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What We Know About the Obesity Epidemic

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Person in red short with overweight stomachOver the last 50 years, global obesity rates have reached such alarming levels that words like “obesity epidemic” and even “pandemic” are being used by respected journals and international bodies like the World Health Organization (WHO) as they try to raise awareness in the public and healthcare sectors. According to the World Health Organization, there are more than two billion adults considered overweight or obese using the Body Mass Index (BMI) method of classification. That’s nearly 40% of adults in the world. Mexico has even more staggering statistics, with about seven out of ten (70%) of all adults classified as being overweight or obese.

What’s more concerning is that the rate has been rising steadily for years. According to the World Obesity Federation, the worldwide prevalence of obesity nearly tripled between 1975 and 2016. What’s more, they estimate the figure of 770 million adults who were affected by obesity in 2020 is anticipated to exceed one billion by 2030 unless action is taken.

What do we know about obesity?

Let’s first define how a person gets to be classified as ‘overweight’ or ‘obese.’

The Body Mass Index, or BMI, is the most commonly used measure of obesity. It is computed by dividing a person’s weight in kilograms by the square of their height in meters. 

BMI scores will classify a person as:

  • Underweight – BMI under 18.5
  • Healthy – BMI 18.5 to 24.9 
  • Overweight – BMI 25 to 29.9
  • Obese (class 1) – BMI 30 to 34.9
  • Obese (class 2) – BMI 35 to 39.9
  • Obese (class 3) or Morbidly obese – BMI 40 or higher

Learning about obesity requires understanding a wide range of subjects because it is a complicated issue. Managing body weight is influenced by hormones, different types of fats, brain pathways, and a complex interplay between genetics and environment. Several theories try to explain why obesity rates are rising, but none can fully account for the entire phenomenon.

Understanding obesity is like assembling a jigsaw puzzle with pieces combined into a single pile but coming from multiple boxes. Scientists have found many pieces, but the complete picture is yet to emerge. This makes obesity a vital and ongoing area of scientific research, one that’s crucial for the health and well-being of society.

What do we know now about how people become obese?

Firstly, the obesity epidemic isn’t just a matter of saying “people are eating too much, so they’re gaining weight.” Scientists have been studying the growing trend toward obesity for decades and have found many pieces of the puzzle. However, they still haven’t found a way to slow it down and are even further from finding how to reverse the change. It’s a complex health crisis that will require significant effort and resources to turn around. 

Here are some factors that seem to be contributing to the obesity epidemic.

  • Hormones like leptin play a key role in telling your body what to do. Leptin is a messenger hormone that tells your brain, “Hey, I’m full, stop eating.”
  • Fats aren’t all bad. As we wrote in an earlier blog, when people hear the word “fat,” it immediately brings up negative emotions.
    • Not all fats are created equal! There’s more than one kind of fat. Brown adipose tissue (BAT) is a kind of fat that actually helps you burn calories instead of storing them, unlike the usual white fat (white adipose tissue, or WAT), which the body uses to store energy for future use. 
    • WAT cells (adipocytes) in the body are constantly being formed and destroyed in what’s known as the adipocyte turnover. It’s a natural process of adipogenesis (creation of new fat cells) and apoptosis (cell death), as well as lipogenesis (fat storage) and lipolysis (fat breakdown).
    • In obese individuals, the adipocyte turnover might be skewed, resulting in more WAT cells being created than destroyed.
    • The amount of fat tissue in the body is regulated by a balance of several processes, including adipogenesis (creation of new fat cells) and apoptosis (cell death), as well as lipogenesis (fat storage) and lipolysis (fat breakdown). 
    • The brain has specific routes (pathways) that control messaging when we feel hungry and want to eat. Think of it like traffic signals for food inside your brain.
  • Genetics plays a significant role. Research increasingly shows that there are genetic factors involved in obesity linked to specific genes. That’s why obesity often runs in families.
    • Mutations of single genes might cause severe obesity that shows up in specific diseases such as Prader-Willi syndrome and Melanocortin 4 Receptor (MC4R) deficiency, which is one of the most common genetic disorders leading to obesity in both children and adults. However, there are thousands of tiny genetic differences that collectively influence BMI.

One common misunderstanding is thinking that obesity is either caused by genes (“It runs in my family”) or the environment (“I gained weight because I went to college”). The truth is, it’s usually both.

In a stable setting, a person’s weight tends to remain the same due to a balance of factors like food intake and energy spent in activities. But this balance can be disrupted by environmental changes like a new job, going to college, or even the recent pandemic that restricted outdoor activities.

Is there progress towards controlling the obesity epidemic?

Recent advances in obesity treatment have targeted brain regions using pharmacological agents like glucagon-like peptide 1 (GLP-1) receptor agonists. These drugs modify the brain’s response to hunger and fullness cues. Medications based on GLP-1 developed to treat type 2 diabetes, such as Ozempic and Mounjaro, resulted in the unforeseen benefit of promoting substantial weight loss. We republished an article by a leading US endocrinologist in August that explained in more detail why you should be talking to your healthcare professional if obesity is a health issue for you.

Questions people ask

Why are the rates of obesity increasing?

That’s the multi-million dollar question! Stated differently, if our bodies have a “set point” that maintains weight, why are more people becoming obese? One theory is the “dynamic equilibrium point,” which suggests that when people gain weight, their bodies somehow set the new weight as the “normal” stable weight. Another weight gain later on again pushes the equilibrium point higher, so there can be a cycle of small increases. 

Obesity isn’t just a straightforward issue of calories in versus calories out; it’s a labyrinthine interplay of genetics, molecular mechanisms, brain signaling, and environmental factors.

Given the global rise of obesity and its associated health risks, comprehending these intricate mechanisms is not just academic; it’s a public health imperative. 

The physical environment, especially the type of food available, plays a significant role in rising obesity rates. Not only does a body require energy, but it also needs specific nutrients. The protein leverage model suggests that diluting protein by excess carbohydrates and fats in our diets could drive us to consume more calories to meet protein needs. Another theory is the carbohydrate-insulin model, which suggests that conventional weight-loss diets that restrict carbs and fats are bound to fail since they worsen the problem by restricting energy sources in the blood, which triggers the starvation response and increases hunger.

How should our bodies manage weight?

There’s a theory that we have a system that senses our overall weight, known as a gravitostat (or sometimes the homeostat.) Cells deep in the weight-bearing bones (osteocytes) can sense the body weight from the strain that the bones are bearing. The homeostasis for body weight regulates body fat mass independently of fat-derived leptin, which means there are two independent negative feedback systems for fat mass regulation. Interestingly, people who are obese almost always have an increase in lean body mass – that’s the weight of all body components except fat, like muscles and bones. The body modifies energy imbalances between creating more lean tissue versus storing fat. However, the precise mechanisms are still under investigation.

Are there social and cultural influences on the obesity epidemic?

Income levels correlate strongly with obesity in high-income countries. Families in lower-income categories tend to consume more high-carb/high-fat foods because they cost less, require less time to prepare, and produce a higher level of satiety (satisfaction) in the short term. However, in low- and middle-income nations, the relationship is often reversed. Upper-income families can afford to eat as much and whatever they want, and obesity is a consequence. For the larger global population, simply getting enough food is a daily challenge, and their health problems relate more to inadequate nutrition.

Intriguingly, obesity tends to occur more frequently in women than in men. According to the Global Obesity Observatory, 38.2% of US adult females are obese compared to 36.7% of adult males. This suggests that gender-specific processes and societal norms may contribute to these trends. Animal studies also indicate that maternal obesity and diet can directly influence the offspring’s susceptibility to obesity. This could explain why the obesity epidemic is occurring and also provide a path to restricting the pattern.

Modern marketing techniques are reinforcing the pressure. Ultra-processed foods have been linked to overconsumption, possibly because they are engineered to be “hyperpalatable.” Foods with high energy density, often rich in fats, can lead to overconsumption of calories. The reduced availability of low-energy-density foods like dietary fiber could be another factor.

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