February 2026 - Food for the Brain

because prevention is better than cure.

because prevention is better than cure.

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Why “Normal” Vitamin D Levels May Not Be Protective for Women’s Brains

Why “Normal” Vitamin D Levels May Not Be Protective for Women’s Brains

Why “Normal” Vitamin D Levels May Not Be Protective for Women’s Brains

Science now recognises Vitamin D as far more than a bone-health nutrient. Over the past decade, it has become increasingly clear that vitamin D acts as a hormone regulator, playing an important role in brain health, immune regulation and inflammation, especially when considering optimal vitamin D levels for women’s brains.

What is discussed far less, is a more nuanced question…

If vitamin D matters for the brain, how much is actually enough and do vitamin D levels differ for women?

A growing body of research links lower vitamin D status with a higher risk of cognitive decline and Alzheimer’s disease. Yet most guidance still relies on population-based “normal” ranges that were never designed to protect the brain. This raises an important prevention question for women, who already carry a higher lifetime risk of Alzheimer’s disease.

What the research shows

A systematic review and meta-analysis in 2025 by Li et al. examined the relationship between circulating vitamin D levels and Alzheimer’s disease risk across multiple observational studies (1).

The findings were consistent:

• Lower vitamin D levels link to a higher risk of Alzheimer’s disease.
• Risk increased progressively as vitamin D levels declined
• Researchers observed this association across different populations and study designs.

Crucially, the authors did not claim that vitamin D deficiency causes Alzheimer’s disease. Instead, vitamin D status appears to track biological vulnerability in the brain and reflects processes such as neuroinflammation, immune dysregulation and vascular dysfunction, all recognised contributors to cognitive decline.

This distinction matters for prevention.

Why these findings matter particularly for women

Women account for around two thirds of Alzheimer’s diagnoses worldwide. Longevity alone cannot explain this difference.

Across midlife and later life, women experience biological changes that alter how the brain responds to metabolic, inflammatory and hormonal stress. The menopausal transition is a key inflection point. Declining oestrogen and progesterone influence immune signalling, cerebral blood flow and brain energy metabolism, all of which intersect with established dementia risk pathways (3). This helps explain why midlife can be a turning point for brain health in women, even when blood test results appear “normal”.

Vitamin D functions as a hormone-like regulator, with receptors widely distributed throughout the brain and immune system. Its actions include modulation of inflammatory responses, immune balance and neuronal protection. Hormonal changes appear to influence how effectively vitamin D signalling is utilised at a tissue level. This is supported by experimental and clinical research showing interactions between oestrogen, vitamin D receptors and immune signalling, although this is not always directly measured in large population studies. In practical terms, this means that a vitamin D level considered “normal” for the general population may not confer the same degree of neuroprotection in the ageing female brain.

This does not mean vitamin D requirements are definitively higher for every single woman, or that everyone should take high-dose supplementation. Excessive intakes via supplementation over time can be harmful, which is why context, testing and appropriate dosing matter. 

Prevention works best when it’s personal, based on what’s happening in your own brain and body, not just what’s considered “normal.”

The problem with “normal” ranges for vitamin D for women’s brains

Researchers established vitamin D reference ranges primarily to prevent overt deficiency-related disease, particularly rickets and osteomalacia. They did not design these ranges to define optimal levels for long-term brain resilience.

Population reference ranges do not account for factors that strongly influence dementia risk, including:

  • Chronic low-grade inflammation
  • Insulin resistance and blood sugar dysregulation
  • Oxidative stress (see our explainer video here)
  • Hormonal transitions across midlife
  • Genetic variation in vitamin D metabolism and receptor activity

As a result, vitamin D levels that fall within the laboratory “normal” range may still exist within a biological environment that favours cumulative brain damage over time. This limitation is not unique to vitamin D. It reflects a broader problem with single-nutrient or single-cause thinking in Alzheimer’s prevention.

Vitamin D does not act alone in protecting women’s brains

Vitamin D is not an isolated lever in brain health. Low vitamin D status frequently clusters with other modifiable biological risk factors, including:

• Low omega-3 fatty acid status
• Raised homocysteine, reflecting impaired B vitamin-dependent methylation, a process essential for maintaining brain cells
• Poor blood sugar control
• Reduced antioxidant capacity, including glutathione availability

Each of these factors independently links to cognitive decline. More importantly, they interact within the brain.

Alzheimer’s disease does not arise from a single deficiency, a single gene or one pathological protein.
It reflects the cumulative impact of multiple biological systems drifting out of balance over years or decades. This is why interventions that target a single marker so often produce disappointing results.

Prevention requires a broader, systems-based view.

Once you see vitamin D in this broader context, it becomes clear why testing a single marker in isolation can only ever give partial answers.

From nutrients to prevention systems

Testing vitamin D alone can identify a deficiency, but it cannot tell you whether the brain’s key protective systems are functioning together.

A prevention-led approach asks different questions:

  • How well is inflammation being regulated?
  • Are brain cell membranes supported by sufficient essential fats?
  • Is methylation, the nutrient-dependent process that supports DNA repair, neurotransmitter balance and brain structure, functioning effectively?
  • To what extent is blood sugar quietly damaging brain neurons over time?

These are not abstract concepts.

They are measurable, modifiable drivers of dementia risk that we assess through our at-home DRIfT blood test.

A smarter way to assess brain health

Many people reading this will have been told their vitamin D is “fine”. They may spend time outdoors, eat well, and still feel tired, foggy or not quite themselves. The problem is not that vitamin D doesn’t matter. It’s that a single number rarely tells the full story.

This systems-based understanding underpins our work at Food for the Brain. It is the heart of prevention.

Prevention is not about chasing one “perfect” nutrient level or one lifestyle change. 

It is about understanding how your body works as one connected system and acting early enough to change the trajectory.

If you want to begin supporting and upgrading your brain today:

Complete the Cognitive Function Test today if you haven’t done so yet.
It is free to everyone, validated and provides personalised insights into your current brain health.

Order your at-home DRIfT blood test to assess the key biological drivers of cognitive decline, including vitamin D, omega-3, homocysteine, blood sugar control and antioxidant status. Together, these results give you the information you need to move from awareness to meaningful prevention.

References:

Further info

Why Gut Health Matters for Brain Health More Than You Think

Why Gut Health Matters for Brain Health More Than You Think

Gut Health Matters for Brain Health More Than You Think

Why Some Brains Improve and Others Don’t

Many people are doing more than ever to protect their brain. They eat well. Take supplements. Exercise. Stay mentally active.

Yet outcomes vary dramatically.

Some improve. Others stall. A few decline despite doing everything “right”.

The missing question is not what else to add, but what environment those interventions are landing in.

Cognitive decline rarely stems from one isolated failure. It emerges when the body’s internal environment no longer supports protection, repair, and resilience. This systems-based understanding underpins the work of Food for the Brain, and explains why gut health plays a central role in our COGNITION brain upgrade programme.

The terrain model of brain health

In medicine, there is a long-established principle that disease does not arise from a trigger alone, but from the biological environment in which that trigger operates. This is often described as the terrain.

From a brain health perspective, terrain includes inflammatory load, metabolic health, immune balance, nutrient availability, and cellular repair capacity. These systems interact constantly. When they stay in balance, the brain shows remarkable resilience. When they become disrupted, vulnerability increases.

Neurodegenerative conditions, including Alzheimer’s disease, are now understood to arise from multiple interacting biological pressures rather than a single pathological process. Many of these systems are shaped upstream by gut related processes.

The gut as a regulator, not a root cause

The gut is often discussed as if it were a standalone digestive organ. In reality, it plays a regulatory role in shaping systemic inflammation, metabolic function, and immune signalling.

When gut barrier integrity is compromised, bacterial components such as lipopolysaccharides can enter circulation. This process increases immune activation and drives chronic low-grade inflammation, a state strongly associated with insulin resistance and cognitive decline [1,2].

In this context, gut dysfunction is not “causing” brain disease. It is influencing the conditions in which brain protection and repair either succeed or struggle.

Why prevention struggles in an inflamed system

Brain health interventions that we talk about here at Food for the Brain do not operate in isolation. Their effectiveness depends on the biological environment in which they are applied.

This is particularly clear in nutritional research.

B vitamin supplementation has been shown to slow brain atrophy, but only in individuals with raised homocysteine levels and a metabolic environment that allows normal methylation processes to function [3]. Similarly, omega 3 fatty acids support neuronal membrane structure and signalling, yet their cognitive benefits are reduced in the presence of inflammation and insulin resistance [4].

Inflammation interferes with digestion, absorption, transport, and cellular uptake of nutrients. Pro inflammatory cytokines also impair intracellular metabolic pathways, shifting the body toward defence rather than repair. In this terrain, even well evidenced interventions may have limited effect.

The same principle applies to lifestyle strategies. Physical activity, cognitive stimulation, and stress reduction are all protective, but their impact is blunted when inflammatory and metabolic pressures remain unaddressed. That is why in COGNITION we target all 8 modifiable nutrition and lifestyle factors, so that you are not just targeting a specific nutrient but you are changing the environment.

cognition 8 domain cogs before and after

Microbes, inflammation, and brain vulnerability

Human studies consistently show that individuals with cognitive impairment or Alzheimer’s disease have altered gut microbiome profiles alongside higher levels of systemic inflammatory markers [5].

This does not demonstrate that microbes cause dementia. What it does show is that microbial imbalance contributes to inflammatory load, which in turn increases brain vulnerability.

Over time, this vulnerability can translate into accelerated cognitive decline.

For this reason, the COGNITION brain upgrade programme actively addresses gut health as one of eight modifiable factors that influence dementia risk. Gut microbes actively shape the internal environment in ways that can either accelerate neurodegeneration or help slow it.

The metabolic bridge between gut and brain

The gut also plays a critical role in metabolic regulation.

Chronic gut driven inflammation worsens insulin resistance, reducing glucose uptake by brain cells. Impaired brain glucose metabolism is a recognised feature of cognitive decline and has led some researchers to describe Alzheimer’s disease as a form of brain specific metabolic failure [6,7].

In this model, the gut is not peripheral. It contributes upstream to the metabolic conditions that determine whether the brain can access adequate fuel to function and repair.

Again, the implication is not that gut health alone determines brain fate. It is that brain health strategies are less effective when the metabolic and inflammatory terrain is unfavourable.

Why Brain Health Advice Works for Some People and Not Others

A terrain based perspective offers something often missing from prevention conversations.

Understanding.

When people follow advice carefully and still do not improve, clinicians too often frame the explanation as lack of compliance or genetics. Systems thinking offers a different interpretation.

The tools may be appropriate but the environment may not yet support repair.

This reframes prevention as a personalised process rather than a universal checklist. Understanding an individual’s internal terrain helps identify where effort should go.

This is why Food for the Brain offers two complementary forms of assessment: the free, validated Cognitive Function Test and optional at home blood testing to assess key modifiable risk markers such as homocysteine, omega 3 status and glutathione.

The answer is not found in one nutrient

Viewing brain health through a terrain lens shifts prevention away from adding isolated solutions and toward restoring balance across systems.

The future of brain health does not lie in targeting one nutrient, one habit, or one molecule.

It lies in creating an internal environment where protection, repair, and resilience are possible.

Brains do not fail because one thing goes wrong. They decline when the terrain no longer supports them.

And that terrain forms quietly and cumulatively long before symptoms appear.

Next Steps

References:

  1. Cani PD, Amar J, Iglesias MA, Poggi M, Knauf C, Bastelica D, et al. Metabolic endotoxemia initiates obesity and insulin resistance. Diabetes. 2007;56(7):1761–72.
  2. Hotamisligil GS. Inflammation and metabolic disorders. Nature. 2006;444(7121):860–7.
  3. Smith AD, Smith SM, de Jager CA, Whitbread P, Johnston C, Agacinski G, et al. Homocysteine-lowering by B vitamins slows the rate of accelerated brain atrophy in mild cognitive impairment. Proc Natl Acad Sci U S A. 2010;107(31):14187–92.
  4. Jernerén F, Elshorbagy AK, Oulhaj A, Smith SM, Refsum H, Smith AD. Brain atrophy in cognitively impaired elderly: the importance of long-chain omega-3 fatty acids and B vitamin status in a randomized controlled trial. Am J Clin Nutr. 2015;102(1):215–21.
  5. Vogt NM, Kerby RL, Dill-McFarland KA, Harding SJ, Merluzzi AP, Johnson SC, et al. Gut microbiome alterations in Alzheimer’s disease. Sci Rep. 2017;7(1):13537.
  6. de la Monte SM, Wands JR. Alzheimer’s disease is type 3 diabetes–evidence reviewed. J Diabetes Sci Technol. 2008;2(6):1101–13.

Further info