movement,” reorienting the primary goal of corporations towards maximizing short-term returns for investors. This placed extraordinary pressure from Wall Street on food companies to post increasing profit growth every quarter to boost their share price. There was already a glut of calories on the market and now they had to sell even more.

    This placed food and beverage CEOs in an impossible bind. It’s not like they’re rubbing their sticky hands together at the thought of luring more Hansels and Gretels to their doom in their houses of candy. Food giants couldn’t do the right thing even if they wanted. They are beholden to investors. If they stopped marketing to kids or tried to sell healthier food or did anything else that could jeopardize their quarterly profit growth, Wall Street would demand a change in management. Healthy eating is bad for business. It’s not some grand conspiracy; it’s not even anyone’s fault. It’s just how the system works.

    As I discuss in my video The Role of Marketing in the Obesity Epidemic, given the constant demands for corporate growth and rapid returns in an already oversaturated marketplace, the food industry needed to get people to eat more. Like the tobacco industry before them, it turned to the ad makers. The food industry spends about $10 billion a year on advertising and around another $20 billion on other forms of marketing, such as trade shows, consumer promotions, incentives, and supermarket “slotting fees.” Food and beverage companies purchase shelf space from supermarkets to prominently display their most profitable products. They pay supermarkets. The practice is also known as “cliffing,” because companies “force suppliers to bid against each other for shelf space with the loser pushed ‘over the cliff.’” With slotting fees costing up to $20,000 per item, per retailer, and per city, you can imagine what types of foods get the special treatment. Hint: It ain’t broccoli.

    To get a sense of what kind of products merit prime shelf real estate, look no further than the checkout aisle. “Merchandising the power categories on every lane is critical,” reads a trade publication on the “best practices for superior checkout merchandising.” It was referring to candy bars and beverages. Just a 1 percent power category boost in sales could earn a store an extra $15,000 a year. It’s not that publicly traded companies don’t care about their customers’ health. They might, but like most of the leading grocery store chains, their “primary fiduciary responsibility is to increase profits” above other considerations.

    For instance, tens of millions of dollars are spent annually advertising a single brand of candy bar. McDonald’s alone may spend billions a year. Now, “the food industry is the biggest spender on advertising of any major sector of the economy.”

    “Reagan-era deregulatory policies removed limits on television marketing of food products to children.” Now, the average child may see more than 10,000 TV food ads a year, and that’s on top of “the marketing content online, in print, at school, at the movies, in video games, or at school,” or even on their phones. “Nearly all food marketing to children worldwide promotes products that can adversely affect their health.”

    Besides the massive early exposure and ubiquity, food marketing has become “highly sophisticated. With the help of child psychologists, companies began to understand the factors that unconsciously influenced sales. They found out, for example, how to influence children and get them to manipulate their parents.” Packaging was designed to best attract a child’s attention, and then those products are placed at their eye level in the store. You know those mirrored bubbles in the ceilings of supermarkets? They aren’t just for shoplifters. Closed-circuit cameras and GPS-like devices on shopping carts are used to strategize how best to guide shoppers toward the market’s most profitable products. Behavioral psychology is widely applied to increase impulse buying, and eye movement tracking technologies are utilized.

    The “unprecedented expansion in the scope, power, and ubiquity of food marketing…coincided with an unprecedented expansion in food consumption in predictable ways.” Some techniques have “skyrocket[ed] from essentially zero to multi-billion-dollar industries” since the 1980s, including “product placement, in-school advertising, event sponsorships.” This led one noted economist to conclude that “the most compelling single interpretation of the admittedly incomplete data we have is that the large increase in obesity is due to marketing.” Yes, innovations in manufacturing and political maneuvering led to a food supply bursting at the seams with close to 4,000 calories a day for us all, but it’s the advances in marketing manipulations that try to peddle that surplus into our mouths. 

    I think the natural reaction to the suggestion of the power of marketing is: I’m too smart to fall for that. Marketing works on other people, but I can see through it. But that’s what everyone thinks! For a splash of cold water to shake us all out of this delusion, I next bring you some data: The Role of Food Advertisements in the Obesity Epidemic. 

    Also, for both the role of marketing and food advertisements, check out Friday Favorites: The Role of Marketing and Food Advertisements in the Obesity Epidemic.

    This is the seventh in an 11-video series. If you missed any of the first six, check out the related posts below. 



    Source link