The Cause and Cure of Overweight and Obesity Prevalence in the USA

Authors: Gary Smith and Keith Belk, Colorado State University

For decades, the medical profession has considered “Obesity” a “Risk Factor”—not a stand-alone disease—and primarily used Body Mass Index (BMI) to diagnose Obesity.¹ In January 2025, a consensus statement in The Lancet Diabetes & Endocrinology formally recognized “Clinical Obesity” as a chronic, systemic, medical disease, and defined it as, “when extra body fat starts to harm organ functions and limit the activities of daily life”.² A “clinical” disease is “a disease founded on actual observation and treatment of patients, as distinguished from theoretical or basic sciences”.³

Clinical Obesity is different from just carrying extra weight; it is directly detrimental to personal health, and much more than just a Risk Factor for predicting development of other chronic diseases.² In the early 1900s, human-health experts believed there was an “Obesity Sextette” (later called the “Metabolic Syndrome”) that was collectively responsible for causing heart disease, diabetes, high blood pressure, arteriosclerosis, stroke, breathing problems, osteoarthritis, gallstones, and some cancers.^4,5 By 2024, Centers for Disease Control and Prevention was calling “Obesity” both a “chronic disease” and a “Risk Factor”—putting people at risk for a plethora of other chronic diseases.⁶ 

BMI is currently the main way to diagnose Obesity, but it neither differentiates between fat and lean mass nor captures variations in body composition and fat distribution.¹ As a result, BMI-based definitions of Obesity may inaccurately estimate actual adiposity among diverse age groups and ethnic populations as well as between men and women.^1,2 A report in The Journal of Clinical Endocrinology & Metabolism shows that the strength of a person’s handshake is a powerful early sign of a person’s risk of developing Obesity-induced organ dysfunction.¹ We must make sure that our diagnoses and treatments for Obesity focus on long-term health.^1,2 

Where are we now? In 1950, 3% of Americans were suffering from a chronic disease; in 1970, it was 11%; at present, it is 76.4%.⁷ Compared to every other country in the world: (a) we are the sickest; (b) we have the highest chronic disease burden; (c) we spend the most on health-care; and (d) we have the worst health outcomes.⁸ We’ve changed from “health-care” to “disease-care”.⁹ Having more of our citizens get sick and stay sick, financially benefits the health-care and pharmaceutical communities; that’s why we’ve morphed into a “sick-care”.⁹ The health-care system spends 8 out of 10 of its dollars treating preventable chronic diseases.¹⁰ We’re in a “War On Chronic Diseases”.¹¹ Obesity is far and away the worst chronic disease that affects Homo sapiens.¹² In 2024, 42.7% of Americans were obese and 32% were overweight.¹³ Bringing down Obesity will bring down almost all chronic diseases.¹⁴ 

When two of our nation’s finest human nutritionists were asked “What caused our Obesity epidemic, and what can we do to conquer it?” (a) Dr. Teresa Davis said: “I think Obesity can largely be explained by Energy-Imbalance, we take in more calories than we expend. We live in an obsogenic environment with continuous stimuli. However, our utilization of the nutrients we consume can be affected by a number of factors, including hormones (predominantly Insulin and Glucagon) and…now…GLP-1s.”¹⁵ (b) Dr. Marc Siegel said: “We lack self-control in what and how often we eat; as a result, we eat too much—especially excessive amounts of ultra-processed food. Our “work” is too sedentary; we don’t exercise enough; we don’t sleep enough; and our bodies don’t produce enough Glucagon.”¹⁶ 

In its list of “Dominant Causes” of childhood Obesity, the American Academy of Pediatrics includes diet, physical activity, and socioeconomic factors (i.e., the poor, disadvantaged, incapacitated, or those under emotional duress).^17,18 Prevalence of overweight and Obesity is 73% among US adults (ages 20 years and older) and 36% among children/adolescents (ages 2 through 19 years).¹⁹ “Obesogenous” means “producing or causing Obesity”; exogenous Obesity is due to overeating while endogenous Obesity is due to metabolic (endocrine) abnormalities.³ The origin of the Energy-Balance postulate lies somewhere in the 1800s and was based on the folklore that “eating too much fat causes a person to be fat.”³ By 1930, it was settled science that those who became obese did so solely because they were lazy, gluttonous, or hedonistic; over-ate or under-exercised; and consequentially took in more calories than they spent.^20,21 

The Energy-Balance model seems simple enough… “Don’t Take In More Calories Than You Spend: Eat Less; Exercise More.” Sounds easy to do; however, it is analogous to those obligatory New Year’s resolutions that last until January 10, in a good year.²² Abiding by a rule that is construed by some as totally intrusive and unsatisfactory and becomes an exercise in futility over the long term.²² When we eat food, we are fulfilling physical and chemical needs for fuel (to produce energy for heat, power, strength, and stamina), replenishment (to replace biochemical and structural components), and mental stability (to assure psychological order of the mind and behavior).²³ The problem is: We don’t know when we’ve eaten enough…but not too much. It’s too easy to start, to continue…and too hard to stop. The eventual solution to the Obesity conundrum rests in taking those decisions out of conscious control.²⁴ 

Attributing Obesity to “overeating” is as meaningless as accounting for alcoholism by ascribing it to “overdrinking”; it transforms a physiological disorder into a behavioral disorder… a character flaw.²⁵ Energy-Balance is difficult to successfully monitor, measure, and manage. “The Father of Statistical Process Control”, W. Edwards Deming is credited with saying, “You can’t manage what you don’t measure”,²⁶ but he did not.²⁷ What he actually said was, “It’s wrong to suppose that if you can’t measure it you can’t manage it; measurement is valuable but over-reliance on metrics can blind you from what really matters.²⁷ Even if you weigh yourself on a bathroom weight-scale, keep daily records, and modify your eating and exercising habits, it’s very difficult to correctly gauge how much less…or more…of each habit you need to manage. It’s a delicate balance; too much exercise may cause you to eat too much.^{28,29,30,31,32} The margin of error is very narrow; overshooting on average by just 10 calories a day—the calories in a single potato chip—translates into gaining a pound of fat yearly, 10 pounds of fat per decade will transform anyone from lean, to obese.²⁵ 

Marc Siegel believes that: (a) To a very large extent, Obesity is caused by the lack of willpower to play by the rules. (b) If you can get to “Net Zero” on the Energy-Balance scale, you won’t get heavier or fatter. (c) Our problem is that we have a hereditary predilection to refuse to eat less or exercise more; we’re always looking for a way to cheat. (d) Anyone who wants to escape Obesity must have energetic resoluteness.^16,33 

Teresa Davis believes that: (a) Perhaps Obesity is not just an Energy-Balance disorder—it is because there are “good calories” and “bad calories”. (b) If the calories you consume come from fat and protein, your pancreas produces Glucagon, and you don’t increase production of Insulin. (c) If your calories come from carbohydrates, you produce Insulin, which sends blood sugar to depots of adipose tissue, and you get fatter. (d) Two hormones control our “urge to eat”; Ghrelin increases appetite and leads to weight gain while Leptin suppresses appetite and contributes to weight loss.^{15,18,34,35,36,37}

Obesity occurs because of biological and behavioral events generated by genetic, mental, and circumstantial (sociodemographic and socioeconomic) factors. What Dr. Siegel says about exogenous Obesity is correct, and so is what Dr. Davis says about endogenous Obesity.^15,16 The nexus of their opinions resides in differentiating between “Good” vs. “Bad” calories (Biological) and between “Good” and “Bad” personal food choices (Behavioral). Neither Dr. Siegel nor Dr. Davis discussed the genetic component of Clinical Obesity.

Obesity has a heritability of 30 to 70%; obese children have a 50 to 85% chance of being an obese adult if one or both parents is/are obese.^38,39,40 It’s higher if the mother is the obese parent because there are more ways biological defects can be passed along and so can parental behavioral traits learned during the child’s adolescence.⁴¹ And, there are some people (e.g., those with an exceptionally high basal metabolic rate; citizens of South and East Asia) who don’t develop Obesity irrespective of what or how much they eat.^29,42 

Dietary Guidelines Advisory Committee data show significant disparities in prevalence of nutrition-related chronic health conditions between sociodemographic groups.¹⁹ Prevalence of obesity is: (a) lower among non-Hispanic Asian children and adults compared to all other racial and/or other ethnic groups; (b) lower among children with higher family income compared to those with lower family income; (c) lower among non-Hispanic Asian and higher in non-Hispanic Black adults; (d) higher among families with lower incomes compared to higher incomes, and (e) lower among adults with higher educational attainment (college or above) than those with lower educational attainment.¹⁹ Socioeconomic status (friends, relatives, communities, economical condition) affects rates of Obesity and early mortality.^43,44,45 

An analysis by the Washington Post of “Who’s Fault Is Obesity?” concluded that: (a) 61% of responsibility goes to the food industry which has developed product-after-product that was deliberately designed to be overeaten; (b) 20% goes to the combined effort of diet purveyors, university scientists, the media, and the federal government to tell us “what to eat” rather than “how much to eat”; and (c) 14% goes to consumers because we (the public) make every event and celebration in life an opportunity to eat too much, and to eat foods that are too rich in calories.⁴⁶ 

In 1999, leaders of the largest processed food companies met to discuss the consumption of craveable foods and the upturn in rates of Obesity; they’ve known for decades that sugary and salty foods are not good for us, yet none has ever changed the content of their “big sellers” (like Doritos® and Twinkies®).^5,47 “Big Food” has pulled all the levers to design processed food products to be addictive. They intentionally make ultra-processed foods as craveable as possible; they do this by including just enough sugar, salt, and crunchy texture to be craveable.^30,48,49,50 Our actual problem is that too much food is too readily available and too accessible.⁵⁰ 

Far too many food purveyors and marketers have exacerbated the problem by capitalizing on the frailty of the human predilection toward hedonism in designed “craveable” products.^51,52 Nutrition scientists have not served us well; almost everything they have told us about the content of a perfect diet has turned out to be wrong.^36,53,54 Too many university scientists have been complicit in giving disingenuous nutrition advice regarding carbohydrates, plant-based diets, and ultra-processed foods.^46,55,56 Our federal government misguided us.^36,57,58 The purpose of Dietary Guidelines For Americans (DGFA) was to hide the truth from the public…to protect the financial interests of “Big Food”.⁵² Following the tenets of the DGFA causes Obesity;^12,53,59 76% of SNAP (i.e., Food Stamps) beneficiaries are overweight or obese because they spend 17% of their Entitlements for soda, candy, and sweets.^36,60,61 

We live in a food carnival and food advertisements are everywhere; billboards, commercials, and celebrity advocates are used to make consumers see, think about, and crave specific food products.⁶² Aside from identified genetic causes of Obesity, almost all other “overeating” problems are behavioral and involve some elements of “personal choice” and food-form availability.⁶³ The “form” of food has changed from “raw” to “processed” and its availability has increased exponentially. Now, vending-machine foods, snacks, and ready-to-eat meals are available anytime, anywhere, and everywhere—and often delivered to your doorstep.⁶⁴ Our overeating problems originate from between-meal snacks, overly rich desserts, and celebratory events. We eat too many snacks.^{32,65,66,67,68} and we eat too much on holidays and at events.^{46,69,70,71,72} 

Following are some things that can be done to mediate the risk of becoming overweight/obese or to lose weight if you are already overweight/obese. (1) Find a better way than use of Body Mass Index to diagnose (and differentiate between) endogenous and exogenous Obesity.^1,29 Those who have endogenous Obesity should be directed to seek a physician’s help rather than trying to self-medicate.^73,74,75 Personalized nutrition advice is much more successful than general population-based dietary guidance in counteracting endogenous Obesity.^76,77 (2) Revise the definition of the Energy-Balance theorem to differentiate between Good and Bad calories as well as between Good and Bad personal food choices.^35,78,79 Simplistically, its admonition should be “Don’t take in more Bad calories than you expend”.^25,42 In actuality, the Bad calories are those that come from refined carbohydrates and sugars (especially sucrose and high-fructose syrups).^42,80,81 (3) Reconsider the merit of Keto Diets in light of the resurrection of DGFA 2025-2030’s approval to eat animal-sourced foods again.^82,83,84 The Low-Carb Diet (especially that of Dr. Atkins) has endured as the best way to lose excess body-fat and prevent obesity.^85,86,87 It’s very hard to overeat (i.e., eat too much) on a Keto Diet because the protein and fat in meat and dairy products promote satiety.^64,88,89 (4) Rethink our recent revisions of the DGFA that turned the original USDA Food Guide Pyramid upside down.^90,91 Consumers now have license to eat “Real Foods” taking advantage of the consumption of animal fats—which meter appetite and satiety as well as provide “Good” calories to fuel our needs for mental and physical energy.^84,92,93 And, we have entered an era in which the federal government’s dietary guidance (DGFA) is no longer almost solely to help Big Food sell what Big Food makes.^5,49,52,94 (5) Restrict the purchase of “Bad” food choices with Entitlement funds is supported by the FDA, the USDA, Republicans in the US Congress, the White House, State authorities, and others.^{36,79,95,96,97} When Entitlements started, 33% of US citizens were overweight or obese; now it’s 73%.⁷⁹ For SNAP alone, 12% of all Americans rely on Entitlements for their food purchases, and they spend 17% of government funds for soda, candy, and other sweets.^36,98,99,100 USDHHS Secretary Kennedy says, “People can eat or drink whatever they wish; we just don’t want to use taxpayer’s dollars to buy (via SNAP, WIC, School Meals, etc.) foods and beverages that we will have to pay-for later (via Medicare and Medicaid).^101,102 (6) Discourage consumption of “Bad” snacks, which is emphasized in DGFA 2025-2030.¹⁰³ Bad snacks called out as problematic are those containing excessive refined carbohydrates and/or sugar as well as those that are ultra- or highly processed.^36,104,105 There have been more than 15,000 observational research studies—all of them demonstrating that eating UDFs (many of which are snacks) is linked to Obesity and overall mortality.^106,107 Other researchers have attributed memory loss, brain health problems, and depression to consumption to UPFs.^108,109,110 Some are saying, don’t eat snacks unless they are made from animal-sourced foods^32,85,111 or fruits/vegetables.1¹² (7) The usefulness of depending on glucagon-like peptide-1 receptor agonists (GLP-1s) for the long-term solution of the Obesity problem is yet to be decided.^85,93,113 Generally, GLP-1s are effective treatments for Obesity and Type II Diabetes by suppressing appetite, quieting “Food Noise”, and inhibiting cravings,^85,114 or by slowing digestion, increasing feelings of fullness, and reducing hunger.^115,116 Consumers using GLP-1 drugs report feeling full faster, experiencing taste aversions to overly sweet and fatty foods, and adopting more structural or mindful eating patterns.¹¹⁷ The American Medical Association’s position on GLP-1s is that use of these agonists can lead to average weight losses of 15 to 20% and are a transformative option for obesity management in appropriately selected patients.¹¹⁸ The present USDHHS considers GLP-1s to be “another arrow in our quiver in the fight against Obesity”.¹¹⁹

The secret to finding a successful long-term treatment or diet is: It must allow a person to maintain a healthy body weight without having to endure hunger; then, and only then, will they be motivated enough to sustain it.⁸⁵