Obesity is a threat to U.S. national security, obesity is the leading medical reason why applicants fail to qualify for military service:
27% of young people aged 17 to 24 are too obese to serve in the armed forces.
Over the last 10 years, the number of states with 40 percent of young adults considered by the CDC to be overweight or obese has risen from one state to 39.
Sensory-specific satiety: the relationship between perceived taste and quantity consumed of food.
As individuals consume more of a food item, they experience diminishing marginal taste perception, which means their level of perceived taste from additional consumption tends to decline (additional consumption becomes less pleasurable). The first bite of chocolate is better than the 10th.
In this study, researchers found that ratings went down after each piece of chocolate consumed with no significant difference in taste perceptions between normal and overweight participants reported. However, participants with obesity had higher levels of initial taste perception, rated subsequent pieces higher than their counterparts without obesity, and their ratings declined at a more gradual rate compared to participants with normal weight and those with obesity.
There is no significant difference in the actual taste perceptions, between those of normal weight and those who are overweight. However, participants with obesity have a greater initial satisfaction from food, which then decreases more gradually. To me, this suggests a significant pleasure or hedonic component to food, consistent with an addiction model of obesity.
Variations in Marginal Taste Perception by Body Mass Index Classification: A Randomized Controlled Trial. Journal of the Academy of Nutrition and Dietetics, 2019.
The experts in processed food addiction in Big Food often manipulate sensory-specific satiety to increase product sales.
It’s the explanation for the phenomenon of “I’m too stuffed to eat another bite. What’s for dessert?” or the 1960’s Lay’s advert “Betcha can’t eat just one!” in which you would eat the whole can of chips.
According to a “NEW” study published in Obesity, “lifestyle interventions focused on altering dietary and physical activity habits using behavioral strategies can produce sustained weight loss among African Americans and Hispanics who have type 2 diabetes (T2D)” Which ivory tower have they been living in or is this new information to their sources of funding?
Maybe some of these researchers could come to visit outpatient clinics that have been successfully doing this for 20 plus years.
Pharmaceuticals have only a short-term role in a long-term lifestyle and behavioral issue.
Bariatric surgery is an induced dietary restriction and malabsorption syndrome, patients often overheat the restriction with liquid calories or develop such significant malabsorption that they develop secondary complications .
I treat obesity, exactly the same as I treat addiction.
The only intervention I have ever found to be successful in the long term was providing the patient with behavioral management tools in altering habits (using substitution and harm reduction), and then a re-education of what was truly “healthy” (and that didn’t include starting the day with a bowl of cereal and skim milk.
In a busy clinical practice, a brief direct interaction, providing just in time information that is “doable” is the only thing that I have found useful. The more esoteric the information or the more complicated the protocol, the worse the adherence.
Download our entire protocol for free on the profile page.
Weight Loss Experiences of African American, Hispanic, and Non‐Hispanic White Men and Women with Type 2 Diabetes: The Look AHEAD Trial. Obesity, 2019; 27 (8): 1275
Obesity doesn’t cause metabolic syndrome; obesity is a marker for metabolic syndrome.
Sugar addiction, especially glucose, leads to obesity because of how it is metabolized. Sucrose (table sugar) is a disaccharide made of 50% fructose and 50% glucose. Sucrose is metabolized primarily in the small intestine, releasing equal parts glucose and fructose. Glucose causes insulin release and is rapidly cleared from the bloodstream by insulin-dependent channels. Fructose is independent of insulin and is rapidly taken up by the liver by a first-pass effect and is preferentially stored as fat.
Further increasing obesity risks, glucose and fructose have different effects on the addiction centers in the brain. Although glucose does not directly activate the brain’s reward center, fructose does produce activation in the brain’s “reward circuit,” and increases the desire for food.
American College of Neuropsychopharmacology. “Fructose and glucose: Brain reward circuits respond differently to two kinds of sugar.” ScienceDaily. ScienceDaily, 10 December 2014. www.sciencedaily.com/releases/2014/12/141210080734.htm
Metabolic syndrome is an early indicator of diabetes even among people of normal weight, and it’s important to take steps to prevent and treat it. During the early phase of metabolic syndrome, the body is compensating for insulin resistance by increasing insulin production to maintain near-normal blood glucose levels. However, when the pancreas and liver overflow with fat from the chronic high insulin levels (the fat-storage hormone), there is a sudden change. Hyperinsulinemia can no longer keep up with the pace of insulin resistance, and the pancreatic beta cells, responsible for insulin production, are also unable to keep up. As this compensatory mechanism fails, the blood glucose rises quickly. It takes only two years or so before the beta cells begin to fail and full-blown type 2 diabetes is diagnosed.
The diagnosis of type 2 diabetes exists on a spectrum. It goes from healthy to metabolic syndrome (with or without obesity) to prediabetes to diabetes. Almost all individuals who are type 2 diabetic for a period of time and treated with insulin become obese due to the fat storage caused by insulin and remain so until they get a secondary complication. However, the metabolic syndrome that precedes the frank diagnosis of diabetes can exist even in normal-weight individuals. The key is preventing metabolic syndrome, whether caused purely by carbohydrate overconsumption or by vegetable oil omega-6 consumption because it will eventually lead to Type 2 Diabetes.
This protocol is relevant for patients who have metabolic syndrome with or without obesity, as they are both risk factors for type 2 diabetes.
Not all food is created equal, and some are even more (ultra) processed than others, thus contributing to gut dysfunction. The purpose of ultra-processing food is to create branded, convenient (durable, ready to consume), attractive (hyper-palatable), and profitable (low-cost ingredients) food products.
Ultra-processed food is made from food-like substances and additives, with little intact natural food. These ingredients are not normally used in natural culinary preparations.
Additives include preservatives, antioxidants, and stabilizers to reduce normal degradation and lengthen shelf life. Some additives enhance the sensory qualities of foods or disguise unpalatable aspects of the final product (dyes and other colors, color stabilizers, flavors, flavor enhancers, non-sugar sweeteners). Processing additives (such as carbonating, firming, bulking, and anti-bulking, de-foaming, anti-caking, and glazing agents, emulsifiers, sequestrants, and humectants) increase gut permeability. Processing with heat extrusion can create de novo compounds, some of which are carcinogens. The preparation and milling of food into shelf-stable acellular materials increases the rapidity of gut absorption, contributing to hepatic dysfunction.
Ultra-processed foods makeup 57.9% of dietary intake and contribute 89.7% of the energy intake from added sugars. These empty-calorie foods contain minimal bioavailable essential nutrients and displace more nutrient-dense foods, which leads to an overfed and yet undernourished population.
Consuming ultra-processed food leads to metainflammation through gut dysfunction. Metainflammation is the root cause of most diseases of Western civilization: obesity, diabetes, heart disease, cancer, cognitive decline, autoimmune dysfunction, and chronic pain.
For years, fat has been targeted as one of the main causes of obesity, but fat in someone’s diet isn’t what makes someone fat. The diet-heart hypothesis falsely attributed eating fat with the development of atherosclerotic heart disease. This anti-lipid agenda led to the low-fat craze, which replaced fat with tasty acellular carbohydrates, paradoxically resulting in a dramatic rise in the obesity rate and a worsening of heart disease, obesity, and diabetes.
Reducing fat intake is not the key to reducing obesity. Re-examining macronutrients in the diet as well as understanding satiety (feeling full) and controlling food intake is the key.
Replacing carbohydrates with avocado increased feelings of satiety, and this was caused primarily by PYY, a peptide hormone secreted by cells lining the ileum and the colon. PYY decreases food intake by inhibiting gut motility, acting as an “ileal brake” to cause a sense of satiety. According to the National Institutes of Health, “replacing carbohydrate with fats and fibers derived from avocados without increasing energy or energy-density enhanced the satiety value of meals in overweight and obese individuals as evidenced by greater hunger suppression.”
Conclusion:
Fat is a potent stimulator of PYY, enhancing satiety and reducing motivation to eat, keeping you full for 6-8 hours. By contrast, carbohydrates increase motivation to eat and don’t significantly increase PYY. Carbohydrates increase insulin, and in obese individuals cause reactive hypoglycemia, making them hungry in 2-3 hours.
That’s why people on whole natural food diets that are higher in fat tend to weigh less and have less heart disease and diabetes.
Lanjun Zhu, et al. Nutrients, 2019; 11 (5): 952
Foods made to taste exceptionally good (hyperpalatable) through combining high fat and high sugar can also lead to behavioral addiction, which can lead to obesity.
Hyperpalatable foods can produce an addiction‐like syndrome. Animals presented with either high‐sugar or high‐fat diets eat excessively but do not gain weight as they offset the increased intake by eating less. It is only the high fat and sugar combination that causes weight gain.
We believe that the obese patients’ relationship to food is more similar to a behavioral addiction like pathological gambling rather than a classic substance addiction, but there is no clear-cut withdrawal mechanism. With “food addiction,” according to the National Institutes of Health, there is a “harmful use that is maladaptive but does not meet the criteria for dependence.” The refeeding cycle is driven by external cues, anticipatory cues, pancreatic training, and loss of fat metabolism adaptation. Specific nutrients do, however, cause an endorphin activation and a neurochemical effect in the brain.
Do you think smoking or obesity would have a higher hazard ratio? When looked at in context, the answer might surprise you. Hazard ratio (HR) is the ratio of the hazard rates corresponding to the conditions described by two levels of an explanatory variable. The HR has also been defined as the ratio of (risk of outcome in one group)/(risk of outcome in another group), occurring at a given interval of time. In the situation where the hazard for an outcome is exactly twice in Group A than in Group B, the value of the hazard ratio would be 2.0.
If I told you that a completely man-made and preventable plague was spreading across the United States and would affect 75% of the population within twenty years, causing countless deaths and cost over $215 billion per year, you might pay attention. Like most epidemics, obesity is accelerating and now affects 17% of all children and adolescents in the United States — triple the rate from just one generation ago.
Obese children are more likely to become obese adults and carry a significantly higher negative lifetime economic and medical burden. If you are overweight or obese, there is a 90% chance you will develop type 2 diabetes; yet, if you smoke for 30-40 years, you have a 10-17% chance of developing lung cancer.
If asked which they were most afraid of, being overweight or smoking, most people would likely think smoking is more deadly. (This is not intended to suggest smoking is beneficial; it’s intended to frame the issue in context.)
In the not-too-distant future, I predict that vegetable oils, refined carbohydrates, and grain-based products will be viewed with the same disdain as cigarette smoking is.