High blood pressure: causes, risks and what biomarkers to check

Primary hypertension: lifestyle and ageing

Around 90-95% of high blood pressure cases are classified as primary (or essential) hypertension, meaning there is no single identifiable cause but rather an accumulation of contributing factors. The most important of these are excess sodium relative to potassium in the diet, excess body weight particularly visceral fat, physical inactivity, excessive alcohol, smoking, chronic stress, and older age. Arterial stiffness increases naturally with age as the walls of large arteries lose elasticity, requiring higher pressure to push blood through them. These lifestyle factors interact with genetic predispositions to produce the blood pressure trajectory of an individual over their lifetime.

Insulin resistance and metabolic syndrome

Insulin resistance and the metabolic syndrome pattern (central obesity, high triglycerides, low HDL, high blood sugar, and high blood pressure) are closely interconnected. Elevated insulin promotes sodium retention in the kidneys, activates the sympathetic nervous system, and stimulates smooth muscle cell proliferation in arterial walls, all of which contribute directly to raised blood pressure. Measuring HbA1c and fasting blood sugar alongside a lipid panel in someone with high blood pressure assesses whether a metabolic driver is part of the picture, because addressing insulin resistance improves blood pressure through mechanisms that medication alone does not cover.

Kidney function: bidirectional relationship

The kidneys regulate blood pressure through their control of blood volume and sodium handling. Chronic kidney disease reduces the kidney's ability to filter blood and excrete sodium, which raises blood pressure. Conversely, sustained high blood pressure damages the delicate filtering units (glomeruli) of the kidneys over time, reducing kidney function, which in turn further raises blood pressure. This bidirectional relationship is one of the reasons that blood tests for kidney function (creatinine, estimated glomerular filtration rate (eGFR)) are an important part of the assessment when high blood pressure is identified. Early kidney involvement is often silent but detectable through blood tests before symptoms develop.

Magnesium and vascular tone

Magnesium plays a direct role in regulating blood vessel tone. It acts as a natural calcium channel blocker in vascular smooth muscle, promoting relaxation of arterial walls and reducing peripheral resistance. When magnesium is low, blood vessels are more prone to constriction, catecholamine responses run more strongly, and the adrenal hormone aldosterone (which promotes sodium and water retention) secretes more readily. Several meta-analyses have found that oral magnesium supplementation produces modest but consistent reductions in blood pressure, particularly in people who are magnesium deficient. Magnesium deficiency is common in the UK, driven by inadequate dietary intake of green vegetables, nuts, seeds, and whole grains.

Secondary hypertension: conditions that raise blood pressure directly

In 5-10% of cases, high blood pressure has a specific identifiable cause. The most important of these are kidney disease (renal artery stenosis or chronic kidney disease), primary aldosteronism (overproduction of the aldosterone hormone by the adrenal glands), and obstructive sleep apnoea (which activates the sympathetic nervous system during repeated overnight oxygen drops). Thyroid disease, both hypothyroid and hyperthyroid, also affects blood pressure: hypothyroidism causes diastolic hypertension, while hyperthyroidism produces a widened pulse pressure with elevated systolic readings. If blood pressure is difficult to control with standard treatment, or if it developed at a young age without obvious lifestyle risk factors, these secondary causes are worth investigating.

Chronic stress and the HPA axis

Chronic psychological and physiological stress maintains elevated levels of cortisol and adrenaline, which act on the sympathetic nervous system to raise blood pressure acutely. When the stress response is sustained, the repeated activation of vasoconstriction and sodium retention can shift baseline blood pressure upward over time. CRP tends to be elevated in people with chronic stress, both because stress directly promotes inflammatory signalling and because the lifestyle patterns associated with chronic stress (poor sleep, poor diet, physical inactivity) compound its inflammatory effects. Addressing stress management as part of blood pressure treatment has measurable biological effects, not just subjective ones.

A blood test cannot diagnose high blood pressure, which requires multiple blood pressure readings taken at rest over time (or 24-hour ambulatory monitoring). What blood tests can do is assess the underlying drivers, rule out secondary causes, and evaluate the impact that elevated pressure is having on key organs.

Creatinine and eGFR assess kidney function. Creatinine is a waste product filtered by the kidneys; when kidney function declines, creatinine rises in the blood and eGFR falls. Tracking these markers over time shows whether blood pressure management is protecting kidney function or whether deterioration is occurring.

HbA1c gives a 3-month average of blood sugar control. Insulin resistance is a driver of high blood pressure through sodium retention and sympathetic nervous system activation. Addressing metabolic health alongside blood pressure treatment produces better outcomes than treating each in isolation.

Full lipid panel (LDL, HDL, triglycerides) assesses cardiovascular risk in the context of high blood pressure. Hypertension and hyperlipidaemia are the two most significant independent cardiovascular risk factors, and their combination multiplies risk substantially more than either alone.

TSH and thyroid function rule out thyroid disease as a secondary cause of blood pressure elevation. Both hypothyroidism (raises diastolic pressure) and hyperthyroidism (raises systolic pressure and heart rate) are treatable causes that should be identified.

CRP measures systemic inflammation. Elevated CRP in someone with high blood pressure confirms the inflammatory dimension of their cardiovascular risk picture and helps direct lifestyle priorities.

Vitamin D is associated with blood pressure regulation through its effects on the renin-angiotensin-aldosterone system, which controls blood volume and blood pressure. Low vitamin D is consistently associated with higher rates of hypertension in population studies.

Magnesium is worth assessing because deficiency is common and contributes directly to increased vascular tone and blood pressure. Standard blood panels often use serum magnesium, which reflects only a small fraction of the body's total magnesium and can appear normal even with intracellular deficiency. Red blood cell magnesium is a more accurate assessment but less widely available.

Homocysteine is relevant because elevated homocysteine damages arterial endothelium and stiffens arteries, compounding the vascular damage caused by high blood pressure itself. It also adds an independent cardiovascular risk signal that is directly addressable.

Sodium, potassium, and the DASH diet

The most evidence-based dietary approach for blood pressure reduction is the DASH (Dietary Approaches to Stop Hypertension) diet, which reduces sodium and increases potassium, magnesium, and calcium through an emphasis on fruits, vegetables, whole grains, low-fat dairy, nuts, and lean proteins. The blood pressure reduction from the DASH diet is comparable to that of a low-dose antihypertensive medication in some trials. The key mechanisms are reduced sodium intake (which reduces blood volume), increased potassium (which counters sodium's effects on blood vessel tone), and increased magnesium (which supports vascular relaxation). Dietary sodium target is below 6g (one teaspoon) of salt per day for people with high blood pressure, with lower targets potentially beneficial for those at higher risk.

Exercise: the dose that makes a difference

Both aerobic exercise and resistance training reduce blood pressure through complementary mechanisms. Aerobic exercise improves arterial compliance (flexibility), reduces resting heart rate, lowers sympathetic nervous system tone, and improves insulin sensitivity. Meta-analyses find that aerobic exercise produces average reductions of 3-5 mmHg in systolic pressure in people with hypertension. Isometric exercises (like wall squats and hand grip exercises) have emerging evidence for particularly strong blood pressure effects. The target of at least 150 minutes of moderate-intensity aerobic activity per week is the minimum evidence-based recommendation for cardiovascular and blood pressure benefit.

Sleep and stress: the underappreciated levers

Sleep quality has a direct bidirectional relationship with blood pressure. Chronic sleep deprivation activates the sympathetic nervous system and impairs the normal nocturnal blood pressure dip (where blood pressure should fall 10-20% overnight). People who do not show this nocturnal dip have significantly worse cardiovascular outcomes. Obstructive sleep apnoea, which causes repeated overnight drops in oxygen saturation and surges in sympathetic activation, is one of the most common secondary causes of resistant hypertension. Treating sleep apnoea with CPAP therapy often produces meaningful blood pressure reductions. Stress management through regular exercise, breathing practices, and adequate recovery time has measurable effects on cortisol, sympathetic tone, and blood pressure regulation.

Magnesium and micronutrient support

Increasing dietary magnesium intake through food sources (dark chocolate, nuts, seeds, leafy greens, whole grains, legumes) or supplementation is a modifiable intervention with specific mechanistic relevance to blood pressure. Meta-analyses of magnesium supplementation trials find average systolic reductions of 2-4 mmHg, with larger effects in people who are deficient. Potassium-rich foods (bananas, sweet potato, spinach, lentils, avocado) counter the blood pressure effects of sodium by promoting its excretion and relaxing blood vessel walls. Vitamin D supplementation in people who are deficient also has evidence for modest blood pressure reduction through its effects on the renin-angiotensin-aldosterone system. Testing these markers gives you a baseline from which to track whether nutritional changes are producing measurable shifts.