An analysis of study data from the Vanderbilt Memory and Aging Project found that a high-fat diet was associated with a rapid decrease in temporal lobe volume in participants without cognitive impairment. However, in people with mild cognitive impairment, adherence to the same type of diet was associated with delayed enlargement of the inferior ventricular region of the brain. The paper is Alzheimer’s disease and dementia.
Although dementia is an inevitable part of normal aging, the risk of developing dementia increases as you get older. Dementia is a disorder characterized by a progressive decline in memory, reasoning, language, judgment, or other cognitive abilities that interferes with daily life. The most common type of dementia is Alzheimer’s disease. The disease is associated with abnormal accumulations of amyloid plaques and proteins called tau tangles in the brain.
In addition to Alzheimer’s disease, dementias include vascular dementia (caused by reduced blood flow and brain tissue damage due to stroke or small vessel disease), Lewy body dementia, and frontotemporal dementia. Although the exact causes of dementia are not fully understood, scientists believe that dementia is caused by a complex interaction between genetic predisposition and the environment. Up to 40% of the risk is due to modifiable lifestyle factors such as diet.
Ray Huang, a researcher at Vanderbilt University Medical Center, and colleagues investigated whether dietary fat intake was associated with changes over time in gray matter atrophy rates detected by neuroimaging in older adults. They were also interested in the interaction of these changes with cognitive status, gender dependence, and whether an individual is a carrier of the APOE ε4 gene variant. APOE ε4 is a genetic mutation that increases the risk of developing Alzheimer’s disease.
These researchers analyzed data from the Vanderbilt Memory and Aging Project. This is a longitudinal observational study investigating vascular and neurological health and aging in older adults without clinical dementia at enrollment. This data was obtained from 758 participants in the Legacy and Expansion Cohorts of the Vanderbilt Memory and Aging Project. Their average age was 67 years. Approximately 47% were male and 35% were carriers of the APOE ε4 gene variant.
Recruitment for the Legacy Cohort began in September 2012, and all participants were required to be at least 60 years old, have good hearing and vision, and have a trusted research partner. The expansion cohort recruits individuals aged 50 and older and began recruitment in August 2021.
Depending on the assessed cognitive status, participants were classified as either non-cognitively impaired or mildly cognitively impaired. Participants completed brain magnetic resonance imaging at the time of study enrollment and at least one more time. They also completed a questionnaire called the Quick Food Scan fat screener, which allowed the study authors to estimate their total dietary fat intake. Data were collected at the beginning of the study, 18 months later, and 3, 5, 7, and 9 years after the start of the study.
As a result, cross-sectional analyzes at baseline showed that neither total fat intake nor the proportion of energy derived from fat was associated with total brain gray matter volume or the volume of specific brain lobes. But over time, over an average of 4.6 years, people who got a higher percentage of their energy from fat tended to have slower volume expansion inside their lateral ventricles. This association was weak, and when the study authors modified the detection threshold for multiple comparisons, the association disappeared.
Further analysis showed that the proportion of energy derived from fat was associated with a faster decline in temporal lobe volume in participants without cognitive impairment. In contrast, in people with mild cognitive impairment, a higher proportion of energy from fat was associated with slower expansion of the inferior ventricular region of the brain.
The temporal lobe is an area of the brain that supports memory and language. The inferior lateral ventricle is a fluid-filled space near the temporal lobe. Their enlargement reflects loss of brain tissue in surrounding areas.
“High-fat diet is associated with accelerated gray matter atrophy in adults (without cognitive impairment), particularly in regions (associated with Alzheimer’s disease) such as the temporal lobe, but with slower atrophy in individuals with (mild cognitive impairment), driven primarily by APOE ε4 carriers and/or women,” the study authors concluded.
“Depending on cognitive status, different mechanisms may be involved in the relationship between fat and neurodegeneration. The cessation of atrophy associated with a high-fat diet was observed only in patients with pre-existing (mild cognitive impairment) and may reflect the role of fat as part of a compensatory mechanism in response to progressive (Alzheimer’s disease) pathology and metabolic challenges.”
This study contributes to the scientific understanding of the link between diet and mental health. However, the design of this study does not allow us to infer causality from the results. It is also limited by the fact that this population was primarily white, educated, and relatively healthy. Furthermore, a single self-reported dietary fat assessment at baseline may not reflect long-term variations in dietary intake.
The paper, “High-fat diet is associated with accelerated gray matter atrophy in older adults without cognitive impairment, but slower atrophy in those with mild cognitive impairment,” was authored by Lei Fan, Yunyi Sun, Dandan Liu, W. Hudson Robb, Kimberly R. Pechman, Niranjana Shashikumar, Yukti Vyas, Bennett A. Landman, Timothy J. Hohman, and Angela. L.Jefferson.
