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What can you do, practically and quickly, to reduce your risk of developing Alzheimer’s?

The International Alzheimer’s Prevention Expert Group, including our founder Patrick Holford, has identified four key areas that could cut your future risk by over 80% – down to less than a quarter – if addressed early.

The four “quick wins”? Increase your vitamin D, omega-3, and B vitamins, and reduce your intake of sugar and refined carbs.

1. Vitamin D: The Sunshine Factor

Vitamin D is primarily made in your skin through sun exposure, particularly at midday in the summer. However, in the winter – especially in the UK and other northern countries – you cannot make enough, so supplementation is essential. A Dutch study found that people with low levels of vitamin D, omega-3s, and B vitamins were over four times more likely to develop dementia¹. Those who supplement with vitamin D have around a third less risk².

Even levels below 62.5 nmol/L (25 ng/mL) increase risk. A French study found that low vitamin D levels tripled Alzheimer’s risk³. The darker your skin, the more sun exposure you need – which makes supplementation all the more vital for many.

2. Omega-3: Feed Your Brain with Fish

Fish is a true brain food – rich in omega-3s, vitamin D, and B12. Eating fish at least once a week reduces Alzheimer’s risk by a third⁴. A recent review confirmed that a daily serving cuts the risk of cognitive decline by 30%⁵.

Omega-3 fats (especially DHA) quite literally build brain cells. The UK Biobank study of over 250,000 people found that those with higher omega-3 levels had a 20% lower risk of dementia⁶. A US study also found that a higher omega-3 index correlated with more white matter in the brain and better cognitive function⁷.

Professor William Harris of the Fatty Acid Research Institute calls it “a safe, simple, cheap and effective tool to forestall Alzheimer’s.”

3. B Vitamins: The Brain Fixers

B6, B12, and folate don’t just support brain function – they’re essential for fixing omega-3s into your brain’s cell membranes. Without them, homocysteine – a toxic amino acid – builds up in your blood. High levels (above 11 μmol/L) are strongly linked to brain shrinkage and Alzheimer’s.

Half of people over 60 in the US have homocysteine levels above 11. The Dutch study found that risk rises even above 8 – a level many people exceed.

As Professor Joshua Miller from Rutgers University says, raised homocysteine is an early warning sign: “a canary in the coal mine.” The good news? It’s easily lowered with a B vitamin supplement – ideally one containing 500 mcg of B12, methylfolate, and B6.

More greens, beans, nuts, and lentils also help. A recent study showed that replacing just one serving of processed meat with nuts or beans (rich in folate) cut dementia risk by 19%⁸.

4. Sugar and Refined Carbs: Silent Brain Saboteurs

The more sugar a person eats – including refined white carbohydrate foods such as bread, pastries, pasta, and rice – the higher their risk of both diabetes and dementia. Fizzy drinks and ultra-processed foods, sweetened with high-fructose corn syrup, are particularly bad for the brain.
“The brain needs the most energy of any organ, so it has the most mitochondria to make it. Sugar damages mitochondria,” says Dr Robert Lustig from the University of California, San Francisco.

A study just published this month in Neurology involving 2 million people shows that those with sugar problems (metabolic syndrome) are 24% more likely to develop dementia early¹⁰.
Keeping blood glucose levels in the low–normal range is reflected by a low glycosylated haemoglobin (HbA1c), which is the blood test doctors use to diagnose diabetes. Having a lower HbA1c is associated with reduced risk for dementia in several studies⁹. A recent study of 374,021 older men with diabetes found that keeping HbA1c stable over three years cut the risk of dementia by a third¹¹.

Want to know what’s driving your brain risk?

Take our free 3-minute Alzheimer’s Prevention Check at alzheimersprevention.info – or, for the full picture, order the four-in-one home blood test to measure your omega-3 index, vitamin D, homocysteine and HbA1c: foodforthebrain.org/tests

Food for the Brain is a not-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.

By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices.

Please support our research by becoming a Friend of Food for the Brain.

References:

1  van Soest APM., et al Alzheimers Dement. 2024 Jul;20(7):4594-4601

2 Ghahremani M, et al. Vitamin D supplementation and incident dementia: Effects of sex, APOE, and baseline cognitive status. Alzheimers Dement (Amst). 2023 Mar;15(1):e12404. doi: https://doi.org/10.1002/dad2.12404

 3 Feart C, et al. Associations of lower vitamin D concentrations with cognitive decline and long-term risk of dementia and Alzheimer’s disease in older adults. Alzheimers Dement. 2017 Nov;13(11):1207-1216. doi: https://doi.org/10.1016/j.jalz.2017.03.003

4 Beydoun MA, et al. Epidemiologic studies of modifiable factors associated with cognition and dementia: systematic review and meta-analysis. BMC Public Health. 2014;14:643. doi: https://doi.org/10.1186/1471-2458-14-643

5 Godos J, et al. Fish consumption, cognitive impairment and dementia: an updated dose-response meta-analysis of observational studies. Aging Clin Exp Res. 2024;61:3731–3739. doi: https://doi.org/10.1007/s40520-024-02823-6

6 Sala-Vila A, et al. Plasma Omega-3 Fatty Acids and Risk for Incident Dementia in the UK Biobank Study: A Closer Look. Nutrients. 2023 Nov;15(23):4896.

7 Loong S, et al. Omega-3 Fatty Acids, Cognition, and Brain Volume in Older Adults. Brain Sci. 2023;13:1278. doi: https://doi.org/10.3390/brainsci13091278

8 Li Y, et al. Long-term intake of red meat in relation to dementia risk and cognitive function in US adults. Neurology.2025;104(3):e210286. doi: https://doi.org/10.1212/WNL.0000000000210286

9 Luchsinger JA, et al. Hyperinsulinemia and risk of Alzheimer disease. Neurology. 2004;63(7):1187–92. doi:https://doi.org/10.1212/01.WNL.0000140292.04932.04932.87;  see also Abbatecola AM, et al. Insulin resistance and executive dysfunction in older persons. J Am Geriatr Soc.2004;52(10):1713–

8. https://doi.org/10.1111/j.1532-5415.2004.52466.x ;see also Xu WL, et al. Uncontrolled diabetes increases the risk of Alzheimer’s disease: a population-based cohort study. Diabetologia. 2009;52(6):1031–

9. doi: 10.1007/s00125-009-1323-x ;see also Hassing LB, et al. Type 2 diabetes mellitus contributes to cognitive decline in old age: a longitudinal population-based study. J Int Neuropsychol Soc. 2004;10(4):599–607. https://doi.org/10.1017/S1355617704104165
; see also Yaffe K, et al. Glycosylated hemoglobin level and development of mild cognitive impairment or dementia in older women. J Nutr Health Aging. 2006;10(4):293–5. https://pubmed.ncbi.nlm.nih.gov/16886099/ ; see also Roberts RO, et al. Diabetes and elevated hemoglobin A1c levels are associated with brain hypometabolism but not amyloid accumulation. J Nucl Med. 2014;55(5):759–64. https://jnm.snmjournals.org/content/55/5/759 

10  Lee JY, Han K, Kim J, Lim JS, Cheon DY, Lee M. Association Between Metabolic Syndrome and Young-Onset Dementia: A Nationwide Population-Based Study. Neurology. 2025 May 27;104(10):e213599. doi: 10.1212/WNL.0000000000213599. Epub 2025 Apr 23. PMID: 40267374.11 Underwood PC, et al. HbA1c time in range and dementia. JAMA Netw Open. 2024;7(8):e2425354. doi: https://doi.org/10.1001/jamanetworkopen.2024.25354

Patrick Holford’s new book claims that almost no one needs to develop Alzheimer’s.

Fewer than 1% of Alzheimer’s cases are genetic, and amyloid deposits – long targeted by new drugs – are neither the cause of the disease nor its cure.

Alzheimer’s is the consequence of a ‘perfect storm’ – a combination of poor diet, unhealthy lifestyle and harmful environmental factors that affect the structure, function or utilisation of the brain, says Patrick Holford,  our founder and author of Alzheimer’s: Prevention is the Cure. He says: “Every single known risk factor affects one of these, and it is combinations of these risk factors – which are under our control – that lead to cognitive decline, first experienced as brain fog and forgetfulness”.

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The book stems from a major global Alzheimer’s prevention project by the charity Food for the Brain, which has assessed the cognitive function of hundreds of thousands of people through a free test, followed by a comprehensive diet and lifestyle questionnaire that calculates their future risk – and shows how to lower it.

“We can detect declining cognitive function from as young as 18. The youngest non-genetic Alzheimer’s diagnosis is just 19,” says Holford, who founded the charity to help prevent Alzheimer’s. “We see a steady decline in cognitive function from the early twenties, with most people starting to show significant cognitive impairment in their seventies and eighties. But this decline cannot only be arrested – it can be reversed with the right diet, supplements and lifestyle choices.”

“Becoming an Alzheimer’s patient is almost always a choice,” says neurologist Dr David Perlmutter, a member of the charity’s Alzheimer’s Prevention Expert Group who also believes that diet and lifestyle, much more than genes, are driving the increase in Alzheimer’s.

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The book  (out today!) explains all the known risk factors we can change – and the extent to which doing so reduces future risk. Particularly important are what Holford calls ‘the four horsemen of the brain health apocalypse’: lack of brain fats, lack of B vitamins, lack of antioxidants, and too much sugar and refined foods. Increasing omega-3 intake from oily fish and supplements cuts risk by about 20%, as does optimising vitamin D levels. Vitamin D is produced in the skin when exposed to sunlight, with some also obtained from oily fish, but supplementation is needed during the winter months. Those who supplement with vitamin D have about one third less risk of developing dementia.

The single biggest–and most easily eliminated–risk factor, is lack of B vitamins, leading to high levels of the toxic amino acid homocysteine. “Homocysteine, if raised above 11 µmol/L, causes brain shrinkage and cognitive decline. If lowered with B vitamins, both shrinkage and decline are arrested. It is the only risk factor for which the evidence is strong enough to say it is causal.” says Holford. “Mine is 7 µmol/L but my wife’s, despite eating the same food, was 15µmol/L – right in the brain-shrinking zone. She now supplements high-dose B12, B6 and folate and her level has dropped to the same as mine. You would never know without testing. We are both in our sixties.” He estimates that half of those over-60 have a homocysteine level above 11, increasing their risk by about one-third.

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“This is why we are now testing people, with a home-test kit, for homocysteine, vitamin D and omega-3 index. If the omega-3 index is below 8% – as it is for many – that predicts cognitive decline and loss of brain density.”

The test kit also measures HbA1c, which GPs use to diagnose diabetes. However, the optimal level for Alzheimer’s prevention is lower than the threshold used to diagnose diabetes. Eating less sugar, fewer refined and ultra-processed foods, and reducing total carbohydrate intake also cuts dementia risk by about 20%.

Another big risk reducer is increasing intake of fruits and vegetables rich in antioxidants, and supplementing with vitamin C. Those in the top third of antioxidant intake have half the risk of cognitive decline, according to a study of 2,716 people over age 60 (1). The home-test kit also measures antioxidant status, specifically glutathione levels.  Greens and beans are rich sources of the B vitamin folate. A recent study found that swapping one serving of processed meat for a serving of nuts or beans – foods high in folate – was associated with a 19% lower risk of dementia (2).

Getting your diet right is only half the story, says Holford. “Minimising alcohol, not smoking, staying physically active, and having a socially and intellectually stimulating lifestyle are all vital parts of dementia-proofing. So too are getting enough sleep, managing stress, and ensuring good hearing and vision. Cataracts, for example, increase risk, but having cataract surgery significantly lowers it. Women also need to support hormonal health after menopause. Often using ‘natural’ HRT makes a big difference.”

The book is out in the UK, EU today and you can pre-order for USA & Australia too (they will be shipped ot you in 3-5 weeks) .

Also join us in May for the Alzheimer’s Prevention Day

Food for the Brain is a not-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.

By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices.

Please support our research by becoming a Friend of Food for the Brain.

By Patrick Holford

Recently, the Telegraph reported: “Statins can reduce the risk of dementia among those who already have low cholesterol.” The article claimed that those on statins were less likely to develop dementia – even Alzheimer’s – and that low LDL cholesterol was somehow protective.

Frankly, this is dangerous misinformation.

Why? Because it contradicts robust scientific evidence that low cholesterol – particularly below 4 mmol/l – increases the risk for dementia. That’s hardly surprising when you consider that 25% of the cholesterol in your body is in your brain. Cholesterol is a vital component of neuronal membranes – it’s not just blood fat, it’s brain fuel.

And as for statins? There’s no credible evidence that they prevent dementia. Quite the opposite: the evidence points to statins lowering brain-essential cholesterol and raising dementia risk. So I asked cholesterol expert Dr Malcolm Kendrick for his take on the study in question.

His response was blunt but justified: “This study is horseshit. Here’s why…”

Dr Kendrick Key Critiques:

LDL measurement was vague. It’s unclear if they even measured LDL directly- most studies use the Friedewald formula, known to be wildly inaccurate, especially with high triglycerides or low HDL.

Only one measurement. LDL was recorded once at the study’s start – never again. That’s like measuring someone’s blood pressure once and claiming to predict their lifetime stroke risk.

Bizarre cohort overlap. Somehow, 170,174 participants were in both high and low LDL groups? That’s statistically and biologically nonsensical.

Alzheimer’s exclusion unexplained. Those with pre-existing Alzheimer’s were removed, but with no breakdown of their LDL levels – crucial missing data.

Propensity score manipulation. This “retrospective matching” excluded over 350,000 people, distorting the natural associations. Diabetes and hyperlipidaemia were artificially balanced between groups, masking real-world relationships.

Key confounder: statin timing. Participants were only included after being prescribed statins, meaning LDL levels were already artificially lowered. So “low LDL” here is post-drug, not natural. The entire premise collapses.

This study, like too many others published today, exemplifies what Drummond Rennie famously criticised:

“There is no study too fragmented, no hypothesis too trivial, no design too warped, no analysis too self-serving for it to be published.”

So what do we actually know? Here is an extract from Patrick’s new book – Alzheimers: Prevention is the Cure.

Cholesterol and the Brain – The Real Story

Your brain needs cholesterol. Low cholesterol (<4 mmol/l) is a clear risk factor for dementia. One biomarker study found that high homocysteine and low cholesterol were the best predictors of dementia risk【1】.

And what’s a common cause of low cholesterol in the elderly? Statins. These drugs have consistently failed to show benefits in preventing cognitive decline【2】.

This fits what we know genetically. The ApoE gene governs how cholesterol gets into neurons. Those with ApoE4 are less efficient at this – that’s why they’re more prone to cognitive decline.

It’s not high cholesterol itself that’s dangerous – it’s cholesterol mismanagement in the brain.

Yes, very high cholesterol (above 6.5 mmol/l) is statistically linked to increased dementia risk – but modest elevations, particularly with a healthy lifestyle, are not a problem【3】. And even that data is shaky. One meta-analysis of over a million people showed only a 14% increased dementia risk with “high” cholesterol. But the thresholds varied – some studies defined “high” as anything over 6.2 mmol/l【3】.

More importantly, people with higher cholesterol often eat more sugar, processed foods, and trans fats – all factors known to fuel inflammation and oxidative stress in the brain.

The Lancet Commission, which makes the anti-cholesterol case, even acknowledged this diet–dementia link: in a cohort of 94,184 Danes, poor diet predicted both high LDL and dementia risk【4】.

So maybe it’s not the cholesterol – it’s what comes with it.

Statins and the Hope for Vascular Dementia 

Originally, statins were hyped for vascular dementia – about 20% of all dementia cases – because of their supposed blood vessel–protective effects. But that theory has fallen flat. A Cochrane review found no benefit from statins for dementia prevention【6】.

And the best independent trial – not funded by drug companies – also found no cardiovascular benefit for statins in older adults【5】.

There’s no data supporting the notion that statins protect the brain. Yet the Lancet Commission listed “high cholesterol” as contributing 7% to dementia risk, which will no doubt spur even more statin prescriptions【4】.

The Optimum Nutrition Perspective

From an optimum nutrition standpoint, we view cholesterol differently.

If your total cholesterol is up to 6.5 mmol/l – but you have high HDL, low triglycerides, low homocysteine, and a healthy diet low in sugar and refined carbs – you’re not at risk. In fact, you’re likely protected.

One recent study showed that higher HDL in midlife predicted significantly lower future dementia risk【7】. Low HDL, not high total cholesterol, is a hallmark of metabolic syndrome – the precursor to diabetes, heart disease, and yes, dementia.

The evidence is clear: cholesterol is essential for brain health. Statins do not prevent dementia – and may contribute to cognitive decline by pushing cholesterol levels too low.

Instead of dumbing down the brain with unnecessary statins, we need to smarten up with nutrients that build brain health: omega-3 fats, phospholipids, B vitamins, and a low-sugar diet.

Doctors prescribing statins as dementia prevention are not only missing the mark – they may be making things worse.

Let’s change the narrative. Let’s put nutrition – not cholesterol fear – at the top of the brain health agenda. Find out more in Patrick’s new book – Alzheimer’s: Prevention is the Cure.

Food for the Brain is a not-for-profit educational and research charity that offers a free Cognitive Function Test and assesses your Dementia Risk Index to be able to advise you on how to dementia-proof your diet and lifestyle.

By completing the Cognitive Function Test you are joining our grassroots research initiative to find out what really works for preventing cognitive decline. We share our ongoing research results with you to help you make brain-friendly choices.

Please support our research by becoming a Friend of Food for the Brain.

References

1  Gong, Q., Xie, L., Bi, M., & Yu, L. (2021). A probability formula derived from serum indicators, age, and comorbidities as an early predictor of dementia in elderly Chinese people. Brain and Behavior 11, e2236. https://doi.org/10.1002/brb3.2236

2 Peters, R, Breitner, J, James, S, et al. Dementia risk reduction, why haven’t the pharmacological risk reduction trials worked? An in-depth exploration of seven established risk factors. Alzheimer’s Dement. 2021; 7:e12202. https://doi.org/10.1002/trc2.12202 

3 Wee J, Sukudom S, Bhat S, Marklund M, Peiris NJ, Hoyos CM, Patel S, Naismith SL, Dwivedi G, Misra A. The relationship between midlife dyslipidemia and lifetime incidence of dementia: A systematic review and meta-analysis of cohort studies. Alzheimers Dement (Amst). 2023 Mar 8;15(1):e12395. doi: 10.1002/dad2.12395. PMID: 36911359; PMCID: PMC9993469.

4  Kjeldsen EW, Thomassen JQ, Rasmussen KL, Nordestgaard BG, Tybjærg-Hansen A, Frikke-Schmidt R. Adherence to dietary guidelines and risk of dementia: a prospective cohort study of 94 184 individuals. Epidemiol Psychiatr Sci 2022; 31: e71. 

5  Han BH, Sutin D, Williamson JD, Davis BR, Piller LB, Pervin H, Pressel SL, Blaum CS; ALLHAT Collaborative Research Group. Effect of Statin Treatment vs Usual Care on Primary Cardiovascular Prevention Among Older Adults: The ALLHAT-LLT Randomized Clinical Trial. JAMA Intern Med. 2017 Jul 1;177(7):955-965. doi: 10.1001/jamainternmed.2017.1442. PMID: 28531241; PMCID: PMC5543335.

6  McGuinness B, Craig D, Bullock R, Passmore P. Statins for the prevention of dementia. Cochrane Database Syst Rev 2016;1: CD003160. 

7 Zhang X, Tong T, Chang A, Ang TFA, Tao Q, Auerbach S, Devine S, Qiu WQ, Mez J, Massaro J, Lunetta KL, Au R, Farrer LA. Midlife lipid and glucose levels are associated with Alzheimer’s disease. Alzheimers Dement. 2023 Jan;19(1):181-193. doi: 10.1002/alz.12641. Epub 2022 Mar 23. PMID: 35319157; PMCID: PMC10078665.

A recent study of 1,178 women found that those carrying the APOE4 gene taking Hormone Replacement Therapy (HRT) had a better delayed memory score compared to APOE4 carriers that were not taking HRT, and to non-APOE4 carriers.[1] They also had slightly larger brain volumes in certain areas. This study suggested that HRT may help to prevent Dementia. This study was an observational trial, not a clinical trial, meaning the statement remains a hypotheses and requires further randomised controlled trials to investigate further. We analysed the paper and provided our comments below.

Clinical Trials on HRT

Clinical trials to date have not shown benefit of HRT with improving cognitive function. A systematic review of the clinical trial evidence for the effect of HRT on cognitive outcomes did not find benefit.[2] The Women’s Health Initiative Memory Study (WHIMS) conducted a double-blind, placebo-controlled clinical trial examining 8300 women 65 years of age or older over a 2- year period to observe the effects of HRTs and dementia progression. The trial failed to find a beneficial effect for HRT in reducing dementia risk, instead finding an increase in all types of dementia.[3]

The ApoE4 Gene

Roughly 1 in 5 people carry the ApoE4 gene, which accounts for 4 to 6% of risk for dementia and can be modified, downregulating the gene, with positive diet, nutritional supplement and lifestyle changes.[1]

Find out your risk for Dementia

In our Dementia Risk Index, as part of the Cognitive Function test, and COGNITION programme to reduce dementia, we excluded HRT because the evidence was not conclusive or consistent.

Have you tried our free Cognitive Function Test yet? Find out your Alzheimer’s disease risk using our evidence backed Dementia Risk Index. If your risk is high, our clever new programme COGNITION can help you make the right nutrition and lifestyle changes to help improve your score.

References

[1] Saleh RNM, Hornberger M, Ritchie CW, Minihane AM. Hormone replacement therapy is associated with improved cognition and larger brain volumes in at-risk APOE4 women: results from the European Prevention of Alzheimer’s Disease (EPAD) cohort. Alzheimers Res Ther. 2023 Jan 9;15(1):10. doi: 10.1186/s13195-022-01121-5. PMID: 36624497; PMCID: PMC9830747.

[2] Marjoribanks J, Farquhar C, Roberts H, Lethaby A, Lee J. Long-term hormone therapy for perimenopausal and postmenopausal women. Cochrane Database Syst Rev. 2017;1(1):CD004143.

[3] Shumaker SA, Legault C, Rapp SR, et al. Estrogen plus progestin and the incidence of dementia and mild cognitive impairment in post- menopausal women: the Women’s Health Initiative Memory Study: a randomized controlled trial. JAMA. 2003;289(20):2651-2662.

Exercise plays an important role in cognition. In this TED talk listen to expert Dr Wendy Suzuki explaining in more detail.

Dr Wendy Suzuki – The Brain Changing Benefits of Exercise (TED).

This study investigate bilingualism & cognition. The study was a meta analysis of studies. Inclusion criteria was studies investigating bilingualism in the elderly with relation to Alzheimer’s disease risk. 6 prospective cohort studies were selected and 8 retrospective studies were selected. Of the 14 studies, only 2 had a monolingual control group. 14 studies selected for analysis. Study indicated that bilingualism may be protective against memory decline in older adults.

Results:

Meta analysis indicates that one exception, the studies support the idea that bilingualism reduces risk of memory decline. . However, only a small sample of studies included, although selected studies generally of a good sample size (>500). Only two of the studies included participants with Alzheimer’s disease diagnosis. Moreover, only two studies had a control group. Further, two of the studies included only Hispanic subjects, which may have impacted results.

A notable limitation of the meta analysis is that it did not include any statistical analysis methods (i.e p value) and this is a significant limitation. Further large scale research is required to explore effects of bilingualism on cognition, and whether bilingualism may be protective against cognitive decline.

Abstract available here

Klimova, B., Valis, M., and Kuca, K. (2017). Bilingualism as a strategy to delay the onset of Alzheimer’s disease. Clin. Interv. Aging 12, 1731–1737.

This study investigated bilingualism & cognition. Study included 28 older adult participants – 14 monolingual participants and 14 bilingual participants (who had been bilingual since before age 11). All participants were subjected to a fMRI and had no diagnosed mental health conditions.

Results indicated:

Bilingual participants performed better on tasks and had better working memory (p<0.01) and better connectivity (p=0.002), compared with the monolingual group (p=0.17)

Results observed for other types of memory were not significant

Study size was small. Further large scale warranted. Study did not specify regarding bilingualism, as to whether participants spoke more than 2 languages, or whether certain type and complexity of language afford greater protection (i.e romance languages, Germanic languages etc.). Further research merited to explore effects of bilingualism on other types of memory.

Abstract available here

Grady, C. L., Luk, G., Craik, F. I., and Bialystok, E. (2015). Brain network activity in monolingual and bilingual older adults. Neuropsychologia 66, 170–181. doi: 10.1016/j.neuropsychologia.2014.10.042

In this study memory change over 6 years was assessed using a large scale sample (16, 638 elderly individuals born <1948) from Health and Retirement Study. Growth curve models were analysed with reference to memory recall of a 10 word list and levels of social integration (i.e with family, volunteering, marital status).

Results indicated:

Socialisation demonstrated as a predictor of slower memory decline (p<.01). 

In individuals with vascular disease, socialisation observed to be protective buffer ( (p< 0.05)

Memory amongst least socialised deteriorated at twice the rate of other participants, with association greatest amongst those with <12 years of education (p<0.07)

The study indicates that socialisation and levels of education may be protective factors for memory decline. The study also suggests that socialisation may reduce risk for memory decline in individuals with vascular diseases. The study did not use a robust means of measuring memory capability, such as MMSE. Results for socialisation as a predictor of slower memory decline not statistically significant. However, socialisation in individuals with vascular disease as a protective factor was observed to be statistically significant. More research required as to the mechanisms of how socialisation reduces risk of memory decline in vascular disease. Findings for education as a protective factor were observed to be statistically significant. More research required into to what level of education is most protective against memory decline.

Abstract can be viewed here

Ertel, K. A., Glymour, M. M., & Berkman, L. F. (2008). Effects of social integration on preserving memory function in a nationally representative US elderly population. American journal of public health, 98(7), 1215–1220.