obesity

Data from 473 adults aged 20-87 has found striking differences in the volume of white matter among middle-aged and older adults, depending on the weight of the individuals. These changes were also associated with greater brain shrinkage. These differences were equivalent to some 10 years in brain age – e.g., an overweight person at, say, 50 years old had a comparable white matter volume to a lean person aged 60 years.

The differences were not found among younger adults. Nor was there any connection between being overweight or obese and an individual’s cognitive abilities, as measured using a standard test similar to an IQ test.

http://www.eurekalert.org/pub_releases/2016-08/uoc-boo080316.php

Ronan, L et al. Obesity associated with increased brain-age from mid-life. Neurobiology of Aging; e-pub 27 July 2016; DOI: 10.1016/j.neurobiolaging.2016.07.010

The connection between higher BMI and greater cognitive decline with age is being blamed on inflammation.

Data from the English Longitudinal Study of Aging, involving some 21,500 older adults (50+) showed that, the higher the BMI at the start, the greater the rise in lovels of C-reactive protein over the next four years. CRP is a marker in the blood of systemic inflammation. This 4-year change in CRP predicted change in cognition six years after the start of the study.

https://www.eurekalert.org/pub_releases/2016-10/uoa-hyb101716.php

Bourassa, K., & Sbarra, D. A. (2017). Body mass and cognitive decline are indirectly associated via inflammation among aging adults. Brain, Behavior, and Immunity, 60, 63–70. https://doi.org/10.1016/j.bbi.2016.09.023

Data from the Advanced Cognitive Training for Independent and Vital Elderly, involving 701 older adults (mean age 73.6) with normal weight, 1,081 overweight, and 902 who were obese, found that memory training provided only one-third the benefit to older adults with obesity compared with the benefit it provided to normal-weight older adults.

Participants were followed for 10 years. Over that time, the effects of training in reasoning and speed of processing didn’t differe between the weight groups. However, the effect of memory training on obese participants was just 38% of that observed in participants with normal-weight BMI.

Memory training focused on improving verbal episodic memory through instruction and practice in strategy use. Reasoning training focused on improving the ability to solve problems that contained a serial pattern. Speed training focused on visual search and the ability to process increasingly more information presented in successively shorter inspection times.

Of the participants, three-quarters were women; three-quarters were white and one-quarter were African-American.

https://www.eurekalert.org/pub_releases/2017-01/iu-oaw011017.php

Clark, D. O., Xu, H., Callahan, C. M., & Unverzagt, F. W. (2016). Does Body Mass Index Modify Memory, Reasoning, and Speed of Processing Training Effects in Older Adults. Obesity, 24(11), 2319–2326. https://doi.org/10.1002/oby.21631

Data from the GENOA study, which began in 1997 and involved African Americans with high blood pressure and their siblings, has found that obesity as such was not linked to cognitive decline. The key factor was abdominal fat rather than BMI.

Having too much belly fat in mid- and late-life was linked to a much higher risk of cognitive decline. Among middle-aged adults, losing weight was linked to higher cognitive scores, while gaining weight was linked to lower scores. However, in later life, losing weight was linked to lower scores (I note that losing weight in old age is often a marker of developing dementia), and gaining weight was linked to better scores.

People in the study ranged in age from 35- to 86-years-old; 78% were women and most were obese. Participants were assessed in 1997-99, 2001-6, and 2009-11.

https://www.eurekalert.org/pub_releases/2017-05/ags-teo050817.php

West, N. A., Lirette, S. T., Cannon, V. A., Turner, S. T., Mosley, T. H., & Windham, B. G. (2017). Adiposity, Change in Adiposity, and Cognitive Decline in Mid- and Late Life. Journal of the American Geriatrics Society, 65(6), 1282–1288. https://doi.org/10.1111/jgs.14786

In one of the largest studies linking obesity with brain dysfunction, brain scans from more than 17,000 individuals (aged 18-94; mean age 40.8) were analyzed to measure blood flow and brain activity. Across all ages, higher BMI was associated with decreased cerebral blood flow. This was seen in almost all brain regions, and particularly so in regions known to be vulnerable to Alzheimer’s: temporal and parietal lobes, hippocampus, posterior cingulate gyrus, and precuneus.

https://www.eurekalert.org/pub_releases/2020-08/ip-bwh080520.php

Amen, Daniel G. et al. 2020. Patterns of Regional Cerebral Blood Flow as a Function of Obesity in Adults. Journal of Alzheimer’s Disease, 1 Jan. 2020: 1–7.

A mouse study explains why excessive weight around our middle affects cognition. It seems that such fat, known as visceral adiposity, generates high, chronic levels of a signal that encourages the formation of inflammasome complexes that amplify the immune response and inflammation.

A protein called NLRP3 is a core component of the inflammasome complex in the fat, and it’s what promotes the production and release of interleukin-1 beta by fat cells. When NLRP3 was blocked in mice, they became protected against such inflammation and cognitive problems. When visceral adipose tissue from obese mice and obese mice missing NLRP3 was transplanted into lean mice, the tissue from those missing NLRP3 had no deleterious effect, but the tissue from the intact obese mice caused increased levels of interleukin-1 beta in the hippocampus, and impaired cognition.

Mice missing interleukin-1 beta’s receptor on the microglia were also protected.

There are indications that interleukin-1 beta also prompts microglia to wrap around synapses, potentially interfering with the communication between neurons.

https://www.eurekalert.org/pub_releases/2020-03/mcog-vfd030220.php

Guo, D.-H., Yamamoto, M., Hernandez, C. M., Khodadadi, H., Baban, B., & Stranahan, A. M. (2020). Visceral adipose NLRP3 impairs cognition in obesity via IL-1R1 on CX3CR1⁺ cells. The Journal of Clinical Investigation, 130(4), 1961–1976. https://doi.org/10.1172/JCI126078

An animal study comparing five diets shows that one diet really doesn't fit everyone, and what works for some may not be best for others.

There were four groups of genetically (almost-)identical animals, with genetic differences between any two of the groups translating to roughly the same as those of two unrelated people. The test diets included: an American-style diet (higher in fat and refined carbs, especially corn); Mediterranean (with wheat and red wine extract); Japanese (with rice and green tea extract); and ketogenic, or Atkins-like (high in fat and protein with very few carbs). The fifth diet was the control group.

One of the four genetic types did very poorly when eating the Japanese-like diet, developing signs of liver damage. Two types did well on the Atkins-like diet, but two did very badly (one became very obese, while the other became 'skinny-fat' — apparently a healthy weight but with a high percentage of body fat.

Two types became very obese, with signs of metabolic syndrome, on the American-style diet, while the other two were less negatively affected. With the Mediterranean diet, some groups were healthy, while others experienced some weight gain.

https://www.eurekalert.org/pub_releases/2017-11/tau-dsm113017.php