top of page

Everything You Need to Know About Blood Pressure

Doctor's Visit
Blood pressure

Posted: 20/10/2017

Updated: 17/09/2018

We all know we should have a healthy blood pressure but what does this exactly mean? How is this even calculated and what can we do to keep it in a healthy range?


Blood pressure is the measure of force being exerted against the walls of the arteries with every heartbeat. This force is vital as it allows nutrients and oxygen to be transported to all of our cells in the body. So how is it calculated? First, we need to understand some terms.


Blood pressure is directly correlated to the amount of blood pumped out of the heart in each minute (cardiac output) and the oppositional force encountered by the blood as it enters the blood vessels (peripheral resistance).


Cardiac output is measured by multiplying the heart rate (HR) with stroke volume (SV).

Blood pressure = Peripheral Vascular Resistance X Cardiac Output

(Heart Rate X Stroke Volume)

BP = PR x CO (HR x SV)

Cardiac output (CO)

the amount of blood that is pumped out of the heart each minute

Peripheral resistance (PR)

resistance of the arteries to blood flow

Heart rate (HR)

refers to the number of times the heart beats every minute (bpm)

Stroke volume (SV)

quantity of blood pumped out of the left ventricle with each beat

  • 1 in 3 adults suffer from hypertension

  • 1 in 3 adults with hypertension do not know they have this disease

  • 1 in 3 adults treating their hypertension cannot keep it under 140/90

Blood pressure can be influenced by the speed of heart rate, the force of each heart contraction and volume of blood by the amount of water in the blood (occurs when salt or water consumption increases).


Hormones and biologically active compounds such as adrenaline, noradrenaline, leukotrienes, endothelin and thromboxane can also act to reduce blood pressure by decreasing the lumen size in the arteries (1).



During blood pressure measurements, two measurements known as systolic (SBP) and diastolic blood pressures (DBP) are taken. The time during which the heart muscle is contracting is called systole and the time during which the heart muscle is relaxing is called diastole.

Diastolic pressure (DBP) 

Pressure within artery between heartbeats


Systolic pressure (SBP)

Pressure generated when the heart ejects blood from left ventricle

High blood pressures, termed as hypertension, causes damage to blood vessels and can contribute to blockages in the arteries. The heart must work harder to pump the blood and the extra effort may lead to heart disease or stroke.


High blood pressure is generally defined as blood pressure above 140/90 mmHg in an adult.


Cut out points are used for the treatment of hypertension are systolic blood pressure (SBP) of 140 mmHg and diastolic blood pressure (DBP) 90 mmHg.

Categorised blood pressure ranges. Source: the American Heart Association (2).

This chart provides a clearer view of blood pressure values from the table above.

Note: Diagnosing high or low blood pressure only requires one measurement (systolic or diastolic) to be outside of the healthy range. 


Source: Vivehealth (3)

Hypertension is also known as the “silent killer” because it exhibits no symptoms.


In fact, astounding 75 million American adults (32%) have hypertension, 1 in every 3 adults do not even know that they have high blood pressure (4). In most cases, hypertension does not cause symptoms for fifteen to twenty years.


The symptoms that occur are due to damage to the organs such as the heart, brain, kidneys, and eyes that may eventually worsen to coronary heart disease, congestive heart failure, heart attacks, strokes, renal failures, blindness and so on.

Both systolic and diastolic blood pressure is measured to determine whether you are hypertensive or within the normal range. Hypertension is symptomless and should be taken seriously as it can cause irreversible damage to our organs.

Types of hypertension


Primary hypertension, or also known as essential hypertension occurs in 95% of all hypertensive cases, whose aetiology is unknown (5). However, there are several potential contributing factors to the development of primary hypertension (6).


Factors such as lifestyle, sleep deprivation, high sodium intake, and atherosclerotic disease are significant contributors to the development of increased pressures.

  • Genetics

  • Salt consumption

  • Obesity

  • Alcohol consumption

  • Poor feotal nutrition

  • Overgrowth of cells in blood vessels that narrow the lumen

  • Insufficient production of nitric oxide

  • Catecholamines, renin, insulin

Secondary hypertension occurs in 5% of all cases that are caused by specific medical and other conditions (7, 8).

Kidney disease

renal disorders

renovascular hypertension


stenosis of renal arteries

polycystic kidney disease


Endocrine disorders


Cushing’s syndrome




pain relievers

oral contraceptives



Drug use

cocaine, amphetamine, methamphetamine

Other less common types


Malignant hypertension is extremely high blood pressure that develops rapidly. This often causes irreversible end-organ damage to the brain (cerebrovascular accidents), eyes (retinal haemorrhages), heart (congestive heart failure) and kidneys (acute/chronic renal failure).


White coat hypertension occurs in a medical environment where a patient's anxiety results in an abnormally high reading. However, they have normal readings at home.


Pulmonary hypertension occurs when pulmonary arterioles (tiny arteries in the lungs) become blocked, narrowed or damaged. As it is harder for the blood to pass through, the heart has to exert more force which eventually leads to hypertension. This is not curable but treatment can help with symptoms.


Resistant hypertension is when 3 or more anti-hypertensive drugs which one of which is a diuretic are taken but still remains higher than normal. This could be due to another secondary cause.

There are 2 main types of hypertension and other less common ones. Primary hypertension occurs when the cause is unknown and secondary hypertension is when it is caused by another disease. Getting the right diagnosis is important in the treatment of hypertension.

Risk Factors

risk factors


Apparent mineralocorticoid excess (AME) is an autosomal recessive genetic disorder which causes severe hypertension at a young age.


Gene mutation causes the deficiency of 11b-hydroxysteroid dehydrogenase which is involved in the conversion of active cortisol to the inactive form.


With elevated concentrations of cortisol in the blood, it can activate the mineralocorticoid receptor on the kidney leading to sodium retention and ultimately, hypertension (9).

Non-modifiable factors





Modifiable factors


Alcohol consumption


Physical activity


Smoking status

Sex and Age

Generally, women have lower blood pressures than men before the age of 55 or until they reach menopause. In addition, women are less likely to experience complications associated with hypertension.

Blood pressure rises steadily with age in both men and women due to stiff arteries, plaque build-ups and higher cardiac rates. Systolic blood pressure is typically 20-30 mmHg higher at age 75 than at age 24 (10).


There is also a definite genetic component in Black Caribbeans, Caucasians and Indians resulting in higher risks.

Genetics, sex, age and ethnicity all affect your risks of having hypertension.



Source: Mayo Foundation for Medical Education and Research (11).




High blood pressure accelerates the development of atherosclerosis. Endothelial cells that line the arteries once damaged, results in monocytes (inflammatory cells that fight infection) entering the blood vessel. These cells engulf LDL cholesterol and ultimately creates a cholesterol plaque. This process is called atherosclerosis or also known as the hardening of the arteries (12).

Cholesterol and plaque build-up in the arteries narrows the arteries. Blood flow becomes restricted and sometimes cut off. Blood pressure will be elevated as the heart is forced to work harder to deliver nutrients and oxygen to cells. Additionally, the plaque can break off and travel to other parts of the body increasing the risk of heart attacks and stroke.

Hyaline arteriolosclerosis


Arterioles, the small blood vessels are prone to hyaline deposition.


Deposits of hyaline in the arterioles are seen more in hypertensive individuals compared with those of the same age who have normal blood pressure.


This extra substance makes the walls of the arterioles thicker and disrupts normal structure. Furthermore, it makes the lumen narrower which easily allows for a clot or plaque (embolus) to be lodged on the wall increasing the chances of a stroke or heart attack. With the weakened wall, it may even result in the arterioles to burst and bleed (13).


Hyperplastic arteriolosclerosis


The arterioles are narrowed due to an extra growth of the cells on the arteriole wall or the basement membrane (lining of arteriole cells). This may cause the deposit of extra proteins such as fibrin. Ultimately, this can lead to a blockage of blood flow (14).




Very small pouches that occur anywhere in the body called aneurysms can protrude from the blood vessels due to the weakening of vessel walls. Under high pressures, these are likely to rupture causing a bleed depending on the location (15).


Heart Disease


The narrowed coronary artery may develop new arteries that go around the blockage to get blood to the heart. However, under some circumstances, the new vessels may not be able to carry sufficient oxygen-rich blood to the heart. The lack of blood supply can cause a heart attack (16).


For the heart to get enough oxygen and nutrients, it needs to exert more effort to push blood around the body. If the heart is unable to pump as well as it should, it can possibly lead to arrhythmia and heart failure.


Brain (17)

Lacunar infarcts


Lacunar infarcts are damaged brain tissue that occurs because of blockages in penetrating arteries that resides deep in the brain.


The symptoms depend on the location and severity of damage. For instance, damage to the pons which is the part of the brainstem results in difficulty in speaking.


Multi-infarct dementia


With multi-infarct dementia, there are several strokes on both sides of the brain in multiple locations. Symptoms vary depending on where the brain is affected.


Hypertensive haemorrhages


The rupture of arteries and haemorrhages (bleeding) can cause brain damage depending on location and size of bleed:


  • Most haemorrhages occur in the putamen in the basal ganglia that is involved in the control of movement which can lead to weakness or paralysis.

  • The thalamus causes a sensory loss.

  • The pons is in the brainstem which is involved in homeostasis (e.g. respiratory system). A bleed can cause a person to fall into a coma and paralysis.

  • The cerebellum is involved in balance, coordination and walking. A haemorrhage can cause an onset of vertigo (dizziness) and difficulty walking. As blood accumulates in the back of the head, this causes nausea. The swelling of the cerebellum can block the normal flow of cerebrospinal fluid (in the brain) causing an increased pressure in the brain. Cerebral herniation may occur which is when the pressure pushes a part of the brain down through the hole at the base of the skull toward the spinal cord. Surgery is required and must be monitored carefully.



High blood pressure can damage blood vessels in the kidneys and cause them to narrow, reducing their ability to work properly.


Eventually, damaged arteries cannot supply enough blood for the kidneys to function and loses the ability to filter waste and fluid from the body. The extra fluid in the blood vessels can further raise blood pressure. This results in a vicious cycle and ultimately the kidneys can fail (18).


Eyes (19)



Blood pressure elevation damages the vessels supplying blood and necrosis in the retina, causing retinopathy. This can lead to blurred vision and eventually a complete loss of vision.


Choroidopathy is the build-up of fluid under the retina due to a leaky blood vessel under the retina. This can result in distorted vision or scarring that impairs vision.


Optic neuropathy occurs when blood flow is blocked which damages the optic nerve. Like retinopathy, this condition can cause bleeding and even vision loss.

Hypertension damages arteries that carry blood all over the body. This can lead to serious complications in organs such as the heart, brain, eyes, and kidney.



Diet Intervention

The Dietary Approaches to Stop Hypertension (DASH) study found that a diet high in fruits, vegetables, and low-fat dairy foods, combined with a reduction of consumption of total fat and saturated fat was helpful in reducing blood pressure.

It also concluded that people can lower their blood pressure significantly by combining these dietary changes with a reduction in salt intake.

Food Group

Low-fat dairy



Grains and grain products

Meat, Poultry and fish

Nuts, seeds and beans

Fats and oils


Daily Servings





2 or fewer

4-5 per week


5 per week

Nutritional Benefit

Ca, K, Mg, protein

K, Mg, fibre

K, Mg, fibre

Carbs and fibre

Protein, Mg

Mg, K, protein, fibre

Applies to all fat

Choose low-fat

More information can be found here. 


Almonds, herring, greens, milk, calcium-fortified soy or almond milk, fat-free yoghurt

Calcium helps to tighten blood vessels and relax when required.


Calcium is found naturally in dairy products, fish with bones and leafy vegetables.


Adults (19-64 years) need 700mg of calcium per day (22, 23). By consuming the RDA for calcium results in lower risk of developing hypertension than consuming lower levels.


Supplementation of calcium of 1 to 2 g/day reduces systolic blood pressure by 1.27 mm Hg but not diastolic blood pressure (24).


However, calcium with supplements shows that even at mega-doses produces only minor changes (25).



Spinach, avocado, pumpkin seeds, almonds, black beans, dark chocolates


Magnesium is a potent inhibitor of vascular smooth muscle contraction and may play a role in blood pressure regulation as a vasodilator.


Studies have shown that hypertensives tend to have lower serum magnesium (26). Hence, magnesium was believed to be of importance in lowering blood pressure.


However, supplemental magnesium has no significant effect on blood pressure in humans (27).



Banana, swiss chard, yellowfin tuna, cantaloupe, green vegetables, potato, sweet potato, tomatoes, watercress, seeds, mint leaves


Normal body levels of potassium are important for the relaxation of the walls of the blood vessels to lower blood pressure. It is also important for the conduction of electrical signals in the heart which protects the heart against an irregular heartbeat (28).


In population studies, dietary potassium and blood pressure are inversely related. High potassium intakes are associated with lower blood pressure (29).


Potassium is difficult to measure intake accurately but excretion is directly related to intake. InterSalt study suggests that a 50 mmol/day increase in potassium excretion would be associated with 3mmHg lower systolic blood pressure and 2mmHg lower in diastolic blood pressure (30).


In conclusion, potassium, but not calcium or magnesium supplements, has a modest blood pressure–lowering effect in normotensive persons with low dietary intake (31).


However, a delicate balance is very important as too much potassium (hyperkalemia) can be deadly and lead to changes in heart rhythms. Certain medications (antibiotics, blood pressure drugs, NSAIDs) can affect your potassium levels and hence, always consult a professional before you consider to increase your potassium intake.




Regular alcohol consumption elevates blood pressure, with global estimates that the attributable risk for hypertensive disease from alcohol is 16% (20).


In the UK, men and women are advised to drink no more than 14 units a week spread evenly over 3 days or more (21).




Sodium intake plays a significant role in regulating blood pressure. On a high salt diet, homeostatic mechanisms ensure that the kidneys will excrete any excess sodium via the urine.


However, excessive salt intake on a regular basis raises the sodium in the bloodstream putting strain and reducing the ability of the kidneys to remove water. The extra fluid overtime can increase blood pressure.

UK guidelines

On average, adults in the UK eat about 8.1g of salt (3.2g sodium)* a day and it is advised by the NHS that adults should be eating less than 6g of salt (2.4g sodium) a day (33). Many other organisations advise us to have less than 3.75g of salt (1.5g sodium) per day.


* Salt contains 60% chloride and 40% sodium so here's the conversion:

Sodium (g) X 2.5 = Salt (g)

Salt (g) / 2.5 = Sodium (g)

0 - 6 month: < 1g a day of salt a day (0.4g sodium)

  1 - 3 years: 2g of salt a day (0.8g sodium)

  4 - 6 years: 3g of salt a day (1.2g sodium)

7 - 10 years: 5g of salt a day (2g sodium)

      11 years: 6g of salt a day (2.4g sodium)

Other methods

Regular physical exercise especially aerobic exercise such as walking, jogging, jumping rope, bicycling, and swimming can be beneficial over time to lowering blood pressure.


By exercising, it can significantly decrease systolic and diastolic daytime ambulatory blood pressure by 6 and 3 mm Hg respectively in one study (34).

However, with severe hypertension, it is best to consult a doctor before engaging in vigorous exercise (35).​


Reducing stress can lower blood pressure. Adopting techniques such as meditation and mindfulness may reduce daily stress (36).


Medication is essential for hypertension when even lifestyle modifications are adapted. Many people do not achieve control with one medication alone and several may be taken for effectiveness. The medical treatment of hypertension is usually long lasting or often for life.

Other methods

Information found here.  Thiazides and thiazide-like drugs (diuretics) are first choice antihypertensive agents.

The DASH diet, eating more potassium-rich foods, limiting alcohol and salt intake can lower your blood pressure levels. In addition to diet intervention, physical exercise and practising relaxation techniques to reduce stress can help. Medication is recommended only when all methods are adapted but levels still remain high.



The large choices of hypertensive drugs are grouped into several classes that act either on the vasoconstriction or volume components of hypertension.


Note: Only a few examples are listed and this is not a complete list.


1. Sympatholytic drugs


Alpha (adrenergic) blockers

Blockade of alpha-1 receptors which then reduces blood pressure by dilating vessels


Beta (adrenergic) Blockers

Reduces cardiac output (heart rate and stroke volume) resulting in lower blood pressure. Furthermore, it acts on the renin-angiotensin system by inhibiting renin release.


2. Angiotensin inhibitors and antagonists


Drugs interfere with the renin-angiotensin system as 15% of patients with primary hypertension exhibits increased plasma renin activity (PRA), 60% have normal activity and 25% have reduced activity (37).


ACE inhibitors

ACE inhibitors inhibit the angiotensin-converting enzyme which then inhibits the creation of angiotensin, a substance that causes tightening of vessels. This results in vascular vessel relaxation and lower blood pressure


ARB blockers

Similar to ACE inhibitors which acts on the renin-angiotensin system, it blocks the receptors of angiotensin II and hence causes vasodilation and increased salt and water secretion


The two types of hypertension can be distinguished by different plasma renin levels.

Type 1 hypertension (vasoconstrictor, high renin)

Renin secretion is inappropriately high for blood pressure and this may be due to a possibility of increased salt sensitivity (small intake of salt causes big changes in blood pressure).


High renin hypertensive patients respond to ACE inhibitors, ARB blockers, and β blockers block the renin-angiotensin system activity which results in vasodilation.

Type 2 hypertension (sodium-dependent, low renin)

Renin secretion is suppressed when the kidney detects that the sodium ions levels are raised.

Low renin hypertensive patients are more responsive to calcium channel blockers and diuretics which are natriuretic (causes sodium excretion) and vasodilating in order to reduce blood pressure (38).

3. Vasodilators

Calcium channel blockers

Relaxes muscles surrounding the blood vessels and decreases vascular resistance resulting in lower blood pressure

4. Diuretics

Thiazides and congeners

Increases amount of urine produced and hence causes falls in sodium stores resulting in lower blood pressure

  • References
    Irritable bowel syndrome [Online] Available at: [Accessed: 22 June 2018]. Saha, L. (2014). Irritable bowel syndrome: Pathogenesis, diagnosis, treatment, and evidence-based medicine. World Journal of Gastroenterology, 20(22), p.6759. D. Cashman, M., K. Martin, D., Dhillon, S. and R. Puli, S. (2016). Irritable Bowel Syndrome: A Clinical Review. Current Rheumatology Reviews, 12(1), pp.13-26. Guidelines--Rome III Diagnostic Criteria for Functional Gastrointestinal Disorders. (2006). Journal of Gastrointestinal and Liver Diseases, 15(3), pp.307-12. Drossman, D. (2016). Functional Gastrointestinal Disorders: History, Pathophysiology, Clinical Features, and Rome IV. Gastroenterology, 150(6), pp.1262-1279.e2. Ikechi, R., Fischer, B., DeSipio, J. and Phadtare, S. (2017). Irritable Bowel Syndrome: Clinical Manifestations, Dietary Influences, and Management. Healthcare, 5(2), p.21. Enck, P., Aziz, Q., Barbara, G., Farmer, A., Fukudo, S., Mayer, E., Niesler, B., Quigley, E., Rajilić-Stojanović, M., Schemann, M., Schwille-Kiuntke, J., Simren, M., Zipfel, S. and Spiller, R. (2016). Irritable bowel syndrome. Nature Reviews Disease Primers, 2, p.16014. Chey, W., Kurlander, J. and Eswaran, S. (2015). Irritable Bowel Syndrome. JAMA, 313(9), p.949. Hungin, A., Chang, L., Locke, G., Dennis, E. and Barghout, V. (2005). Irritable bowel syndrome in the United States: prevalence, symptom patterns and impact. Alimentary Pharmacology and Therapeutics, 21(11), pp.1365-1375. Gibson, P., Varney, J., Malakar, S. and Muir, J. (2015). Food Components and Irritable Bowel Syndrome. Gastroenterology, 148(6), pp.1158-1174.e4. Card, T., Canavan, C. and West, J. (2014). The epidemiology of irritable bowel syndrome. Clinical Epidemiology, p.71. Occhipinti, K. and Smith, J. (2012). Irritable Bowel Syndrome: A Review and Update. Clinics in Colon and Rectal Surgery, 25(01), pp.046-052. Chey, W., Kurlander, J. and Eswaran, S. (2015). Irritable Bowel Syndrome. JAMA, 313(9), p.949. Zhou, Q. and Verne, G. (2011). New insights into visceral hypersensitivity—clinical implications in IBS. Nature Reviews Gastroenterology & Hepatology, 8(6), pp.349-355. Ghoshal, U., Kumar, S., Mehrotra, M., Lakshmi, C. and Misra, A. (2010). Frequency of Small Intestinal Bacterial Overgrowth in Patients with Irritable Bowel Syndrome and Chronic Non-Specific Diarrhea. Journal of Neurogastroenterology and Motility, 16(1), pp.40-46. Ghoshal, U., Shukla, R. and Ghoshal, U. (2017). Small Intestinal Bacterial Overgrowth and Irritable Bowel Syndrome: A Bridge between Functional Organic Dichotomy. Gut and Liver, 11(2), pp.196-208. Ghoshal, U. (2014). Irritable bowel syndrome and small intestinal bacterial overgrowth: Meaningful association or unnecessary hype. World Journal of Gastroenterology, 20(10), p.2482. Marshall, J., Thabane, M., Garg, A., Clark, W., Moayyedi, P. and Collins, S. (2010). Eight year prognosis of postinfectious irritable bowel syndrome following waterborne bacterial dysentery. Gut, 59(5), pp.605-611. Marshall, J., Thabane, M., Garg, A., Clark, W., Salvadori, M. and Collins, S. (2006). Incidence and Epidemiology of Irritable Bowel Syndrome After a Large Waterborne Outbreak of Bacterial Dysentery. Gastroenterology, 131(2), pp.445-450. Spiller, R. and Campbell, E. (2006). Post-infectious irritable bowel syndrome. Current Opinion in Gastroenterology, 22(1), pp.13-17. Ericsson, C., Hatz, C. and DuPont, A. (2008). Postinfectious Irritable Bowel Syndrome. Clinical Infectious Diseases, 46(4), pp.594-599. Grenham, S., Clarke, G., Cryan, J. and Dinan, T. (2011). Brain?Gut?Microbe Communication in Health and Disease. Frontiers in Physiology, 2. The Brain-Gut Connection [Online] Available at: [Accessed: 24 June 2018]. Folks, D. (2004). The interface of psychiatry and irritable bowel syndrome. Current Psychiatry Reports, 6(3), pp.210-215. Fichna, J. and Storr, M. (2012). Brain-Gut Interactions in IBS. Frontiers in Pharmacology, 3. El-Salhy, M. and Gundersen, D. (2015). Diet in irritable bowel syndrome. Nutrition Journal, 14(1). Irritable Bowel Syndrome - National Library of Medicine - PubMed Health [Online] Available at: [Accessed: 24 June 2018]. Folks, D. (2004). The interface of psychiatry and irritable bowel syndrome. Current Psychiatry Reports, 6(3), pp.210-215. Ikechi, R., Fischer, B., DeSipio, J. and Phadtare, S. (2017). Irritable Bowel Syndrome: Clinical Manifestations, Dietary Influences, and Management. Healthcare, 5(2), p.21. Rao, S., Yu, S. and Fedewa, A. (2015). Systematic review: dietary fibre and FODMAP-restricted diet in the management of constipation and irritable bowel syndrome. Alimentary Pharmacology & Therapeutics, 41(12), pp.1256-1270. Moayyedi, P., Quigley, E., Lacy, B., Lembo, A., Saito, Y., Schiller, L., Soffer, E., Spiegel, B. and Ford, A. (2014). The Effect of Fiber Supplementation on Irritable Bowel Syndrome: A Systematic Review and Meta-analysis. The American Journal of Gastroenterology, 109(9), pp.1367-1374. FRANCIS, C. (1994). Bran and irritable bowel syndrome: time for reappraisal. The Lancet, 344(8914), pp.39-40. Vazquez–Roque, M., Camilleri, M., Smyrk, T., Murray, J., Marietta, E., O'Neill, J., Carlson, P., Lamsam, J., Janzow, D., Eckert, D., Burton, D. and Zinsmeister, A. (2013). A Controlled Trial of Gluten-Free Diet in Patients With Irritable Bowel Syndrome-Diarrhea: Effects on Bowel Frequency and Intestinal Function. Gastroenterology, 144(5), pp.903-911.e3. Ford, A., Quigley, E., Lacy, B., Lembo, A., Saito, Y., Schiller, L., Soffer, E., Spiegel, B. and Moayyedi, P. (2014). Efficacy of Prebiotics, Probiotics and Synbiotics in Irritable Bowel Syndrome and Chronic Idiopathic Constipation: Systematic Review and Meta-analysis. The American Journal of Gastroenterology, 109(10), pp.1547-1561. Basturk, A., Artan, R. and Yilmaz, A. (2016). Efficacy of synbiotic, probiotic, and prebiotic treatments for irritable bowel syndrome in children: A randomized controlled trial. The Turkish Journal of Gastroenterology, 27(5), pp.439-443. Zhang, Y., Li, L., Guo, C., Mu, D., Feng, B., Zuo, X. and Li, Y. (2016). Effects of probiotic type, dose and treatment duration on irritable bowel syndrome diagnosed by Rome III criteria: a meta-analysis. BMC Gastroenterology, 16(1). Guandalini, S., Magazzù, G., Chiaro, A., La Balestra, V., Di Nardo, G., Gopalan, S., Sibal, A., Romano, C., Canani, R., Lionetti, P. and Setty, M. (2010). VSL#3 Improves Symptoms in Children With Irritable Bowel Syndrome: A Multicenter, Randomized, Placebo-Controlled, Double-Blind, Crossover Study. Journal of Pediatric Gastroenterology and Nutrition, 51(1), pp.24-30. Paineau, D., Payen, F., Panserieu, S., Coulombier, G., Sobaszek, A., Lartigau, I., Brabet, M., Galmiche, J., Tripodi, D., Sacher-Huvelin, S., Chapalain, V., Zourabichvili, O., Respondek, F., Wagner, A. and Bornet, F. (2007). The effects of regular consumption of short-chain fructo-oligosaccharides on digestive comfort of subjects with minor functional bowel disorders. British Journal of Nutrition, 99(02). Khanna, R., MacDonald, J. and Levesque, B. (2013). Peppermint Oil for the Treatment of Irritable Bowel Syndrome. Journal of Clinical Gastroenterology, p.1. Peppermint Oil for IBS: Does it Work? [Online] Available at: [Accessed: 24 June 2018]. Grigoleit, H. and Grigoleit, P. (2005). Peppermint oil in irritable bowel syndrome. Phytomedicine, 12(8), pp.601-606. Khanna, R., MacDonald, J. and Levesque, B. (2013). Peppermint Oil for the Treatment of Irritable Bowel Syndrome. Journal of Clinical Gastroenterology, p.1. IBS Diet: What to Do and What to Avoid [Online] Available at: [Accessed: 24 June 2018]. Johannesson, E., Simrén, M., Strid, H., Bajor, A. and Sadik, R. (2011). Physical Activity Improves Symptoms in Irritable Bowel Syndrome: A Randomized Controlled Trial. The American Journal of Gastroenterology, 106(5), pp.915-922.

There are numerous anti-hypertensive drugs on the market that helps lower blood pressure primarily by dilating blood vessels or reduce blood present in the arteries.

bottom of page