Anxiety: could your biology be a factor? Biomarkers worth investigating

Thyroid dysfunction

The link between thyroid function and anxiety is well established in research. An overactive thyroid (hyperthyroidism) produces symptoms that closely resemble an anxiety disorder: racing heart, tremor, sweating, difficulty sleeping, restlessness, and a sense of being unable to switch off. These symptoms are driven directly by excess thyroid hormone accelerating metabolic processes throughout the body. Even subclinical hyperthyroidism, where thyroid hormone levels are mildly elevated without a formal diagnosis, can produce significant anxiety-like symptoms. The UK Biobank prospective study, following nearly 350,000 participants, found significant associations between anxiety and subsequent thyroid disease risk, reflecting the bidirectional relationship between the two systems.

Equally, hypothyroidism does not always present as classically low-energy. In some people, particularly in early stages, the body's attempt to compensate for falling thyroid hormone can produce anxiety, palpitations, and emotional dysregulation before the more expected symptoms of fatigue and weight gain become dominant. Testing the full thyroid panel, including TSH, Free T4, Free T3, and thyroid antibodies, provides a more complete picture than TSH alone.

Magnesium deficiency

Magnesium is one of the most well-researched biological contributors to anxiety. It acts as a natural regulator of the nervous system, moderating the activity of NMDA receptors, which, when overactivated, contribute to a heightened stress response. Research consistently shows that magnesium deficiency is specifically and strongly associated with anxiety, more so than with depression or other mood presentations. Magnesium depletion is accelerated by chronic stress itself, creating a self-reinforcing cycle: stress depletes magnesium, low magnesium lowers the threshold for the stress response. Modern dietary patterns, particularly those low in leafy vegetables, legumes, and whole grains, combined with high caffeine and alcohol intake, which increase urinary magnesium excretion, make suboptimal magnesium status common.

Blood sugar instability

Drops in blood glucose trigger the release of adrenaline and cortisol, hormones that are also the primary drivers of the physiological anxiety response. This mechanism explains why some people experience sudden anxiety, racing heart, trembling, and a sense of impending doom in the mid-morning or mid-afternoon, patterns that correlate with glucose troughs rather than any external stressor. People with insulin resistance or reactive hypoglycaemia experience these episodes more intensely and frequently. Checking HbA1c alongside fasting glucose identifies whether metabolic instability is contributing to anxiety-like episodes.

Elevated cortisol and chronic stress activation

Cortisol, the primary stress hormone, follows a diurnal rhythm: it peaks shortly after waking and declines through the day, supporting energy and alertness. When chronic stress sustains cortisol at elevated levels, particularly in the evening when it should be low, the result is persistent physiological arousal, difficulty switching off, sleep disruption, and anxiety. Sustained high cortisol also suppresses TSH and impairs thyroid hormone conversion, creating thyroid-like symptoms even in the absence of primary thyroid disease. It also depletes magnesium, vitamin D, and B12 over time, creating multiple intersecting biological contributors to anxiety.

Vitamin D deficiency

Vitamin D receptors are found throughout the brain, including in regions that regulate the fear response and stress reactivity. Research has found associations between low vitamin D and anxiety, with some studies reporting that people with anxiety disorders have lower average vitamin D levels than age-matched controls. The proposed mechanism involves vitamin D's role in regulating serotonin production and moderating neuroinflammation, both of which affect anxiety threshold. In the UK, where sunlight-driven vitamin D synthesis is limited for six months of the year, deficiency is particularly common.

Gut health and the gut-brain axis

The gut produces approximately 90% of the body's serotonin, and the gut-brain axis, a bidirectional communication system between the enteric nervous system and the central nervous system, plays a significant role in anxiety regulation. Gut dysbiosis, an imbalanced microbiome, is associated with increased intestinal permeability, elevated systemic inflammation, and altered neurotransmitter production. Research using UK Biobank data found that anxious individuals showed higher levels of systemic inflammation markers, suggesting an inflammatory component in anxiety that may partly originate from gut dysfunction. People whose anxiety worsened after a period of gut illness, antibiotics, or dietary change may find that microbiome assessment adds useful information alongside a blood panel.

Anaemia and iron deficiency

UK Biobank data analysis found that anxious individuals showed higher rates of anaemia than non-anxious controls. Iron deficiency, even without frank anaemia, affects the synthesis of dopamine and serotonin, and the physiological effects of low ferritin, including heart palpitations, breathlessness on exertion, and increased heart rate, can trigger or worsen anxiety in people who are already predisposed. Checking ferritin as part of a comprehensive panel provides important context, particularly for women with heavy periods or anyone following a plant-based diet.

Standard GP assessments for anxiety rarely include comprehensive blood testing. A basic blood count may identify severe anaemia, and TSH may be checked, but the most informative markers for a biological anxiety investigation are typically absent from routine panels.

A comprehensive blood panel for investigating biological contributors to anxiety covers:

Full thyroid panel including TSH, Free T4, Free T3, and Anti-TPO antibodies to assess for both hypo- and hyperthyroidism, early autoimmune thyroid disease, and impaired thyroid conversion.

Vitamin D to identify the most common UK deficiency and its relationship to neuroinflammatory and serotonergic pathways relevant to anxiety.

Ferritin to assess iron stores, which affect neurotransmitter synthesis and produce physiological symptoms that can worsen anxiety.

HbA1c and fasting glucose to assess whether blood sugar instability is driving episodic anxiety-like symptoms.

CRP and homocysteine to identify systemic inflammation and B-vitamin pathway disruption, which are independently associated with anxiety presentations.

Vitamin B12 and folate to assess the methylation capacity needed for neurotransmitter production.

For people who suspect their anxiety has a strong thyroid component, or whose anxiety significantly worsened during a period of high stress or poor nutrition, a blood panel is a practical first step. It provides information that informs rather than replaces any psychological or psychiatric support.

Optimise magnesium and key nutrients

Magnesium is among the most accessible and evidence-supported nutritional interventions for anxiety. Dietary sources include dark leafy vegetables (spinach, kale), legumes, nuts, seeds, and whole grains. Supplementation is typically well tolerated, with magnesium glycinate and magnesium malate being the forms most commonly used for anxiety rather than gut symptoms. Testing before supplementing, while not strictly necessary for magnesium given its safety profile, helps distinguish genuine deficiency from high-normal status and allows you to track whether dietary changes are sufficient.

Stabilise blood sugar

Reducing glucose variability through dietary choices has a direct bearing on the frequency and intensity of physiological anxiety episodes driven by blood sugar troughs. Eating protein with each meal, choosing lower glycaemic index carbohydrates, avoiding long gaps between meals, and limiting caffeine on an empty stomach are the most practical starting points. HbA1c provides a three-month average that tells you whether the pattern is changing.

Support thyroid and reduce cortisol load

If thyroid markers show early dysfunction, the co-factors that support healthy thyroid metabolism are worth addressing: selenium (found in Brazil nuts, eggs, and oily fish), iodine (found in dairy and seafood), and ferritin. For cortisol dysregulation, the most evidence-supported interventions are consistent sleep timing, regular moderate exercise, and reducing stimulant intake, particularly caffeine after midday. Neither yoga nor meditation appears on the list as a dismissal; both have measurable effects on HPA axis activation. The point is that cortisol patterns are trackable and responsive to consistent lifestyle changes.

Address gut health

Dietary patterns that support microbiome diversity, including 30 different plant foods per week, fermented foods, and adequate dietary fibre, are associated with reduced anxiety scores in prospective research. Reducing alcohol, which disrupts the gut lining and depletes magnesium, vitamin B1, and folate, addresses multiple biological anxiety contributors simultaneously. If gut dysbiosis is suspected as a primary contributor, microbiome testing provides a baseline from which to measure improvement.