Brain atrophy, or brain shrinkage, is the opposite of neurogenesis. Brain atrophy describes a loss of neurons and the connections between them.
Figure 1. Normal brain versus Atrophic brain (Source)
Brain atrophy can be categorized as either general or focal. With general brain atrophy, all of the brain shrinks. With focal brain atrophy, shrinkage of the brain affects a limited area of the brain which often results in decreased functions in the area that area controls. For example, if the cerebrum atrophies, then conscious thought and voluntary processes may be impaired.
Even if you do not have a chronic disease, you may be losing as much as 0.4% of your brain mass every year. 1 The rate of brain shrinkage increases with age and is a major factor in early cognitive decline and premature death. 2 Age related cognitive decline occurs in tandem with the physical degradation of brain structure.
Figure 2. Brain atrophy in Advanced Alzheimer’s Disease (Source)
By the age of 60, approximately .5 to 1% of brain volume is lost per year. By the time you reach age 75, your brain is on average of 15% smaller than it was when you were in your mid-20’s.
Even though brain shrinkage is progressive, a growing number of neuroscientists believe that brain shrinkage can be slowed or even reversed. 3
Medical science has recognized a number of conditions and behaviors that cause brain atrophy:
Homocysteine is a risk factor for brain atrophy. Supplementation with B vitamins that lower levels of plasma total homocysteine can slow the rate of brain atrophy in subjects with mild cognitive impairment. 4
Poor sleep quality was associated with reduced volume within the right superior frontal cortex in cross-sectional analyses, and an increased rate of atrophy within widespread frontal, temporal, and parietal regions in longitudinal analyses. 5
Studies have shown that both high and low blood pressure (BP) may play a role in the etiology of brain atrophy. High BP in midlife has been associated with more brain atrophy later in life. 6
Normal aging is associated with diminished blood flow to the brain. This pathology is known as hypoperfusion and causes cell injury and death. The combination of hypertension and hypoperfusion is associated with smaller brain volume. 7
Type 2 Diabetes
New research has shown that cognitive decline in people with type 2 diabetes is likely due to brain atrophy, or shrinkage, that resembles patterns seen in the early stages of Alzheimer’s disease. 8
Higher body mass index (BMI, a measure of obesity) is associated with lower brain volume in obese and overweight people. 9
Any lifetime history of smoking (even if you currently do not smoke) is associated with faster brain shrinkage in multiple brain regions, compared with people who never smoked. 10
Heavy drinkers are 80% more likely than nondrinkers to sustain frontal lobe shrinkage, compared with nondrinkers,49 and 32% more likely to have enlargement of the ventricles, indicating shrinkage from within. 11
Preventing Brain Atrophy with Omega-3 Fatty Acids and B Vitamins
A study published in July 2015 in The American Journal of Clinical Nutrition entitled “Brain atrophy in cognitively impaired elderly: the importance of long-chain ω-3 fatty acids and B vitamin status in a randomized controlled trial”, revealed some interesting new findings on brain atrophy.
The researchers investigated whether plasma omega-3 fatty acid concentrations (eicosapentaenoic acid and docosahexaenoic acid) modify the treatment effect of homocysteine-lowering B vitamins on brain atrophy rates in a placebo-controlled trial.
The study included 168 elderly people (≥70 y) with mild cognitive impairment, randomly assigned either to placebo (n = 83) or to daily high-dose B vitamin supplementation formula consisting of:
- folic acid (800 mcg)
- vitamin B6 (20 mg)
- vitamin B12 (500 mcg)
The subjects underwent cranial magnetic resonance imaging scans at baseline and 2 years later.
In the group of subjects who took the B vitamin formula and that had a high baseline omega-3 blood levels (>590 μmol/L), the mean brain atrophy rate slowed by 40% compared to the placebo group.
In the placebo group there was no slowing of brain atrophy even when this group had a high baseline of omega-3 fatty acids.
In the group receiving the B vitamin formula with a low baseline omega-3 blood levels (390μmol/L), there was no significant effect on the rate of atrophy among subjects.
The researchers conclusion demonstrates the importance to supplement with both omega-3 fatty acids and the B-complex vitamins:
“The beneficial effect of B vitamin treatment on brain atrophy was observed only in subjects with high plasma ω-3 fatty acids. It is also suggested that the beneficial effect of ω-3 fatty acids on brain atrophy may be confined to subjects with good B vitamin status.” 12
Prevention of Cognitive Decline with Omega-3 Fatty Acids and B Vitamins
A more recent study published in January 2016 in the Journal of Alzheimer’s Disease entitled “Omega-3 Fatty Acid Status Enhances the Prevention of Cognitive Decline by B Vitamins in Mild Cognitive Impairment”, investigated whether baseline omega-3 fatty acid status interacts with the effects of B vitamin treatment slowed the rate of cognitive and clinical decline.
For this study 266 participants with MCI aged ≥70 years were randomized to B vitamins (folic acid, vitamins B6 and B12) or placebo for 2 years.
Baseline cognitive test performance, clinical dementia rating (CDR) scale, and plasma concentrations of total homocysteine, total docosahexaenoic and eicosapentaenoic acids (omega-3 fatty acids) were measured.
Final scores for verbal delayed recall, global cognition, and CDR sum-of-boxes were better in the B vitamin-treated group according to increasing baseline concentrations of omega-3 fatty acids, whereas scores in the placebo group were similar across these concentrations.
The results were intriguing among those with good omega-3 status. In this group, 33% of those on B vitamin treatment had global CDR scores >0 compared with 59% among those on placebo.
For all three outcome measures, higher concentrations of docosahexaenoic acid (DHA) alone significantly enhanced the cognitive effects of B vitamins, while eicosapentaenoic acid (EPA) appeared less effective.
When omega-3 fatty acid concentrations are low, B vitamin treatment has no effect on cognitive decline in MCI, but when omega-3 levels are in the upper normal range, B vitamins interact to slow cognitive decline.
The concluding remarks from the researchers reinforces the necessity to consume both omega-3 fatty acids, preferably in the form of EPA and DHA (fish oil) and the B-complex vitamins:
“In conclusion, when plasma omega-3 fatty acid concentrations are low, B vitamin treatment does not slow cognitive decline in people with MCI. In contrast, when omega-3 fatty acid levels are in the upper range of normal, the slowing effects of B vitamins on both brain atrophy  and cognitive decline are enhanced. We suggest that the effects of this interaction between the two nutrients on brain atrophy and cognition is consistent with the view that they slow down the disease process in MCI.” 13