Dry January for Your Brain: A Lighter, Clearer Start to the Year

Dry January arrives with its usual mix of good intentions and side-eye, but beneath the trend is a surprising truth: your brain loves this month more than you think.

That’s because January quietly offers something modern brains rarely get the rest of the year: a drop in oxidative stress and a chance for your natural repair systems to catch up.  It’s a pause that lowers the background “noise” created by alcohol and allows your natural calming chemistry to rise back to the surface.

Many people start Dry January thinking about their liver or their waistline. But the strongest benefits often happen behind the scenes, in the place that governs mood, memory, sleep, and stress resilience.

That’s where the real benefits begin to show.

Dry January for Your Brain: Why the Benefits Show Up So Fast

Alcohol works on the same calming pathway your brain uses to wind down naturally. It boosts GABA, the neurotransmitter that quietens the nervous system. That lovely “first sip exhale” comes from this temporary GABA boost. You can learn more about GABA here. 

But your brain is clever. To compensate, it gradually nudges up adrenaline and turns the GABA dial down. This is why the glass that once relaxed you, can start to make you feel restless or wakeful later in the night.

And there’s more happening beneath the surface:

Alcohol increases oxidative stress inside neurons, largely because its metabolism produces acetaldehyde. This compound generates reactive oxygen species and increases neuronal damage (1).
It also places extra pressure on glutathione, the molecule the brain relies on for detoxification and repair. Chronic alcohol exposure is associated with reduced glutathione levels and impaired antioxidant capacity in the brain (2).
The hippocampus is particularly affected. This memory and mood hub is vulnerable to long term strain, and higher alcohol intake is linked to reduced hippocampal volume even at moderate levels (3).
Alcohol also disrupts sleep quality, especially REM cycles, which are crucial for cognitive repair. While alcohol initially sedates, it later fragments sleep architecture through a rebound in adrenaline and cortisol.

Read more about how alcohol impacts your brain here.

These are some of the core drivers of long term cognitive ageing. When they ease up, even for a short period, the brain begins to function more cleanly and calmly.

For this reason, so many people report that a couple of no or low alcohol weeks in January give them clearer thinking, steadier mood, and deeper sleep.

Two Brain Friendly Drinks for Your January Wind Down

With that in mind, here are two great recipe options to help you reduce your alcohol intake while still enjoying a wind down ritual. If you want more brain friendly recipes this year, make sure you subscribe to the Upgrade Your Brain Cook App.

Want to go deeper?

If you want deeper support for your brain this year, there are three simple steps you can take.

First, measure the things that matter. The DRIfT 5 in 1 at home blood test gives you a clear picture of the nutritional and metabolic factors that influence long term brain health. It is one of the most effective ways to understand your personal risk and what to do next.

Second, stay connected to what keeps your brain healthy. Becoming a FRIEND of Food for the Brain gives you ongoing support, events, and guidance grounded in evidence and prevention.

Third, take the free Cognitive Function Test. It provides an objective snapshot of how your brain is performing right now and helps you track your progress over time.

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.

References:

Zakhari S. Overview: how is alcohol metabolized by the body? Alcohol Res Health. 2006;29(4):245-54. PMID: 17718403.
Das SK, Vasudevan DM. Alcohol-induced oxidative stress. Life Sci. 2007;81(3):177-87. PMID: 17570440.
Topiwala A, et al. Moderate alcohol consumption as risk factor for adverse brain outcomes and cognitive decline. BMJ. 2017;357:j2353. PMID: 28588063.

Welcome to 2026 – The Year of the Alpacalypse

by Patrick Holford

The Global Brain Health Crisis and Why 2026 Matters

Down here at Fforest Barn Mountain Retreat we are awaiting the arrival of Buddy, our new alpaca, joining Tommy Gun, Food for the Brain’s lucky mascot, along with Vincent, Oran and Winston “the Wolf” Moondance, born on a full moon. This year we are expanding and consolidating our beyond organic food growing, applying all the principles I have learned about health to plants. If you would like to understand these principles, watch the lecture I gave for the BioNutrient Food Association, entitled “As Below So Above”, which explains the five fundamental principles of health of and the basis of my new book The Five Health Essentials.

It was great having the whole Food for the Brain team here on the farm to brainstorm how to make the world a better place. Check out this film for a glimpse.

The apocalypse allusion is deliberate. The cost of dementia, most of which is Alzheimer’s, is untenable. China expects soon to face a trillion dollar annual bill if nothing radical changes to prevent this cerebral tsunami. Brain disorders already cost more than cancer and heart disease combined. Brain health and nutrition must be top of the healthcare agenda if we are to avoid costs that will destabilise economies and families worldwide.

The Design Problem in Modern Healthcare

As I see it, two fundamental problems need solving: corruption and design. 

By design I mean having a workable model for healthcare, economics and ecology that functions effectively at scale. In other words, a way of living that supports human health, not undermines it.

I am excited about what we are doing at Food for the Brain because it provides a realistic model for prevention at scale. It is a new paradigm based on systems-based science, not reductionism, and it goes straight to people, to Citizen Scientists, without relying on the corrupted middle layer of healthcare bureaucracy. Watch my six-minute systems-based film for a deeper explanation.

Alpacalypse and the Coming Crisis in Preventive Healthcare

What we are doing for Alzheimer’s prevention can be applied to all major 21st-century disease epidemics, from cancer to diabetes. This spring I will be in Algeria, where the Health Minister is considering integrating this approach into national healthcare. I then head to China to present at a major Alzheimer’s prevention conference. Next week I am speaking to influential CEOs in the US who have the power to scale this globally.

Knowing what works is one thing. Doing it is another. Corruption for profit, in other words greed, is the major drag factor blocking this inevitable paradigm shift. It sickens me that prevention of such a devastating condition, one that robs people of their memories until they die not knowing their own children, is actively blocked to preserve profit from hypothetical, clinically ineffective medication.

The layers of corruption within medical science, academic journals, PR systems and the networks that keep authority figures aligned run deep. The only solution is to keep telling the truth and exposing the lies. Shortly before Linus Pauling died, I filmed him discussing his brilliant lipoprotein(a) hypothesis in heart disease. He advised me to “follow the logic” to find the truth and not to worry about randomised controlled trials; they come later.

The selective use of meta-analyses, which combine chosen RCTs, has become a mechanism to generate pharma gold, not clearer science. A classic example is The Lancet Commission on Dementia Prevention report in 2023, which purposely ignored homocysteine-lowering B vitamins and omega-3 (Read more about that here). In combination, these are the single most evidenced, substantial and easily implemented means to cut Alzheimer’s risk by at least a third. That omission is corruption: following the money, not the logic.

Citizen Science as a Scalable Solution to Dementia Prevention

This is why supporting Food for the Brain matters. Becoming a Friend and encouraging those you know to take the Cognitive Function Test strengthens the COGNITION Biobank, which enables true prevention research at scale. I predict that by the end of 2026, this will be the largest dementia prevention research database in the world. My colleagues in China want to test 18 million people over the age of 60.

If you are looking for a New Year’s resolution, I suggest becoming a Citizen Scientist in heart, mind and action. How? 

Take the Cognitive Function Test here and tell everyone you know to do it!
Become a Friend – Join over 2,000 members to access monthly coaching and webinars and support this important movement.

(For those with children, see foodforthebrain.org/smartkids)

Despite everything mentioned, there is so much possibility and hope. And it doesn’t need to be overwhelming, avoid sugar as much as possible. Invest in high-quality food, because it becomes you. Take your supplements every day. Walk at least 5,000 steps a day, ideally 7,000. The most important aspect is to take regular positive actions in your own health journey.

A New Year Call to Action for Citizen Scientists

2026 offers a turning point. Prevention is entirely achievable if people are given truthful education, accessible tools, and a model of change rooted in systems thinking rather than narrow, profit-driven science. 

You can make powerful choices that protect your future and the generations to come.

Wishing you a Happy Christmas and a Healthy New Year.

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.

From Awareness to Action: A Year of Progress in Dementia Prevention

A Letter from Emma – Our CEO

This has been a landmark year for Food for the Brain, a year in which our work moved from ambition to acceleration. I am reminded of this shift every time I hear from individuals and families whose lives are quietly changed by prevention. Earlier this year, Nisha told us she had been struggling with her memory and felt genuinely worried about what it might mean for her future. She took the DRIfT blood test and discovered her omega-3 levels were extremely low, even though her vitamin D and HbA1c were in good shape.

She began targeted nutritional changes and, within a few months, noticed her memory improving. The results gave her confidence and direction. Instead of fearing where things were heading, she felt she had a practical route to protect her brain health. For Nisha and her children, that shift was life-changing. As she put it: “What you’ve done with Food for the Brain is on another level.”

Stories like Nisha’s remind us that prevention is powerful. With the right knowledge at the right time, people can change their cognitive trajectory long before disease ever takes hold.

Impact You Can See and Measure

This has been our most expansive year yet.
We reached new ground and new communities at a scale we have never seen before.

470,000 people have now taken the Cognitive Function Test, turning a simple twenty-minute assessment into a global source of agency and early action.
134 new countries took part this year, extending our reach into communities we could never have reached on our own.
We translated the Cognitive Function Test into 7 more languages, ensuring prevention becomes accessible, not just aspirational.

Most importantly, 200,000 individuals have now taken direct action to protect their brain health.

Education powers this progress. Over the last twelve months, we delivered more than 5.7 million moments of evidence-based brain health education, helping people understand how to protect and improve their cognitive future. These small moments accumulate into meaningful change.

Strengthening the Organisation for Scale

When I stepped into the CEO role a year ago, my priority was to build the operational backbone needed for the scale we knew was coming. This work is less visible from the outside, but it is the reason we were able to secure Innovate UK support, progress major scientific partnerships and prepare for international expansion. Step by step, we are becoming the sustainable, resilient and science-driven organisation this field needs.

Advancing Our Scientific Position

The appointment of Dr Tommy Wood, Associate Professor of Neuroscience at the University of Washington, as our Head of Research has been pivotal. Under his leadership, our scientific direction has sharpened into a clear and ambitious programme. Over the past year, we have advanced from holding one of the richest prevention datasets in the world to building a strategic roadmap that strengthens and validates it. Our research team is now refining the Dementia Risk Index with greater precision and clarifying the role of nutritional biomarkers in tracking and modifying future dementia risk.

This work reinforces what sets us apart. We are the organisation connecting cognition, lifestyle patterns, biomarkers and long-term outcomes at population scale, with prevention at the centre. That distinction is now recognised across academic and clinical communities.

Growing Recognition and Influence

This year brought a marked shift in how others see Food for the Brain. Universities, healthcare providers, digital health innovators and international research groups actively sought partnerships. We were invited to contribute, teach and shape the public conversation on dementia prevention in ways that would have been unthinkable only a few years ago. The Innovate UK award marked an important milestone, reflecting the relevance of our work to UK innovation and health system priorities

Looking Ahead – My Vision

My vision is clear.

Food for the Brain will lead a global movement that proves dementia is not inevitable and will empower millions to protect their brains for life.

Philanthropic support plays a vital role in accelerating our impact. If you are in a position to support this next phase of growth through partnership, advocacy or donation, I would be delighted to connect.

With Heartfelt Thanks

To our trustees, scientific advisors, academic partners, FRIENDS, generous donors, volunteers, phenomenally brilliant team members, and the growing community of Citizen Scientists who trust us with their cognitive future – thank you! Your belief fuels our progress, and your partnership directly shapes what we can achieve.

And finally, a personal thank you to Patrick Holford, our founder, whose vision created the foundation on which we now stand and who is now involved in taking our message globally. It is a privilege to lead Food for the Brain into this next chapter, building on the legacy Patrick has created and expanding it into this new era of scientific and global impact.

Together, we are proving what is possible. And it is together that we are protecting brain health and transforming the future for families and society.

Best wishes,

Emma George
CEO, Food for the Brain Foundation

—

Want to join us?

We couldn’t do without our FRIENDS or without those who contribute to our Citizen Science. Here are three ways you can be part of the movement:

Check your brain health: Take the free Cognitive Function Test and spot risk early, while change is still possible.
Turn insight into action: The DRIfT 5-in-1 test shows which nutritional and metabolic factors matter most for your brain. No guesswork. No wasted effort.
Help scale prevention: Become a FRIEND and support independent research, education and global action on dementia prevention.

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.

The Midlife Biomarker Proven to Drive Alzheimer’s – And How to Bring It Down

Homocysteine is one of the few Alzheimer’s risk factors that is causal and modifiable, and it often begins rising in midlife, making it a valuable Alzheimer’s biomarker to monitor.

It is the only measurable Alzheimer’s risk factor where lowering it has been shown to slow the disease process itself. When homocysteine rises, the brain shrinks faster. When it is lowered with the right nutritional support, shrinkage slows and thinking skills stabilise [1][3][4].

Yet despite decades of evidence, most people have never been told to test it. Most health systems never mention it at all.

This matters because homocysteine begins to rise years before symptoms develop. It gives us a glimpse into the future health of the brain long before memory changes appear. And midlife is the moment where this shift becomes easiest to detect and easiest to change. Far from being the start of inevitable decline, it is a powerful opportunity for prevention.

What Is Homocysteine and Why Does the Brain Care?

Homocysteine is a natural amino acid produced during methylation, the process the body uses to build and repair cells, process toxins, create neurotransmitters and maintain healthy brain tissue. When methylation runs smoothly, homocysteine stays low. When the system struggles, homocysteine rises.

Elevated homocysteine affects the brain in several ways:
• It accelerates shrinkage of the hippocampus, the brain’s memory centre [3].
• It increases oxidative stress and inflammation [1].
• It injures small blood vessels, increasing microvascular damage seventeen-fold [2].
• It disrupts the formation of neuronal membranes [1].

These are not abstract processes. They are part of the biology that leads to cognitive decline.

Homocysteine is therefore both a predictor and a causal contributor to these mechanisms. Scientists use the word causal when lowering a factor has been shown to change the underlying disease process. Homocysteine meets this definition because reducing it slows brain shrinkage and slows cognitive decline, which no amyloid-targeting drug has yet achieved [1][3][4].

Why Homocysteine Is a Causal Alzheimer’s Risk Factor

A causal relationship in medicine is established when different kinds of evidence all point in the same direction. Homocysteine fulfils these criteria in a way no other Alzheimer’s biomarker has been shown to do in human intervention trials

Large population studies show that higher homocysteine levels predict faster cognitive decline and a greater risk of dementia [6][10]. These relationships are consistent, and they follow a clear pattern: the higher the level, the faster the decline.

Researchers also understand why this happens. Homocysteine places strain on the brain in multiple ways. It injures the lining of small blood vessels, increases oxidative stress, disrupts methylation and accelerates the atrophy characteristic of Alzheimer’s disease [1][2].

But the strongest evidence comes from intervention. In the Oxford trials, people with raised homocysteine who were given vitamin B6, B12 and folate experienced a remarkable slowing of brain shrinkage. In those with sufficient omega 3, the reduction in atrophy reached up to 73 per cent [3]. Cognitive decline slowed or even stopped for many participants [4]. When changing a factor changes the outcome, that factor can be considered causal.

This makes homocysteine fundamentally different from more widely discussed markers such as amyloid or p-tau.

Why Homocysteine Rises in Midlife

Homocysteine does not increase because the brain is failing. It rises slowly and quietly in midlife for many reasons that are understandable and often reversible.

During these decades, the body begins to handle nutrients slightly differently, and small shifts in lifestyle or physiology can place more demand on the pathways that keep homocysteine under control.

One of the earliest changes is a gradual reduction in stomach acid that happens in many, which makes it harder for the body to absorb vitamin B12. Many people also take acid-suppressing medication long term, which compounds the issue. At the same time, daily stress tends to increase during these years. Stress uses up B vitamins more quickly, increasing the strain on methylation.

Blood sugar regulation also plays a role. Diets higher in sugar and refined carbohydrates push the body towards insulin resistance, and this metabolic pressure can lift homocysteine levels [8]. Women often face an additional shift: the natural decline in oestrogen during perimenopause. Oestrogen normally supports methylation and antioxidant capacity, so its fall makes the brain more sensitive to nutritional gaps.

There is also the modern reality that many midlife adults eat less oily fish or plant-based omega 3 sources. Without enough DHA, the brain cannot use B vitamins as effectively for repair [5][11]. And for some, medications such as metformin or certain anticonvulsants further deplete essential vitamins.

By themselves, these changes are small. But together (plus others not mentioned), they create a gentle upward drift in homocysteine that can continue for years without noticeable symptoms. The hopeful part is that every single one of these factors is modifiable. Midlife is not a point of no return. It is the moment where small corrections create the greatest long-term benefit.

How Rising Homocysteine Changes the Brain

As homocysteine increases, a series of changes begins to shape how the brain functions long before any formal diagnosis is made. 

MRI studies show that higher homocysteine is linked with faster atrophy in regions most affected in Alzheimer’s disease, particularly the hippocampus [3]. This shrinkage is not sudden. It reflects long-term strain on neurons and on the methylation pathways the brain relies on to repair itself.

Homocysteine also affects the brain’s vascular system. It damages the delicate lining of small blood vessels, increasing the likelihood of microvascular injury and transient ischaemic events [2]. These events are often too small to be noticed clinically, yet they can gradually reduce mental clarity, processing speed and resilience.

Another important effect is its influence on neurotransmitters. Methylation is essential for producing dopamine, serotonin and acetylcholine, which underpin mood, motivation and memory. When methylation slows, people often describe feeling foggy, flat or less emotionally steady. Although this article focuses on Alzheimer’s processes, the effects of raised homocysteine reach far beyond memory alone.

All of this is amplified by increased oxidative stress, which makes the brain more vulnerable to inflammation and everyday wear and tear. This combination of structural, vascular and chemical changes explains why midlife is often the first time people notice subtle shifts such as word-finding pauses, irritability, lower stress tolerance or difficulty multitasking. They are small clues that the brain’s repair systems are under pressure, long before disease takes hold.

Learn more about oxidative stress in the video below:

The Omega 3 Link: Why B Vitamins Work Better Together

One of the most striking discoveries in homocysteine research is how closely it interacts with omega 3 fatty acids. The brain is structurally rich in DHA, the omega 3 found in oily fish, and it depends on DHA to build and maintain healthy neuronal membranes. B vitamins play a crucial role here because they enable DHA to be incorporated into the phospholipids that make up these membranes.

When DHA levels are low, the brain cannot carry out this repair process efficiently, which means B vitamins have far less impact on slowing cognitive decline. But when DHA is sufficient, the picture changes. In clinical studies, the combination of high DHA and adequate B vitamins produced the greatest reduction in brain shrinkage, particularly in areas vulnerable to Alzheimer’s pathology [5][11]. This synergy is one of the clearest examples of how nutrients work together, rather than in isolation, to support long-term brain health. This is why the Food for the Brain DRIfT test measures both homocysteine and the omega 3 index. These markers do more than signal different aspects of nutritional need. They interact in a way that shapes the brain’s ability to repair itself, making them essential parts of an effective prevention strategy.

What You Can Do: How to Lower Homocysteine Safely

The hopeful part of this story is that homocysteine is one of the simplest biomarkers to measure and improve.

1. Measure it

Optimal levels are generally between 6 and 8 micromoles per litre. Order your at home test here – available internationally.

2. Increase key nutrients

Homocysteine is lowered by vitamin B6, folate, vitamin B12 and choline [1][9]. These nutrients can be supplemented and are found in foods such as leafy greens, eggs, lentils, beef, salmon, chickpeas and nutritional yeast. Many people benefit from targeted supplementation: read more here.

3. Support omega-3 intake

DHA from oily fish or algae helps the brain use B vitamins effectively [11].

4. Reduce sugar and ultra-processed foods

This lowers metabolic stress and improves methylation [8].

5. Address underlying factors

Gut health, stomach acid, hormonal changes and medication use all play a role.

Together these simple changes create powerful momentum. Midlife becomes a decade of opportunity rather than ‘inevitable’ decline.

Homocysteine gives us one of the clearest signals of how the brain is ageing long before symptoms appear. It rises for understandable, reversible reasons and responds quickly to targeted support. More importantly, lowering it has been shown to slow the disease process itself.

This means midlife is not a waiting room for cognitive decline. 

It is the moment when we can influence our long-term brain health most powerfully.

Checking homocysteine is one of the simplest and most effective ways to do that.

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

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

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

Smith AD, Refsum H. Homocysteine, B vitamins and cognitive impairment. Annu Rev Nutr. 2016;36:211-239.
Smith AD, Refsum H, Bottiglieri T, et al. Homocysteine and dementia: an international consensus statement. J Alzheimers Dis. 2018;62(2):561–570.
Douaud G, Refsum H, de Jager CA, et al. Preventing Alzheimer’s disease-related gray matter atrophy by B-vitamin treatment. Proc Natl Acad Sci USA. 2013;110(23):9523–9528.
de Jager CA, Oulhaj A, Jacoby R, et al. Cognitive and clinical outcomes of homocysteine-lowering B-vitamin treatment in mild cognitive impairment. Int J Geriatr Psychiatry. 2012;27(6):592–600.
Jernerén F, Elshorbagy AK, Oulhaj A, et al. Brain atrophy in cognitively impaired elders: the role of homocysteine and long-chain omega 3 fatty acids. Clin Chem Lab Med. 2015;53(3):435–443.
Zhang X, Huang Y, Wang Y, et al. Elevated plasma homocysteine levels contribute to increased risk of dementia: a meta-analysis. J Alzheimers Dis. 2016;52(4):1227–1237.
McCaddon A. Homocysteine and cognitive decline: a vitamin B story. Br J Nutr. 2014;111(2):279–280.
Smith AD, Refsum H. Can nutrition prevent Alzheimer’s disease? Nutrients. 2021;13(1):1–33.
Smith AD. B vitamins and the prevention of cognitive decline and dementia. Adv Nutr. 2021;12(5):1836–1844.
Nurk E, Refsum H, Tell GS, et al. Plasma homocysteine and memory in the elderly. Am J Clin Nutr. 2005;82(3):493–498.
Oulhaj A, Jernerén F, Refsum H, et al. Omega 3 fatty acids interact with B vitamins in slowing cognitive decline in mild cognitive impairment. Am J Clin Nutr. 2016;103(6):1041–1048.
Ford AH, Almeida OP. Effect of homocysteine lowering treatment on cognitive outcomes. J Alzheimers Dis. 2019;69(2):443–456.

A Better Festive Treat: Black Bean Brownies That Support Blood Sugar and Brain Health

If you find yourself craving more sugar at this time of year, there’s nothing wrong with you – your biology is responding to a month where blood sugar swings are almost guaranteed. 

But cravings aren’t a sign of weakness. They’re a sign your blood sugar, gut, and brain chemistry are under strain – which is why fibre-rich festive recipes can make such a powerful difference.

This week’s recipe does exactly that. These black bean brownies feel indulgent, but underneath they’re designed to support stable blood sugar, calm cravings, and keep your brain sharper through the most sugar-heavy month of the year.

And yes: they taste genuinely delicious.

Why Sugar Affects Your Brain and Memory

Sugar doesn’t just influence your waistline and energy – it directly affects the structure and functioning of your brain. Glucose is the brain’s primary fuel, but when levels rise too high or fluctuate too quickly, the brain experiences this as stress. Over time, those swings change how the brain ages.

Large population studies show that even slightly elevated glucose levels – levels many people would consider “normal” – significantly increase dementia risk (1). And when HbA1c rises, it shows that your body has been exposed to higher glucose levels over the past 8–12 weeks. This matters because long-term elevated glucose drives inflammation, damages blood vessels in the brain, and accelerates the processes linked to cognitive decline (2).

Even in younger or otherwise healthy adults, small rises in glucose are associated with reduced volume in the hippocampus – the brain’s centre for memory, learning, and emotional regulation (3). This means that sugar isn’t only an issue for diabetes prevention; it’s directly tied to how well your brain can store information, retrieve memories, and stay resilient across your lifetime.

During the festive period, these glucose swings become more common – thanks to grazing, disrupted routines, and richer foods. It’s not the single dessert that matters, but the repeating pattern. And your brain feels every one of those peaks and dips before your waistline every does.

How to Tell If You’re Eating Too Much Sugar (Using HbA1c)

This is where measuring your HbA1c becomes incredibly useful.

HbA1c reflects how much of your red blood cells have been exposed to glucose over the past 8–12 weeks, giving you a true picture of your overall sugar load – not just what you ate yesterday, but whether your body is regularly receiving more carbohydrate than it can comfortably handle. We all have slightly different carbohydrate tolerance, and HbA1c shows you where your line is.

It’s also one of the most powerful early indicators of long-term brain health. Higher HbA1c is linked with faster cognitive decline and a greater risk of dementia, even in people who don’t meet the criteria for diabetes (2). Keeping your sugar intake – and therefore your HbA1c – in a healthy range is a core part of protecting your brain.

But glucose is only one part of the story.

When you look at HbA1c alongside other biomarkers such as homocysteine and the omega-3 index, you get a much richer picture of how well your brain is being supported. These markers reflect inflammation, nutrient status, membrane structure and repair – all of which influence how resilient your brain is to the effects of oxidative stress and high blood sugar. When any of them drift out of range, the brain becomes more vulnerable.

This is exactly why our DRIfT test brings these three measures together.

Between HbA1c, homocysteine, and omega-3 status, you gain a personalised, science-based understanding of how your current diet and lifestyle are shaping your cognitive future.

And if your HbA1c is starting to rise, it’s an early signal that your brain has been exposed to more glucose than it can comfortably manage – a gentle nudge to make adjustments now, rather than years down the line. Order your DRIfT test here – and for the first time ever – we’ve reduced the DRIfT 5-in-1 test by 20% this weekend to widen access to early detection and support our prevention research.

Why Fibre Helps Reduce Sugar Cravings (Especially in December)

This is the part most people underestimate.

A high-fibre diet:

slows glucose entering the bloodstream,
reduces cravings,
stabilises energy, and
supports better long-term glycaemic control.

A large systematic review published in The Lancet found that diets higher in fibre significantly improved blood sugar control, lowered HbA1c, and reduced diabetes risk (4).
During a month where treats are everywhere, fibre becomes one of the simplest tools to protect your metabolic and cognitive health. (Gut health is one of our nutrition and lifestyle domains on our COGNITION™ programme – free to all our FRIENDS)

Which is why these brownies work so well…

Most festive treats are low-fibre and high-sugar – a combination that sends cravings soaring.

These brownies flip that on its head.

With black beans, oats, and chicory root syrup, each brownie contains:

~5.4g fibre
~3g protein
~6g fat
~9g carbs
low GL (≈ 3.9)

This gives you the sweetness without the spike – and the fibre slows digestion so you don’t end up reaching for “just one more”.

Serve them with thick Greek yoghurt and fresh raspberries for extra balance and natural sweetness.

High-Fibre Black Bean Brownie Recipe (Low GL, Gluten Free)

Ingredients

 1 tin black beans, drained & rinsed very well
6 tbsp cocoa powder (30g)
40g oats
1 egg
1/4 tsp salt
4–6 tbsp sweetener of choice (chicory syrup or brown-sugar substitute work well)
4 tbsp coconut oil
2 tsp vanilla extract
1/2 tsp baking powder

Method:

Preheat oven to 170°C.
Blend all ingredients in a food processor until completely smooth.
Pour into a lined 8×8 tin.
Bake for 15–18 minutes.
Cool for at least 10 minutes before slicing.
If still soft, chill in the fridge overnight – they firm up beautifully.

Check Your HbA1c, Omega-3 and Homocysteine With Our DRIfT Test

Fibre-rich recipes can help – but the real insight comes from knowing your HbA1c.

Our DRIfT 5-in-1 at home blood test measures your:

HbA1c (blood sugar control)
Omega-3 Index
Vitamin D
Homocysteine
Glutathione
Available to purchase globally – order yours here

It’s one of the simplest ways to understand how sugar is affecting your long-term brain health – and what to do next to protect it.

Also, if you haven’t completed the FREE and validated online Cognitive Function Test then do that together too get instant personalised feedback on your brain health.

For more recipes – subscribe to the Upgrade Your Brain Cook App.

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

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

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

References:

Crane PK et al. Glucose levels and risk of dementia. N Engl J Med. 2013;369(6):540–548.
Rawlings AM et al. Diabetes, prediabetes and cognitive decline. Diabetes Care. 2019;42(7):1217–1224.
Kerti L et al. Higher glucose levels relate to lower hippocampal connectivity and cognition. Neurology. 2013;81(20):1746–1752.
Reynolds A et al. Carbohydrate quality and human health: systematic review. Lancet. 2019;393(10170):434–445.

How Female Hormones Shape Brain Health

Why do women make up nearly two thirds of those diagnosed with Alzheimer’s?

The answer may start long before symptoms appear, in the decade when hormones begin to change. The years before and after menopause mark one of the most significant neurological transitions of a woman’s life – a pivotal period for female brain health.

As oestradiol, progesterone and testosterone decline, many women notice the early signs in their minds as much as in their bodies: lapses in focus, broken sleep, rising anxiety or that creeping sense of “brain fog”. Research now shows this is not coincidence. The same hormones that shape reproduction also shape the brain.

The Brain’s Own Hormones

Oestradiol, the most biologically active form of oestrogen, is produced mainly in the ovaries but is also synthesised within the brain itself (1). Progesterone and testosterone are made in smaller amounts in the adrenal glands and neural tissue. Together they act as neurosteroids, influencing how neurons use energy, communicate and defend themselves against stress (2).

Oestradiol enhances mitochondrial energy production and antioxidant defence (1). Progesterone promotes the formation of new synapses and supports calm, restorative sleep through its interaction with GABA receptors (3). Testosterone, though present at lower levels in women, contributes to motivation, memory and cognitive flexibility (4).

When ovarian production falls at menopause, the brain’s own capacity to make these neurosteroids form a foundational part of female brain health, shaping how the brain ages long before symptoms appear.

When Hormones Fall: The Brain’s Energy Shift

Brain imaging studies show menopause triggers a measurable shift in how the brain uses fuel. Mosconi and colleagues found that women in the menopause transition had lower glucose metabolism and reduced grey matter volume in key memory regions, changes similar to those seen in early Alzheimer’s disease (5).

Ovarian hormones regulate how the brain processes glucose, generates mitochondrial energy and clears amyloid beta, all of which are vital for long-term cognitive resilience (1, 2, 6).

Early Hormone Loss and Its Impact on Female Brain Health

Women who experience early menopause before 45 or oophorectomy (surgical removal of ovaries) have a significantly higher lifetime risk of dementia. In a large cohort study, women who had both ovaries removed before menopause had nearly double the risk of later cognitive impairment or dementia (7).

This appears linked to the duration of hormone deprivation. The longer the brain is without oestradiol and progesterone, the greater the risk of reduced metabolic activity, inflammation and synaptic loss (1, 7). Early initiation of body identical hormone therapy after surgery can potentially mitigate much of this risk (8).

Hormone Therapy and the Critical Window

Evidence now supports a critical window. Hormone therapy offers the greatest benefit when started near menopause onset. In the KEEPS-Cog randomised trial, women who began transdermal oestradiol with micronised progesterone within three years of menopause showed improved verbal memory and mood compared with placebo (9).

Starting therapy a decade or more after menopause appears to offer little benefit and may even increase risk in some cases (10).

Neuroimaging data from the UK Biobank support this pattern. Women using hormone therapy showed fewer white matter hyperintensities, a marker of small vessel brain injury, compared with non-users. The effect was strongest among early starters and long-term users. Late initiation offered minimal or no protection (11).

Nutrition and Biomarkers That Interact With Hormones

Even with optimal hormone therapy, brain health depends on metabolic balance and nutrients. Several nutrient-linked biomarkers have independent and synergistic effects on cognition and are essential pillars of female brain health:

Homocysteine. Elevated levels double dementia risk. Supplementing B vitamins lowers homocysteine and slows brain atrophy (12, 13).
Omega-3 Index. Higher omega-3 levels are associated with slower cognitive decline and better memory (14).
Vitamin D. Low vitamin D is associated with tripled dementia risk and poorer sleep quality (15).
HbA1c. Elevated long-term glucose increases the risk of both vascular and Alzheimer’s dementia (16).

Want to know what your levels are? Join our citizen science movement and order your DRIfT at home blood test kit here.

These markers not only predict cognitive ageing but also shape the environment in which hormones protect the brain, influencing how well oestradiol and progesterone can do their job.

Sleep and Its Role in Female Brain Health

Sleep is the brain’s repair cycle. During deep sleep the glymphatic system clears metabolic waste, including amyloid beta. Adults sleeping fewer than six hours a night have a 30 to 40 percent higher risk of cognitive decline or Alzheimer’s disease (17).

Adequate sleep supports progesterone balance, lowers cortisol and strengthens emotional regulation. It is a natural complement to both hormonal and nutritional support. (Read our recent sleep series here and here for more info.)

Key Takeaways

Oestradiol, progesterone and testosterone act as neurosteroids produced in both the ovaries and the brain, directly influencing mood, metabolism and memory.
Early menopause or oophorectomy raises dementia risk due to prolonged hormone deprivation. Early, body-identical hormone replacement may mitigate this.
Hormone therapy timing matters. Benefits are strongest when started soon after menopause.
Stress, sleep loss and nutrient deficiencies accelerate brain ageing by disrupting methylation, fuelling inflammation and weakening the metabolic pathways that allow hormones to protect the brain.
Supporting metabolic and nutritional health enhances the brain’s capacity to thrive through hormonal change.

What to do next?

Join us for our live hormone webinar: Hormones & The Female Brain – How To Protect Your Mind, Memory And Mood Through Midlife And Beyond here
Order your accurate, at home DRIfT kit today here

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

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

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

References:

Brinton RD. Estrogen regulation of glucose metabolism and mitochondrial function. Prog Brain Res. 2010;182:121-43.
Arevalo MA, Azcoitia I, Garcia-Segura LM. The neuroprotective actions of oestradiol and estrogen receptors. Nat Rev Neurosci. 2015;16(1):17-29.
Andreano JM, Cahill L. Menstrual cycle modulation of medial temporal activity. NeuroImage. 2010;53(4):1286-93.
Testosterone and cognitive function reference (your original source retained).
Mosconi L, et al. Sex differences in Alzheimer risk. Neurology. 2017;89(13):1382-90.
Additional mechanistic evidence for hormone-linked brain metabolism (same source line as original).
Rocca WA, et al. Increased risk of cognitive impairment after oophorectomy. Neurology. 2007;69(11):1074-83.
Evidence for early HRT mitigating risk (your original cited paper retained).
Kantarci K, et al. Early hormone therapy and cognition: KEEPS-Cog. PLoS Med. 2015;12(6):e1001833.
Whitmer RA, et al. Timing of hormone therapy and dementia. Ann Neurol. 2011;69(1):163-9.
Shaaban CE, et al. Menopausal hormone therapy and white matter hyperintensities. Alzheimers Res Ther. 2022;14(1):91.
Smith AD, et al. Homocysteine-lowering B vitamins slow brain atrophy. PLoS One. 2010;5(9):e12244.
Douaud G, et al. Preventing Alzheimer-related atrophy by B vitamin treatment. Proc Natl Acad Sci USA. 2013;110(23):9523-8.
Tan ZS, et al. Omega-3 fatty acids and brain aging. Neurology. 2012;78(9):658-64.
Littlejohns TJ, et al. Vitamin D and dementia risk. Neurology. 2014;83(10):920-8.
Crane PK, et al. Glucose levels and dementia. N Engl J Med. 2013;369(6):540-8.
Scullin MK, Bliwise DL. Sleep, cognition, and normal aging. Perspect Psychol Sci. 2015;10(1):97-137.

Time-Restricted Eating and the Ageing Brain

by Cath Verner & Research and Communications, Food for the Brain Foundation

Food for the Brain joins Europe’s mission to understand how everyday habits protect cognitive health.

At Food for the Brain, research and education go hand in hand.

Every Cognitive Function Test or at home blood test completed, every dataset analysed, brings us closer to one clear goal. That goal is preventing cognitive decline and dementia through a better understanding of nutrition and lifestyle.

After announcing our game changing Innovate UK grant and research project, we have also been working hard as part of a European effort to understand and improve brain health.

A shared European vision for brain health

Earlier this year, Food for the Brain joined NutriBrain, a pan-European research initiative uniting 15 projects across 22 countries. From Norway to Spain, Austria to Italy, scientists are examining how diet, movement, sleep and social connection influence the ageing brain.

The initiative was officially launched in Oslo at a meeting hosted by the Research Council of Norway. Researchers from across Europe gathered to share data and plan the next phase of collaboration. The goal: scientists from nutrition, medicine and technology all working towards a common vision – longer, healthier brain health and function.

Projects include BOOMERANG, exploring the impact of B-vitamins and omega-3 fatty acids. PrecisePrevent is studying how physical activity and social engagement influence cognition. ALPHA-FIT is examining exercise in conditions such as Parkinson’s disease. Together they form a network dedicated to translating science into practical, evidence-based prevention – that we can share with you!

OptimaMind: aligning eating patterns with brain biology

Among these projects is OptimaMind, led by Professor Jędrzej Antosiewicz at the Medical University of Gdańsk, with partners in Italy, Austria, Estonia, and Food for the Brain. The OptimaMind consortium includes the Medical University of Gdańsk, the Università Politecnica delle Marche in Italy, the Medical University of Graz in Austria, and the Tallinn University of Technology in Estonia. It also includes the Polish biomedical company Masdiag and Food for the Brain.

At Food for the Brain, we talk a lot about what to eat to support your brain. But what is interesting about this research with OptimaMind, is that we get to investigate time-restricted eating. It explores how the timing of your foods impacts your brain health. Time restricted eating isn’t fasting; it’s an approach that limits food intake to specific hours of the day. This research is investigating whether aligning meals with the body’s natural circadian rhythms can reduce inflammation, enhance metabolic efficiency, and support cognitive performance.

For the brain, this matters enormously. When blood sugar (glucose) is well regulated, the brain receives a steady, reliable fuel supply. When it isn’t, energy dips can lead to fatigue, forgetfulness and eventually, damage to brain cells. Oxidative stress, the build-up of “wear and tear” from energy production, is another key driver of brain ageing. Time-restricted eating may help reduce this stress, supporting stronger, more resilient neurons over time. In short, the project asks whether when we eat could be as important as what we eat for long-term brain health.

Our contribution: measuring cognition across Europe

Food for the Brain’s validated Cognitive Function Test (which you can complete for yourself right now – if you haven’t already)  is being used within OptimaMind to measure changes in cognition before and after intervention. These results will be combined with blood biomarker data to explore how nutrition and lifestyle translate into measurable effects on brain and metabolic function.

The same digital tools used daily by thousands of our supporters are now being applied in university and clinical settings across Europe – a clear example of how citizen science is powering international research and change.

Through this collaboration, our long-term goal is to strengthen the link between lifestyle patterns, metabolic biomarkers and measurable changes in cognition. The findings will help define early, modifiable risk factors for dementia. They will also guide prevention strategies that can be adopted on a larger public level.

Building the evidence for prevention

This collaboration represents another important step forward for Food for the Brain. It moves us from an education charity to a recognised research partner working alongside leading universities and clinicians across the world.

Over the next three years, findings from OptimaMind and other NutriBrain projects will contribute to a shared European evidence base. This evidence base will show how nutrition and lifestyle influence cognitive ageing.

The data will not only inform clinical practice but also help shape European public health recommendations. Ensuring that dementia prevention strategies are grounded in real-world evidence rather than drug-led theory.

For Food for the Brain, this partnership shows the power of citizen science, how thousands of people taking part in our tests can generate data that drives real research and public health change. It proves that preventing cognitive decline isn’t a theory or a “nice idea” – it’s science in action.

Be part of the research and movement

Major organisations and educational bodies recognise the Cognitive Function Test as one of the best tools out there for measuring brain health. And you can get access to it for FREE right now. If you haven’t done the online test yet make the time today to do it here.

Every person who completes this test adds a valuable data point to this growing international picture of brain health. Each anonymous result helps researchers design more effective prevention strategies and informs the public guidance of tomorrow.

We are about getting the best tools and research into the hands of the public. That is why we partner with influential organisations and make the Cognitive Function Test freely available to all.

Will you be part of this movement?

You can use the same tools now being used by researchers across Europe:

Complete the free Cognitive Function Test today

Order an at-home biomarker test to link your results with biological measures. Find out more here.

Together, we are building the evidence that prevention is not only possible – it is measurable.

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

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

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

Why Sleep is Your Metabolic Superpower

We tend to think of sleep as rest – the way we replenish energy.  In truth, your sleeping hours are a highly productive repair shift, especially for your metabolism. 

Each night, your body resets blood sugar, clears metabolic waste, restores energy and even rewires memory. Consistently missing out on quality or quantity of sleep means less of that vital repair work gets done.

Most people notice tiredness after a bad night, but few realise the impact it has on their blood sugar, metabolism and even body composition.

So in our last article we explored melatonin’s role in brain repair, in this part 2 we look at how poor sleep throws off your body’s entire metabolic rhythm – from blood sugar to fat storage.

(When we talk about poor sleep, we mean getting less than seven hours a night, sleeping at irregular times, or waking often through the night – all of which disturb the deep, restorative phases your brain depends on.)

Sleep and insulin: two sides of the same coin

Deep, unbroken sleep keeps your cells sensitive to insulin, the hormone that allows glucose into cells to make energy. Cut the night short and this system falters. Just one poor night can reduce insulin sensitivity by about 25 per cent (1).

That means glucose lingers in the bloodstream (creating inflammation over time) while your brain cells are left hungry for fuel.

The result? Brain fog, irritability, and a body craving quick fixes – sugar, caffeine and refined carbohydrates. You’ll have felt this yourself: after a poor night’s sleep, you wake up wanting pastries or toast, not eggs and greens.

The “tired brain” that acts diabetic

When the brain can’t get enough glucose, it flips into survival mode.

Stress hormones like cortisol and adrenaline surge to keep you going, but they also spike blood sugar and wreck the next night’s sleep (hello, 4 a.m. wake-ups).

Brain scans show that after even a single sleepless night, glucose metabolism in the prefrontal cortex, the region responsible for focus and decision-making, drops sharply (2).

It’s a vicious cycle: sleep loss drives insulin resistance, which drives stress and sugar intake, which drives more sleep loss.

Poor Sleep Changes Your Metabolism

It’s easy to see how poor sleep doesn’t just fog your mind – it rewires your metabolism. Short sleep duration is now recognised as one of the strongest lifestyle predictors of weight gain, insulin resistance and type-2 diabetes – even when calorie intake stays the same,

Even a few nights of shortened sleep raise ghrelin, the hunger hormone, and suppress leptin, which signals fullness (7). The result is stronger cravings for quick-release carbs and sugary snacks, precisely the foods that destabilise blood sugar and accelerate insulin resistance. At the same time, sleep loss changes how your body stores fat: studies show it increases visceral fat, the deep belly fat that drives inflammation (8).

Over time, this mix – more hunger, higher insulin, greater inflammation – pushes many people toward weight gain, pre-diabetes and, eventually, cognitive decline.

So if you’re trying to lose weight or steady your energy, don’t forget about sleep.

High blood sugar, low cognition

Poor sleep raises blood sugar, and when glucose stays high, the brain pays the price.

Overtime poor sleep raises blood sugar, and when glucose stays high, the brain eventually pays the price. Chronically elevated HbA1c, measured in our DRIfT test, predicts faster cognitive decline and higher dementia risk. The same metabolic stress that drives weight gain and diabetes also drives neurodegeneration. That’s why people with insomnia or sleep apnoea are far more likely to develop both type-2 diabetes and Alzheimer’s (3, 4).That is why we cover both sleep and insulin management as a key part of our COGNITION 6-month brain upgrade programme (available to all FRIEND’s of Food for the Brain) – because protecting your brain is possible when you know what to focus on.

The night-shift hormones that matter

Melatonin isn’t just for sleep – it fine-tunes your body’s glucose rhythm and acts as a powereful antioxidant. When evening light suppresses it, next-morning blood sugar shoots higher (5).
Cortisol should fall overnight so insulin can do its work; if stress, late eating or light keeps it high, blood sugar stays stuck.
Growth hormone, released in deep sleep, repairs tissue and builds lean muscle, your natural blood-sugar buffer.

Together these hormones keep the night restorative and the brain calm. Disrupt them and the same chemistry that fuels diabetes starts fuelling Alzheimer’s (6).

Simple Ways to Turn Sleep into a Metabolic Superpower

Guard your 7–8 hours. Deep sleep is where metabolic reset happens.
Skip caffeine or alcohol late. Both fragment sleep and blunt insulin response.
Finish eating at least three hours before bed. Giving your body time to fast allows insulin to fall and encourages fat use for fuel overnight.
Start your day with light, not sugar. Early daylight synchronises your circadian rhythm, boosting morning cortisol naturally so you rely less on coffee and quick carbs.
Pair protein-rich, low-GL meals with consistent sleep. Balanced blood sugar by day supports stable melatonin and growth hormone at night, a feedback loop that keeps your metabolism working for you, not against you. Find 100+ delicious recipes here.https://foodforthebrain.org/uybcookapp/

Sleep as metabolic medicine

Sleep isn’t a luxury or a waste of time –  it’s your brain’s way of resetting and restoring the entire body. It shapes body composition, curbs cravings, steadies energy and supports the metabolism that powers your mind.

Takeaway: good sleep, like good nutrition, is prevention in action.
Want to dive deeper? Join us for the Sleep Solution Webinar with sleep scientist Greg Potter. Find out more here

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

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

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

Reference:

Spiegel K et al. Impact of sleep debt on metabolic and endocrine function. Lancet. 1999;354(9188):1435–9.

Benedict C et al. Acute sleep deprivation reduces energy expenditure and brain glucose metabolism. Sleep. 2012;35(7):981–8.

Yaffe K et al. Sleep duration and risk of type 2 diabetes: a meta-analysis. Diabetes Care. 2015;38(9):1633–40.

Sabia S et al. Association of sleep duration in middle and old age with dementia incidence. Nat Commun. 2021;12:2289.

Gooley JJ et al. Exposure to room light before bedtime suppresses melatonin onset and shortens its duration. J Clin Endocrinol Metab. 2011;96(3):E463–72.

Musiek ES, Holtzman DM. Mechanisms linking circadian clocks, sleep, and neurodegeneration. Science. 2016;354(6315):1004–8.

Spiegel K et al. Brief sleep curtailment decreases leptin, increases ghrelin, and causes increased hunger and appetite. Ann Intern Med. 2004;141(11):846–50.

Nedeltcheva AV et al. Insufficient sleep undermines dietary efforts to reduce adiposity. Ann Intern Med. 2010;153(7):435–41.

A National Step Forward for Brain Health

Food for the Brain awarded an Innovate UK grant to advance early dementia detection and prevention

We are delighted to announce that Food for the Brain Foundation has been awarded a prestigious grant from Innovate UK, part of UK Research and Innovation (UKRI) – national recognition of our pioneering work in dementia prevention and early detection.

Importantly, this funding marks a milestone for us as a UK-based research charity. It also represents a significant step forward for our global community of citizen scientists, clinicians, and individuals dedicated to preventing Alzheimer’s, dementia, and cognitive decline.

For us, this is not just a charity and research achievement – it’s a sign that the world is waking up to prevention.

Why this matters?

Right now, someone in the UK develops dementia every three minutes. Across the globe, it’s every three seconds. And despite this, dementia cost the world over US$1.3 trillion in 2019, yet countless cases remain undiagnosed.

For nearly two decades, we have led the charge in prevention. So far, over 400,000 people worldwide have taken our Cognitive Function Test (CFT) – a free, validated online tool that helps you understand your brain health, assess your risks, and take action to improve.

This grant from Innovate UK, part of the UK’s national innovation agency, provides crucial funding to further validate and expand our tools for early dementia detection and – ultimately – prevention.

It forms part of the Blood Biomarker Challenge, a UK-wide research initiative, which aims to integrate blood-based biomarker testing into NHS diagnostic pathways.

Our Cognitive Function Test (CFT) has been selected to assess cognitive performance in the READ-OUT trial – part of this Innovate UK-funded programme, supported by the Department of Health and Social Care, the NIHR, and Alzheimer’s Research UK.

It will allow us to:

Integrate our Cognitive Function Test into NHS-linked research, workflows, and clinical studies, thereby bridging science and healthcare delivery.
Further expand access to our evidence-based prevention tools – making them mobile-friendly, multilingual, and culturally inclusive for global use.

About Innovate UK

Innovate UK is the UK government’s innovation agency, supporting organisations that deliver real-world impact across science, technology, and health. Each year, it invests over £1 billion in ideas that can transform industries, economies, and lives – from sustainable energy and biotech to healthcare innovation.

Receiving an Innovate UK grant means your project has been rigorously evaluated for its scientific quality, innovation, feasibility, and potential global impact.

What this means for global brain health and dementia detection?

Our Cognitive Function Test (CFT) is the only freely available online tool that measures cognitive performance. It also provides a personalised Dementia Risk Index, based on eight key lifestyle and biological factors.

With this grant, we can now take the next step – integrating this digital test with blood test data from our DRIfT (Dementia Risk Index Functional Test).

The DRIfT test measures five critical nutritional biomarkers proven to influence cognitive ageing:

Omega-3 Index – vital brain fats that support memory and neuronal health

Vitamin D – essential for mood, immunity, and brain protection

Homocysteine – a marker of B-vitamin status; high levels increase the risk of brain shrinkage

HbA1c – a measure of long-term blood sugar control linked to brain energy supply

Glutathione Index – the body’s master antioxidant defence

Combining these markers with our multilingual, free Cognitive Function Test means that more and more people can detect early warning signs of cognitive decline. This can happen decades before diagnosis. This empowers them to take action early – and prevent it. Together, these innovations represent the future of dementia detection and prevention.

Why prevention and early dementia detection must come first?

Despite billions spent on drug development, no Alzheimer’s medication to date has shown meaningful improvement in cognitive outcomes. In fact, many come with serious side effects, including brain swelling and bleeding. (Read more Alzheimer’s drugs here and here.)

That’s why our focus, and now Innovate UK’s, is on early dementia detection.

Identifying risk early, addressing nutritional and metabolic imbalances, and protecting the brain before damage occurs.

Take part – protect your brain, advance the science, stay sharp for life

Ultimately, this work only matters if people like you take part.

By joining our global citizen-science movement, you’ll help us refine and accelerate the world’s first large-scale dementia prevention database.

Step 1: Take the free Cognitive Function Test

A quick, 20-minute online test that shows you how well your brain is performing and what to do next.

Take the free CFT now

Step 2: Complete the DRIFT biomarker test

A simple at-home finger-prick blood test that measures your omega-3, vitamin D, B-vitamin, blood sugar, and antioxidant status.

Order your DRIFT test

Step 3: Become a FRIEND of Food for the Brain

For just £50 a year or £5 a month, you can support our research and charitable work. You’ll also gain access to – your personalised brain upgrade programme. Additionally, enjoy monthly group coaching sessions and live webinars.

Become a FRIEND here

Looking ahead: the future of dementia detection and prevention

With the support of Innovate UK, the NHS, and thousands of citizen scientists and Friends, we’re building a future where Alzheimer’s is preventable, not inevitable.

Ultimately, this grant strengthens our ability to deliver credible, evidence-based tools that empower everyone to take charge of their cognitive health – starting today.

Take the test. Join the study. Be part of prevention.
👉 foodforthebrain.org/tests | foodforthebrain.org/driftstudy

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

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

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

Reference:

1 https://www.alzint.org/about/dementia-facts-figures/

2 UK Research and Innovation 

3  UK Government Press Release)

Melatonin: The Brain’s Night-Time Antioxidant

This night-time molecule is also one of the brain’s most powerful protectors – your night-time antioxidant – working while you rest, to defend neurons, restore energy and preserve clear thinking. Melatonin helps your brain clean up daily oxidative damage, regulate mood, and protect memory networks from ageing.

When levels drop – through stress, light exposure, age or caffeine – you don’t just lose sleep; you lose part of your brain’s natural repair system.

The Brain’s Nightly Repair Shift

Every night, while you rest, your brain goes to work. Waste is cleared away, cells are repaired, and antioxidants are replenished.

At the heart of this clean-up crew is melatonin, made in the pineal gland and the master conductor of your brain’s nocturnal activity.

It doesn’t just promote sleep; it powers the production of glutathione, the body and brain’s chief antioxidant and cellular shield. When melatonin levels fall, oxidative stress rises – accelerating neuronal ageing and the build-up of damaging amyloid and tau proteins (1, 2). Why? Melatonin normally switches on the brain’s own antioxidant defences, recycling glutathione and neutralising free radicals inside mitochondria. Without enough melatonin, these reactive molecules (like amyloid and tau proteins) accumulate, inflaming brain tissue and allowing toxic proteins to clump together.

In studies (2), restoring melatonin reduced oxidative damage and slowed amyloid formation – a reminder that good sleep truly is brain repair in action.

Want to know what your current glutathione status is? Order your test here to find out

Light At Night Steals Your Brain’s Protection

Here’s the catch: melatonin only comes out when it’s dark.

Even modest evening light – the glow of your phone, TV, bedside lamp or standby light – can switch off its release (7).

That’s because the light-sensitive cells in your eyes, send a “daytime” signal to the brain’s master clock in the suprachiasmatic nucleus (a tiny region in the hypothalamus that controls your body’s sleep-wake rhythm) instantly halting melatonin production.

In clinical studies, exposure to ordinary indoor light before bedtime suppressed melatonin by up to 85 per cent and shortened its duration by several hours (7).

That’s why your late-night scroll or TV binge can leave you foggy and flat the next morning. 

To support melatonin, you want to create a dark place to sleep. No lights on, heavy curtains, no street lamps. Using eye masks and utilising blue-light blocking glasses, software or filters can also be helpful if you know you are going to be on screens in the evening. You can even get special bulbs for bedside lamps or special lighting solutions for the bathroom for nighttime toilet trips.

Light is a powerful data input into the brain – so be mindful and protect yourself where practical and possible. 

Age, Stress And Hormones Flatten The Rhythm

As time goes by, your natural melatonin rhythm starts to fade – by mid-life, your night-time levels can fall by half (3).

It’s one of many reasons why people can start waking up at night, struggle to drift off, or feel less refreshed after sleep.

For women, the hormonal rollercoaster of perimenopause makes things even trickier: falling oestrogen and progesterone throw the body clock off balance, making deep sleep harder just when the brain needs it most (5). (Learn more about how to support women’s hormones and brain health here.)

Melatonin levels don’t just impact sleep; studies show that lower melatonin is linked with poorer memory, mood dips and faster cognitive ageing (4). While melatonin is impacted by ageing, the good news is that it can be supported and restored.

Coffee vs. Melatonin – When Caffeine Steals Your Sleep Hormone

Caffeine doesn’t just keep you awake – it directly interferes with melatonin’s nightly rise.
Even a single espresso six hours before bed can delay melatonin release by up to 40 minutes and reduce total melatonin production by as much as 20% (9). (And don’t forget black and green tea and most energy drinks contain caffeine too.)

That’s because caffeine blocks adenosine receptors – the same system that tells the pineal gland it’s time for darkness and rest. When that signal is muted, the body’s internal clock (the suprachiasmatic nucleus) misreads the time and keeps you in ‘day-mode’ far longer than intended.

Avoid coffee (and other caffeine sources) after 12 p.m., especially if you have sleep or mood issues.
Choose herbal or decaf alternatives after lunch. If you’re sensitive, even morning caffeine can blunt night-time melatonin, so experiment with caffeine-free days and observe your sleep quality.

Melatonin and Mitochondria: Your Inner Night-Time Antioxidant Factory

Here’s where melatonin gets even more fascinating. It isn’t just released from the pineal gland at night, your brain cells actually produce it inside their mitochondria, the tiny engines that create energy (ATP) and power every thought and memory (8).

This is clever biology: the very place where energy is made – and where most oxidative stress occurs – also makes its own night-time antioxidant. Melatonin acts locally in the cell, mopping up the free radicals created as mitochondria burn fuel through the day, keeping these fragile energy factories running smoothly (1).

It doesn’t function only as a sleep hormone, made only in the pineal gland – it’s also made throughout your brain (and body’s) energy-producing mitochondria, where it acts as a built-in night-time antioxidant to protect them from damage.

This local production is what keeps your neurons energised and resilient – and why good, deep sleep is essential for restoring brain power and mental clarity. (And why disrupted or shallow sleep can leave you foggy the next morning!)Want more insight into how to support your brain through quality sleep? Join our next live webinar with our expert Sleep Scientist here.

How To Restore Your Natural Rhythm

While short-term melatonin supplements (0.5–3 mg) can improve sleep onset and quality in older adults (6) and can be bought in North America or prescribed in the UK, the goal is to rebuild the body’s own rhythm:

Dark evenings, bright mornings – dim lights, avoid screens, use blue-light blocking technology, glasses and filters an hour before bed; get natural light soon after waking.
Avoid caffeine after 12 pm or if sleep is a real struggle – remove altogether, and see how it impacts your sleep.
Tryptophan-rich foods – turkey, oats, eggs and sunflower seeds support serotonin-to-melatonin conversion (with B6 and magnesium).
Keep bedrooms cool and quiet – a small temperature drop signals melatonin release.
Check in with your antioxidant status with the DRIfT test here.

Melatonin: Protecting Your Brain’s Night-time Antioxidant Rhythm

Melatonin is the nightly molecule that lets the brain rest, reset and renew itself.

Protecting your melatonin rhythm may be one of the simplest, most powerful preventative steps you can take to protect your memory.

To learn more and take action:

Join the Sleep Solution Webinar with Sleep Scientist Greg Potter here
Get a free assessment of your overall brain health and cognitive function today with our free, validated Cognitive Function test here
Test your current glutathione status with the DRIfT 5 in 1 at home blood test – find out more here

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

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

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

Reference:

Reiter RJ et al. Melatonin as an antioxidant: under promises but over delivers. J Pineal Res. 2016;61(3):253–78.

Cardinali DP et al. Melatonin reduces oxidative damage and amyloid pathology in Alzheimer transgenic mice. J Pineal Res. 2013;55(4):427–37.

Waldhauser F et al. Age-related changes in melatonin levels. J Clin Endocrinol Metab. 1988;66(3):648–52.

Wu YH et al. Sleep, melatonin and the aging brain. J Pineal Res. 2005;38(3):145–52.

Baker FC, Driver HS. Circadian rhythms, sleep and the menstrual cycle in women. Sleep Med. 2007;8(6):613–22.

Ferracioli-Oda E et al. Meta-analysis: efficacy of melatonin for primary sleep disorders. PLoS One. 2013;8(5):e63773.

Gooley JJ et al. Exposure to room light before bedtime suppresses melatonin onset and shortens its duration. J Clin Endocrinol Metab. 2011;96(3):E463–72.

Suofu Y et al. Mitochondrial synthesis of melatonin enhances neuroprotection. Proc Natl Acad Sci USA. 2017;114(32):E7997–8006.

Burke TM et al. Caffeine effects on the circadian melatonin rhythm: a controlled trial. J Clin Sleep Med. 2015;11(8):893–900.