Prevent or delay 40% of dementia cases by addressing lifestyle factors: Here is what you need to know
According to a recent report by the Lancet commission of dementia prevention, intervention and care, up to 40% of an individual’s risk of dementia is potentially modifiable1. But which are the factors that need to be addressed? And how does dementia prevention work?
Think of dementia as a disease of the young: Brain damage appears decades before the first symptoms
Dementia is generally perceived to be a disease of the old- but it is now recognized that late-onset Alzheimer’s disease (the most common form of dementia) begins decades before a diagnosis of dementia is made. Even in about one fifth of 25 year old’s, mild changes typical for the first neuropathological stages of Alzheimer’s disease can be found in routine autopsies2.
This earliest stage of the disease is called “preclinical Alzheimer’s disease”, and during this phase no symptoms are experienced. Because Alzheimer’s pathology progresses very slowly in the brain, the long preclinical phase offers a large window of opportunity for intervention to prevent or delay dementia symptoms3.
We all have the power to influence our odds of developing dementia
While age is the single biggest risk factor for dementia, dementia is not inevitable. An estimated 42% of people will develop Alzheimer’s disease by age 85, but this also means that 58% of older adults don’t develop dementia, even if they have damage typical for Alzheimer’s disease in their brains. The reason for this can in part be explained by the effect of risk factors which we are exposed to during our life4,5.
Some risk factors we can’t change, such as our age, gender and genetics. But up to 40% of dementia cases might be preventable by changing modifiable factors. These are the risk- and protective factors which we can actively influence1. Look for a list of modifiable risk and protective factors here.
However, it is important to note that adopting measures to reduce risk is no guarantee for prevention. Even with the best preventative measures, one might still develop dementia: It is the likelihood that decreases. Preventative measures can also help to delay the onset of dementia compared to when no preventative steps were taken.
Sometimes we cannot say with certainty whether a risk factor causes dementia, or whether what we see is a consequence of (early) disease, or both. This concept is referred to as “reverse causality”. For example, social isolation, depression or sleep disturbances might be caused by and cause, cognitive decline6.
disturbances might be caused by and cause, cognitive decline6.
It’s best to tackle multiple lifestyle factors at once
Many interrelated risk- and protective factors are at play for the development of dementia. It therefore doesn’t come as a surprise that multimodal interventions (these are interventions that target not one, but many risk factors at once) are deemed necessary for an optimal preventive effect7.
Risk and protective factors influence the brain via multiple ways.When talking about protective factors, one important concept is that of cognitive reserve: Such reserve means that one can tolerate more damage in the brain without experiencing a cognitive deficit. Think of cognitive reserve as having “more brain”, in the sense that better connections exist between brain cells but also, the ability to use these connections more effectively8.
Risk factors can do damage via multiple ways, and vascular damage, direct neurotoxic damage, inflammation, and oxidative stress all play a role. The most prominent mechanisms by which each factor influences the brain is described in more detail under the individual risk factors.
It matters when risk and protective factors are at play
The effect that risk- and protective factors depends on when in the lifespan we are exposed to them: For example, hypertension and obesity at middle age (<65) predict future dementia. On the other hand, a low blood pressure and weight in later life (>75) are found in those who are developing dementia9. Thus, a lower weight and blood pressure in later life could be a sign of illness, and not just absence of risk.
Or take education: education protects the brain from dementia by increasing cognitive reserve. Most of the clinical reserve is built up until late adolescence, and relative smaller gains are made with education after the age of 20 years. This is why education is more important in early life1,10.
Dementia risk can be calculated:
The Australian National University has created and validated the Alzheimer’s Disease Risk Index (ANU-ADRI) score, which is based on 11 risk factors and 4 protective factors11,12. The score is accessible here. The test takes 10-15 minutes, is free of charge, and a paper version is also available.
Other validated scores are the Cardiovascular Risk Factors, Ageing and Dementia (CAIDE) risk score, and the Lifestyle for Brain Health (LIBRA) score.
CAIDE is based on 7 midlife risk factors and can predict late life dementia (20 years later). The score is also available as mobile app in Europe13.
LIBRA is based on 12 risk and protective factors. It was developed in The Netherlands and was used in the innovative midlife intervention for dementia deterrence In-MINDD project14.
APOE is not destiny
There are several genes that increase a person’s risk to develop Alzheimer’s disease. The apolipoprotein E (APOE) is the major risk gene for late onset Alzheimer’s disease and comes in several different forms or alleles; people with a form known as APOE ɛ4 have an increased risk of cognitive impairment and Alzheimer’s disease.
People who carry one ɛ4 allele are estimated to have a lifetime risk of up to 35%, and people who carry two ɛ4 alleles are estimated to have a 68% risk at age 85. However, genes are neither a prerequisite for, nor sufficient cause for Alzheimer’s disease15,16. This is because genes interact with the environment, and this interaction determines the risk – by modifying the effect that genes have.
Overall, more cases of Alzheimer’s disease can be explained by lifestyle risk factors (around 40%) than by APOEɛ4 carrier status (around 7%)1,17.
Lifestyle interventions are even more important in risk gene carriers
Harmful environmental and lifestyle factors do more damage to the brain in APOE ɛ4 carriers than in people who don’t have a risk gene for Alzheimer’s. APOE ɛ4 can magnify the risk of lifestyle factors such as high saturated fat intake, physical inactivity, alcohol drinking, smoking or diabetes by at least 3 times. Thus, lifestyle interventions are particularly important in risk gene carriers18,19.
The good news is that protective factors can “buffer” the negative effects of risk genes. For example, formal high education can half the risk of dementia due to APOE ɛ420.
In Australia, the biggest lifestyle risk factor for dementia is physical inactivity
About 50% of Australia’s dementia cases can be attributed to seven risk factors (physical inactivity, midlife obesity, midlife hypertension, low educational attainment, smoking, depression, and diabetes). Physical inactivity is the biggest contributor to dementia cases with 18%, directly followed by midlife obesity, low educational attainment and hypertension21.
And now it’s your turn: educate, educate, educate!
Knowledge about modifiable risk factors in the population are low. However, 70% would like to receive more information about the relationship between lifestyle and brain health. In fact, the biggest barrier for adopting a brain healthy lifestyle is a lack of knowledge, followed by a lack of motivation according to a population based study in Holland22.
So what do people know? About 10% of people cannot identify a single risk factor, and the majority (around 70%) of people know fewer than 5. Most commonly people cited social isolation, depression, cognitive activity, exercise, and healthy diet as risk or protective factors. However, the link between “heart health” and “brain health” and associated variables such as high blood pressure, cholesterol and coronary heart disease are not well understood in the general population22,23.
Remember, reducing risk factors by 25%, could prevent up to 3 million dementia cases worldwide24. And you can help make this happen.
- Livingston G, Huntley J, Sommerlad A, et al. Dementia prevention, intervention, and care: 2020 report of the Lancet Commission. Lancet 2020; 396: 413–446.
- Braak H, Braak E. Frequency of Stages of Alzheimer-Related Lesions in Different Age Categories. 1997.
- Mortimer JA, Borenstein AR, Gosche KM, et al. Very Early Detection of Alzheimer Neuropathology and the Role of Brain Reserve in Modifying Its Clinical Expression. Journal of Geriatric Psychiatry and Neurology; 18. Epub ahead of print December 29, 2005. DOI: 10.1177/0891988705281869.
- Dementia Statistics hub, Alzheimer’s research UK. Alzheimer’s research UK, https://www.dementiastatistics.org/statistics/prevalence-by-age-in-the-uk/ (accessed June 17, 2021).
- Galvin JE. Prevention of Alzheimer’s Disease: Lessons Learned and Applied. Journal of the American Geriatrics Society 2017; 65: 2128–2133.
- Livingston G, Sommerlad A, Orgeta V, et al. Dementia prevention, intervention, and care. Lancet 2017; 390: 2673–2734.
- Kivipelto M, Mangialasche F, Ngandu T. Lifestyle interventions to prevent cognitive impairment, dementia and Alzheimer disease. Nature Reviews Neurology 2018; 14: 653–666.
- Stern Y. What is cognitive reserve? Theory and research application of the reserve concept. J Int Neuropsychol Soc 2002; 8: 448–460.
- Singh-Manoux A, Dugravot A, Shipley M, et al. Obesity trajectories and risk of dementia: 28 years of follow-up in the Whitehall II Study. Alzheimer’s & Dementia; 14. Epub ahead of print February 2018. DOI: 10.1016/j.jalz.2017.06.2637.
- Kremen WS, Beck A, Elman JA, et al. Influence of young adult cognitive ability and additional education on later-life cognition. Proceedings of the National Academy of Sciences; 116. Epub ahead of print February 5, 2019. DOI: 10.1073/pnas.1811537116.
- Anstey KJ, Cherbuin N, Herath PM. Development of a New Method for Assessing Global Risk of Alzheimer’s Disease for Use in Population Health Approaches to Prevention. Prevention Science 2013; 14: 411–421.
- Anstey KJ, Cherbuin N, Herath PM, et al. A Self-Report Risk Index to Predict Occurrence of Dementia in Three Independent Cohorts of Older Adults: The ANU-ADRI. PLoS ONE; 9. Epub ahead of print January 23, 2014. DOI: 10.1371/journal.pone.0086141.
- Sindi S, Calov E, Fokkens J, et al. The CAIDE Dementia Risk Score App: The development of an evidence‐based mobile application to predict the risk of dementia. Alzheimer’s & Dementia: Diagnosis, Assessment & Disease Monitoring; 1. Epub ahead of print September 2, 2015. DOI: 10.1016/j.dadm.2015.06.005.
- Schiepers OJG, Köhler S, Deckers K, et al. Lifestyle for Brain Health (LIBRA): a new model for dementia prevention. International Journal of Geriatric Psychiatry; 33. Epub ahead of print January 2018. DOI: 10.1002/gps.4700.
- Genin E, Hannequin D, Wallon D, et al. APOE and Alzheimer disease: a major gene with semi-dominant inheritance. Molecular Psychiatry; 16. Epub ahead of print September 10, 2011. DOI: 10.1038/mp.2011.52.
- Bettens K, Sleegers K, van Broeckhoven C. Genetic insights in Alzheimer’s disease. The Lancet Neurology; 12. Epub ahead of print January 2013. DOI: 10.1016/S1474-4422(12)70259-4.
- Ritchie K, Carriere I, Ritchie CW, et al. Designing prevention programmes to reduce incidence of dementia: prospective cohort study of modifiable risk factors. BMJ; 341. Epub ahead of print August 5, 2010. DOI: 10.1136/bmj.c3885.
- Kivipelto M, Rovio S, Ngandu T, et al. Apolipoprotein E 4 magnifies lifestyle risks for dementia: a population-based study. J Cell Mol Med 2008; 12: 2762–2771.
- Strand BH, Rosness TA, Engedal K, et al. Interaction of Apolipoprotein E Genotypes, Lifestyle Factors and Future Risk of Dementia-Related Mortality: The Cohort of Norway (CONOR). Dementia and Geriatric Cognitive Disorders; 40. Epub ahead of print 2015. DOI: 10.1159/000431218.
- Wang H-X, Gustafson DR, Kivipelto M, et al. Education halves the risk of dementia due to apolipoprotein ε4 allele: a collaborative study from the Swedish Brain Power initiative. Neurobiology of Aging; 33. Epub ahead of print May 2012. DOI: 10.1016/j.neurobiolaging.2011.10.003.
- Ashby-Mitchell K, Burns R, Shaw J, et al. Proportion of dementia in Australia explained by common modifiable risk factors. Alzheimer’s Research & Therapy; 9. Epub ahead of print December 17, 2017. DOI: 10.1186/s13195-017-0238-x.
- Heger I, Deckers K, van Boxtel M, et al. Dementia awareness and risk perception in middle-aged and older individuals: Baseline results of the MijnBreincoach survey on the association between lifestyle and brain health. BMC Public Health; 19. Epub ahead of print June 3, 2019. DOI: 10.1186/s12889-019-7010-z.
- Barak Y, Gray AR, Rapsey C, et al. The Dunedin dementia risk awareness project: Pilot study in older adults. International Psychogeriatrics 2020; 32: 241–254.
- Barnes DE, Yaffe K. The projected effect of risk factor reduction on Alzheimer’s disease prevalence. The Lancet Neurology; 10. Epub ahead of print September 2011. DOI: 10.1016/S1474-4422(11)70072-2.
This article has been written for the Australasian Society of Lifestyle Medicine (ASLM) by the documented original author. The views and opinions expressed in this article are solely those of the original author and do not necessarily represent the views and opinions of the ASLM or its Board.