Based on studies conducted in a kinder environment, overeating behavior and lifestyle are no longer looked upon as the contributing factors to obesity. Other factors such as genetics, hormones, food addiction to engineered junk foods, western pattern diet (WPD) that promotes insulin resistance, medications, leptin resistance, and the insidious prevalence of sugary foods also come into play.
Some people are predisposed to obesity as it has a strong genetic component1. Having a family history of obesity increases the odds. For example, children of obese parents are much more likely to become obese than children of parents with normal healthy weight, although it is not completely predetermined.
What you eat can have a major effect as well. An unhealthy diet may change the environment and the signals sent to the genes, which can affect your susceptibility to gaining weight. Studies on identical twins have shown this factor2.
Many sugar-sweetened, high-fat junk foods stimulate the reward centers in your brain, which can cause addiction to susceptible individuals3. You eat more when you lose control over your eating behavior, similar to people struggling with alcohol addiction losing control over their drinking behavior.
The western pattern diet (WPD) is defined as “a modern dietary pattern that is characterized by high intakes of red meat, processed meat, pre-packaged foods, butter, fried foods, high-fat dairy products, eggs, refined grains, potatoes, corn (and high-fructose corn syrup) and high-sugar drinks”. WPD promotes insulin resistance, a condition in which elevated insulin levels cause energy to store in fat cells. While insulin’s role in obesity is controversial, several studies suggest that high insulin levels have a causal role in the development of obesity4,5.
Certain pharmaceutical drugs can cause weight gain as a side effect, such as antidiabetic medications, antidepressants, antipsychotic drugs, stimulant drugs for children suffering from hyperactivity. These drugs alter the function of your body and brain, reducing metabolic rate or increasing appetite6,7,8,9.
Fat cells produce leptin. Leptin is a hormone that plays an important role in obesity by signaling your brain on the sense of satiety, resulting in reduced appetite, which prevents an individual from overeating. However, leptin levels increase with higher fat mass, therefore its levels are especially high in obese. This caused a decreased function of the hormone, called leptin resistance, as it cannot cross the blood-brain barrier10.
When consumed sugar in excess, changes the hormones and biochemistry of your body, which contributes to weight gain. Added sugar is half glucose, half fructose. People get glucose from a variety of foods, including starches, but most fructose comes from added sugar. Excess fructose intake may cause insulin resistance and elevated insulin levels. It also doesn't promote satiety in the same way glucose does11,12,13.
- Xia, Q., & Grant, S. F. (2013). The genetics of human obesity. Annals of the New York Academy of Sciences, 1281(1), 178–190. https://doi.org/10.1111/nyas.12020
- Bouchard, C., Tremblay, A., Després, J. P., Nadeau, A., Lupien, P. J., Thériault, G., Dussault, J., Moorjani, S., Pinault, S., & Fournier, G. (1990). The response to long-term overfeeding in identical twins. The New England journal of medicine, 322(21), 1477–1482. https://doi.org/10.1056/NEJM199005243222101
- Avena, N. M., Rada, P., & Hoebel, B. G. (2008). Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, excessive sugar intake. Neuroscience and biobehavioral reviews, 32(1), 20–39. https://doi.org/10.1016/j.neubiorev.2007.04.019
- Templeman, N. M., Skovsø, S., Page, M. M., Lim, G. E., & Johnson, J. D. (2017). A causal role for hyperinsulinemia in obesity. The Journal of endocrinology, 232(3), R173–R183. https://doi.org/10.1530/JOE-16-0449
- Esmaillzadeh, A., Kimiagar, M., Mehrabi, Y., Azadbakht, L., Hu, F. B., & Willett, W. C. (2007). Dietary patterns, insulin resistance, and prevalence of the metabolic syndrome in women. The American journal of clinical nutrition, 85(3), 910–918. https://doi.org/10.1093/ajcn/85.3.910
- McFarlane S. I. (2009). Antidiabetic medications and weight gain: implications for the practicing physician. Current diabetes reports, 9(3), 249–254. https://doi.org/10.1007/s11892-009-0040-7
- Patten, S. B., Williams, J. V., Lavorato, D. H., Khaled, S., & Bulloch, A. G. (2011). Weight gain in relation to major depression and antidepressant medication use. Journal of affective disorders, 134(1-3), 288–293. https://doi.org/10.1016/j.jad.2011.06.027
- Correll, C. U., Lencz, T., & Malhotra, A. K. (2011). Antipsychotic drugs and obesity. Trends in molecular medicine, 17(2), 97–107. https://doi.org/10.1016/j.molmed.2010.10.010
- Butte, N. F., Treuth, M. S., Voigt, R. G., Llorente, A. M., & Heird, W. C. (1999). Stimulant medications decrease energy expenditure and physical activity in children with attention-deficit/hyperactivity disorder. The Journal of pediatrics, 135(2 Pt 1), 203–207. https://doi.org/10.1016/s0022-3476(99)70023-5
- Sáinz, N., Barrenetxe, J., Moreno-Aliaga, M. J., & Martínez, J. A. (2015). Leptin resistance and diet-induced obesity: central and peripheral actions of leptin. Metabolism: clinical and experimental, 64(1), 35–46. https://doi.org/10.1016/j.metabol.2014.10.015
- Basciano, H., Federico, L., & Adeli, K. (2005). Fructose, insulin resistance, and metabolic dyslipidemia. Nutrition & metabolism, 2(1), 5. https://doi.org/10.1186/1743-7075-2-5
- Page, K. A., Chan, O., Arora, J., Belfort-Deaguiar, R., Dzuira, J., Roehmholdt, B., Cline, G. W., Naik, S., Sinha, R., Constable, R. T., & Sherwin, R. S. (2013). Effects of fructose vs glucose on regional cerebral blood flow in brain regions involved with appetite and reward pathways. JAMA, 309(1), 63–70. https://doi.org/10.1001/jama.2012.116975
- Teff, K. L., Elliott, S. S., Tschöp, M., Kieffer, T. J., Rader, D., Heiman, M., Townsend, R. R., Keim, N. L., D'Alessio, D., & Havel, P. J. (2004). Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women. The Journal of clinical endocrinology and metabolism, 89(6), 2963–2972. https://doi.org/10.1210/jc.2003-031855