The number of people with diagnosed overweight or obesity is rapidly growing worldwide. The problem concerns both, children and adults. According to World Health Organization, there is 1,6 bn overweight and 522 m obese people around the world. The latest research conducted in the United States showed that high-fat diet impairs cognitive processes of human organism such as memory or learning.
One of the most common problems connected with human’s lifestyle is excessive body weight. Overweight or obesity are risk factors leading to development of many diseases such as type 2 diabetes, arterial hypertension, ischemic heart disease, stroke and a certain cancers, what in consequence results in premature death. New scientific research show that health risk connected with excessive fat tissue increases not only with significant obesity, but even with relatively low increase in body weight.
Scientists from Georgia Regents University in United States discovered that high-fat diet destroys nerve-nerve synapses which are connections enabling communication between neurons. It was stated that damages involve brain structure called hippocampus which has a major role in transferring information from short-term to long-term memory and is responsible for spatial cognition. It was experimentally proved on animals that damage to hippocampus significantly impairs learning abilities.
American research was conducted on mice which were divided into two groups: one group was fed with diet containing about 10% of calories and the other one with 60% of calories coming from saturated fats. Low-fat diet was reflection of a healthy diet in human, whereas high-fat diet resembled fast-food intake. Both diets contained similar amount of proteins and micronutrients.
Scientists assessed chosen parameters in 4th, 8th and 12th week of the research. In 4th and 8th week, level of synaptic markers in hippocampus was the same in both groups of mice. In 12th week scientists observed lowered level of synaptic markers and increased level of cytokines – proteins taking part in inflammatory process, what indicated devastation of synapses in hippocampus. Mechanism of this phenomenon may be explained as follows: excess of fat in organism induces chronic inflammation causing autoimmune response of microglia cells in the central nervous system. The cells lose their ability to move with shoots and start to digest surrounding synapses through phagocytosis. After 12 weeks of the research high-fat diet was replaced with low-fat one in half of the mice from the high-fat diet group. As a result, there was inhibition of degenerative processes in the brain, while in the group which continued high-fat diet further damages were observed.
It is assumed that some drugs used in Crohn’s disease and in rheumatoid arthritis, which block inflammatory cytokines, may positively influence nervous tissue in people with overweight or obesity thus preventing degeneration of cognitive functions. However, we should try to maintain proper body weight and healthy eating habits in order to keep our nervous system functional.
Written by: Karolina Gasińska, Anna Szajerska
1. Behl C, Lezoualc’h F, Trapp T, and al. Glucocorticoids enhance oxidative stress-induced cell death in hippocampal neurons in vitro. Endocrinology. Published online 1 July 2013.
2. Hao S, Dey A, Yu X, et al. Dietary obesity reversibly induces synaptic stripping by microglia and impairs hippocampal plasticity. Brain, Behavior and Immunity. doi:10.1016/j.bbi.2015.08.023. Published online 31 August 2015.
3. Lynch MA. Long-term potentiation and memory. Physiological Reviews. 2004;84:87–136.
4. Puszkarska A, Głuszek J. Zwiększenie skuteczności terapii nadciśnienia tętniczego poprzez redukcję otyłości (Czy utrata nadwagi zawsze powoduje normalizację ciśnienia tętniczego?). Arterial Hypertension. 2011;15:118–124.
5. Silverthorn DU. Human physiology: an integrated approach (4th ed.). San Francisco: Pearson/Benjamin Cummings 2007, p. 271.
6. Sturm R. The effects of obesity, smoking, and drinking on medical problems and costs. Health Aff. 2002;21:245-253.