What makes you fat?

We take a look at some theories about the causes of obesity.
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CHOICE looks at the science of overweight and obesity and provides an overview of some of the latest theories about what makes people gain weight.

At its simplest, we gain weight and get fat if we suffer an energy imbalance – that is, if the energy we eat exceeds the energy we burn off through metabolic processes and physical activity. But it's clearly more complex than that, and some people gain weight far more readily than others with an apparently similar lifestyle.

It's generally accepted that while some genes may predispose people to obesity, obesity is not inevitable. Rather, it's an interaction between genetics, lifestyle and environment. Some of the more recent avenues of research into obesity include looking at systemic inflammation, the role of our gut bacteria and environmental contaminants. Here we look at some of this research, and how it relates to the modern obesity crisis.

For more information about weight loss, see Diet and exercise.

Systemic inflammation

Research over the last two decades has shown that obesity and other metabolic diseases such as diabetes and cardiovascular disease, are linked with a chronic low-grade systemic inflammation. This inflammation, also called 'metaflammation' because of its relationship to metabolic processes, has various physiological effects, including changes to glucose and fat metabolism which lead to insulin resistance and weight gain.

Inflammation can be detected by measuring inflammation-related chemicals in the blood. Researchers have found that a diet high in saturated and trans fats, sugar and high glycaemic index foods, and modern processed or modified foods, is associated with this inflammation. Fruit and vegetables, fish and fish oil, nuts, olive oil and herbs and spices seem to have an anti-inflammatory effect. Drinks including tea, wine and beer appear to have anti-inflammatory effects as well, though too much alcohol has been associated with increased inflammation.

Foods with high energy density and/or low satiety – which feature prominently among so-called pro-inflammatory foods – can result in weight gain and, ultimately, obesity ¬– which itself has a pro-inflammatory effect. Weight loss, however, has an anti-inflammatory effect. Your overall diet, particularly energy balance, is therefore important, and can contribute to inflammation.

Physical activity can have an anti-inflammatory effect, although the dose makes the poison: too much (in terms of duration and intensity) or too little (independent of weight) exercise can be inflammatory. An increasing body of research shows that the amount of sitting we do, irrespective of other activity, causes inflammation.

EDCs and other environmental contaminants

Obesogens, which are stored in fatty tissue, are thought to act via an inflammatory effect, but may also exert their effects on the genetics of a developing foetus, consequently affecting future generations.

Chemicals known to have an endocrine (hormonal system) disrupting effect, called endocrine-disrupting chemicals or EDCs, may also be linked with obesity. 

These include certain phthalates, which are found in plastics, cosmetics and fragrances.

  • Dichlorodiphenyldichloroethylene (DDE), which is a chemical formed from the breakdown of the once widely used dichlorodiphenyltrichloroethane (DDT) organochlorine pesticide
  • Polychlorinated biphenyl (PCB), a persistent organic pollutant now banned but once used on various industrial and manufacturing applications; 
  • Dioxins, industrial and combustion-related chemicals
  • Possibly bisphenol A
And it’s not just in humans – studies have found that low-level environmental contamination of these so-called “obesogens” may be linked with weight gain in other mammals.

Obesogens, which are stored in fatty tissue, are thought to act via an inflammatory effect, but may also exert their effects on the genetics of a developing foetus, consequently affecting future generations.

The gut bacteria of the microbiome

Most people are aware that we have lots of bacteria living in our gut – for example, the so-called good bacteria and bad bacteria, which may get out of balance if we’re sick or take certain medications. We’re born with them, though the types and numbers are modified over our lifetime. Collectively called the microbiome – and considered by some to be an ‘organ’ in its own right – the bacteria in and on us comprise about two kilograms of our body weight and these bacteria outnumber human cells 10 to one. The importance of the microbiome is gaining more and more attention, and different assortments of bacteria have been associated with intestinal and bowel conditions such as ulcerative colitis and irritable bowel syndrome, and also immune disorders such as allergies and type 1 diabetes.

But it’s becoming increasingly apparent that the microbiome is linked with metabolism and metabolic diseases, including type 2 diabetes and obesity. It’s known that obese people and lean people have different bacterial profiles, though whether this is a cause or effect of obesity is unknown. For example, when sterile (bacteria-free) lean mice exposed to non-sterile obese mice, they get fat, despite there being no change to their energy intake – suggesting it’s the bacteria that causes obesity. The use of antibiotics in human and veterinary medicine has also been linked with obesity.

There are several suggestions as to how the microbiome may cause obesity. Certain bacteria, the ones more predominant in obese people, are better at extracting energy from food for the host, leading to weight gain. It’s also been suggested that the microbiome is linked with obesity through inflammation (see above). Other theories relate to chemical or hormonal communications between the host and the microbiome, or the regulation by the microbiome of host genes related to energy expenditure and storage. Most likely it’s a combination of several effects.

Small trials in which microbe-rich faecal matter (that’s poo to you) is transplanted from healthy individuals into the lower intestine of people with colitis have been successful in treating the disease, leading some to suggest similar treatment for obesity and type 2 diabetes. However, there are far too many unknowns at this point, such as which bacteria are beneficial and which pathogenic, and whether artificially changing someone’s microbiome may cause other problems. More likely scenarios are the development of microbial supplements of helpful bacteria, perhaps in combination with antibiotics targeting undesirable bacteria, or else drugs that mimic their actions.



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