Share on PinterestVisceral fat could contribute to Alzheimer’s risk. Could shedding that fat help prevent cognitive decline? Image credit: Adrian Rodd/Stocksy.
- Obesity has previously been linked to Alzheimer’s disease risk.
- Researchers from Mallinckrodt Institute of Radiology have recently presented research at the Radiological Society of North America conference suggesting organ fat in midlife could contribute to Alzheimer’s risk due to its role in neuroinflammation.
- They looked at small groups of midlife adults for the three studies presented.
Visceral fat has been shown to contribute significantly to the relationship between high body mass index (BMI) and the accumulation of proteins associated with Alzheimer’s disease.
Researchers from Mallinckrodt Institute of Radiology at Washington University School of Medicine in St. Louis, MO, presented results from three small studies at the Annual Meeting of the Radiological Society of North America, held between December 1–5.
They looked at fat and muscle distribution in a small cohort of people around the age of 50, as well as at blood flow in the brain, and the accumulation of proteins associated with Alzheimer’s disease, including amyloid and tau.
This research builds on previous findings presented at the same conference last year. None of these studies have been published in peer-reviewed journals yet.
This previous research showed that visceral fat, found around the organs in the abdomen, was associated with higher accumulation of amyloid protein in parts of the brain, up to 15 years before disease onset.
Author Mahsa Dolatshahi, MD, PhD, a researcher at Mallinckrodt Institute of Radiology at Washington University School of Medicine in St. Louis told Medical News Today that “midlife obesity is known as a risk factor for Alzheimer’s disease decades later.“
“However, different kinds of fat have variable effects on inflammation and metabolic abnormalities, where visceral fat has a stronger effect on inflammation,“ she explained. “We wanted to see whether the roles of different kinds of fat in Alzheimer disease differ.”
Is visceral fat linked to toxic protein accumulation in the brain??
In one study of 62 midlife individuals with an average age of 50 presented at the conference, researchers found that individuals with obesity had higher amyloid accumulation compared to those without obesity.
However they also found that visceral fat was responsible for most of this, and that it mediated most of the effect of BMI on amyloid accumulation, which is often a marker of cognitive decline.
Researchers also measured insulin resistance, and found this had some, but less effect on amyloid accumulation. Thigh and liver fat was not shown to have an effect on amyloid accumulation.
Does liver fat lead to brain inflammation?
Another abstract presented by the team contained analyses of 67 cognitively normal middle-aged participants with an average age of 50, and an average BMI of 32.
Researchers looked at thigh fat-to-muscle ratio, insulin resistance, systemic inflammation, and brain histology using Diffusion Basis Spectrum Imaging.
They found that liver fat, but not thigh fat or insulin resistance, resulted in increased inflammation in the brain.
In a final study, researchers looked at abdominal fat alongside brain scans. A total of 66 middle-aged cognitively normal adults with an average age of 50 were observed.
The researchers found that obesity and increased visceral abdominal fat are associated with a lower blood flow in the brain. A prominent decrease was seen in an area of the brain called the middle temporal cortex, an area associated with Alzheimer’s disease.
The researchers looked at adiposity and BMI, but did not adjust their findings for lifestyle factors.
“We have not studied or controlled for these factors. We cannot ignore the role of these factors but diet and physical activity act upstream to body adiposity. We aim to assess ApoE genotype [associated with a heightened Alzheimer’s risk] in our longitudinal study and control for it in our analysis,” said Dolatshahi.
The authors argue that their findings suggest excess fat could increase the risk of Alzheimer’s disease due to inflammation in the brain, and that reducing fat and obesity in midlife could reduce Alzheimer’s disease later on.
Dolatshahi went on to note that “lifestyle factors like diet and physical activity can affect the body fat distribution and the recently approved anti-obesity drugs are recognized to have differential effects on various body adipose tissues, and preventing Alzheimer disease.“
She pointed out we have no evidence that tackling obesity in midlife could reduce risk of Alzheimer’s disease “but as these effects are cumulative, it is better to be prevented as early as possible.“
“We plan to do a longitudinal version of this study to see if the pattern of adiposity changes and how it affects Alzheimer pathology and cognitive function. Also we aim to include assessments of social and structural determinants of health and genetic factors,” added Dolatshahi.
Why could obesity contribute to Alzheimer’s disease?
Verna Porter, MD, a board-certified neurologist and director of the Dementia, Alzheimer’s Disease and Neurocognitive Disorders at Pacific Neuroscience Institute at Providence Saint John’s Health Center in Santa Monica, CA, who was not involved in the research told MNT that other research had linked obesity, adiposity and Alzheimer’s disease before.
“Obesity and adiposity have been strongly linked to an increased risk of Alzheimer’s disease. This connection is attributed to the metabolic, inflammatory, and vascular consequences of excessive body fat, especially visceral adipose tissue,“ Porter noted.
“Visceral fat is more closely associated with Alzheimer’s disease pathology than subcutaneous fat or general obesity. Studies have shown higher amyloid deposition in the brain, a hallmark of Alzheimer’s disease, in individuals with elevated visceral adipose tissue levels,“ she added.
As to why obesity could contribute to the risk of Alzheimer’s disease, Porter explained that:
“Obesity promotes systemic inflammation, insulin resistance, and oxidative stress, all of which contribute to neurodegenerative processes. Excess adiposity, particularly visceral adipose tissue, is linked to reduced cerebral blood flow, which may impair brain function and facilitate Alzheimer’s disease progression. Therefore, overall, adiposity, particularly visceral obesity, is a significant risk factor for Alzheimer’s disease development.”
She agreed that midlife could be a critical time for dealing with some of the lifestyle factors that could contribute to obesity.
“Midlife is a pivotal period for addressing modifiable risk factors that contribute to Alzheimer’s disease, including obesity,“ Porter said.
“In cognitively normal midlife adults, higher visceral fat correlates with greater amyloid burden and lower cerebral blood flow, particularly in Alzheimer-sensitive regions like the temporal cortex,“ she detailed. “The detrimental effects of midlife obesity, such as increased amyloid deposition and brain hypoperfusion, may precede cognitive decline by decades, thus emphasizing the importance of early intervention.“
“Midlife presents a critical opportunity to address modifiable factors like obesity, physical inactivity, and poor cardiovascular health to reduce the risk of Alzheimer’s disease. As a neurologist, the focus on visceral fat reduction, lifestyle interventions, and early detection can provide patients with tangible steps to safeguard brain health over time,” Porter advised.
