A new study suggests high-fat diet destroys synapses (connections between neurons that help them communicate) in the hippocampus of the brain. This action may lessen memory and learning because hippocampus is the part of the brain which is essential in forming memories.
Nonetheless, the researchers suggest that the brain-damaging effects of a high-fat diet can be countered through switching to low-fat diet for 2 months.
Problems with obesity
An adult with Body Mass Index (BMI) 30 or more is considered obese.
Obesity is a major public health concern all over the developed world. Obesity is responsible for disease like heart disease, stroke, high blood pressure, diabetes, gallbladder disease, osteoarthritis and some type of cancers.
More than a third of adults in the United States are considered obese.
In England, the prevalence of obesity among adults rose from 14.9% to 24.9% between 1993 and 2013. In UK and Ireland, data from 2013 showed that around 62.1% of adults were overweight or obese (67.1% of men and 57.2% of women).
Many studies have shown that fatty food is not only responsible for weight gain; it is also harmful for brain. Dr. Alexis M. Stranahan, a neuroscientist at the Medical College of Georgia and her team decided to explore this association further.
The researchers studied normal male mice. They randomized the mice to one of two groups: One group consumed a diet where saturated fat was the source of approximately 10% of the calories, and the group ate a diet that was 60% fat. The chows had similar levels of macronutrients and protein. The chows were similar to what humans consume as healthy diet and fast-food diet.
A string of metabolic measures, like food intake, weight, insulin levels and blood glucose of the mice were checked at 4, 8 and 12 weeks after the start of diet.
The researchers also measured the hippocampus of the brain – the part of the brain responsible for learning and forming memory – and levels of synaptic markers, examined proteins present at synapses that correspond with the synapse count.
Additionally, they measured inflammatory cytokine levels; these are produced by microglia when they start to get angry.
In both groups, all levels were approximately the same at four weeks. At 8 weeks the mice with high-fat diet gained weight, but the other measures were same.
By 12 weeks, however, the fat-consuming mice were obese, possessed higher levels of cytokine and had a decreased number of synapse and their function,indicating that synapses were being destroyed in the hippocampus.
According to researchers, too much fat in the body leads to chronic inflammation, triggering an autoimmune response from microglia. Microglia are the glial cells that is responsible for primary immune defense in the central nervous system.
Microglia, which is responsible for helping the brain get rid of harmful agents and help protect and strengthen neurons, seems to become less effective in carrying on with the process when there is too much fat in the body.
At the next phase, the researchers reversed mice’s diet. Half the mice on the high-fat-diet were switched to low-fat diet to see its impact on the brain.
After the switch in diets, the mice returned to their normal weight within 2 months, however, their ‘fat pad’ – a layer of fat that simplifies future weight gain – remained larger than the mice with low-fat diet who had never experienced weight gain. As with most humans, the mice consuming a low-fat diet slowly gained weight as they aged.
Mice on high-fat diet lost more synapses
Moreover, while the mice on high-fat diet continued to get fatter, experience more inflammation and lose more synapses, these functions were restored among the mice that switched to low-fat diet. This suggests switching to a low-fat diet may balance neurological damage caused by a high-fat diet.
Cognitive impairment due to synapse los is caused by microglia eating synapses. Although, it’s scary, it is also reversible. If one switches to a low-fat diet that doesn’t entirely eliminate the adiposity, it is possible to reverse these cellular processes and maintain cognition, concluded Dr. Stranahan.
The findings also suggest some potential new objectives for existing medications used to treat rheumatoid arthritis and Crohn’s disease, which stop particular inflammatory cytokines and tumor necrosis factor alpha. In the brains of the obese mice, both of these are heavy.
Dr. Stranahan notes that the mice in the fat-eating group actually consumed less chow and had the same volume of calories as the mice in low-fat diet.
The complete metabolic phenotype is propelled by the composition of diet rather than the calorie count, said Dr. Stranahan.
The study was published in the journal Brain, Behavior and Immunity.
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