Brain shrinkage, known as ‘cerebral atrophy’ in the scientific community, is a process that describes the gradual loss of neurons (brain cells). Akin to the way that we lose height or muscle mass as we age, cerebral atrophy is an ongoing process and is more common in aging individuals. Aging has widespread effects on the brain – from the neurotransmitters that control memory and thought processing to the blood supply and overall size of the brain.
Even in those who are otherwise healthy, some shrinkage is quite normal. After age 40, the volume of the brain shrinks by around 5% per decade, with rates increasing further over age 70. However, rates of atrophy are notably higher amongst those with cognitive impairment, particularly in those who progress to have Alzheimer’s disease.
However, brain aging and shrinkage are not tied to our chronological age, meaning that despite the 
turning pages of the calendar, it may be possible to slow the process of cerebral atrophy with diet, exercise, and moderating alcohol intake. Interestingly, these lifestyle-based changes may have a greater impact than some of the newest drugs on the market.
Led by the University of Oxford Professor David Smith, director of the Oxford Project to Investigate Memory and Ageing (OPTIMA), a clinical trial highlighted vitamin B’s role in preserving brain volume in older adults with mild cognitive impairment.
Certain B vitamins (particularly folate, B6 and B12) are essential in breaking down a substance called homocysteine. This amino acid serves as a building block for proteins in the body. Previous research has demonstrated that elevated homocysteine levels may be associated with an increased risk of dementia, heart disease, and stroke. Thus, Professor Smith’s team set out to investigate whether vitamin B, which plays a critical role in lowering homocysteine levels, could reduce the rate of brain atrophy in older adults.
The clinical trial, published in PLoS One in 2010, included 271 individuals aged 70+ who had identified pre-
existing concerns with their memory. The volunteers included in this study were defined as having ‘mild cognitive impairment,’ which indicates challenges with memory, recall, or word-finding that do not interfere with day-to-day function. Participants underwent MRI imaging of their brains at the start and end of the study to assess overall brain size and volume. Over two years, study participants were randomly assigned to receive either high-dose vitamin B supplements (consisting of folic acid, vitamin B12 and vitamin B6) or to the placebo group.
As expected, the researchers found that treatment with vitamin B tablets led to a notable 22.5% reduction in homocysteine levels in the blood – already a promising finding! The brain imaging revealed that those who received B vitamins had a reduced rate of brain atrophy – 30% less than the placebo group. Importantly, those individuals who received the vitamin B tablets did not report any adverse side effects, suggesting that this is likely a safe and reasonable treatment to slow the accelerated rate of brain shrinkage in older adults with mild degrees of cognitive impairment.
To highlight how impactful these dietary changes can be, and perhaps more so than a pharmaceutical intervention, a 2019 study published in Translational Research & Clinical Intervention investigated a highly touted new medication, solanezumab, on brain shrinkage. In a class of drugs known as monoclonal antibodies, solanezumab binds to and clears amyloid proteins from the brain, which are known to play a role in the development of Alzheimer’s dementia. Surprisingly, the study results failed to demonstrate any difference in brain atrophy rates between those who received the medication and those who were taking the placebo pill.
This is an important, early study highlighting how simple supplements like Vitamin B can slow the rate of progression of mild cognitive impairment associated with brain atrophy. Nearly 1 in 6 adults over the age of 70 have troubling concerns with their memory, and a proportion of these will advance to develop Alzheimer’s Disease. Therefore, it is critical to identify safe interventions that will delay or prevent the progression of memory impairment.
