Recent research supports the preventive promise of simple changes
Until they reach their 50s, most people don’t dwell on the risk of dementia.
But cognitive decline begins long before symptoms like memory loss begin to manifest.
According to the The Lancet Commission on Dementia prevention, intervention, and care, a handful of simple steps can help reduce the risk of dementia — possibly by as much as 35% (Livingston G et al. 2017).
Let’s examine five key lifestyle tactics, starting with one of the easiest steps anyone can take.
Step #1: Eat fatty fish
The first step is the easiest and simplest, because it doesn’t require significant self-discipline or medical intervention.
All you need to do is eat seafood — preferably fatty fish — at least twice a week, as recommended by U.S. and international health authorities.
There’s ample epidemiological (population-diet-health) and clinical evidence linking diets rich in fish with reduced risks for dementia and milder forms of cognitive decline. For example, see Fishy Diets Linked to Less Dementia in 3rd World.
Why would fishy diets help protect brain health? They do two important things:
- Provide omega-3 fats and vitamin D, which are linked to brain health.
- Limit consumption of meats, which aren’t linked to better brain health.
To learn more about research on omega-3s and brain health, see these and other reports from the Omega-3s & Brain Health section of our news archive:
- Omega-3 Deficiency Predicts Faster Brain Decline
- Fish Oil Aided the Size and Health of Aging Brains
- Middle-Aged Brain Boost Linked to Omega-3s
- Brain Health in Middle Age Tied to a Fishy Omega-3
- Omega-3 Seen to Preserve Memory in Healthy People
Likewise, many studies link low vitamin D levels to cognitive problems … you'll find these and more in the Brain Health section of our news archive:
- Vitamin D May Boost Aging Brains
- Vitamin D Lack Linked to High Dementia Risk
- Brain-Killing Plaque Cleared by Omega-3s, Vitamin D
- Vitamin D Shows More Brain Protection Potential
- Alzheimer's Linked to Vitamin D Lack
Unfortunately — compared with people in Japan, Europe, and many other places — Americans eat very little seafood.
And much of the seafood Americans eat is shrimp, the skipjack or tongol in most canned tuna, and the pollock used in most fish sticks and sandwiches.
Compared with fatty fish like sardines, salmon, sablefish, mackerel, and albacore (“white”) tuna, shrimp and pollock don’t provide nearly as much omega-3 fat or vitamin D.
Our Seafood Nutrition chart shows the average omega-3 and vitamin D content of most species sold at Vital Choice. You’ll also find comparative omega-3 content data at the Seafood Health Facts website — a joint project of six American colleges and universities.
For those who don't like seafood, or can't get their families to eat it frequently, it makes sense to take omega-3 and vitamin D supplements.
Step #2: Get a good night’s sleep as often as you can
The results of several studies published this year and last combine to stress the importance of sleep to brain health.
And poor sleep doesn’t just damage brain health: see Junk Sleep Hurts You As Much As Junk Food.
We covered some of the proven strategies for helping to ensure good sleep in Suffering a Lack of Sleep? Try Seven Secrets.
Let’s take a close look at two of the most recent, comprehensive reports on the role lifestyle can play in raising or lowering dementia risk.
Loss of REM sleep promotes dementia
Last year, Australian researchers published a study involving 321 people (average age of 67) from Massachusetts who’d participated in the famous Framingham Heart Study.
During their study, sleep cycles were measured for each participant.
There are five stages of sleep:
- Light sleep
- Preparation for deep sleep
- Deep sleep part one
- Deep sleep part two
- REM or “dreaming” sleep, during which the eyes move rapidly, brain activity increases, body temperature rises, and pulse and breathing rates quicken.
REM sleep begins about an hour to an hour-and-a-half into sleep and recurs periodically throughout the night.
The Australian researchers collected sleep data from the participants and then followed them for an average of 12 years.
During that time, 32 people were diagnosed with some form of dementia and of those, 24 were determined to have Alzheimer’s disease.
The people who developed dementia spent an average of 17 percent of their sleep time in REM sleep, compared to 20 percent for those who did not develop dementia.
After adjusting for age and sex, researchers found links between both a lower percentage of REM sleep and a longer time to get to the REM sleep stage and a greater risk of dementia.
In fact, for every percent reduction in REM sleep there was a 9 percent increase in the risk of dementia.
Sleep deprivation promotes Alzheimer’s-related plaque
The results of a recent study from the National Institute on Alcohol Abuse and Alcoholism (NIAAA) also support the importance of sleep.
Researchers from the NIAAA conducted a small brain-scan study, and its results showed that losing just one night of sleep immediately raised brain levels of beta-amyloid protein, high levels of which occur in most Alzheimer’s patients (Shokri-Kojori E et al. 2018).
Beta-amyloid protein plaques impair communication between brain cells (neurons), and beta-amyloid levels are typically about 40% higher in Alzheimer’s patients, compared with healthy older adults.
Sleep deprivation elevates brain beta-amyloid levels in mice. And the new brain-imaging study from the NIAAA seems to confirm that good sleep helps control beta-amyloid plaque buildup — probably by enabling optimal performance by the brain’s own “trash removal” processes.
The NIH team used positron emission tomography (PET) to scan the brains of 20 healthy subjects (aged from 22 to 72 years), after a night of restful sleep and after being awake for about 31 hours (i.e., losing a night of sleep).
Losing a night of sleep raised beta-amyloid levels by about five percent in the thalamus and hippocampus — brain regions especially vulnerable to damage in the early stages of Alzheimer’s disease.
The researchers also found that study participants with larger increases in beta-amyloid reported worse mood after sleep deprivation.
The study wasn’t designed to determine whether the increase in beta-amyloid in sleep deprived participants would subside after a night of rest.
According to study co-author Dr. Ehsan Shokri-Kojori, Ph.D., “Even though our sample was small, this study demonstrated the negative effect of sleep deprivation on beta-amyloid burden in the human brain.”
Interestingly, the link between sleep disorders and Alzheimer's risk is believed to be “bidirectional,” because elevated beta-amyloid levels may also lead to sleep disturbances.
Disordered breathing during sleep linked to dementia
Three research papers presented at the 2017 Alzheimer’s Association International Conference look for links between breathing problems during sleep and physical markers of Alzheimer’s disease.
Adults who suffer from sleep disordered breathing (SDB) experience hypopnea (under-breathing) and apnea (not breathing).
The three studies presented at the Alzheimer’s Association meeting came to these conclusions:
- SDB increased the build-up of beta-amyloid (a marker of Alzheimer’s disease) in normal individuals and individuals with mild memory impairment
- Obstructive sleep apnea (OSA), the most common type of SDB, was associated with increased brain build-up of beta-amyloid, lower levels of cerebrospinal fluid (CSF), and higher levels of tau protein levels – 3 markers of Alzheimer’s disease
As Dean M. Hartley, Ph.D., of the Alzheimer’s Association said, “The Centers for Disease Control and Prevention says more than one third of American adults do not get enough sleep on a regular basis. Clearly this is not good for brain health or overall health.”
And he added an important, encouraging point: “Sleep disordered breathing is treatable in many cases … and effective treatment of these sleep disorders [presents] the potential to improve cognition and possibly reduce dementia risk.”
Steps #3, 4, and 5: Control weight, control blood pressure, get ample exercise
Last year witnessed the release of two comprehensive reports on the efficacy of using various lifestyle measures to reduce dementia risk.
And the results of a first-ever clinical trial seem to support their conclusions: see Can Dementia be Defeated Naturally?.
Lancet commission report
A commission of 24 international experts — convened by the medical journal Lancet — presented a report on dementia treatment and prevention at the Alzheimer’s Association International Conference.
The commission listed nine risk factors, ranging from early-life choices to those in later life, that show promise for helping to minimize or prevent dementia.
Importantly, the commission estimated that about one-third — 35% to be precise — of all cases of dementia could be prevented by improving these lifestyle factors.
The nine lifestyle factors include:
- Hearing loss
- Social isolation
- Physical inactivity
- Diabetes in late life
- High blood pressure
- Obesity in middle age
- Years of education before age 15
Out of these nine factors, six can be modified by personal actions and/or medical treatment: high blood pressure, obesity, smoking, depression, social isolation, diabetes late in life, and physical inactivity.
The commission also calculated risk reduction associated with two groups of factors:
- Education in early life and managing hearing loss, hypertension and obesity in midlife, dementia rates could reduce the risk by as much as 20%.
- Stopping smoking, treating depression, increasing physical activity, increasing social contact and managing diabetes could reduce dementia risk by an additional 15%.
Commission member Lon Schneider, M.D., from the Keck School of Medicine at California’s USC stress the meaning of their findings: “There’s been a great deal of focus on developing medicines to prevent dementia, including Alzheimer’s disease. But we can’t lose sight of the real major advances we’ve already made in treating dementia, including preventive approaches.”
And as she said, “The potential magnitude of the effect on dementia of reducing these risk factors is larger than we could ever imagine the effect that current, experimental medications could have. Mitigating risk factors provides us a powerful way to reduce the global burden of dementia.”
National Academies report
The second report — a 180-page book — came from the U.S. National Academies of Sciences, Engineering, and Medicine.
The National Academies convened a 17-member panel of university experts to examine lifestyle factors believed to slow mental decline and dementia (NAS 2017).
Their findings and recommendations were based mostly on findings from an evidence review commissioned by the U.S. Agency for Healthcare Research and Quality, and were more conservative than those of the Lancet commission (Kane RL et al. 2017).
The National Academies report, entitled Preventing Cognitive Decline and Dementia: A Way Forward, concludes that scientific evidence is not robust enough to justify “an assertive public health campaign aimed at widespread adoption of any such intervention”.
While there are gaps in the available research, the committee concluded that three interventions look encouraging:
- Increased physical activity
- Blood pressure management
- Cognitive training – This includes education focused on improving reasoning and problem solving, memory and processing speed (many of these training exercises are computer-based)
The clinical evidence is somewhat inconsistent, but generally indicates that cognitive training can improve performance on a trained task, while long-term benefits for memory and reasoning are not yet known.
Blood pressure management, particularly between the ages of 35 to 65 years, shows promising but inconclusive results. However, the heart-health benefits of controlling blood pressure make this dementia-prevention tactic a — pardon the pun — “no-brainer”.
The NAS panel concluded that increased physical activity can delay age-related cognitive decline, although the results of research aren’t entirely consistent. Like blood pressure management, the broader health benefits of physical activity are well-documented.
According to the committee chairperson Alan I. Leshner, Ph.D., “Even though clinical trials have not conclusively supported the three interventions discussed in our report, the evidence is strong enough to … help inform [people’s] decisions about how they can invest their time and resources to maintain brain health with aging.”
- Bubu O et al. Effect of Obstructive Sleep Apnea (OSA) on Rate of Change of AD Biomarkers in Cognitive Normal, MCI and AD Elderly: Findings from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) Cohort. Presented at the Alzheimer’s Association International Conference 2017. 18 July 2017.
- Hogan M, et al. Obstructive Sleep Is Associated with Longitudinal Increases in Amyloid Burden in Elderly Mild Cognitive Impairment Individuals. Presented at the Alzheimer’s Association International Conference 2017. 18 July 2017.
- Kane RL et al. Interventions to Prevent Age-Related Cognitive Decline, Mild Cognitive Impairment, and Clinical Alzheimer’s-Type Dementia [Internet]. Rockville (MD): Agency for Healthcare Research and Quality (US); 2017 Mar.
- Livingston G et al. Dementia prevention, intervention, and care. Lancet. 2017 Jul 19. pii: S0140-6736(17)31363-6.
- National Academies of Sciences (NAS), Engineering, and Medicine, Health and Medicine Division, Board on Health Sciences Policy, Committee on Preventing Dementia and Cognitive Impairment; Downey A, Stroud C, Landis S, Leshner AI, editors. Preventing Cognitive Decline and Dementia: A Way Forward. Washington (DC): National Academies Press (US); 2017 Jun 22. Accessed at https://www.ncbi.nlm.nih.gov/books/NBK436397/
- Shim A, et al. Sleep Disordered Breathing, APOE4 and β-Amyloid Deposition in Cognitive Normal Elderly. Presented at the Alzheimer’s Association International Conference 2017. 18 July 2017.
- Shokri-Kojori E et al. β-Amyloid accumulation in the human brain after one night of sleep deprivation. Proc Natl Acad Sci U S A. 2018 Apr 24;115(17):4483-4488. doi: 10.1073/pnas.1721694115. Epub 2018 Apr 9.