Diet
Deconstructing Obesity: A New Perspective
Mounting evidence suggests a link to threat load.
Posted February 21, 2023 Reviewed by Hara Estroff Marano
Key points
- Obesity is more than excess eating.
- What one eats is important, and starvation is not a cure.
- There are different phenotypes of obesity.
- Toxic obesity, accompanied by metabolic and other disorders, is associated with chronic threat.
Fundamentally, obesity is an excess of fat. The excess fat can have adverse effects on quality of life, health, and longevity. Obesity is associated with an increased incidence of type 2 diabetes, kidney disease, cardiovascular disease, autoimmune disease, dementia, mental illness, and cancer. Obesity is a major risk factor for faring poorly with a Covid-19 infection, including increased risk of hospitalization and Long Covid and much higher risk of death.
In addition to the effects on quality of life, health and longevity, obesity is expensive. Per the CDC, the population cost of obesity in the United States now exceeds $180 billion annually.
Being overweight or obese in the United States is so common it has become a norm and is being normalized. Are we failing to affect this pandemic due to a misunderstanding of the cause of the condition, thus leading to ineffective interventions?
Our historical belief is that obesity is caused by taking in too many calories—eating too much—and not expending enough calories—lack of activity or exercise. This model has some merit, and eating a lot and lack of activity add weight as fat.
Researchers are now trying to figure out different types—phenotypes—of obesity. They have characterized the “hungry gut,” in which the gut doesn’t know when to stop eating; the “hungry brain,” in which the brain doesn’t know when to stop eating; “the emotional eater,” for whom food provides comfort; and the “low-energy expender,” who doesn’t burn enough calories. Three of the four types represent too many calories in, while the fourth represents not enough calories out.
These classifications are likely to spur considerable search of our genetics to define the types by differences in DNA. There are likely to be pills and procedures designed to work on the gut, brain, and the emotional and metabolic networks
Historical practices for weight reduction have included starvation diets that deplete the body and lower the metabolic rate, placing people at risk for illness and rebound weight gain.
Additionally, pharmacologic, procedural and surgical manipulation of the gastrointestinal system has been used for weight loss. The strategies make eating uncomfortable and absorption of calories and nutrients difficult. Although weight loss is achieved with such fewer-calorie-in interventions, they have significant risks to overall health and quality of life and poor long term outcomes.
What if the calories-in versus calories-out strategy is wrong?
Japanese sumo wrestlers notoriously eat a lot and carry a high proportion of fat relative to height. They qualify as obese and yet they don’t suffer from the multitude of comorbidities that the overweight U.S. population suffers from. Acknowledging this difference allows us to conclude that obesity has different forms, and calories-in in excess of calories-out is inadequate to define the illnesses and diseases of the obese.
What is it that distinguishes toxic from nontoxic obesity?
The American diet has a role to play in the obesity pandemic. Foods high in salt, sugar, and animal proteins bias our systems towards inflammation, fat storage, illness, and disease. One particular sugar, fructose, is an additive in many of our processed foods and it is particularly problematic.
From an evolutionary perspective, high fructose intake from ripened fruits in the late summers and early fall signaled our bodies to store fat to prepare for harsh and scarcely resourced winters. High fructose intake was historically cyclical and of short duration. Whereas, in the modern world, fructose is in a constant and excessive supply.
The ability of fructose to signal fat storage is different than the caloric content of fructose. Fructose is unique as a sugar in its ability to signal fat storage. In addition, all sugar intake stimulates the release of insulin, which subsequently promotes the storage of fat as well.
It isn’t just calories-in versus calories-out but the type of foods that can determine fat accumulation, as well.
The parts of our country that suffer the most from obesity are the poorer indigenous, rural, and urban communities where whole organic foods are rare. Cheaper, processed, high-salt and -sugar edible (foods?) are the norm in these communities. That’s a problem for health.
However, there is more to the obesity problem than lack of exercise, excess consumption, and a terrible diet.
These same communities that disproportionately suffer from obesity have much else in common— limited educational opportunities, restricted job opportunities, societal disenfranchisement, and financial stress, if not abject poverty. These communities live with chronically high threat loads.
A high threat load is correlated with the illnesses and diseases that are the comorbidities of obesity.
Could this high threat load actually cause obesity, as well?
The threat response modifies and interprets our genetic code to express a phenotype that tells us to eat easily digestible, sugary and salty foods and alters gut, brain, emotional, and metabolic functions. In severe or chronically sustained threat,the threat response will lower our activity and metabolism to conserve energy and protect us from a harsh and scarcely resourced world.
At the same time, the threat response increases inflammation and insulin resistance within the body. The threat response impairs the cell’s metabolism of fat and facilitates the accumulation of fat. Every cell in the body changes its phenotype within a threat response, so we, as whole human beings, change our phenotype, too. Threat can make us ill, diseased, and fat.
If we want to cure obesity and all of its comorbidities, we can search the genome for the phenotypes of obesity. But perhaps a better strategy is to understand the phenotypes of threat versus safety and their relationship to obesity.
The best strategy to use against obesity may be to reduce actual threat and increase safety within the U.S. and the world—provide clean air, water, and soil to grow whole, unprocessed foods and nourish people; educational and job opportunities to re-enfranchise the forgotten and discriminated against; a social safety net below which no one can fall, with child care, elder care, health care, basic income, and secure housing. Peace on earth would be nice, too.
Reflecting on the Japanese sumo wrestlers who qualify as obese yet lack the illnesses and diseases associated with obesity requires us to consider how the wrestlers differ from the obese in the United States. Japan is regarded as the safest country with the best health and greatest longevity in the world. Maybe weight is the wrong target?
Yes, we can still work on balancing calories in versus calories out, but what we really need is to weight the scale heavily towards safety versus threat to impact the pandemic of obesity.
References
CDC, National Center for Chronic Disease Prevention and Health Promotion, Division of Nutrition, Physical Activity and Obesity.
Monostra, M. Phenotyping, genetics hold keys to precision medicine in obesity treatment. Healio.com. 2023 Feb 16.
Johnson RJ, Tolan DR, Bredesen D, Nagel M, Sánchez-Lozada LG, Fini M, Burtis S, Lanaspa MA, Perlmutter D. Could Alzheimer’s Disease Be a Maladaptation of an Evolutionary Survival Pathway Mediated by Intracerebral Fructose and Uric acid Metabolism?. The American Journal of Clinical Nutrition. 2023 Jan 11.
Lustig RH, Mulligan K, Noworolski SM, Tai VW, Wen MJ, Erkin‐Cakmak A, Gugliucci A, Schwarz JM. Isocaloric fructose restriction and metabolic improvement in children with obesity and metabolic syndrome. Obesity. 2016 Feb;24(2):453-60.
Naviaux RK. Perspective: Cell danger response Biology—The new science that connects environmental health with mitochondria and the rising tide of chronic illness. Mitochondrion. 2020 Mar 1;51:40-5.