Obesity is linked to serious health problems like hypertension, coronary heart disease, Type 2 diabetes and stroke. But a study has found that, on top of these conditions, obesity in midlife is also a major contributor to cognitive aging.
For their study, researchers at Iowa State University (ISU) analyzed data collected over the span of six years from a cohort of cognitively unimpaired adults who were in their late midlife. They found that the participants’ cognitive performance was greatly influenced by two things: the amount of lean muscle mass they had and the amount of visceral adipose tissue they managed to accumulate.
Visceral adipose tissue refers to the deeply hidden “belly fat” that surrounds important organs, such as the stomach, liver and intestines. This type of fat is different from subcutaneous fat, which lies just beneath the skin and is not harmful in normal amounts.
Also called “active fat” because of its considerable influence on hormone function, adults often accumulate visceral adipose tissue around the abdomen as part of aging. In fact, this development, together with age-related muscle loss, starts in middle age and continues into advanced age.
How obesity alters the human brain
Earlier studies have established a clear relationship between obesity and cognitive decline. Clinical evidence suggests that aside from being a predictor of mild cognitive impairment in old age, mid-life obesity is also a risk factor for late-life dementia.
According to a review published in Frontiers in Neuroscience, this link may be explained by the loss of brain volume (atrophy), particularly in the hippocampus, observed in middle-aged adults who are obese. The hippocampus is a small but complex brain structure that plays a crucial role in learning and memory.
Brain atrophy occurs in the hippocampus as a consequence of an unhealthy diet. Specifically, following a high-fat diet, which is linked to an increased risk of obesity, has been shown to reduce the production of molecules involved in the formation and growth of new brain cells. At the same time, high intake of dietary fats has been found to trigger apoptosis (programmed cell death) in hippocampal brain cells.
Meanwhile, in another brain region known as the prefrontal cortex, excessive consumption of fats also wreaks havoc by reducing the levels of dopamine and acetylcholine — two chemical messengers involved in memory, mood and behavior — and increasing oxidative stress. This cell-damaging event, which triggers inflammation (a significant component of obesity), plays an important role in the development and progression of neurodegenerative diseases and brain aging.
Another possible mechanism underlying obesity’s impact on the brain features the thickening and hardening of blood vessels — a condition known as atherosclerosis. Animal studies show that a high-fat diet promotes atherosclerosis in large cerebral arteries, which hinders blood flow to the brain. This disruption is even observed in the small blood vessels in the hippocampus and cerebral cortex. Reduced blood flow to the brain is a significant contributor to cognitive decline and dementia.
Chronic low-grade inflammation induced by the accumulation of fat is also linked to the cognitive decline observed in obese older adults. Human and animal studies show that elevated blood levels of inflammation-related chemicals not only disrupt neural circuits involved in cognition and memory but also impair the brain’s processing speed and executive function.
Belly fat and loss of muscle mass reduce fluid intelligence
Prompted by these earlier findings, the ISU researchers set out to investigate the changes caused by obesity in an age-sensitive cognitive domain like fluid intelligence. Fluid intelligence encompasses the ability to think in an abstract way, reason quickly and solve unfamiliar problems.
The researchers also looked at how obesity-induced changes to fluid intelligence correspond to the amount of visceral fat, subcutaneous fat and lean muscle mass in men and women. The data they analyzed belonged to 4,431 late middle-aged adults who were part of the U.K. Biobank prospective cohort.
Their six-year endeavor revealed that having more lean muscle mass correlated with favorable fluid intelligence scores in both older men and women. On the other hand, having more visceral or subcutaneous fat was associated with a decline in fluid intelligence.
The researchers noted that inflammation may have played a huge role in these obesity-induced changes to fluid intelligence, as evidenced by the higher eosinophil counts in women with more visceral fat and the lower lymphocyte counts in women with more lean muscle mass.
A high eosinophil count usually indicates an infection, allergic reaction or a serious health condition, while a high lymphocyte count signifies chronic inflammation.
In men, reductions in fluid intelligence were correlated with high basophil counts in those with more visceral fat. In contrast, lower basophil counts were observed in men with more lean muscle mass. A high basophil count may be an indication of an allergic reaction or chronic inflammation caused by an autoimmune disease, rheumatoid arthritis, lupus or diabetes.
“Chronological age doesn’t seem to be a factor in fluid intelligence decreasing over time,” said Auriel Willette, an assistant professor at ISU and one of the study authors. “It appears to be biological age, which here is the amount of fat and muscle.”
To maintain optimal cognitive performance, Willette advises middle-aged adults to switch to a healthy diet and start exercising. This advice is based on the protective effects of lean muscle mass against cognitive decline that they observed in their study.
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