“The clinical management of hypertension is one of the most common interventions in primary care, accounting for approximately £1 billion in drug costs alone in 2006” (NICE, 2011).
Nevertheless, according to the British Heart Foundation there are an estimated 7 million people in the UK living with undiagnosed high blood pressure. This is a concern as high blood pressure may give no symptoms but increases the risk of heart attack, heart failure, stroke, dementia, kidney failure, diabetes and peripheral vascular disease.
Thirty percent of the population has high blood pressure, and another 30 percent has pre-hypertension. Before the age of 45, men are more likely than women to have high blood pressure but after 65 the ratio reverses. Diagnosis is often as a result of routine health monitoring, although for some people undiagnosed hypertension may produce symptoms of headaches and visual or respiratory difficulties.
This week’s blog discusses causes of hypertension and nutrition and lifestyle approaches to address the underlying causes.
What is hypertension?
Blood pressure is measured in millimeters of mercury and is recorded as two figures:
Systolic pressure: the pressure of the blood when the heart beats
Diastolic pressure: the pressure of the blood when the heart is at rest, between beats
The NICE guidelines’ criteria for a diagnosis of hypertension is when blood pressure readings are consistently 140/90 mmHg or higher in clinic. The diagnosis should then be confirmed using ambulatory blood pressure monitoring (APBM, ie a blood pressure cuff which takes intermittent readings is worn for a period) or home blood pressure monitoring (HPBM) where the former is not possible.
A blood pressure reading between 120/80 mmHg and 140/90 mmHg could mean you’re at risk of developing high blood pressure (ie this is the pre-hypertension range). An ideal blood pressure is considered to be between 90/60 mmHg and 120/80 mmHg. Low blood pressure is 90/60mmHg or lower.
Hypertension is often divided into two forms: essential (primary) hypertension and secondary hypertension.
Essential hypertension is the most common form and the causes are multifactorial. The NHS website lists age, obesity, African/Caribbean descent, genetics, sedentary lifestyle, high alcohol, coffee or salt consumption, lack of fruit and vegetables, smoking and poor or insufficient sleep as increasing the risk of high blood pressure.
Essential hypertension is the most common risk factor for cardiovascular diseases; it is also recognised as a primary cause for cerebrovascular and cardiovascular mortality.
Secondary hypertension accounts for a relatively small number of those with hypertension, and is secondary to a specific abnormality in one of the organs or systems of the body.
The renin-angiotensin-aldosterone system (RAAS)
The RAAS is a key regulator of blood pressure and fluid homeostasis. When plasma sodium concentration is lower than normal or renal blood flow is reduced, pro-renin (the inactive enzyme) is converted to renin which is then secreted into the circulation. Renin activates angiotensinogen to angiotensin I and this is then further converted to angiotensin II by the enzyme angiotensin converting enzyme (ACE) which is found in capillary endothelial cells throughout the body.
Angiotensin II is a potent vasoconstrictor that results in increased blood pressure. It also stimulates the secretion of the hormone aldosterone from the adrenal cortex, which causes increased reabsorption of sodium ions by the kidneys (at the same time as increased potassium excretion). Prescription drugs to lower blood pressure interrupt different steps in this system.
Causes of Hypertension
Hypertension is considered a result of endothelial dysfunction – a chronic condition which usually predates the diagnosis of cardiovascular conditions – in some cases by many years. Endothelial dysfunction can be caused by:
Atherosclerosis: (a narrowing of the arteries) due to inflammation and an accumulation of fatty deposits on the lining referred to as atheroma. Thus, factors that increase the risk of atherosclerosis such as hyperhomocysteinaemia and hyperglycaemia will also increase the risk of hypertension
Increased arterial tension: due to an imbalance in vasoactive mediators that are involved in relaxation of blood vessels (ie the vasodilator response).Electrolytes and nitric oxide (see below) are important for arterial tension
The thickness of the blood: if the blood is thicker or stickier than normal this can cause small increases in blood pressure.
Electrolytes: The balance of minerals – sodium, potassium, calcium and magnesium – controls arterial tension. The more sodium inside the cells and the less potassium the higher the tension, which raises blood pressure. Similarly, the more calcium inside the cells and the less magnesium the higher the blood pressure.
Blood pressure can therefore be controlled by reducing sodium and increasing potassium consumption, that is eating less salt to reduce sodium and increasing vegetable consumption to increase potassium; and by increasing magnesium intake (nuts, seeds and dark green leafy vegetables). NB calcium channel blocker drugs work on this mechanism by stopping calcium from entering cells.
Nitric Oxide: Nitric oxide (•NO) is a free radical produced by the vascular endothelium that mediates arterial relaxation, inhibits platelet aggregation and protects the endothelium from atherosclerosis. Loss of NO-driven vasodilatory control or ‘endothelial dysfunction’ hence causes vasoconstriction that increases vascular resistance (and thereby blood pressure). •NO is subject to rapid inactivation by the superoxide anion, a product of normal oxidative metabolism.
Usually superoxide in tissues is kept at low levels by the enzyme superoxide dismutase (SOD). However excess vascular levels of superoxide are linked to hypertension. Thus •NO-mediated arterial relaxation depends on SOD activity to limit the availability of superoxide. In addition to SOD other compounds can reduce the tissue availability of superoxide including antioxidants such as vitamins C, E and glutathione.
Nitric oxide production can be stimulated by both beetroot juice (which is high in nitrates that are metabolised to produce nitric oxide) and the action of sunlight on the skin. Studies have shown both as being effective in increasing levels of nitric oxide and lowering blood pressure.
Nutrients important for endothelial function
B vitamins – Homocysteine is a naturally occurring amino acid produced in the body as part of the methylation cycle. Adequate dietary intake of the nutrients betaine, choline, vitamins B6, B12 and folate are required to maintain low homocysteine levels. Elevated homocysteine can contribute to endothelial dysfunction and high blood pressure.
Vitamin C – Vitamin C is an aqueous-phase antioxidant that reduces oxidative stress and enhances endothelial function through effects on nitric oxide production. Vitamin C is also a natural blood thinner. Observational studies have shown an inverse association between plasma vitamin C concentrations and vitamin C intake with blood pressure. A 2012 meta-analysis of small studies concluded vitamin C may have a useful role in lowering BP and larger clinical trials are needed.
Vitamin D – There are many potential mechanisms for vitamin D deficiency to produce hypertension. Direct effects are mediated via the renin-angiotensin system. Indirect effects may include increased occurrence of atherosclerosis. The NHANES III study looked at serum 25(OH)D levels in relation to CVD risk factors in approximately 13,000 US adults and found vitamin D status was inversely associated with blood pressure.
Magnesium – Arterial tension is controlled by the balance of calcium, magnesium and potassium in relation to sodium. Magnesium and potassium are often lacking in the diet. One of the ways that magnesium may influence blood pressure is by activation of the cellular membrane pump that pumps sodium out of, and potassium into, the cell. Thus, low intracellular potassium may be the result of low magnesium intake. Population studies show a strong relationship between a high intake of magnesium and low blood pressure.
Coenzyme Q10 – An antioxidant and an essential component of the mitochondria. Although CoQ10 can be synthesised in the body, deficiency states have been reported including in people with hypertension. In several studies CoQ10 therapy has been shown to lower blood pressure in patients with hypertension. However, results have been mixed and a 2016 Cochrane review concluded that more trials are needed.
Omega 3 fatty acids – Many studies have shown increasing intake of omega 3 fatty acids can lower blood pressure. In one double blind trial 4 g per day of DHA reduced 24-hour systolic blood pressure by 5.8 mmHg and diastolic 3.3 mmHg. Flaxseed oil has also been shown to have a blood pressure lowering effect.
Polyphenols – Vegetable consumption is important in relation to potassium content as discussed. It has been suggested that the flavonoid content of fruit and vegetables may also lower blood pressure. Studies have evaluated foods including: grapes, berries, cocoa and tea. Results have been conflicting – probably due to the heterogeneity of study design, polyphenol source and population characteristics. The best results have been obtained from cocoa and black/green tea.
Lifestyle and Diet
Maintaining a healthy body weight, exercise and physical activity, avoiding smoking, limiting alcohol consumption, managing stress levels and adopting a good quality diet have all been found to have a beneficial effect on lowering blood pressure.
Therapeutic diet models have included the DASH (Dietary Approaches to Stop Hypertension) diet and Mediterranean diet. Both emphasise a wholefood diet based on lots of vegetables, fruit, nuts/seeds (so high in fibre). The DASH diet also includes sodium restriction and weight loss if needed. The DASH diet led to a mean systolic blood pressure that was 7.1 mmHg lower in participants without hypertension and 11.5 mmHg lower in participants with hypertension. A significant intake of wholegrains is included in the DASH diet models, which may not be appropriate for everyone especially if gluten intolerance or carbohydrate sensitivity (ie blood sugar issues) are relevant.
Other factors to consider
Gluten intolerance nutrient deficiency: Gluten intolerance could result in nutrient deficiencies leading to high blood pressure. In a case reported by Lim et al (2001), the patient had raised homocysteine and low B12 levels. The patient was described as sub-clinical coeliac which was identified as the cause of her nutrient deficiencies. Adhering to a gluten free diet along with supplementing folate, B6 and B12 normalised blood pressure within 15 months (improvement was seen after 6 months)
Toxins: Exposure to heavy metals like cadmium, mercury and lead may also be a significant factor for some people. The mechanism for this may be via damage to the kidney (ie affecting the renin-angiotensin system of blood pressure control), as well as mitochondrial damage affecting energy production (and thereby electrolyte balance).
Hormone imbalances: Oestrogens stimulate the release of endothelium vasodilators such as NO and inhibit the renin-angiotensin system and pre-menopause women are less likely to suffer high blood pressure. Post menopause(when oestrogen declines) blood pressure levels increase and the prevalence of high blood pressure becomes similar to that seen in men.
Both hypothyroidism and hyperthyroidism may also lead to increased blood pressure. In the case of hyperthyroidism this is associated with increased systolic pressure and normal diastolic pressure.
Social connectedness: A recent study revealed that frequent socialising with friends was inversely associated with the presence of high blood pressure in elderly.
If you have any questions regarding the topics that have been raised, or any other health matters please do contact me (Clare) by phone or email at any time.
firstname.lastname@example.org, 01684 310099
Clare Daley and the Cytoplan Editorial Team: Helen Drake, Joseph Forsyth and Chris Skal.
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Georgousopoulou E N et al (2017) – Mediterranean lifestyle and cardiovascular disease prevention. Cardiovasc Diagn Ther, 7(Suppl 1): S39–S47.
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Juraschek S et al (2012) – Effects of vitamin C supplementation on blood pressure: a meta-analysis of randomized controlled trials. Am J Clin Nutr, 95(5): 1079–1088.
Lim PO, Tzemos N, Farquharson CA, et al. Reversible hypertension following coeliac disease treatment: the role of moderate hyperhomocysteinaemia and vascular endothelial dysfunction. J Hum Hypertens. Jun 2002;16(6):411-415.
Lugg S T et al (2015) – Optimal vitamin D supplementation levels for cardiovascular disease protection. Dis Markers. 2015; 2015: 864370.
Lyrio dos Santos R et al () – Sex hormones in the cardiovascular system.
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NICE Clinical guideline [CG127] (2011) – Hypertension in adults: diagnosis and management https://www.nice.org.uk/guidance/cg127/chapter/Introduction
Suh S and Kim D K (2015) – Subclinical hypothyroidism and cardiovascular disease. Endocrinol Metab (Seol), 30, 3, 246-251
Vamvakis A et al () – Between celiac disease and irritable bowel syndrome: the “no man’s land” of gluten sensitivity. Am J Gastroenterol. Jun 2009;104(6):1587-1594.