Above: Bioengineered obese mouse, Aberdeen, Scotland, 1998. This mouse lacked the gene responsible for the production of leptin. As a result, it ate voraciously and continually gained weight. (Wikimedia Commons/Wellcome Images)
Did you know? According to Statistics Canada, 15% of the country’s children were obese or overweight in 1978. By 2007, the figure had nearly doubled to 29%.
What pops into your head when you see an obese person passing by on the street? Do you think they should eat less and exercise more? You are not alone. Many people assume that obesity is the result of poor personal habits.
It is true that an inactive lifestyle, genetics, and smoking are risk factors for obesity. But the biggest factor is hormonal changes. These changes are related to a diet high in sugar and low in fibre. For example, an imbalance in levels of the hormones leptin and insulin can promote both gluttony (excessive eating and drinking) and sloth (laziness). Abnormal levels of other hormones, such as cortisol and serotonin, can also contribute to obesity. Leptin and insulin are the key players, though.
Leptin and the hypothalamus
Did you know? Obesity means having too much body fat. It is generally diagnosed using the body mass index (BMI), which takes into account a person’s body weight and height.
Leptin is secreted by fat cells into the bloodstream. It then travels to the brain. In the brain, leptin binds to receptors in the hypothalamus, an area of the brain that coordinates many bodily functions. Organs affected by a specific hormone have receptors to which only that hormone can bind. It is like a key in a lock. When the hormone that “fits” attaches to the receptors, it causes the organ to perform its functions.
Leptin sends two signals to the brain. The first turns on the sympathetic nervous system, which is responsible for muscle activity and fat burn. The second signal turns off the vagus nerve, which promotes appetite and fat gain.
In people who are obese, normal communication between leptin and the hypothalamus is interrupted. This can be the result of either leptin deficiency or leptin resistance. Leptin deficiency can be treated by taking hormone supplements.
Insulin and leptin resistance
Did you know? To increase the shelf life and enhance the taste of processed foods, manufacturers add salt and sugar. They also reduce or remove fibre.
Treating leptin resistance is more complicated. In some cases, the hypothalamus can be permanently damaged by a brain tumour or by treatments for a tumour, such as radiation therapy. However, leptin resistance can also occur when the hypothalamus simply cannot “see” the leptin. This may happen because the hormone is being blocked by high levels of insulin.
Insulin is secreted by the pancreas when blood sugar levels are high. This sends a signal that there is an excess of sugar in the blood that needs to be stored. Added sugar is a very common ingredient in processed foods. It’s often in the form of sucrose (table sugar) or high-fructose corn syrup. It is also found in fast food, soda, fruit drinks and sports drinks. And the more sugar you consume, the more sugar you crave. More sugar means more insulin, which in turn blocks leptin. As a result, the brain cannot “see” the leptin and thinks your body is starving! To prevent you from starving, the brain signals for you to eat unnecessarily and reduce your amount of physical activity. This results in weight gain.
Did you know? Worldwide, the number of obese and overweight people has more than doubled from 857 million in 1980 to 2.1 billion in 2013.
Fibre is the antidote to too much sugar. First and foremost, fibre slows down the absorption of sugar from the gut into the bloodstream. When sugar gradually enters the bloodstream, the increase in insulin levels is less sharp. This prevents leptin from being blocked. Fibre also helps digestion, so you feel full more quickly. This reduces your desire to eat more food.
There is a strong connection between obesity and an imbalance in hormonal levels. This imbalance can make you eat more and move around less. Your diet plays an important role in keeping your hormones balanced. You can reduce your risk of becoming obese or overweight by eating more fruit, vegetables, and healthy homemade meals. You should also limit the amount of processed food (including fast food) and sugary drinks you take in each day.
So next time you have a choice between an orange and orange juice, go with the orange. You will still get plenty of sugar, but the extra fibre in the orange will slow down your absorption of sugar. This will help keep your hormones in balance!
This article was updated by Let's Talk Science staff on 2016-10-17 to improve readability by reducing the reading grade level.
Childhood Obesity Foundation (2015)
Website with information and resources related to the causes and prevention of childhood obesity in Canada.
Defining Overweight and Obesity (2012)
US Centers for Disease Control
Explanation of how obesity is diagnosed using the body mass index, with information on risks associated with obesity and links to additional information.
M. E. Haahr, P. M. Rasmussen, K. Madsen, L. Marner, C. Ratner, N. Gillings, W. F. Baaré, G. M. Knudsen. (2012). Obesity is associated with high serotonin 4 receptor availability in the brain reward circuitry. Neuroimage 61(4), 884-888.
Article discussing the importance of serotonin to the brain’s reward system and the regulation of people’s food intake. An abstract is available on the publisher’s website. A subscription is required to view the full text.
J. F. Davis, D. L. Choi, S. C. Benoit. (2009). Insulin, Leptin and Reward. Trends in Endocrinology & Metabolism 2(20), 68-74.
Article describing how insulin and leptin levels affect appetite and energy. An abstract is available on the journal’s website. A subscription is required to view the full text.
P. Björntorp, R. Rosmand. (2000). Obesity and Cortisol. Nutrition 16(10), 924–936.
Article discussing the role of cortisol in obesity, as well as the influence of other neuroendocrine pathways and environmental factors. An abstract is available on the publisher’s website. A subscription is required to view the full text.