Project Abstract

Project Overview

<p> </p><p><strong>INTRODUCTION</strong></p><p>Sodium chloride (NaCl) is a prototypical stimulant that elicits salty taste. Sodium chloride is a commonly used food ingredient which provides many technological functions such as Flavor enhancement, preservation and texture modification (Hutton, 2002). Sodium (Na) also performs a number of vital roles in the body including maintaining the volume of extracellular fluid, osmotic pressure, acid-base balance and transmission of nerves impulses (Geerling and Loewy, 2008).</p><p>Unlike other essential minerals such as calcium, we do not have large stores of sodium in the body and need to constantly replenish sodium via the diet (Reddy and Marth, 1991). While sodium is essential for normal human body functioning, current sodium intakes far exceed recommendation for good health (Brown and Tzoulaki, 2009). This is a problem because there is a strong positive relationship between sodium intake and raised blood pressure.</p><p>Raised blood pressure is a major cause of cardiovascular diseases, responsible for 62% of stroke and 49% of coronary heart disease (He and MacGregor, 2010). Excess sodium consumption has also been linked to numerous other negative health effects including gastric cancer (Tsugane <em>et al</em>., 2004), decreased bone mineral density (Devine <em>et al</em>., 2000) and obesity (He <em>et al</em>., 2008).</p><p>In general attempts to reduce dietary sodium intake through sodium restricted diets have shown short term success but have lacked long term sustainability and practicality for large populations due to high level of sodium in processed foods and the significant contribution of processed foods to our diet (James <em>et al.,</em>&nbsp;1987). Also, a reduction of sodium chloride in foods is accompanied by a loss of palatability of those foods (Mattes, 2007). The ideal solution would be to reduce the concentration of sodium in the food while retaining optimum saltiness for palatability. One strategy to reduce sodium is to replace with potassium salts, and while potassium chloride elicits weak saltiness at higher concentrations it also elicits metallic and bitter taste limiting its utility in foods (Ainsworth and Plunkett, 2007).</p><p>However, minimizing those ‘off-flavors’ means potassium could be an effective salt taste replacer. Arguably, the human diet has undergone more significant changes in the past 50 years than in the past 10 million years (Cordian <em>et al</em>., 2005). One of such modification is the molar ratio consumption of sodium to potassium. Historically, hominid diet contains high potassium and low sodium concentration due to a diet consisting largely of fruit, vegetables and whole grains (Cordian <em>et al., </em>2005). Our evolutionary forbears had a need to consume sodium, and the sodium was a scarce dietary element, we developed an appetitive response to sodium via salt taste (Mela, 2006). Although the taste mechanism for sodium has not changed, the food supply has developed to suit our appetitive desire and the modern western diet contains a high proportion of processed food with high levels of sodium, which is inherently appealing to humans (Mattes, 2001).</p><p>Moreover, fruit and vegetables are the major source of dietary potassium but they are not much consumed in the diet. High consumption of processed food has resulted in a decrease intake of potassium and increase intake of sodium which has much negative health effect including raise blood pressure, obesity and decreased mineral density etc. In recognition of the risks posed by the excessive consumption of sodium, a new daily consumption limit of less than 5g/day (&lt;87mmole per day) has been set for high risk groups, including adults of black African origin. Therefore, this research is aimed at estimating the daily salt intake of healthy ambulant Nigerian adults.</p><p>The high risk of hypertension and its related complications in both developed and developing countries has been attributed to the sociological, political and economic changes and the associated alterations in people’s lifestyles (Ukoh <em>et al</em>., 2004). This research is aimed to investigate what is known from previous studies relating to the relationship between hypertension and:</p><ul><li>Risk factors including age, gender, genetics, diet, and weight, alcohol, smoking, lack of activity and co- morbidity</li><li>Mediating factors including economic factor, stress or personality and medication</li><li>Management of hypertension through life style modification</li><li>Complimentary therapy: foot reflexology and foot message</li></ul><p>&nbsp;</p><p><strong>1.1 Sodium</strong></p><p><strong>1.1.1 &nbsp; Source of Dietary Sodium</strong>&nbsp;<strong>in the Body</strong></p><p>In developed countries, large proportion of the sodium ingested is added (as sodium chloride) in food manufactured and foods eaten away from home. Ralph <em>et al</em>., 2000) estimated that for the United Kingdom and USA, about 75% of sodium intake was from processed or restaurant foods, 10–12% was naturally occurring in foods and the remaining 10–15% was from the discretionary use of salt in home-cooking or at the table. Sodium content of a takeaway cheeseburger and chips (French fries) is estimated at 1240 mg (54 mmol) compared with homemade steak and chips at 92 mg (4 mmol), sodium content of a ‘ready-meal’ risotto is estimated at 1200 mg (52 mmol), while that of its homemade equivalent at &lt; 2 mg (&lt; 0.1 mmol).</p><p>In some cases, for example chick peas, sweet corn and peas which naturally have very low sodium content. More so, processed food increases the sodium content by 10–100-fold and foods such as corned beef, bran flakes or smoked salmon have sodium intakes of 1–2%, equivalent to, or more than the sodium concentration of Atlantic seawater (MacGregor and De Waedener, 2005). Cereals and cereal products including bread, breakfast cereals, biscuits and cakes, contribute about 38% of estimated total intake, meat and meat products 21%, and other foods such as soups, pickles, sauces and baked beans a further 13%. Bread, ready-to-eat cereal and cakes, cookies, quick-breads and doughnuts contribute 16-17% of sodium intake, ham, beef, poultry, sausage and cold cuts about 13%, milk and cheese 8–9%, condiments, salad dressing and mayonnaise about 5%, other foods including potato chips, popcorn, crackers and pretzels, margarine, hot dogs, pickles and bacon a further 23–25% (Mattes, 2001).</p><p>All the products listed alone contain over 2.3 g (100 mmol) sodium, i.e. the recommended daily tolerable upper intake level (UL) for the USA (Institute of Medicine, 2004). However, some foods contain twice the recommended Upper Level. Some children foods are extremely high in sodium. For example the estimated salt content of one large slice of pizza or two thin fried pork sausages is around 1g (391mg, 17mmol sodium).</p><p>In the United Kingdom, cereals contribute 38–40% of sodium present in the diets of children and young people ages 4–18 years, meats 20–24%, vegetables 14–17%, and dairy products 7–9%. In the USA, girls reporting that they ate fast foods at least four times per week had higher sodium intakes than girls having fast foods &lt; 1–3 times per week (Schmidt <em>et al</em>., 2005). A different picture with regard to dietary sources of sodium is apparent in some Asian countries. In China and Japan, a large proportion of sodium in the diet comes from sodium added in cooking and &nbsp; 25% from various sauces, including soy sauce and miso (in Japan).</p><p>In china, 75% of dietary sodium comes from sodium added as salt in cooking, and a further 8% from soy sauce. In Japan, the main sources were soy sauce, fish and other sea food, soups and vegetables (66% in total) with a further 10% being contributed by salt added during cooking. Some foods commonly consumed in Malaysia are also very high in sodium for example a bowl of Mee curry and a bowl of Mee soup available from ‘hawker’ markets contain about 2.5 g (109 mmol) and 1.7 g (74 mmol) sodium, respectively (Campbell <em>et al</em>., 2006) .</p><p><strong>1.1.2 &nbsp; &nbsp; Significance of Sodium</strong></p><p>Excess sodium consumption has been linked to numerous adverse health conditions and is a major public health concern in the USA, Nigeria and worldwide (Medicine, 2010). Previous strategies to reduce sodium chloride consumption have shown to be effective in health care settings but are not practical at the population level due to the large contribution of processed foods to sodium intake. Strategies aimed at lowering the sodium content of processed foods have the potential to decrease sodium in the food supply, thereby decreasing population wide sodium consumption. Even small decreases in diastolic blood pressure could reduce the prevalence of hypertension by 17% (Cook <em>et al.</em>, 2001). While decreasing sodium intake invariably decreases the risk of hypertension (World Health Organization, 2003), the totality of existing evidence suggests that low sodium intakes are necessary for the greatest protection against high blood pressure and development of cardiovascular disease. The mechanism of hypertension resulting from the excessive consumption of salt and it’s retention in the body which stimulates the sympathetic nervous system in the brain to increase adrenaline production. The increased adrenalin being circulated throughout the body causes the arteries to constrict which results in resistance to blood flow and a decrease in circulatory volume. (INTERSALT Cooperative Research Group, 2008).</p><p>&nbsp;</p><p><strong>1.1.3 &nbsp; &nbsp; Physiological Roles of Sodium</strong></p><p>Sodium is responsible for regulating extracellular volume, maintaining acid-base balance, neural transmission, renal function, cardiac output and myocytic contraction (Dotsch <em>et al.</em>, 2009). While there is variability in individual sodium requirements the World Health Organization recommends that an adult adequate sodium intake is &lt;87 mM/day (&lt;5g) (World Health Organization, 2003). The average US sodium intake is estimated to be 140-160 mM/day (8-9.5 g/day) (Wright <em>et al.</em>, 2003) and United Kingdom (161 mM/day (9.5g/day). These show that Nigerians consume high level of sodium more than the required quantity for a healthy life (Ukoh <em>et al.,</em>&nbsp;2005).</p><p><strong>&nbsp;</strong></p><p><strong>1.1.4 &nbsp; Health Effects of Sodium</strong></p><p>Health hazards of excessive consumption of sodium in the diet.</p><p><strong>&nbsp;</strong></p><p><strong>1.2 &nbsp; &nbsp; &nbsp; Blood Pressure</strong></p><p>The relationship between sodium intake and blood pressure is well established. Numerous systematic reviews and meta-analysis have been found to support a positive linear association between sodium intake and increasing blood pressure (INTERSALT Cooperative Research Group, 2002). This association was depicted in the large worldwide epidemiological study (INTERSALT) which reported the relationship between sodium and potassium excretion and blood pressure of 10,079 men and women across 52 centers. A significant positive linear relationship was found between sodium intake and systolic blood pressure when adjusted for age, sex, BMI and alcohol consumption (P&lt;0.001) (INTERSALT Cooperative Research Group, 2002). The linear relationship is supported by another meta-analysis which illustrates significant reduction in blood pressure with a decline in sodium intake. He and Mac Gregor (2002) found that sodium decrease by 78 mM/day (1.8g/day) in hypertensive individuals equated with 4.96mmH fall in systolic blood pressure (P&lt;0.001). In addition, in normotensive individuals 74mmol/day (1.7g/day) reduction in sodium caused a decrease of 2.03mmHg (P&lt;0.001). The meta-analysis findings are supported by previous conclusions that a reduction in sodium decreases the affect of hypertension in individuals to a greater degree. (Geleijnse <em>et al</em>., 2001). Furthermore, these findings were based on modest sodium reduced diets in adults over a minimum intervention period of four weeks which demonstrates that there is likely to be a long term effect of sodium reduction on blood pressure.</p><p><strong>&nbsp;</strong></p><p><strong>1.2.1 &nbsp; &nbsp; &nbsp; Cardiovascular Disease </strong></p><p>High blood pressure is a strong risk factor for cardiovascular disease and stroke (World Health Organization, 2002). It has been estimated that a decrease in systolic blood pressure of 2mmHg would result in a 4 % reduction in cardiovascular disease risk and overall mortality by 3% (Chobanian <em>et al</em>., 2003). Studies linking sodium intake and reduced cardiovascular disease risk have shown conflicting results. A possible reason for this is the inconsistency of definitions used to describe cardiovascular events, different methodological approaches used due to differences in population groups and sodium measurement methods (Hooper <em>et al</em>., 2002). However, a meta-analysis study of 14 prospective subjects shows an association between higher sodium intake and cardiovascular disease risk (Strazzullo <em>et al.,</em>&nbsp;2009).</p><p><strong>&nbsp;</strong></p><p><strong>1.2.2 Stroke</strong></p><p>A meta-analysis of prospective studies on the effects of sodium intake on stroke and cardiovascular disease illustrated that a high sodium intake was associated with greater risk of stroke (P=0.007) (Strazzullo <em>et al</em>., 2009). Results from prospective studies of stroke risk and potassium intake have shown inconsistent findings however, majority supports a direct relationship between stroke risk and increased dietary sodium intake. Epidemiologic follow-up study of 9805 men and women who participated in NHANES, it was found that those who had decrease sodium intake had 5% risk of stroke compared to people with high sodium intake who had 30% risk of stroke (Bazzano <em>et al</em>., 2001).</p><p>&nbsp;</p><p><strong>1.3 &nbsp; &nbsp;Risk Factors of Hypertension </strong></p><p>Research has demonstrated that many factors including age, gender, genetic, diet, smoking and alcohol have effect on hypertension. Some of these effects are as follows:</p><p><strong>&nbsp;</strong></p><p><strong>&nbsp;</strong></p><p><strong>&nbsp;</strong></p><p><strong>1.3.1 &nbsp; Age and Gender</strong></p><p>Increased age and gender difference have been shown as risk factors for cardiovascular diseases (National Heart Foundation of Australia 2002). Males have a gene that influences hypertension more than females, when compared at the same age. Interestingly, however in postmenopausal women and men of the same age, there is no difference in findings (Williams <em>et al.,</em>&nbsp;2000). A study based on a semi-rural Michigan population examined ambulatory blood pressure, related to the effects of age and sex, in 131 patients who had more than two prior office diastolic blood pressure measurements greater than 90 mmHg and less than 115 mmHg. Blood pressure measurements were taken every 10 to 60 minutes over a 24 hour period using the Space Labs 90207 computerized ambulatory blood pressure monitor. The results showed that patients aged 65 years or over had a higher mean systolic and lower mean diastolic blood pressure (p &lt; 0.001) in the office than those aged less than 65 years. Office mean arterial blood pressures were also higher (p &lt; 0.001) in the older patients. For mean ambulatory blood pressure, older patients had higher mean ambulatory systolic blood pressures than the younger age group, but there were no differences in mean ambulatory diastolic blood pressure between the two groups. Men had higher mean ambulatory diastolic and mean arterial blood pressures than women. However, women had higher systolic (p &lt; 0.008) and mean arterial office blood pressures than men (Khoury <em>et al.,</em>&nbsp;2007).</p><p>&nbsp;</p><p>A similar result was gained in a study of 24 hour ambulatory blood pressure monitoring in 352 healthy Danish subjects aged 20 to 79 years. These participants were divided into groups of 25 to 30 subjects, of each sex, across all age groups. Blood pressure monitoring was measured on the left arm every 15 minutes from 7am to 11pm and every 30 minutes from 11pm to 7am. The study found that systolic blood pressure increased only slightly with age and was significantly higher in men than in women. On the other hand, the diastolic blood pressure increased only slightly with age in both sexes until the 50 to 59 years age group, declined thereafter and was not statistically different between sexes (Wiinberg <em>et al.,</em>&nbsp;2003).</p><p>&nbsp;</p><p>Research in animals also supports these findings. In one study, blood pressure and heart rates were measured continuously at ten minute intervals for one week in six-month-old spontaneously hypertensive and normotensive rats, using biotelemetry transmitters implanted in the abdominal cavity with the pressure-sensing catheter inserted into the descending aorta below the renal artery. The study showed that male hypertensive rats had significantly higher systolic and diastolic blood pressures compared with hypertensive female rats. Normotensive male and female rats had similar diastolic blood pressure, but males had slightly higher systolic blood pressure than females (Maris <em>et al</em>., 2005).</p><p>&nbsp;</p><p>In summary, males have higher systolic blood pressure than females of the same age and systolic blood pressure in both sexes increases with age while diastolic blood pressure is likely to be similar in both sexes at the same age. &nbsp;<strong>&nbsp;</strong></p><p><strong>&nbsp;</strong></p><p><strong>1.3.2 &nbsp;Genetics</strong></p><p>Genetics is also claimed to contribute to hypertension. A study of 591 Japanese participants, aged 20 to 59 years, showed that family history was strongly related to the incidence of hypertension especially in older people (Naruse <em>et al</em>., 2008). It has been shown that in humans, chromosome 17q is associated with the incidence of hypertension (Baima and Beaucham, 2004), and also that the Gsα gene (Gs protein α-subunit) is a factor in blood pressure changes (Jia <em>et al</em>., 2009).</p><p>&nbsp;</p><p>Another study found that genes were related to a change of blood pressure in between 30% and 50% of individuals (Dominiczak <em>et al</em>., 2000). A study of the genetic effects on hypertension in 6000 British patients found approximately 3.5 times the risk for hypertension as a sibling of hypertensive person, compared with the risk in the general population (Brown, 2006). Data showed that the gene identified as influencing hypertension was found more frequently in hypertensive than normotensive people, and more frequently in normotensive people with hypertensive parents than in those with normotensive parents. In addition, study also found this gene more often in hypertensive siblings (Williams <em>et al</em>., 2000).</p><p>&nbsp;</p><p>In animal trials, it was found that, compared to normotensive rats, hypertensive rats displayed abnormal growth and death of vascular smooth muscle cells resulting from DNA synthesis and apoptosis. Research thus demonstrates that the risk for hypertension can be passed on by hereditary means (Devine <em>et al</em>., 2000).</p><p>&nbsp;</p><p><strong>1.3.3 &nbsp; Diet and Weight</strong></p><p>Consumption of food high in saturated fat, salt or sodium, the level of alcohol intake, and weight gain play an important role in contributing to hypertension (Breien and Marshall, 2000). Australian Institute of Health and Welfare (2004) concluded that obesity, saturated fat intake and consumption of food high in salt or sodium contribute to the incidence of hypertension.</p><p><strong>&nbsp;</strong></p><p><strong>1.3.4 &nbsp; Obesity and Body Mass Index</strong></p><p>As the body mass index increases, blood pressure also increases. Research found that body mass index was a contributory factor for high blood pressure (Kotsis <em>et</em>&nbsp;<em>al</em>., 2005). A cohort study of 300 Japanese-Americans, using a 10 to 11 year follow-up, found that intra-abdominal fat measured using computed tomography was significantly related to hypertension (Hayashi <em>et al</em>., 2004). A similar result was found by Poirier <em>et al. </em>(2005). This study supported the finding that abdominal obesity as measured by waist circumference related to the increase of systolic blood pressure in both sexes. Another study by Niskanishi <em>et al</em>. (2004) showed that an increase in waist circumference was strongly associated with the development of hypertension. This cohort study investigated the effects of abdominal obesity and smoking on the development of hypertension in 379 middle-aged normotensive men over an 11 year follow-up period. It found that 124 participants (33%) developed hypertension factors which substantially relate to the incidence of hypertension were cigarette smoking and waist circumference. Singh <em>et al</em>. (2007) studied 984 Indian men and 951 Indian women to find the risk factors for hypertension. The study found that being overweight or obese and living a sedentary lifestyle were significant risk factors for hypertension. Obesity not only significantly increased systolic blood pressure but also decreased insulin sensitivity and vasodilatation (De Jong <em>et al</em>., 2004). Furthermore, an additional study in the area showed that an increase in body mass index and systolic blood pressure contributed to deaths in both genders, but especially in men (Bender <em>et al.,</em>&nbsp;2002). There is strong evidence that overweight is a significant risk factor for hypertension.</p><p><strong>&nbsp;</strong></p><p><strong>1.3.5 &nbsp; Consumption of Food High in Sodium </strong></p><p>High sodium intake is found to be a factor influencing hypertension development. In animal trials, it was found that a high sodium intake contributed to an impairment of renal blood flow, a decrease of the glomerular filtration rate and filtration fraction, and also induced albuminuria and hypertension in rats (Sander <em>et al.,</em>&nbsp;2005). A similar result was detailed in Yu <em>et al. </em>study (2007) which indicated that a high salt diet caused fibrosis and hypertrophy in the left ventricle and kidney in both hypertensive and normotensive rats. In a human study, high sodium intake was related to an increase in systolic blood pressure (Hajjar &nbsp;<em>et al.,</em>&nbsp;2001) and also contributed to hypertensive renal disease, cerebrovascular disease and impairment in the elasticity of large arteries (Schmieder and Matthew, 2000).</p><p>&nbsp;</p><p><strong>1.3.6. &nbsp; Alcohol Consumption</strong></p><p>Several studies have demonstrated a non-linear relationship between alcohol and blood pressure. Both blood pressure and the heart rate significantly increased in healthy normotensive men after drinking 40 grams of red wine or beer (Ziikens <em>et</em>&nbsp;<em>al</em>., 2005). In a study by Ashton and Wood, (2000), the risk of hypertension was also found to increase in people who drank more than 15 alcoholic units a week. Other studies have found that drinking more than 210g alcohol a week induced hypertension (Fuches <em>et al</em>., 2001), especially drinking every day or drinking without food (Stranges <em>et al</em>., 2004). Consumption of large amounts of alcohol contributes to other health issues.</p><p>&nbsp;</p><p>Reynolds <em>et al</em>. (2003) found that heavy alcohol consumption (more than 60g of alcohol a day) increased the incidence of stroke, however light to moderate consumption of alcohol (less than 15 units a week) decreased the incidence of cerebrovascular accident or cerebrovascular disease (Malinski &nbsp;<em>et al</em>., 2004). Seminke <em>et al</em>. (2005) found that drinking less than 80g per day of alcohol helped to decrease the thickness of the carotid artery in men, resulting in a decreased incidence of cerebrovascular disease and stroke. Moderate wine consumption (less than 60g of alcohol a day) has been demonstrated to decrease deaths in patients with hypertension (Renaud <em>et al</em>., 2004).</p><p>&nbsp;</p><p>In conclusion, excess alcohol consumption is related to high blood pressure and its complications, whereas light to moderate alcohol consumption is a factor in maintaining good health. This may be particularly relevant in individuals where high alcohol intake is linked to poor nutrition, obesity and other risk factors such as smoking.</p><p><strong>&nbsp;</strong></p><p><strong>1.3.7 &nbsp; Smoking </strong></p><p>Smoking plays a role as a risk factor for hypertension. A study of the effects of heavy smoking on blood pressure was conducted on 16 normotensive smokers. Ten participants were asked to smoke one cigarette every 15 minutes for one hour, then no cigarettes for one hour. Their blood pressure and heart rates were continuously monitored during the smoking period and during the non-smoking hour. Six other participants were asked to smoke two cigarettes per hour for eight hours. Their blood pressure and heart rates were monitored every ten minutes in ambulatory conditions using the Finapres device. The results showed that blood pressure and heart rates were persistently higher during the smoking times than the non-smoking times in both groups (Groppelli <em>et al</em>., 2001).</p><p>&nbsp;</p><p>Another study of the relationship between smoking and hypertension in 12 417 men from 10 medical centers in Western and Central France found that smokers had significantly greater risk of hypertension compared to non-smokers (Halimi <em>et al.,</em>&nbsp;2002). Conversely, the two studies showed that smoking had some positive effects on blood pressure.</p><p>&nbsp;</p><p>Primatesta <em>et al</em>. (2001) studied the relationship between smoking and blood pressure and found that smoking caused high systolic blood pressure only in men aged more than 45 years. Women who were light smokers (up to nine cigarettes a day) had lower systolic blood pressure than those who were heavy smokers or who did not smoke.</p><p>Another study found an inverse association between smoking and blood pressure in 352 participants, including 161 smokers. Smokers, as compared with non-smokers had statistically significant lower clinical blood pressure, day ambulatory blood pressure, and night ambulatory blood pressure (Mikkelsen <em>et al</em>., 2007). Although it cannot be assumed from these studies that cigarette smoking contributes to hypertension, smoking in patients with hypertension contributes to complications such as thickness, narrowness and stiffness of the carotid artery (Liang, 2007), subarachnoid hemorrhage (Feigin <em>et al</em>., 2001), and decreased lifespan (Simons, 2005).</p><p><strong>1.3.8. &nbsp; Lack of Activity</strong></p><p>A decrease in daily activity is related to hypertension. A seven year study of 2548 middle-aged Japanese men who either had no hypertension or took hypertensive drugs assessed the relationship between daily activities and the risk of hypertension. The study found that daily activity was inversely related to the incidence of hypertension (Nakanishi, 2005). The same result was found by Singh and Stamler (2007) study of 984 men and 951 women in North India. The authors concluded that a sedentary lifestyle was an important risk factor for hypertension.</p><p><strong>&nbsp;</strong></p><p><strong>1.3.9 &nbsp;Co-morbidity</strong></p><p>Many clinical conditions such as diabetes, cerebrovascular disease, heart disease and chronic kidney disease are co-morbidities of hypertension. However, the most common causative co-morbidity of hypertension is diabetes mellitus. The diabetes disorder induces two times the risk of vascular diseases including coronary artery disease, stroke and peripheral vascular disease (Manica, 2002). Patients with hypertension and diabetes mellitus are more likely to have chronic kidney disease and end-stage renal disease contributing to increasing blood pressure (Lea and Nicholas, 2002).</p><p><strong>&nbsp;</strong></p><p><strong>1.4 &nbsp; Mediating Factors for Hypertension</strong></p><p>In addition to the risk factors discussed above, there are mediating factors which affect the lifestyle or quality of life in patients with hypertension. These elements include economic factors, personality or stress and medications.</p><p><strong>1.4.1 &nbsp; Economic Factors</strong></p><p>Chronic diseases, incur costs for drugs, health insurance, medical consultations, laboratory tests, transportation and food are some challenges of low socioeconomic hypertensive individuals (Costa <em>et al</em>., 2002). Low socio-economic status and financial difficulties were found to be associated with high blood pressure. Kalimo and Vuori (2001) outlined the negative relationship between socio-economic status and hypertension. This study was undertaken in an urban area of Jamaica, a middle-income developing country. It was found that blood pressure was substantially higher in poor men with a low level of education. Conversely, women with a high income experienced higher blood pressure than those with a low income (Shaw <em>et al.,</em>&nbsp;2003)</p> <br><p></p>