What if protecting your brain health became as accessible as popping into your local pharmacy?

Author: Catherine Verner · Published: 14/10/2026

We know that many of the factors linked to dementia risk are modifiable. But knowing what can help prevent cognitive decline and making that knowledge accessible to everyone are two very different things. That’s something we’re determined to change.

For many people, the community pharmacy is the part of the health service they see most often. There is no appointment to book, and the staff are familiar faces. For many people managing blood pressure or diabetes, it is a regular stop. This autumn, that everyday visit becomes the starting point for an exciting new research project.

We’re delighted to have been awarded funding from the National Institute for Health and Care Research (NIHR), through its Invention for Innovation (i4i) Funding At the Speed of Translation (FAST) scheme to test whether our dementia prevention pathway can be offered through community pharmacies. The 12-month project began in September 2026 and will run across seven pharmacy branches in Northern Ireland, working with a delivery partner. It aims to involve 300 adults.

About this research

Project period: September 2026 to August 2027
Funder: National Institute for Health and Care Research (NIHR)
Research sponsor: Aberystwyth University
Study location: Seven community pharmacy branches in Northern Ireland
Target participation: 300 adults

Why prevention, and why the pharmacy?

Around 982,000 people in the UK are living with dementia (1). The 2024 Lancet Commission estimated that around 45% of cases worldwide are linked to 14 risk factors that can be modified, including high blood pressure, diabetes, physical inactivity and hearing loss (2). That figure describes whole populations and is not a promise for any one person, but it makes a strong case for acting earlier. You can explore the science behind these findings in our evidence-based dementia prevention recommendations. It brings together research on the lifestyle factors linked to cognitive health.

Evidence from clinical trials also supports this approach. In the Finnish FINGER trial, a two-year programme combined diet, exercise, cognitive training and vascular risk monitoring. The programme improved or maintained cognitive function in older adults at risk, compared with general health advice (3).

Yet most services still identify dementia only once symptoms appear. People who live a long way from specialist services, or who rarely see their GP, have even fewer chances to learn about their risk early. Community pharmacies are often close to home and already part of people’s routines.

For us, this is at the heart of our mission. We want to move dementia prevention out of the research papers and into everyday life, giving more people the knowledge and practical support to take charge of their brain health before problems develop.

How the pathway works

Pharmacy teams will not administer the cognitive assessments. Their role is to let people know the study is there, through materials in the branch and leaflets included in prescription bags for patients receiving medication deliveries

Participants then complete everything at home. They take our Cognitive Function Test, the online assessment already completed by more than 400,000 people worldwide. This is followed by a questionnaire on diet and lifestyle. Their results lead into COGNITION, our personalised brain health programme. The programme supports people to make small, specific changes across eight areas of brain health, from sleep to blood sugar balance. COGNITION draws on the COM-B model of behaviour change. This recognises that a new habit takes hold only when a person has the capability, the opportunity and the motivation to act (4). At the end of the programme, participants repeat the assessments. This allows the research team to see what has shifted over time.

The check is not a diagnosis for dementia. Where a result suggests someone should talk to their GP, they are given clear information and encouraged to do so. Results are shared with a GP practice only if the participant chooses.

What the project will show

This is an implementation study. It will not show whether the pathway prevents dementia, which no 12-month project could. It asks a more practical question: can this approach fit into the working day of a busy pharmacy, and do people from different backgrounds find it acceptable? The team will also look at how well it connects with existing health services and what it costs to deliver.

A Lived Experience Advisory Group is helping to shape the invitation materials and the routes into the study.

The project is led by Food for the Brain, with Aberystwyth University as research sponsor. Dr Amanda J Lloyd of Aberystwyth University manages the project, working with Cath Verner, our Head of Research, and Kim Close, our Head of COGNITION. Dr Tommy Wood of the University of Washington provides scientific oversight.

“Community pharmacies could provide a really accessible way to help people understand and reduce their dementia risk, particularly in rural communities,” said Dr Amanda Lloyd, project lead. “We’re looking forward to sharing the work at the Rural Health and Care Wales Conference this November.”

By August 2027, we aim to have the evidence a health commissioner would need to decide whether a pharmacy-led model is worth adopting more widely.

Our hope is that this is another step towards a future where dementia prevention becomes a normal part of healthcare, rather than something people only think about once memory problems begin.

We’ll share progress with you as the project develops.

How you can be part of it

The pharmacy study is recruiting only through its participating branches, but you don’t need to be part of this study to start taking action for your brain health.

Our Cognitive Function Test is free for anyone to take at foodforthebrain.org, helping you understand your cognitive health and identify areas where you may be able to reduce your risk.

Research like this is also made possible by the thousands of people who have already taken part in our citizen science work, and by our community of supporters who believe, as we do, that prevention deserves a much bigger place in healthcare.

If you’d like to help us continue this work, becoming a FRIEND of Food for the Brain is one way to support the research that comes next.

Related reading:

From Awareness to Action: A Year of Progress in Dementia Prevention (A Letter From Emma – our CEO)
Groundbreaking New Research: The Key to Reducing Dementia Risk
Preventing Alzheimer’s

Sugar and Cognitive Function: What We Found in Nearly 29,000 People

Food for the Brain’s first peer-reviewed study using data from nearly 29,000 people found that more frequent consumption of sugary snacks and drinks was associated with lower cognitive function scores. Researchers analysed anonymised data from people who completed our validated Cognitive Function Test alongside questions about their diet and lifestyle.

Researchers analysed anonymised information from almost 29,000 people who completed our validated Cognitive Function Test alongside questions about their diet and lifestyle, creating an unusually large real-world dataset through which to explore the relationship between what we eat and how well we think. Among the dietary patterns examined, one stood out particularly strongly: people who reported consuming sugary snacks and drinks more frequently tended to have lower cognitive function scores.[1]

There is another reason this paper matters so much to us. These findings were made possible by people just like you. Thousands of people have chosen to test their cognitive function and contribute their anonymised information to this research, so if you were one of them, you were not simply gathering information and tools for your own brain. Collectively, you were helping us ask much bigger questions about what influences cognitive function and, ultimately, how we might protect it.

Research at a glance

Published: Frontiers in Nutrition (2026)
DOI: 10.3389/fnut.2026.1830204
Participants: ~29,000
Research: Food for the Brain / Conti et al.
Measured: Self-reported diet + Cognitive Function Test performance
Key finding: Frequent sugary snack/drink consumption associated with poorer cognitive performance
Study type: Observational
Read the peer-reviewed paper →

Nearly 29,000 people, one remarkable dataset

Since November 2022, people completing our free Cognitive Function Test have also been able to answer questions about their diet, sleep, activity and health. The test itself is validated against established cognitive measures and has been shown to distinguish between healthy individuals and those with mild cognitive impairment.[2] Over time, those individual contributions have created something scientifically valuable: a large dataset connecting measures of cognitive function with information about how people actually live.

For this first published study, researchers led by Federica Conti, working with our Head of Research Dr Tommy Wood and colleagues, analysed almost 29,000 anonymised records.[1] Rather than beginning with an assumption about which foods should matter most, they used a statistical approach called the Bias-reduced Regression Analysis in Nutrition, or BRAiN, index. In simple terms, this allowed patterns within the data to identify which reported dietary behaviours were most strongly associated with cognitive performance, rather than assigning importance to particular foods in advance.[1]

This distinction matters because nutrition research is complicated. We do not eat nutrients in isolation, foods themselves contain complex combinations of nutrients and compounds, and our food choices sit alongside differences in age, health, activity and many other aspects of our lives. No statistical method can remove all of that complexity, but analysing a dataset of this size gives researchers an opportunity to look for patterns that may be difficult to see in much smaller studies.

(It’s worth noting that this research paper explored a much broader range of dietary factors than sugar alone, with several other interesting patterns emerging from the analysis. For this article, we are focusing on one finding in particular because of its strength, its relevance across age groups and how it connects with the wider evidence around glucose regulation and brain health.)

What did the study find about sugar and cognitive function?

Of the dietary behaviours examined, the frequency of sugary snacks and drinks emerged as one of the strongest dietary factors associated with cognitive performance.[1] This category included foods and drinks such as biscuits, cakes, chocolate, sweets, fizzy drinks and fruit juice, rather than the naturally occurring sugars contained within whole fruit.

The pattern became particularly interesting when researchers looked at frequency. People reporting sugary snacks or drinks twice a day or more tended to have lower cognitive scores, while lower reported frequencies did not show the same strength of association.[1] Because the questionnaire measured how often these foods were consumed rather than exactly how much sugar people ate, we cannot turn this into a precise daily sugar limit or say that two occasions represents a biological threshold. What we can say is that, within this large group of people, more frequent consumption was associated with poorer cognitive performance.

For those who have followed Food for the Brain for some time, our focus on sugar and blood glucose will not be new. Reducing sugar and refined carbohydrates, choosing whole foods and following lower glycaemic load principles have long been part of the approach we teach through COGNITION, based on the wider evidence around glucose regulation and brain health. What is exciting about this study is that when researchers analysed our own community data, frequent consumption of sugary foods and drinks emerged as one of the strongest dietary factors associated with cognitive performance.[1] It gives us new evidence from our own research community to add to a much larger body of science examining the relationships between sugar intake, glucose regulation and cognitive health.

This does not mean sugar is something to dismiss under an “everything in moderation” banner. We want whole, minimally processed foods to make up the foundation of what we eat, with sugary and highly processed foods being the exception rather than an everyday staple. At the same time, protecting your brain does not have to become another source of pressure to achieve dietary perfection. What this research highlights is the potential importance of the choices we make repeatedly over time.

Was sugar associated with cognitive function at different ages?

Perhaps one of the most interesting aspects of the study is that sugar did not emerge as relevant only among older participants. It remained among the leading dietary predictors of cognitive performance across the age groups examined, suggesting that the relationship between diet and how well we think may be relevant much earlier in adult life than conversations about dementia sometimes imply.

This matters to us because prevention should not begin only at the point when memory is already failing. Dementia develops over many years, and the biological processes that influence brain health do not suddenly appear in our seventies or eighties. This study cannot specifically tell us that reducing sugar in younger adulthood will prevent dementia decades later, but it adds to the case for thinking about cognitive health throughout life, an approach that has long been central to Food for the Brain. (Want to understand more then make sure you read our founder Patrick Holford’s Alzheimer’s: Prevention is the Cure.)[3]

The brain you have later is, in part, shaped by the life you live now.

Why might sugar and glucose regulation matter?

This study was designed to identify associations, not to establish the biological mechanism behind them. To understand why the finding is so interesting, however, we can place it alongside what previous research has already told us about sugar, glucose regulation and the brain.

Previous population research has found associations between habitual sugar intake and cognitive function,[4] while higher dietary glycaemic load has also been associated with poorer cognitive performance.[5] Longer-term research has found an association between higher glucose levels and increased dementia risk, including among people without diabetes.[6] Taken together, this gives us good reason to continue investigating how sugar intake and glucose regulation may influence the brain throughout life.

Professor Robert Lustig, a member of Food for the Brain’s Scientific Advisory Board and an international authority on sugar and metabolic health, explores the wider science in much more depth in his article Is Sugar Killing Your Brain?. There he looks beyond cognitive performance to research around insulin resistance, brain energy metabolism and brain structure. That wider evidence helps explain why sugar has been an important part of our prevention work, while this new study adds something different: evidence of a relationship between reported sugary food and drink frequency and cognitive performance within our own large research dataset.

Nor does any of this mean that all foods containing carbohydrate or sugar are metabolically equivalent. Whole fruit comes packaged with fibre, water and a complex mixture of nutrients and plant compounds, which is very different from consuming a sugary drink with little or no fibre. Our metabolic responses also differ, which is another reason to look beyond a single food or nutrient and consider the wider diet, lifestyle and health of the individual. The overall pattern of the diet matters, but food is only one part of the picture. Physical activity, metabolic health and keeping the brain challenged and stimulated through the “Use It or Lose It” approach are all part of protecting cognitive function throughout life, an approach explored further in Dr Tommy Wood’s book The Stimulated Mind.

There are also limits to what any observational study can tell us, and acknowledging them is part of doing good research. Participants reported their own diets and the questionnaire measured frequency rather than the exact quantity of sugar consumed. An observational study like this can also identify associations, it cannot establish that sugary foods caused the differences in cognitive performance. Other factors may contribute to the relationship, and further research will be needed to understand cause and effect. 

How can you reduce sugar to support cognitive health?

Reducing sugar will look different for different people, but a useful place to begin is by looking honestly at how frequently sugary and highly processed foods are appearing in your day. If biscuits, sweets, cakes, chocolate, fruit juice or sugary drinks are showing up several times a day, reducing those occasions is a practical first step.

For many people, focusing on replacement rather than restriction can make that change easier to put into practice. Could an afternoon biscuit become yoghurt with blueberries and nuts, or a drive-through sugary coffee become coffee from home alongside a whole-food snack? These are starting points, not necessarily the end point. Some people may benefit from reducing sugar and high-glycaemic foods much more substantially, depending on their metabolic health and individual response, but shifting repeated choices away from sugar and towards whole, minimally processed foods is a practical place to begin.

This is why COGNITION focuses on lower glycaemic load principles and making whole, minimally processed foods the foundation of the diet. Vegetables, pulses, whole fruit, nuts, seeds, quality sources of protein and intact whole grains where appropriate provide much more than carbohydrate alone, including fibre and a wide range of nutrients. We also look at how foods are combined, because the effect of a meal on blood glucose is influenced by the whole meal, not simply one ingredient. These particular strategies were not tested by this study, but they draw on the wider evidence around metabolic health and turn that science into everyday habits.

You can also learn something about how well your own body has been managing blood sugar. HbA1c is a blood test that measures the proportion of haemoglobin in your red blood cells that has glucose attached to it. Because red blood cells live for around three months, this gives us a useful picture of your average blood sugar over the previous two to three months. Put very simply, the higher your average blood sugar has been, the more haemoglobin becomes glycated, or “sugar-coated”, and the higher your HbA1c is likely to be. 

(HbA1c is one of the biomarkers included in our DRIfT 5-in-1 test – find out more here) 

Our first paper. Just the beginning.

For Food for the Brain, this publication represents something bigger than a single finding about sugar. We are a research charity built around a simple but ambitious idea: that by understanding more about the modifiable influences on cognitive decline, we can find better ways to protect brain health and move prevention further up the health agenda.

Every Cognitive Function Test completed, every questionnaire answered and every person who chooses to contribute their anonymised information helps make that research possible. One person’s results can help them understand more about their own brain, but tens of thousands of people contributing together create something much more powerful: a growing research resource through which scientists can investigate the patterns that may matter for all of us.

So if you have taken our Cognitive Function Test and contributed your information to research, this paper belongs partly to you. Your data have moved beyond your individual result and become part of a much bigger effort to understand how we can keep our brains working better for longer. This is citizen science in action, and you helped build it. Thank you.

And we are only just beginning. Because the more people who take part, the more we can learn, and together we have an opportunity to change how we understand, protect and care for our brains for generations to come.

Could your diet be affecting your brain health? Take the Cognitive Function Test and discover how your cognitive function measures up.

An Enlightening Double Whammy For Alzheimer’s 

By Jerome Burne

Hundreds of billions of dollars have been spent by pharmaceutical companies developing drugs that clear them out. But while they do the job, the clean-up does remarkably little to smarten up your mental processes and come with undesirable side-effects, such as bleeding in the brain.  

So, research attention has been turning to ways of manipulating the clean-up squads already present in the brain. One way of doing this is with NIR, another is to target the patterns of brain activity, known as gamma oscillations, linked with such vital mental activities as attention, memory, consciousness and dreaming. The brains of cognitively intact individuals sing in harmony with these gamma brain waves while cognitively impaired brains do not. 

Research has shown that exposing the brain to oscillations of 40Hz light, delivered by looking at or being in the field of a light screen, can reduce the build-up of amyloid plaques and tau, as well as improve thinking and memory.

This is because it affects the immune cells of the brain known as microglia, which have a number of remarkable properties.  

One type, sometimes described as “the butler to the brain” or M2, can clear plaques and tangles and the left-over fats and proteins involved in making energy and running the body’s multiple processes.  

But recently research at the Massachusetts Institute of Technology has discovered that sometimes those butlers can go rogue if they are not getting enough resources or dirty fuel from the powerhouses of the cells, the mitochondria. These make the energy that powers the brain but when they become clogged up and inefficient, a scenario created by an unhealthy diet with too much sugar, smoking, burnt fats, and not enough B vitamins and antioxidants, they trigger a transformation trick worthy of a horror movie changing the function of the normally friendly microglial cells into the brain’s enemy. They begin destroying vital protective features of the brain such as the blood brain barrier or the system for controlling sugar and insulin in the blood, transforming from the supportive M2 ‘butler’ mode into M1, known as the “evil twin”.  

One of the valuable effects of 40Hz oscillation is that it can reverse the evil twin effect. Recent research, however, suggests that those less desirable M1 microglial cells may also have benefits. The M2 “butler” is very valuable when all well in the brain, but of little use when it comes under attack from the viruses or bacteria which it is designed to destroy. 

These attacks, which cause damaging inflammation, often originate from what is called “barrier tissue” which is in contact with the outside world, such as the lungs, gut bacteria, the mouth – periodontal disease -, liver and kidneys.  

The implication of the new view is that targeting the build-up of the sticky proteins plaque and tau in the brain as we age, may be the wrong target. Instead focusing on keeping body’s systems and organs healthy, as Food for the Brain does, emerges as a much better protective strategy. 

Another is that when microglia are in M2 mode they can swell to a size large enough to munch up the damaging plaque and tau. But if this ability is overworked, it can stop, causing brain cells to become inflamed and making plaque even more toxic. Exposure to 40Hz oscillations is likely to be able to reverse this too.  

Another of the natural clean up systems that can benefit from a boost is called the ‘glymphatic flush’, a deep clean that uses cerebrospinal fluid to clear out cluttering proteins left by energy creation. 

This is a new and sophisticated form of preventative medicine that is delivered by wearing a type of ear and eye headset, called Cognito, worn often before bed, with eyes closed, for 30 minutes to an hour a day, asleep or awake. The first human clinical trial conducted by scientists at Yale University’s Department of Comparative Medicine, has shown remarkable effects in arresting both cognitive decline and brain shrinkage in a group of 76 of patients with mild to moderate Alzheimer’s given either the 40Hz therapy for an hour a day or a sham treatment over a six month period. While those given the sham treatment had the usual steady decline in cognitive function, determined by a Mini-Mental State Exam (MMSE) and a measure of functional abilities called ADAS-ADL, those given the real 40Hz therapy barely declined at all. Also, their brain shrinkage was substantially less, with the usual reduction in whole brain volume, which is the hallmark of Alzheimer’s, being 69 per cent less. 

Another 40Hz device, called EVY, made by optoceutics.com, is in the trial phase in a race to achieve a licensed medical device. I also found a device available on Amazon called Digipace that delivers 40Hz therapy but without substantiated trial results.

But targeted gamma oscillation is only part of a new and radical idea about how best to cut Alzheimer’s risk. It is one approach that I first became aware of in a new book Brain Defenders (Hodder and Stoughton) by Neurologist Dr David Perlmutter, a New York Times best-selling author and part of Food for the Brain’s think tank.

Besides the NIR helmet or 40Hz devices I have also been following a protocol devised by the Alzheimer’s prevention charity, foodforthebrain.org that aims to ensure you have a heathy brain in a healthy body. This fits much better with the latest research about the threat from “barrier tissue” problems and how the brain defencers itself from threats. Think of it as a sort of biochemical gamma stimulation.

This involves strategies such as regular exercise, getting enough sleep, upping your intake of omega-3 from fish and fish oil, supplementing B vitamins, dramatically reducing sugary foods and drinks, plus two tablespoons of Ketofast, a ketogenic fuel called C8, all designed to switch your brain towards running on ketones. Ketones are an alternative fuel for defective brain cells, gunked up from too much glucose. and following a ‘ketogenic’ diet which means you cut back on carbohydrates – especially sugar, cereals, and sugar-sweetened beverages – now dominating much of the modern diet. 

The result is that you start producing energy packets known as ketones, which the brain can use for energy rather than glucose. It’s been used since the 1920’s to treat brain disorders such as epilepsy and more recently Alzheimer’s anorexia and Parkinsons. Ketones, which are created in the liver from a type of fat known as C8, derived from coconut oil, also help give defective mitochondria a full service, which has the knock on effect of bringing M2 microglial cells, the brain’s butlers, back to life and turning off the more aggressive  evil twin – the M1 microglia. 

Ketones are also fuel for your energy- making mitochondria which often are dysfunctional in people with Alzheimer’s. 

Food for the Brain’s strategy is being adopted in China as part of a nationwide ‘Silver Haired Healthy Lifestyle Popularisation’ campaign to prevent Alzheimer’s and their free online Cognitive Function Test is being trialled both in China and in the NHS to give GPs instant access to a digital assessment that anyone can do on a computer or smartphone. In China 10 million ‘silver haired’ Chines citizens attended or watched a conference broadcast across twenty TV stations with Food for the Brain’s founder, Patrick Holford, presenting the way forward for prevention. With over 300 million people over 60, almost a quarter of their population, preventing Alzheimer’s in China has become a government imperative. 

There are two more key ingredients of the Food for the Brain recipe for brain and physical health – B vitamins to bring down the level of an amino acid called homocysteine, linked with brain shrinkage, and omega three oil, which boosts the vitamin’s effect. 

So, the dream team to ensure Alzheimer’s has a hard time getting a grip on your brain would be a combination of 40hz gamma oscillations and the nutrition and the healthy lifestyle protocol advocated by and developed by foodforthebrain.org.

About the author

Jerome Burne has been a health journalist for twenty years and has written for most of the UK’s national newspapers, as well as a variety of magazines. Before becoming a health journalist, he edited the extensive reference work Chronicle of the World. Prior to that, he was co-editor of Time Out in the mid-1980s.

In recent years, he has written mainly for the Daily Mail. He has also contributed regularly to Reader’s Digest and occasionally to the Times Literary Supplement.

In 2012, Jerome won the Medical Journalist’s Association award in the category of Medical Science Explained. He was also runner-up in the Best National Newspaper Feature category.

To find out more read Dr David Perlmutter’s book ‘Brain Defenders: harness the power of your immune cells to safeguard your brain’s destiny’ while the nutritional approach being adopted in China is explained in the book ‘Alzheimer’s:Prevention is the Cure’ by Patrick Holford.

What is Alzheimer’s?
Amyloid isn’t Alzheimer’s – How NOT to Study a Disease
The 8 Domains to improve your COGNITION
Melatonin: The Brain’s Night-Time Antioxidant

Magnesium for Brain Function

When people think about nutrients that support the brain, omega-3 fats, B vitamins, and vitamin D usually get most of the attention. However, magnesium for brain function, including focus and memory, is just as important and often overlooked.

Yet there is another nutrient that may deserve a place on that list.

Magnesium is involved in more than 300 biochemical reactions throughout the body. It helps regulate nerve signalling, supports energy production, influences sleep quality, helps control blood sugar, and plays a critical role in the brain’s ability to learn, adapt, and form memories.

Despite this, many people consume less magnesium than they need.

As rates of cognitive decline, anxiety, sleep problems, and metabolic disease continue to rise, researchers are increasingly investigating whether magnesium status could play a role in protecting brain health throughout life.

Why does magnesium matter for the brain?

Your brain is an energy-hungry organ.

Although it accounts for only around 2% of body weight, it uses approximately 20% of the body’s energy supply. To function well, brain cells require a constant supply of nutrients that support energy production, communication between neurons, and protection from oxidative stress.

Magnesium contributes to all three.

It helps regulate neurotransmitters, supports healthy nerve-cell communication, and is required for the production of ATP, the molecule that powers every cell in the body. Magnesium also influences NMDA receptors, which are involved in learning, memory formation, and neuroplasticity, the brain’s ability to adapt and create new connections.¹

Low magnesium levels have been linked to increased inflammation, greater oxidative stress, and impaired glucose regulation, all of which are recognised contributors to cognitive decline and dementia risk.²

Magnesium and cognitive decline

One of the most interesting areas of research concerns magnesium and long-term cognitive health.

Several large population studies have found that people with higher magnesium intake or higher blood magnesium levels tend to have a lower risk of cognitive impairment and dementia.³⁻⁵ In a study published in Neurology, individuals with optimal blood magnesium levels had a significantly lower risk of developing dementia compared with those with lower levels.⁴

A recent systematic review concluded that magnesium appears to play an important role in maintaining cognitive health throughout ageing, although researchers emphasise that more intervention studies are needed to establish cause and effect.²

This does not mean magnesium is a magic bullet for preventing dementia, but it does suggest that ensuring adequate magnesium intake may be one of several important factors that help support a healthy brain as we age.

Could magnesium help with brain fog?

Many people first become interested in magnesium because they feel mentally tired, forgetful, or unable to concentrate.

While brain fog is not a medical diagnosis, it is often associated with poor sleep, chronic stress, blood sugar instability, and low energy production, all areas in which magnesium plays an important role. It also helps regulate the body’s response to stress. Chronic stress can deplete magnesium stores, while low magnesium levels may make us more vulnerable to the effects of stress, creating a vicious cycle.⁶

For some people, improving magnesium status may help support mental clarity simply by improving sleep quality, reducing stress reactivity, and supporting stable energy production.

Magnesium, mood and sleep

The relationship between magnesium and mental wellbeing has been studied for decades.

Research suggests that magnesium may help support healthy mood regulation and stress resilience, particularly in individuals with inadequate magnesium intake.⁶

Magnesium is also commonly used to support sleep. It helps regulate the nervous system and appears to influence melatonin production and GABA activity, both of which are involved in sleep regulation.

While magnesium is not a sleeping tablet, some people report improvements in sleep quality, reduced nighttime waking, and a calmer mind when magnesium intake is optimised.

Since poor sleep is increasingly recognised as a risk factor for cognitive decline and Alzheimer’s disease, supporting healthy sleep may be one of the ways magnesium contributes to long-term brain health.

Food First: Magnesium-Rich Foods to Try Before Supplements

Many people can substantially improve their magnesium intake simply by eating more magnesium-rich foods, including leafy greens, beans, nuts and seeds. Although modern farming and soil quality may have reduced the magnesium content of some foods compared with the past, food should still be your first source wherever possible. Supplements are best considered a complement to diet, not a replacement for it.

Which type of magnesium is best?

One of the most confusing aspects of supplementation is the number of different forms available.

The truth is that there is no single “best” magnesium. Different forms may be more suitable, depending on your goals.

Magnesium glycinate: a gentle option often used for sleep and relaxation

Magnesium glycinate combines magnesium with the amino acid glycine. It is well absorbed and gentle on the stomach. Although it is widely recommended to support sleep and relaxation, there is currently little direct evidence that it is more effective than other well absorbed forms of magnesium. Its popularity is based largely on its favourable absorption, the calming properties of glycine, and positive clinical experience.

Magnesium l-threonate: the leading choice for magnesium for brain function

Magnesium L-threonate has attracted attention because it appears to increase magnesium levels within the brain more effectively than some other forms.

Animal studies have shown improvements in learning and memory, while early human studies suggest potential benefits for cognitive function.¹ ⁷

The evidence remains preliminary, but this is currently the form generating the most interest for memory and cognitive health.

Magnesium citrate: widely available and well absorbed

Magnesium citrate is widely available and generally well absorbed. It is often used when constipation is also an issue because it can have a mild laxative effect.

Magnesium malate: sometimes chosen for energy support

Magnesium malate combines magnesium with malic acid, a compound involved in cellular energy production.

Some practitioners favour this form for people experiencing fatigue, although the evidence supporting its superiority for energy is limited.

Magnesium oxide: common, but less efficiently absorbed

Magnesium oxide contains a high amount of elemental magnesium but is relatively poorly absorbed.

For brain health purposes, there are usually better options available.

Magnesium for Brain Function: Quick Comparison by Form

The bottom line: what this means for you

Magnesium is not a miracle nutrient, nor is there one form that’s right for everyone. The best choice depends on your individual needs, goals, and overall health. For some people, simply eating more magnesium-rich foods may be enough, while others may benefit from supplementation.

What the evidence does tell us is that magnesium is fundamental to healthy brain function. It supports energy production in every cell, helps nerve cells communicate, contributes to healthy sleep and stress regulation, and plays an important role in learning and memory. Maintaining healthy magnesium levels may therefore be one of the many ways we can support our brains as we age. (2-8)

Brain health is rarely transformed by a single nutrient, supplement, or food. It’s the result of consistently supporting the systems your brain depends on through good nutrition, regular movement, restorative sleep, stable blood sugar, social connection, and other healthy lifestyle habits.

Magnesium isn’t the whole picture, but it is an important piece of it. Making sure you’re getting enough, whether through your diet or, where appropriate, a well-chosen supplement, is one simple step towards supporting your brain for years to come.

Further reading:

Want to learn how nutrition supports brain health from the very beginning of life? Explore our article Building Young Brains: Shaping Your Child’s Future

Disclaimer: This article is for general information only and is not medical advice. It is not a substitute for consultation with a qualified healthcare professional, and should not be used to diagnose or treat any condition. Always speak with a GP, pharmacist, or registered nutritionist before starting a new supplement, particularly if you are pregnant, breastfeeding, taking medication, or managing a health condition.

The Best Foods to Help Lower Homocysteine Naturally

Of all the blood markers linked to dementia risk, homocysteine may be one of the most important and one of the easiest to improve. There are certain foods that lower homocysteine, making it possible to have a positive impact through your diet.

If you have searched online for foods that lower homocysteine, you have probably found plenty of articles recommending spinach, broccoli, eggs and salmon. They are all excellent foods, but they are only part of the story.

The truth is that no food lowers homocysteine directly. Your body is the one that does that. Every second of every day, it is recycling homocysteine through a series of biochemical reactions that depend on a steady supply of essential nutrients. The foods you eat simply provide the vitamins and nutrients those reactions need to work efficiently.

Understanding that difference changes the conversation completely. Instead of searching for a miracle food, the goal becomes giving your body the nutrients it needs to keep homocysteine in a healthy range.

For a full explanation of what homocysteine is and why elevated levels matter, read our guide to homocysteine.

Combined with appropriate testing and, where needed, targeted supplementation, improving your diet is one of the most practical ways to support long-term brain health.

Can food lower homocysteine?

No food lowers homocysteine directly. Instead, foods provide the folate, vitamin B12, vitamin B6, riboflavin, choline and betaine your body needs to recycle homocysteine efficiently.

Improving your intake of these nutrients may help support healthier homocysteine levels, particularly if your diet has previously been low in leafy green vegetables, legumes, fish, eggs or other nutrient-rich whole foods.

However, the effect of diet depends on why homocysteine is elevated. Poor vitamin B12 absorption, medications, kidney disease, thyroid problems and genetic factors may mean that dietary changes alone are not enough.

The key nutrients involved in homocysteine metabolism

Why homocysteine matters?

Homocysteine is a naturally occurring amino acid produced whenever your body breaks down methionine, an amino acid found in protein-rich foods.

Under healthy conditions, homocysteine does not remain in the bloodstream for long. It is quickly recycled into other useful compounds that support normal cellular function.

Problems arise when that recycling process slows down. Homocysteine begins to accumulate, increasing oxidative stress, inflammation and damage to blood vessels.

Over the last three decades, elevated homocysteine has consistently been associated with a higher risk of cognitive decline, dementia, stroke and cardiovascular disease.¹

Unlike high blood pressure or raised cholesterol, however, homocysteine rarely causes obvious symptoms. People often discover it is elevated only after having a blood test, by which time it may have been quietly increasing for years.

That is why homocysteine can be such a valuable biomarker. It gives you an opportunity to identify a potential problem early and take appropriate action.

You can learn more about the evidence linking homocysteine and dementia risk.

Why these foods work?

Your body has evolved an elegant system for dealing with homocysteine. Rather than allowing it to build up, it continually recycles it through two interconnected pathways.

One pathway converts homocysteine back into methionine so it can be reused. The other converts it into cysteine, an amino acid used to produce glutathione, often described as the body’s master antioxidant because of its role in protecting cells from oxidative damage.

Neither pathway works without the right nutrients. Folate, vitamin B12, vitamin B6, riboflavin, choline and betaine each have specific jobs within this recycling process.

If one or more of these nutrients becomes limiting, the whole system becomes less efficient and homocysteine starts to rise.

For a more detailed explanation of these biological pathways, read our guide to methylation and homocysteine.

This explains why two people eating apparently similar diets can have very different homocysteine levels. One may absorb vitamin B12 less efficiently as they get older. Another may carry a common genetic variant that increases their riboflavin requirement. Someone else may consume large amounts of caffeine or alcohol, increasing their need for certain B vitamins.

It is rarely one factor in isolation. More often, several small influences combine over many years.

The good news is that these pathways can be responsive. Give your body the nutrients it needs, remove some of the obstacles that interfere with the process, and homocysteine may begin to fall.

Foods that lower homocysteine: folate-rich foods

When researchers study nutrition and homocysteine, one nutrient consistently stands out: folate.

Folate plays a central role in recycling homocysteine back into methionine. Without enough folate, this pathway slows, making it much harder for your body to keep homocysteine within a healthy range.

Numerous intervention studies have demonstrated that improving folate status lowers homocysteine, particularly in people whose intake has previously been low.¹

Fortunately, folate is abundant in many whole plant foods.

Leafy green vegetables

Beans and lentils

Foods that lower homocysteine with vitamin B12

Folate rarely works alone. Vitamin B12 is equally important because it enables homocysteine to be converted back into methionine.

When vitamin B12 is lacking, this recycling process slows, regardless of how much folate is available.

One reason this matters is that vitamin B12 deficiency becomes increasingly common with age. Stomach acid, which helps release vitamin B12 from food, naturally declines over time. Some medications can further reduce absorption, while vegetarians and vegans may consume too little through their diet.

As a result, homocysteine may begin to rise years before the more familiar symptoms of vitamin B12 deficiency appear.

Fish and seafood

Eggs and dairy

Meat and liver

Foods that lower homocysteine with vitamin B6

Although folate and vitamin B12 receive most of the attention, they are only part of the story.

Vitamin B6 helps direct homocysteine down a different pathway, converting it into cysteine, which is then used to produce glutathione.

Good dietary sources include:

Poultry
Salmon
Tuna
Potatoes
Bananas
Chickpeas
Fortified cereals

Vitamin B6 is found in a wide range of foods, so a varied whole-food diet will usually provide more than relying heavily on one source.

Vitamin B2 foods that lower homocysteine

Riboflavin, better known as vitamin B2, is another nutrient that deserves greater recognition.

It is particularly important for people carrying the common MTHFR C677T genetic variant, where an adequate riboflavin intake may help the recycling process work more efficiently.

Foods containing riboflavin include:

Eggs
Yoghurt
Milk
Mushrooms
Almonds
Beef
Fortified cereals

Looking at nutrients individually is helpful for understanding the biology, but this is not how we eat. Meals contain dozens of vitamins, minerals and plant compounds working together, which is one reason whole-food dietary patterns consistently outperform approaches focused on isolated foods alone.

Choline and betaine foods that lower homocysteine naturally

Your body has a second way of recycling homocysteine that receives far less attention.

This alternative pathway depends on choline and betaine.

Choline supports normal methylation, helps build healthy brain cell membranes and is used to produce acetylcholine, a neurotransmitter involved in learning and memory.

Betaine acts as a methyl donor, allowing homocysteine to be converted back into methionine through a different biochemical route.

Eggs are one of the richest dietary sources of choline, while liver, fish and soybeans also provide significant amounts.

Beetroot, spinach, quinoa and wholegrains contribute valuable sources of betaine.

Thinking about these nutrients together helps explain why no single food can claim to lower homocysteine. Instead, the most effective dietary approach is built around a wide variety of nutrient-dense whole foods, each contributing different pieces of the puzzle.

Foods and habits that may make high homocysteine harder to manage

Supporting healthy homocysteine is not only about what you add to your plate. Certain everyday habits can also make it harder for your body to keep levels under control.

A diet low in vegetables naturally reduces your intake of folate and other B vitamins.

Diets dominated by ultra-processed foods often provide fewer of the vitamins needed for efficient methylation.

Excess alcohol can interfere with the absorption and metabolism of several nutrients involved in homocysteine recycling.

Smoking increases oxidative stress and is associated with higher homocysteine levels.

Coffee deserves a brief mention because the evidence is more nuanced. Moderate coffee consumption has been associated with several health benefits, yet some studies have also shown that high coffee consumption can increase homocysteine.

This does not mean everyone needs to give up coffee, but it strengthens the case for maintaining a good nutritional status if you drink several cups each day.

The aim is not dietary perfection. It is creating the best possible environment for your body’s own recycling system to work efficiently.

Diet is only one part of the picture. Regular exercise, stopping smoking, managing alcohol intake and correcting nutritional deficiencies can all help support healthy homocysteine levels. Learn about these and other evidence-based strategies in our guide to Eight Ways to Lower Your Homocysteine.

A Sample Day of Eating with Foods That Lower Homocysteine

The best foods to support healthy homocysteine

There is not a single food that lowers homocysteine. Eating a variety of whole foods provides the nutrients your body needs to recycle it efficiently.

Leafy green vegetables such as spinach, kale and broccoli are among the richest sources of folate, while fish, seafood and eggs provide vitamin B12.

Eggs also supply choline, an important nutrient for healthy methylation, and beans and lentils contribute folate and vitamin B6.

Beetroot, spinach and wholegrains provide betaine, which supports an alternative pathway for recycling homocysteine.

Rather than searching for a superfood, build meals around these foods consistently. Together they provide the nutrients your brain and body need to maintain healthy homocysteine metabolism.

Is diet enough to lower high homocysteine?

Improving your diet should always be the foundation. Every meal and snack is an opportunity to provide your body with the nutrients it needs to recycle homocysteine efficiently.

Many people may see meaningful improvements simply by eating more leafy greens, legumes, seafood, eggs and other nutrient-dense whole foods.

However, diet has its limits.

If a blood test shows your homocysteine is above the optimal range, food alone may not be enough to bring it back down.

Poor vitamin B12 absorption becomes increasingly common with age, certain medications interfere with B-vitamin metabolism, and some people have genetic variations that increase their need for specific nutrients.

Even someone eating what appears to be an excellent diet may still require additional nutritional support.

Rather than viewing food and supplements as competing approaches, think of them as working together. A nutrient-rich diet provides the foundation for lifelong health, while targeted supplementation may help correct a nutritional imbalance when diet alone does not achieve the desired result.

Read our complete guide to lowering homocysteine for a broader explanation of diet, lifestyle, testing and targeted nutritional support.

You can also learn more about B vitamins for lowering homocysteine.

How long does it take to lower homocysteine?

One of the encouraging things about homocysteine is that it can respond relatively quickly to the right intervention.

Improvements may begin within a few weeks of increasing key nutrients, although this depends on the underlying cause and how elevated homocysteine was to begin with.

Dietary changes may begin affecting homocysteine within weeks, but retesting after an appropriate interval can show whether the changes have been sufficient.

Food for the Brain recommends a simple approach.

First, test your homocysteine to establish your starting point. If you’re unsure which test to choose or how testing works, read our guide to homocysteine testing.

Next, improve your diet by increasing foods naturally rich in folate and other B vitamins while introducing targeted supplementation where appropriate.

Finally, repeat the test after around three to six months to confirm whether your homocysteine has moved towards a healthier range.

Without measuring it, you do not know whether your strategy is working.

Read more about how and when to test homocysteine.

Already have a result? Learn how to understand your homocysteine result.

Frequently asked questions

The bigger picture

Homocysteine is more than another blood test. It can indicate whether your body has the nutrients needed to support healthy methylation and long-term brain health.

Unlike many risk factors for cognitive decline, it is measurable, modifiable and measurable again after you have taken action.¹

A nutrient-rich diet should always be the starting point, but if testing shows your homocysteine is above the optimal range, targeted supplementation may be needed alongside dietary changes.

The goal is not simply to eat more spinach, although eating more vegetables is rarely a bad idea.

The goal is to understand what your body needs, measure your progress and know whether the steps you are taking are actually working.

Next steps

If you have not measured your homocysteine, that is the best place to start.

Knowing your level takes the guesswork out of deciding whether dietary changes alone are enough or whether targeted supplementation may be needed.

You can order our accurate at-home Homocysteine Test or choose the DRIfT 5-in-1 Test, which measures homocysteine alongside vitamin D, omega-3 index, HbA1c and glutathione, giving you a broader picture of your brain health.

You can also read our complete guide to lowering homocysteine for the next practical steps.

‘Our Children No Longer Need to Worry About Our Cognitive Decline‘

What one family learned from living through dementia and why they decided to take action.

When dementia affects a family, the impact often extends far beyond the person who receives the diagnosis. Many people begin to worry about cognitive decline, wondering whether it is an inevitable part of ageing or whether there is anything they can do to reduce their risk.In this story, Peter shares how watching his mother develop dementia changed the way he and his wife thought about ageing, why they decided to take a more proactive approach to their brain health, and how that decision ultimately gave their children something they hadn’t expected: peace of mind.

Most people do not start thinking seriously about dementia until it touches someone they love. Yet every day in the UK, around 790 people receive a dementia diagnosis, the equivalent of seven double-decker buses full of families beginning a journey they never expected to take.

Why One Family Decided Not to Worry About Cognitive Decline

For Peter and his family, dementia was not something they read about in the news or encountered through awareness campaigns. It arrived at their front door.

As his mother’s dementia progressed, the family witnessed first-hand how profoundly the condition could affect daily life. For a period, she lived with Peter and his wife, giving them a close-up view of the challenges, heartbreak, and uncertainty that often accompany cognitive decline.

Their children were young when their grandmother first became unwell and were old enough to witness much of what followed. They saw the gradual changes in her memory, independence, and ability to live the life she had once enjoyed. Like many families affected by dementia, they adapted as best they could, but experiences like these leave their mark.

Should You Worry About Cognitive Decline if Dementia Runs in Your Family?

At first, the family’s focus was entirely on supporting a much-loved mother and grandmother. Then, as they watched dementia unfold over many years, the children naturally started asking questions about the future. What would happen to their parents? Was this simply what ageing looked like? Could anything be done to reduce the risk of dementia?

For Peter, this became one of the most difficult parts of the journey.

When his mother died in 2016, he and his wife found themselves reflecting on everything the family had been through. They knew there were no guarantees when it came to health and ageing, but they also felt increasingly uncomfortable with the idea of simply hoping for the best.

Instead, they made a decision. Rather than focusing on what they could not control, they would focus on what they could.

That decision marked the beginning of a journey that continues today.

What to Do Instead of Worrying About Cognitive Decline

Peter’s interest in health had not appeared overnight.

Years earlier, they had discovered Patrick Holford’s work and become increasingly interested in nutrition and healthy ageing. Like many people, they had spent years trying to understand how food, lifestyle, and everyday habits influence long-term wellbeing.

Dementia, however, gave that interest a new urgency, as brain health was no longer an abstract topic. It had become deeply personal.

Instead of feeling powerless, they wanted to understand more about the factors associated with cognitive decline and, more importantly, what practical steps they could take to support healthy brain ageing. This led them to Food for the Brain’s educational resources, the Cognitive Function Test, and DRIfT biomarker testing.

They were not looking for guarantees or predictions about the future. They wanted a clearer understanding of where they stood and, perhaps more importantly, what they could actually do about it.

Measuring What Matters

The first steps? Understanding where they actually stood.

After years of watching dementia affect someone they loved, they wanted more than good intentions. They wanted a clearer picture of their current health and a better understanding of where they should focus their efforts.

The Cognitive Function Test provided one piece of that picture. Having first completed the assessment many years ago, Peter returned to it years later with a renewed interest in dementia prevention and healthy ageing. His score improved from 51 to 73.

The score itself was only part of the story. What mattered more was having a way to check in on how things were going. After everything the family had been through, it felt reassuring to have something tangible to measure rather than simply wondering whether their efforts were making a difference.

Alongside cognitive testing, they also began monitoring several biomarkers associated with brain health through DRIfT testing and implementing the guidance they were given along the way. The results showed encouraging changes across a number of areas:

Key Changes Over Time

His homocysteine level proved particularly useful information. Although he had already made a number of dietary and lifestyle changes, his levels remained higher than he would have liked, hovering at around 12 µmol/L across several tests. Regular testing allowed him to identify the issue, make further adjustments, and see how his body responded over time. After introducing vitamin B12, his homocysteine eventually reduced from 11.9 µmol/L to 7.16 µmol/L.

Without testing, he would never have known that this important marker remained elevated, as it is not something you can feel. Equally, without repeating the test, he would never have known whether the changes he made were having the desired effect. never have known whether the changes he made were having the desired effect.

Lifestyle Changes That Reduced Their Worry About Cognitive Decline

There was no single intervention that transformed their health overnight. Instead, they gradually reshaped the way they lived. Ultra-processed foods disappeared from the shopping trolley, wheat was removed from the diet, fermented foods became a regular feature at mealtimes, and targeted supplements were added where testing suggested they might be beneficial. Alongside this, they stayed physically active, walked regularly, and continued to challenge themselves mentally through activities such as completing The Times crossword.

Like many people who successfully improve their health over the long term, they did not follow a perfect plan or look for a magic solution. They focused on making changes they could sustain and enjoy, building habits that fitted naturally into the life they wanted to lead in retirement.

In many ways, their experience reflects what the research increasingly tells us about brain health: it is rarely one single intervention that matters most, but the cumulative effect of multiple factors working together over time, from nutrition and exercise to sleep, metabolic health, social connection, and lifelong learning.

The Difference It Made

Over time, they began to notice subtle shifts. Their thinking felt clearer, they felt more optimistic about ageing, and they gained confidence from seeing improvements in some of the markers they were tracking. Yet perhaps the biggest change was not physical at all. For years, dementia had been something that happened to their family. Now, instead of feeling defined by that experience, they felt they were actively shaping what came next.

The conversations within the family began to change, too. Their children and their children’s partners became more interested in brain health, nutrition, and prevention, turning what began as one family’s experience of dementia into a wider conversation about healthy ageing. Rather than seeing cognitive decline as an inevitable part of getting older, the family started to see it through a different lens, one that recognised the role informed choices can play in supporting long-term brain health.

When asked what has mattered most, Peter does not talk about biomarkers, supplements, or cognitive test scores. He returns instead to the concern that first motivated him and his wife to take action. Watching their grandmother’s decline had left a deep impression on the children, who naturally worried about what the future might hold for their parents. Those concerns did not disappear overnight, but they gradually eased as they saw their parents taking positive action, learning more about brain health, and making it a priority.

Reflecting on everything that had changed, Peter felt one thing stood out above all the others. He said “our children no longer need to worry about our cognitive decline.”

For Peter, that is the result that matters most.

Want to understand your own brain health?

Peter’s experience is not really about a test score, a supplement, or a blood result. Those were simply tools that helped him and his wife better understand their health, make informed decisions, and feel more confident that they were moving in the right direction.

At its heart, this is a story about a family who experienced dementia first-hand and decided not to leave the future entirely to chance. It is about protecting independence, preserving memories, staying connected to the people we love, and approaching later life with greater confidence and optimism.

At Food for the Brain, we believe more people deserve the opportunity to do the same. As a research and education charity, our mission is to make dementia prevention and optimal brain health possible by translating the latest science into practical, accessible actions that people can take today. Through research, education, testing, and behaviour-change programmes, we help people understand their brain health and take positive action while there is still time.

Related reading:

25 Daily Habits To Reduce Dementia Risk
Four Quick Wins to Reduce Your Risk of Alzheimer’s
Preventing Alzheimer’s Disease

Algae Oil vs Fish Oil for Brain Health: What’s the Difference?

If you’ve spent any time reading about brain health, you’ve probably come across omega-3s. When it comes to choosing a source of these essential nutrients, many people weigh up Algae Oil vs Fish Oil. They are one of the most researched nutrients in dementia prevention, cognitive function and healthy ageing, yet one surprisingly common question remains:

Does it matter where your omega-3s come from?

For years, fish oil was considered the gold standard. More recently, algae oil has emerged as an alternative that is popular with vegetarians, vegans and those who simply prefer a tasteless supplement. But does algae oil offer the same brain health benefits as fish oil, or is one genuinely better than the other?

The answer is more interesting than you might think.

Why Omega-3s Matter for Brain Function and Healthy Ageing

When we talk about omega-3s and brain health, we are mainly referring to two fatty acids: EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid).

DHA is particularly important because it forms part of the structure of brain cells themselves. In fact, DHA is one of the most abundant fats found within the brain, helping maintain healthy cell membranes and supporting communication between neurons.

EPA appears to play a slightly different role. It is involved in regulating inflammation, blood flow and a number of processes linked to mood and cognitive function.

Research has consistently linked higher omega-3 status with better cognitive performance, healthier brain ageing and a lower risk of cognitive decline. Some of the most fascinating findings come from the Oxford VITACOG studies, which examined the relationship between omega-3s, B vitamins and brain ageing.

Researchers found that participants with higher blood levels of omega-3s gained significantly greater benefits from homocysteine-lowering B vitamins than those with lower omega-3 levels. Those with both adequate omega-3 status and B vitamin support experienced slower rates of brain atrophy and reduced cognitive decline compared with those who had lower omega-3 levels [3,4].

Interestingly, emerging research suggests that maintaining adequate omega-3 levels may be particularly important for women. Hormonal changes associated with ageing can influence brain health, inflammation and cognitive resilience, making omega-3 status an important consideration throughout later life. You can learn more in our article on why women’s brains need omega-3 now.

The simple takeaway is that omega-3s appear to be an important part of protecting the brain as we age. They also do not work in isolation. Like most nutrients, they seem to be most effective when part of a wider network of nutrients and healthy lifestyle factors.

Want a quick overview before we compare algae oil and fish oil? This short video explains why omega-3s are so important for brain health and healthy ageing.

Algae Oil vs Fish Oil: What’s the Difference?

Fish oil is extracted from oily fish such as sardines, anchovies and mackerel and has been the most widely used source of EPA and DHA for decades.

Algae oil, on the other hand, is derived directly from marine microalgae.

This distinction is important because fish do not actually produce omega-3 fats themselves. Instead, they accumulate EPA and DHA by consuming algae and other organisms within the marine food chain [5].

In other words, algae are the original source of the omega-3 fats found in fish.

From a nutritional perspective, both fish oil and algae oil can provide the same biologically active forms of omega-3. The main differences relate to dietary preference, manufacturing methods and the specific balance of EPA and DHA provided by individual products.

If you’re considering an omega-3 supplement, it’s worth understanding the differences between EPA and DHA, how much you may need, and what to look for when choosing a quality product. Our comprehensive guide to omega-3 supplements covers the evidence, recommended intake levels and key considerations before you buy.

Algae Oil vs Fish Oil: Key Differences

Is Algae Oil as Effective as Fish Oil?

Fish oil still has one clear advantage: it has been studied for much longer.

As a result, there is currently a larger body of research investigating fish oil supplementation and health outcomes. That does not necessarily mean fish oil is superior, only that it has a longer research history.

More recently, scientists have started directly comparing fish oil and algae oil. A 2025 human trial found that algae-derived EPA and DHA were absorbed just as effectively as omega-3s from fish oil when equivalent doses were provided [6].

This is an important finding because it suggests the body is able to utilise EPA and DHA from algae in much the same way as EPA and DHA from fish oil. For people who do not eat fish, follow a plant-based diet or simply prefer a tasteless source of marine omega-3s, algae oil appears to be a credible alternative rather than a compromise.

Omega-3s, B Vitamins and Dementia Prevention

There are two topics we love talking about at Food for the Brain: omega-3s and homocysteine. While they might seem unrelated, some of the most exciting dementia prevention research suggests they may be more connected than we once thought.

One reason omega-3s have become such an important focus in dementia prevention research is their relationship with homocysteine. Homocysteine is a naturally occurring amino acid that, when elevated, is associated with a greater risk of cognitive decline and dementia. B vitamins, particularly folate, vitamin B12 and vitamin B6, help keep homocysteine levels under control.

In the landmark VITACOG trial, homocysteine-lowering B vitamins significantly slowed the rate of brain shrinkage in older adults with mild cognitive impairment [1]. Further analysis showed that these benefits were strongest among participants with higher omega-3 levels [3,4].

This helps explain why many practitioners now assess both homocysteine and omega-3 status when considering an individual’s long-term brain health. This highlights an important lesson in nutrition: it is rarely one nutrient acting alone. The greatest benefits usually come from the interaction between multiple nutrients and healthy lifestyle factors working together. (Which is why we have our 8 nutrition and lifestyle domains in the COGNITION online community and programme.)

Don’t Guess Your Omega-3 Status

One of the biggest misconceptions about omega-3 supplementation is that taking a supplement automatically means your levels are optimal.

In reality, omega-3 status varies considerably from person to person. Genetics, absorption, diet, dosage and supplement quality can all influence the amount that ultimately reaches your bloodstream. Two people taking the same supplement may achieve very different results.

That is why, at Food for the Brain, we believe testing is often more useful than guessing.

The DRIfT test measures several important biomarkers linked to brain health, including omega-3 status, homocysteine, vitamin D, HbA1c and glutathione. Rather than assuming your current diet or supplement routine is working, testing can help identify where support is needed and allow you to take a more personalised approach to protecting your brain health.

Algae Oil and Fish Oil: Key Takeaways for Cognitive Health

Both fish oil and algae oil provide the EPA and DHA associated with healthy brain ageing and cognitive function.

Fish oil remains the most extensively studied source and continues to have the largest body of evidence behind it. However, current research suggests that algae oil can raise blood levels of EPA and DHA just as effectively, making it a viable option for those who prefer not to use fish-derived products [6].

Perhaps the most important lesson from the research is that taking an omega-3 supplement is only part of the story. What ultimately matters is whether those omega-3s are reaching meaningful levels in your bloodstream and, ultimately, your brain.

The real question might not be whether your omega-3 comes from fish or algae.

The real question is whether your brain is getting enough.

Next Steps:

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. This allows them 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.

Related reading:

Alzheimer’s: Why prevention is better than drugs – but less profitable
How to Keep Building Brain Cells at Any Age

Chromium, Blood Sugar and Brain Health: The Overlooked Connection

How Blood Sugar Regulation Affects Brain Function?

When people think about protecting their brain, they often focus on keeping mentally active, reducing alcohol, or hoping they avoid dementia as they get older, somehow? But nutrients and minerals like chromium may also play a role in brain health.

Few think about blood sugar.

Yet every thought, memory, conversation, and decision relies on a constant supply of energy. Increasingly, researchers are discovering that how effectively we regulate blood sugar and respond to insulin may play an important role in how our brains function and age. (1)

This is where chromium enters the story.

Although only required in tiny amounts, chromium plays an important role in normal carbohydrate, fat, and protein metabolism. Its best understood role is helping insulin do its job more effectively. Insulin is the hormone that helps move glucose from the bloodstream into cells, where it can be used for energy, and chromium appears to support this process. (2)

The Brain’s Energy Demand and Glucose Supply

The brain represents only around 2% of body weight, yet uses roughly 20% of the body’s energy. (3) To function properly, brain cells require a continuous supply of fuel. Most of the time, that fuel comes from glucose, although the brain can also use ketones under certain circumstances.

When insulin is working well, glucose can be transported efficiently to the cells that need it. When cells become less responsive to insulin, a state known as insulin resistance develops. Blood sugar levels may rise, inflammation can increase, and energy production becomes less efficient.

Importantly, insulin resistance does not just affect muscles, fat tissue, and the liver. It also affects the brain.

Researchers have linked impaired insulin signalling with changes in brain structure and function, while people with type 2 diabetes consistently show a higher risk of cognitive decline and dementia than those with healthy glucose regulation. (4)

This growing body of evidence is changing how scientists think about brain health. Protecting the brain is not only about keeping it stimulated and active. It also depends on how effectively the body produces, regulates, and delivers energy to brain cells throughout life.

Chromium and Blood Sugar Regulation

Chromium is found naturally in foods including shellfish, meat, eggs, broccoli, and whole grains.

In terms of how it works, you can think of insulin as a key trying to unlock the door to a cell, and chromium appears to help that key work more efficiently, allowing glucose to move where it is needed and be used for energy. (2)

This has led researchers to investigate whether chromium supplementation might support healthy blood sugar regulation. Results have been mixed, but overall, the evidence suggests chromium may help improve fasting glucose in some individuals, particularly those with impaired glucose control or type 2 diabetes. (5)

That does not make chromium a miracle nutrient, nor does it mean everyone should supplement with it. What it does suggest is that even relatively small nutrient deficiencies may influence how effectively the body’s blood sugar regulation systems operate.

Insulin Resistance, Dementia and Brain Health

Unlike omega-3 DHA and B vitamins, which work together to support the formation, maintenance, and communication of brain cells, chromium’s role appears to be less about building brain tissue directly and more about helping to regulate the energy supply those cells depend upon.

Its potential relevance lies in the fact that the brain is one of the most energy-demanding organs in the body. If insulin resistance increases the risk of cognitive decline, it is reasonable to ask whether nutrients involved in healthy insulin function might also matter for long-term brain health.

We do not yet have evidence that chromium supplementation directly reduces dementia risk. However, the connection between insulin resistance and brain health is now difficult to ignore, making nutrients that support healthy glucose regulation increasingly worthy of attention. This metabolic connection is also reflected in research examining glycaemic load and dementia risk.

In other words, chromium is interesting not because it is a brain nutrient, but because it sits within a system that appears to be highly relevant to how the brain functions and ages.

Chromium, Mood and Sugar Cravings

Interestingly, chromium’s effects may extend beyond glucose regulation.

Several small studies have explored chromium supplementation in people with atypical depression, particularly where symptoms include fatigue, increased appetite and carbohydrate cravings. Some reported improvements in mood and reductions in cravings, while researchers have also proposed possible effects on neurotransmitter systems involved in mood regulation. (6)

These studies are small and far from definitive, but they point towards something that is becoming increasingly clear: metabolism and mental health may be far more connected than we once believed. So much so that entire fields such as metabolic psychiatry and nutritional psychiatry have emerged in recent years. Researchers including Christopher Palmer and Georgia Ede are helping to challenge the idea that mental health exists solely in the brain, highlighting the important role that blood sugar regulation, nutrient status, inflammation and cellular energy production may play in our mental health and resliency.

Why Metabolic Health and Chromium Matters for the Brain

The story of chromium is not really about chromium.

It is about systems.

For decades we have tended to separate brain health from metabolic health. We talk about memory, dementia and cognition on one side, and blood sugar, insulin and diabetes on the other.

Increasingly, the science suggests these systems are deeply interconnected.

Reducing excess sugar intake remains one of the most important things we can do for long-term health. Following a low glycaemic load diet can help reduce blood sugar spikes and support healthier glucose regulation. But this also raises an interesting question. What if someone is already eating relatively well, yet their blood sugar regulation remains less than optimal?

Chromium is unlikely to be the missing piece for everyone. In fact, many multivitamins already contain small amounts. But it serves as a useful reminder that healthy insulin regulation depends on more than simply avoiding sugar. It relies on a network of nutrients, hormones and metabolic processes working together.

This is one reason we include HbA1c in the DRIfT blood test. HbA1c provides insight into how effectively blood sugar has been regulated over the previous two to three months and can help identify an often-overlooked aspect of brain health long before symptoms appear.

Next Steps:

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. This allows them 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.

Related reading:

Depression
Make Eating Less Sugar Easier (& a FREE Recipe!)

Is China’s Alzheimer’s Nightmare Becoming Our Reality?

Patrick Holford examines how China is advancing Alzheimer’s prevention through nutrition, lifestyle and digital health initiatives, while questioning the pace of policy action in the UK.

The Race to Prevent Alzheimer’s in China

If there is one country that has to move fast to prevent Alzheimer’s, it is China. And it is.

With almost a quarter of its population over 60, some 320 million people, and an estimated 20 million expected to have Alzheimer’s by 2030, costing close to a trillion dollars a year, government health officials are taking prevention very seriously indeed.

Those over 60 are not called old, elderly, or senior, but “silver-haired“, a growing community that is at the heart of China’s health prevention strategies.

The doctor in charge of the Silver-Haired Healthy Lifestyle campaign is Dr Zhang Lei. He is a famous TV doctor and former surgeon.

I asked him if he believed there would ever be a cure for Alzheimer’s.

“Prevention is the cure,” he said. “And I want to make a special announcement. Next year, when your excellent book Alzheimer’s: Prevention is the Cure is published in Chinese, we will use this book as the cornerstone of our national prevention campaign. We already have direct access to 20 million people through our networks, but our ambition is to reach as many as 100 million. We will encourage everyone to take the online Cognitive Function Test from Food for the Brain. This book and this tool together will be our roadmap for a prevention revolution in China.”

Prevention-First Approach

I attended and spoke at the 2nd Silver-Haired Healthy Lifestyle Conference, where I met hundreds of silver-haired people like myself. The event was attended by 2,500 people and broadcast to 10 million people across twenty TV channels.

Other speakers included leading professors of public health, nutrition, gerontology and geriatrics, all delivering positive and progressive messages about prevention, including eating more seafood and vegetables, stopping smoking, cutting right back on sugar, sleeping better and taking 10,000 steps a day.

I spoke about the essential need for, and codependence of, omega-3, phospholipids and B vitamins. If omega-3 were the man and phospholipids, rich in eggs and seafood, were the woman, then B vitamins are the priest, I said. When they are married in your brain, magic happens. Together, they are the three building blocks of every brain cell.

You could have heard a pin drop. Everyone was listening and, in China, action is taken quickly.

The former Health Minister said that “diet, supplements and lifestyle” are the cornerstones of prevention. “We need education, not medication.“

No one was talking about anti-amyloid treatments.

Prevent Alzheimer’s at Scale

Next year, when the 3rd Healthy Lifestyle Conference coincides with the Chinese publication of my book Alzheimer’s: Prevention is the Cure, I have been invited to speak at universities and health departments across China.

Many silver-haired people in China do not have computers, but they all have smartphones. There are virtually no physical wallets. Communication and payment are conducted through the WeChat app.

The professors and public health officials were therefore very excited about our online digital test. They want to get everyone using Food for the Brain’s Cognitive Function Test. The COGNITION questionnaire then helps people understand which specific prevention steps are most relevant to them.

The experts, health authorities and policymakers understand that changing behaviour is the hardest part, and that this kind of personalised digital technology is key to motivating individuals and measuring change to find out what really works. It is big-data science helping to sharpen prevention strategies.

Why China Is Embracing Nutrition Over Medication for Brain Health

Traditionally, Chinese culture sees food as medicine, which may be one reason people are more open to optimum nutrition. There is also a long tradition of using natural compounds to support health, so supplements are a natural extension of this way of thinking.

Not one person repeated the old myth that “you can get all the nutrients you need from a well-balanced diet“.

The stark ignoring of established scientific facts about, for example, B vitamins and omega-3, which have outperformed anti-amyloid treatments, by our politicians and health ministers is verging on outrageous when the lives and brains of so many are at stake.

China’s High-Speed Lesson for Alzheimer’s Prevention

As I sat on a high-speed train travelling 1,200 kilometres from Shanghai to Beijing in just 3.5 hours, faster than taking a plane, and capable of speeds of 650 kilometres an hour, I found myself contemplating how the UK has yet to deliver the promised high-speed rail line from London to Birmingham, a little over 100 miles, despite more than a decade of work, a projected cost of over £100 billion, and a journey time saving of less than half an hour.

If this same failure to translate prevention science into policy continues, as it has over the past two decades, offering platitudes about the importance of prevention but little action, while continuing to avoid the scientific evidence of what actually works, then China’s nightmare of a large proportion of its silver-haired population slipping into dementia will become our reality.

Alzheimer’s is preventable. That is a fact, not a belief.

Those who say it cannot be done should not stand in the way of those who are doing it.

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. This allows them 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.

Related reading:

Dementia Prevention Goes Global
China Is Taking Prevention Seriously In The ‘silver-haired’ Economy
Alzheimer’s: Why Prevention is Better than Cure

Amyloid isn’t Alzheimer’s – How NOT to Study a Disease

by Patrick Holford

Alzheimer’s disease has, for decades, been framed primarily as a problem of amyloid plaques building up in the brain.

It is a compelling idea. It is measurable, visible on brain scans, and has shaped billions in research funding and drug development. There’s just one problem.

It doesn’t adequately explain what we see in people.

Many individuals with significant amyloid in their brains remain cognitively normal. Others develop clear dementia with little or no amyloid present (1). Treatments that successfully reduce amyloid have, at best, produced only modest effects on slowing decline, with no meaningful reversal of symptoms (2).

Amyloid is associated with Alzheimer’s disease, but association is not the same as causation.

And that distinction changes everything.

This growing tension between theory and evidence is explored in depth by neurobiologist Karl Herrup in How Not to Study a Disease, where he challenges how the field has come to define and pursue Alzheimer’s.

Some people develop increasingly severe cognitive decline as they age. This affects roughly one in ten older adults. We call this dementia. In some cases, brain scans show clear shrinkage in key regions, particularly the medial temporal lobe, which is then used to diagnose Alzheimer’s disease. So we have two observable features: a decline in cognitive function and measurable loss of brain tissue.

The question that follows is simple, but critical.

What is actually causing this process?

What causes Alzheimer’s?

Amyloid has long been positioned as the answer. Yet the evidence tells a more complicated story.

A significant proportion of older adults have amyloid plaques in their brains and remain cognitively normal. At the same time, some individuals with clear dementia show little or no amyloid pathology. Amyloid is associated with Alzheimer’s, but that is not the same as being the cause.

If amyloid were the primary driver, then reducing it should meaningfully change the course of the disease. However, interventions designed to reduce amyloid have consistently lowered amyloid burden in the brain, yet produced, at best, modest effects on slowing decline, often measured as very small changes on cognitive scales. There has been no meaningful reversal of symptoms. In some cases, safety concerns have emerged, including brain bleeding and swelling.

Recent large-scale evidence (6) now reinforces this point. A 2026 Cochrane review concluded that although anti-amyloid monoclonal antibodies can remove amyloid from the brain, this does not appear to translate into clinically meaningful effects for people with mild cognitive impairment or mild dementia due to Alzheimer’s disease, while increasing the risk of amyloid-related imaging abnormalities.

From a scientific perspective, this adds to an already substantial body of evidence suggesting that amyloid accumulation, on its own, does not explain the disease process. It may be part of the picture, but it is not the engine driving it.

And yet, the field has remained heavily focused on this single pathway.

When a hypothesis becomes a lens

Research tends to follow what is measurable, fundable, and already established. Over time, this can narrow the lens rather than expand it.

Amyloid has become that lens. As Karl Herrup argues in his book, once a hypothesis becomes dominant, it can begin to shape not just what is studied, but how results are interpreted and what gets funded next.

The result is that vast resources have been invested in understanding and modifying amyloid biology, while other avenues have received comparatively less attention. We have learned a great deal about amyloid itself, but we are not significantly closer to preventing or reversing the condition that matters most to patients, which is cognitive decline.

This is not unusual in science. Once a model becomes dominant, it shapes the direction of funding, research questions, and even how people interpret results.

A similar pattern is now emerging with another biomarker, p-tau.

Tau is a normal protein that, under certain conditions, becomes altered and associated with the tangles seen in Alzheimer’s pathology. Higher levels of p-tau are linked with increased risk, but again, association does not establish causation. Many individuals have elevated levels without clinical symptoms.

As with amyloid, the risk is that a marker becomes mistaken for the mechanism.

What does influence the disease process?

This is where the picture becomes more interesting.

There are factors that sit upstream of both amyloid and tau, influencing the environment in which brain cells function or fail. One of the most studied is homocysteine, a marker of methylation and B vitamin status.

Unlike amyloid, intervention trials have shown that homocysteine influences outcomes. In the VITACOG study, lowering elevated homocysteine with targeted B vitamins significantly slowed the rate of brain atrophy in individuals with mild cognitive impairment, with corresponding effects on cognitive decline. This is much closer to what we would describe as a disease-modifying effect (3,4). It also raises questions explored in Apparently healthy but diagnosed with Alzheimer’s about whether current diagnostic models are identifying true disease drivers or simply biomarkers.

That does not mean homocysteine is the only cause. It is one piece of a larger system. But it illustrates an important point. When you influence the underlying biology of the brain, rather than a downstream marker, you begin to see meaningful change.

For more on this approach, see our article on early diagnosis of Alzheimer’s: amyloid protein vs homocysteine testing.

A systems problem, not a single cause

Alzheimer’s does not behave like a single-cause disease.

It is better understood as the result of multiple interacting processes. These include inflammation, oxidative stress, insulin resistance, mitochondrial dysfunction, and impaired methylation, among many others (5). Each of these affects how brain cells are built, maintained, and powered. Emerging research is also exploring how 40 Hz light and sound stimulation may affect Alzheimer’s-related processes, including microglial activity, amyloid and tau.

Individually, they may not be sufficient to cause disease. Together, they can create the conditions in which the brain becomes vulnerable.

This is closer to how we understand most chronic conditions. Not as a single fault, but as a convergence of pressures that eventually exceed the system’s ability to compensate. A more useful way to think about it is not as one switch flipping, but as several dials turning in the wrong direction at the same time.

Why this matters

If we continue to focus primarily on downstream markers such as amyloid or p-tau, we risk missing the broader picture.

If instead we look at the upstream drivers, the factors that influence brain structure, function, and energy supply, we open up a different set of possibilities. Not just for treatment, but for prevention.

These are not fringe ideas. They are part of a growing shift in how Alzheimer’s is being understood, questioned, and re-examined. Researchers like Karl Herrup are helping to bring that conversation into the open, challenging long-held assumptions and asking more useful questions about what truly drives the disease.

It’s a conversation that is only just beginning to reach wider audiences.

This is exactly what we’ll be exploring at Alzheimer’s Prevention: New Frontiers conference, where leading researchers and clinicians will come together to look beyond single-cause models and towards a more complete understanding of brain health and cognitive decline.

Is prevention the real solution?

The prevailing model in medicine has been to identify a single cause and target it with a treatment. That works well for some conditions. It is less suited to complex, multifactorial diseases like Alzheimer’s.

A systems-based approach asks a different question.
What combination of factors leads to decline, and how do we shift that combination in the opposite direction?

This is the approach we take at Food for the Brain. By combining cognitive testing with blood testing and lifestyle information, it becomes possible to see patterns, not just isolated variables. Over time, this allows us to understand what drives resilience as well as risk.

It is likely that we will not find a single primary cause of Alzheimer’s. What we may find is something more useful: a set of modifiable factors that, together, determine whether the brain maintains function or begins to decline.

In that sense, prevention may not just be part of the solution.

It’s the solution.

Find out more with Alzheimer’s: Prevention is the Cure book here

Learn more about our Alzheimer’s Prevention: New Frontiers Conference here.

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Thank you for reading!

Food for the Brain is a non-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.

Related reading

Apparently Healthy, but Diagnosed with Alzheimerʼs? 
Why “Normal” Vitamin D Levels May Not Be Protective for Women’s Brains
Early Diagnosis of Alzheimer’s – Amyloid Protein vs Homocysteine Testing
‘My Relative Has Memory Problems, Possibly Dementia. What Do You Recommend?’
Homocysteine & Alzheimer’s Disease (2002)