Evolution and Obesity

A century ago, obesity was rare. Now people all over the world are gaining weight, with 69% of adults in the US currently overweight or obese. Obesity is linked to rising rates of health problems such as cardiovascular disease and diabetes. Why the sudden change? Is obesity in our genes, or has something in our environment made us fat in recent decades?

The answer is both. People vary in how easily they gain weight, and much of that variation is coded in genes and passed down through families. However, the rise of obesity has happened too quickly to be caused by genetic changes. Genetic variations linked to obesity have been with us for millennia, but only in combination with the modern environment do they make us obese.

For example, FTO (also known as “Fatso”) is the gene with the strongest known effect on common types of obesity. Some variants of the gene increase obesity risk, while others lower it. However, the effects of FTO depend on environment. Even high-risk forms of FTO have little effect on body fat among people who get lots of exercise or eat low-fat diets.

Changes shaped by early experience interact with our genes and with environmental and lifestyle factors throughout our lives. For thousands of years, these interactions helped people maintain a healthy body weight. But in the last few decades, our environment has changed, unbalancing our biology and pushing more and more of us toward obesity.

While obesity rates are rising in our society, many people remain lean, and this variation is not just a matter of willpower. People vary widely in how easily they put on fat and how difficult it is for them to lose it.

Genes

Genetic variation between people accounts for 50 to 70% of variation in BMI, but the genetics are complex. Amount of body fat is affected by many different factors, including how efficiently the digestive system extracts nutrients from food, how readily nutrients are stored as fat or burned as fuel, and how hungry we feel. Each of these factors is influenced by hundreds of genes.

While there are a few gene variants that dramatically increase obesity risk, these are uncommon. For most of us, each gene contributes only a tiny amount to risk, but all of them combined can make the difference between being naturally thin and having to struggle to maintain a healthy weight.

Even people with a similar obesity risk may have different genetic reasons for that risk. Because of this, different people may need different approaches to weight management.

Epigenetics

When a baby is conceived, the sequence of their genes is set for life. However, the activity of those genes is flexible. Signals from the environment influence our genes, guiding them down different developmental pathways. Some of those developmental decisions influence how easily people put on fat later in life.

Either too little or too much nutrition in the womb can “program” fetuses to gain weight as children and adults. Women who undergo food shortages during pregnancy tend to have small babies, but if food is available after birth, the babies catch up and put on large amounts of fat. Such babies often go on to suffer from obesity, diabetes, and cardiovascular disease. Women who are overweight or who gain excess weight during pregnancy tend to have larger, fatter babies, and those babies are also at increased risk of developing obesity.

Microbiome

A person’s intestines contain two to three pounds of microorganisms, most of which are bacteria. These bacteria help us get more energy from food by breaking down nutrients that we can’t digest on our own. They can have other effects too, such as protecting the intestinal lining or stimulating the production of appetite-controlling hormones. Different people have different types of bacteria, and these differences may play a role in obesity.

Obese people tend to have fewer species of gut bacteria than thin people do, and the bacterial species are in different proportions. Transplanting bacteria between the intestines of fat and slim mice can change how efficiently the mice digest food, and similar experiments are ongoing in humans. Human babies with certain gut bacteria are more likely to become obese as children. Researchers are now studying whether humans can fight obesity by supplementing their diet with healthy bacteria, or "probiotics."

Much remains unknown about how gut bacteria interact with body fat. This is partly because different bacteria feed on different kinds of nutrients, so the populations in your gut are largely determined by which foods you eat. When diet, weight, and gut bacteria are all changing, it’s hard for researchers to separate cause from effect.

Human lifestyles have changed dramatically through the course of history. The timeline below shows changes that may be important in understanding our current obesity epidemic. Further down, you will find explanations of how these changes may interact with our biology to make us fat. Each explanation has some researchers who support it and others who are skeptical.

Until the last century, people were at more risk from malnutrition or starvation than they were from obesity. This lopsided pressure may have shaped humans to be more prone to store fat than to lose it. The ability to store extra calories as fat during times of plenty could help someone stay healthy and fertile when food was scarce.

Over thousands of generations, selective pressure from food scarcity could cause many different kinds of adaptations to evolve. These adaptations could make us crave rich foods that are easy to digest, or drive us to keep eating after we’ve had enough. They could act on our desire to exercise, making us inclined to sit still and conserve energy. They could allow us to extract more nutrients from food, or channel those nutrients to fat cells and away from other body functions. Unreliable food supplies have likely shaped our evolution in all these ways and more.

The same adaptations that let our ancestors succeed now predispose people to gain dangerous amounts of fat. Most people in the developed world can get as much food as they want without working up a sweat. Humans are still evolving, but evolution is a slow process, and widespread obesity has been possible for only a tiny sliver of our history. We get fat because our bodies are adapted to overcome our ancestors’ challenges.

Among most mammals, only babies drink milk. The same is true of most humans, but in some societies, people have the ability to digest milk throughout their lives. Why, and when did this ability evolve?

Milk contains a unique sugar called lactose, and baby mammals digest it with an enzyme called lactase, which they stop producing after they are weaned. Genetic and archaeological evidence shows that the ability to produce lactase throughout life, a condition known as lactase persistence, evolved around the same time as dairy farming. Today, around 35% of adults can digest milk, and they are concentrated in populations with a history of dairying.

Lactase persistence allows people who raise cows to get more calories from the resources available to them. The mutations for lactase persistence spread rapidly through populations, which shows that they helped people to survive and reproduce. Now most people have no trouble getting enough calories, but Europeans with lactase persistence still tend to be heavier than those who are lactose intolerant. The ability to digest milk is an adaptation shaped by the food scarcity of past generations.

The body has an internal clock known as the “circadian rhythm.” This clock regulates daily cycles of activity on every level, from molecular processes inside cells to behaviors like sleeping. Under natural circumstances, the circadian rhythm is set by sunlight entering the eyes during the day. Each cycle is about twenty-four hours, with body processes matched to the rising and setting of the sun.

We no longer live under natural circumstances. Artificial light exposure has increased 100,000 times since the kerosene lamps of the 1800s, and it shines on us at every time of the day and night. Many people have disrupted sleep schedules, and there is growing evidence that the disruptions go beyond sleep, predisposing people to obesity and a wide variety of illnesses.

People who regularly don’t get enough sleep are more likely to be obese, and two nights of bad sleep can cause hormonal changes that increase hunger. Sleep deprivation and shifts in schedule both cause changes in the body similar to those seen in diabetes, and shift workers are at increased risk for obesity regardless of food intake and exercise. In today’s world, a light in the darkness may be more of a threat than a beacon.

Synthetic chemicals are everywhere, and our exposure has been increasing exponentially since the 1800s. We add synthetic chemicals to food and manufactured products, use them in industrial processes, and release them into our air and water. During the 20th century, people evaluating the safety of these chemicals generally didn’t look for weight gain over long periods of time, and the effects of the chemicals on body weight are only now coming to light.

A variety of common chemicals have recently been linked to weight gain. Most of them are “endocrine disruptors”—substances that interfere with the regulatory molecules known as hormones. The doses that cause weight gain are often small, similar to amounts many people are exposed to. Many such chemicals accumulate in fat, and when people lose weight they are released back into the blood. Their effects vary with age, and exposure in the womb or early childhood can cause life-long changes.

Some endocrine disruptors have been banned after decades of use, while others, such as phthalates and bisphenol A, are still being produced and added to products like plastics and can linings. According to the World Health Organization, hundreds of chemicals are known endocrine disruptors, while thousands more have not been adequately studied.