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ESTIMATION OF DAILY SALT INTAKE OF HEALTHY AMBULANT NIGERIAN ADULTS

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ABSTRACT

Data on the current levels of sodium consumption of Nigerian  adults are  urgently needed  to  determine  the  contribution  of  dietary  sodium  as  a  risk  factor  in  the increasing incidence of hypertension and related complications  in the country. The aim of this study was  to  estimate  the daily salt  intake of healthy ambulant Nigerian adults  using  the  24-hour  urinary  sodium ion excretion method (the gold standard) and  spot urine  sodium  ion excretion  method  (a proposed  convenient  alternative). Eighty  adult  Nigerians  aged  between  20  and  50 years  made  up  of 60% males and  40%  females  were  the  subjects  that  provided  24-hour  urine  and  spot  urine samples.  Urinary  sodium  excretion  was  estimated  using  the  atomic  absorption spectrophotometer (AAS). Measured 24-hour urinary sodium excretions for male and female  subjects  were 4.7+0.5  and 4.0+0.6  g/day respectively.  This  translates  to a dietary salt intake of 11.8+1.3 g/day for male subjects and 10.1+1.5 g/day for female subjects. A significant decrease (p<0.01) was observed between the values obtained by 24-hour  urinary  sodium  excretion  method  and  spot  urinary  sodium  excretion method. Estimated 24-hour urinary sodium ion excretion positively correlated (r=+61) with spot urinary sodium excretion.  Age  dependent  increase was observed  in both measured and estimated 24-hour urinary sodium ion excretion. Systolic and diastolic blood pressure  increased  significantly (p<0.05) with increase  in measured  24-hour urinary sodium ion excretion. Based on these results, the salt intake of all the subjects as determined  by both methods far exceeded the recommended daily salt limit of < 5.0g/day. The positive correlation (r= +0.61) between the results obtained from both methods suggests that notwithstanding the differences between the values obtained, the spot urinary excretion method  can be used to determine  the daily  dietary salt intake of Nigerians.

CHAPTER ONE

INTRODUCTION

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).

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.

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  et  al.,  2004),  decreased  bone  mineral  density (Devine et al., 2000) and obesity (He et al., 2008).

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 et al., 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).

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 et al., 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 et al., 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).

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 (<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.

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 et al., 2004). This research is aimed to investigate what is known from previous studies relating to the relationship between hypertension and:

 Risk  factors  including  age,  gender,  genetics,  diet,  and  weight,   alcohol, smoking, lack of activity and co- morbidity

 Mediating   factors  including   economic  factor,  stress  or  personality   and medication

 Management of hypertension through life style modification

 Complimentary therapy: foot reflexology and foot message

1.1 Sodium

1.1.1   Source of Dietary Sodium in the Body

In developed countries, large proportion of the sodium ingested is added (as sodium chloride) in food manufactured and foods eaten away from home. Ralph et al., 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 < 2 mg (< 0.1 mmol).

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).

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).

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 < 1–3 times per week (Schmidt  et al., 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     25% from various sauces, including soy sauce and miso (in Japan).

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 et al., 2006) .

1.1.2     Significance of Sodium

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 et al., 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).

1.1.3     Physiological Roles of Sodium

Sodium  is  responsible  for  regulating  extracellular  volume,  maintaining  acid-base balance, neural transmission, renal function, cardiac output and myocytic contraction (Dotsch et al., 2009). While there is variability in individual sodium requirements the World Health Organization recommends that an adult adequate sodium intake is <87 mM/day (<5g) (World Health Organization, 2003). The average US sodium intake is estimated  to be 140-160  mM/day (8-9.5  g/day)  (Wright  et al., 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 et al., 2005).

1.1.4    Health Effects of Sodium

Health hazards of excessive consumption of sodium in the diet.

1.2       Blood Pressure

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<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<0.001).  In addition,  in normotensive  individuals  74mmol/day  (1.7g/day)  reduction  in sodium caused a decrease of 2.03mmHg (P<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 et al., 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.

1.2.1       Cardiovascular Disease

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 et al.,  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   et  al.,  2002). However,  a  meta-analysis  study of  14  prospective  subjects  shows  an association between  higher  sodium  intake  and  cardiovascular  disease  risk  (Strazzullo  et  al., 2009).

1.2.2  Stroke

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 et al., 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 et al., 2001).

1.3    Risk Factors of Hypertension

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:

1.3.1   Age and Gender

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 et al., 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 < 0.001) in the office than those aged less than 65 years. Office mean arterial blood pressures were also higher (p < 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 < 0.008) and mean arterial office blood pressures than men (Khoury et al., 2007).

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 et al., 2003).

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  biotelemetr 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 et al., 2005).

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.

1.3.2  Genetics

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 et al., 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 et al., 2009).

Another study found that genes were related to a change of blood pressure in between 30% and 50% of individuals (Dominiczak et al., 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 et al., 2000).

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 et al., 2000).

1.3.3   Diet and Weight

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.

1.3.4   Obesity and Body Mass Index

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  et al.,

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 et al., 2004).    A  similar  result  was found by Poirier et al. (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 et al. (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 et al. (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 et al., 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 et al., 2002). There is strong evidence that overweight is a significant risk factor for hypertension.

1.3.5   Consumption of Food High in Sodium

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 et al., 2005). A similar result was detailed in Yu et al. 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    et  al., 2001)  and  also  contributed  to hypertensive renal disease,   cerebrovascular disease and impairment in the elasticity of large arteries (Schmieder and Matthew, 2000).

1.3.6.   Alcohol Consumption

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 et al.,

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  et  al.,  2001),  especially  drinking  every  day  or  drinking  without  food (Stranges et al., 2004). Consumption of large amounts of alcohol contributes to other health issues.

Reynolds  et al.  (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  et al., 2004).  Seminke et al. (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 et al., 2004).

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.

1.3.7    Smoking

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 et al., 2001).

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 et al.,

2002). Conversely, the two studies showed that smoking had some positive effects on blood pressure.

Primatesta et al. (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. 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 et al., 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  et  al.,  2001),  and  decreased  lifespan  (Simons, 2005).

1.3.8.   Lack of Activity

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.

1.3.9  Co-morbidity

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).

1.4    Mediating Factors for Hypertension

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.

1.4.1   Economic Factors

Chronic  diseases,  incur  costs  for  drugs,  health  insurance,  medical  consultations, laboratory tests, transportation and food are some challenges of low socioeconomic hypertensive   individuals  (Costa  et  al.,  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 et al., 2003)

1.4.2   Stress and Personality

Stress is claimed to contribute to development of hypertension through its stimulation of  the  sympathetic  nervous  system  (Lieberman  and  Neal,  2001).  A  longitudinal observation study of stress on blood pressure in 144 nuns (Intervention Group) and

138 females from the general population (Control Group) showed that during the 30 year follow-up period, there was a statistically significant difference in blood pressure between the two groups. Compared to the control group, none of the nuns showed an increase in diastolic blood pressure over 90 mm Hg where blood pressure increased in the control group (Timo et al., 2010).  Chronic stress in caregivers combined with low expression  of this stress is also  risk factors for  hypertension  (Shaw  et al., 2003). Particularly  in  women,  suppression  of  anger  increased  systolic  blood  pressure (Helmers,  2000). Stress from work  contributed  to the risk of hypertension  in men (Pickering,  2006).  Unemployment  and  job  insecurity  were  also  associated  with increased  blood  pressure in men (Smith and Kaplan,  2001). Some studies did not support   the   relationship   between   hypertension,   personality   and   psychological characteristics such as Type A behavior, anger, anxiety and depression. Friedman et al. (2001), when studying a group of mild hypertensive men and normotensive men aged   30  to  60   years,   found   no   difference   in  personality   and   psychological characteristics. On the other hand, highly defensive people tended to have high blood pressure. A study by Rutledge and Linda (2003) demonstrated that during three years of study, high-defensive participants (a total of 125  American participants) showed higher ambulatory blood pressure than in low-defensive group.  In summary, although the research is mixed, there is  evidence  that stress is an important  risk factor for hypertension.

1.4.3   Hypertension Medications

Hypertensive drugs are useful and effective in treating hypertension and preventing its complications, particularly in men (Gueyffier, 2007). It was reported that the rate of using antihypertensive drugs in hypertensive Americans was higher because of their effectiveness (Glynn et al., 2005).  Death rates and complication rates from stroke and coronary heart disease were decreased by using antihypertensive drugs (Glynn et al.,

2005). However,  although  hypertensive  drugs do reduce blood  pressure, they  also have many side effects which can affect the quality of life of individuals taking it.

1.4.3.1   Diuretics

Low-dose  diuretics  are recommended  as the drug of choice  to  treat  hypertension (Fretheim, 2003). Diuretics are more effective in reducing blood pressure than other antihypertensive drugs such as beta blockers (Antonios et al., 2000). They also help to reduce health costs since they are less expensive  than other antihypertensive  drugs (Aaserud and Oxman, 2003).  Thiazide diuretics not only effectively decrease blood pressure but also help to decrease the risk of cardiovascular morbidity and mortality by mean of a decrease in left ventricular  mass (Gotidiener  et al., 2007). Low-dose thiazide (25mg/day) combined with potassium sparer’s help to reduce the incidence of cardiac arrest (Siscovick et al., 2004). Diuretics can cause ventricular arrhythmias and sudden  death   (Hoes   et   al.,  2005).   Glucose   intolerance   and  hyperinsulinemia particularly when combined with angiotensin converting enzyme inhibitors (example captopril)  (Hunter  et  al.,  2001).  In  contrast,  however,  Gress  et  al.  (2002)  study showed  that thiazide diuretics did not induce diabetes in patients with hypertension. Hypercholesterolemia  is another  side effect of thiazides  and should  be avoided  in patients with hypertension and hyperlipidaemia (Beevers and Marshall, 2005). Other side   effects   of   diuretics   include   hypokalemia,   hyperuricemia,   hypercalcemia, hyponatremia,  hypomagnesemia,  erectile dysfunction  (Lieberman  and Neal, 2001). Shahinfar  et  al.  (2007)  found  that  to  reduce  side  effects   (hyperuricemia)   on angiotensin II receptor blockers, losartan is recommended as a combination drug.

1.4.3.2   Adrenergic inhibitors

Adrenergic   inhibitors   have   been   found   to   reduce   blood   pressure   effectively (Dickerson and Gibson, 2005). This group is made up of peripheral inhibitors, central alpha 2 (α2) agonists, alpha blockers and beta blockers. The side effects of peripheral inhibitors  are nasal  congestion,  depression,  an increase  in gastric acid,  orthostatic hypotension, diarrhea, fluid retention and failure of ejaculation (Lieberman and Neal,

2001).

Central α2 agonists may cause sedation, a dry mouth and depression. Many patients experience  hypotension  in addition to sodium and water  retention  (Dickerson  and Gibson, 2005). Alpha blockers can cause headache, drowsiness, fatigue and weakness (Lieberman  and Neal, 2001). Beta blockers were reported  to reduce mortality and morbidity  in older  patients  with  hypertension  (Dickerson  and  Gibson,  2005),  the

symptoms  of angina  pectoris  (Wright,  2000)  and  coronary  events  (Berglund  and Tuomilehto, 2002). Therefore, these drugs are suitable for patients with hypertension and myocardial infarction or angina and heart failure (Dickerson and Gibson, 2005). However,  these  drugs  can  cause  bronchospasm,  hypoglycemia,  depression,  poor peripheral circulation,  insomnia,  bradycardia,  fatigue, decreased  exercise tolerance, hypertriglyceridemia, and decreased HDL cholesterol (Lieberman and Neal, 2001). Shorr  et  al.  (2000)  found  no   significant  increase  or  decrease  in  the  risk  of hypoglycemia when using these drugs in hypertensive diabetic patients. In contrast, another  study by  Gress  et al.  (2002)  found  that  beta blockers  contributed  to  the development of diabetes in patients with hypertension.

1.4.3.3   Vasodilators

This  group  consists  of  direct  vasodilators,  calcium  channel  blockers,  angiotensin converting  enzyme  (ACE)  inhibitors  and  angiotensin  II  receptor  blockers.  Direct vasodilators  cause  headaches,  tachycardia,   flushing,   hirsutism   and  a  lupus-like syndrome (Lieberman and Neal, 2001).

Calcium channel blockers were found to be the first-line drugs for African-Americans as opposed to thiazides (Sareli and Keast 2001). These  drugs may induce nausea, headache, hypotension, palpitation, conduction defects, flush, local ankle oedema and constipation (Lieberman and Neal, 2001).  ACE inhibitors and angiotensin II receptor blockers  significantly  decreased  clinical  and  ambulatory  blood  pressure  and  also significantly decreased albuminuria  (Lacourciere  et al., 2000).   However, the ACE inhibitors significantly increased  the incidence of cough (Lacourciere et al., 2000), hypotension,  loss of taste,  skin rash, a rare leukopenia, hypoglycemia and impaired renal function (Lieberman and Neal, 2001).

In addition, angiotensin II receptor blockers contribute to hyperkalemia, hypotension, renal  impairment  and,  rarely,  angioedema  (Lieberman  and  Neal,  2001).  Using  a combination of hypertensive drugs is recommended in patients with hypertension and co-morbidities  or risk factors (Dickerson and Gibson,  2005). Several studies  have shown that using a combination of drugs significantly reduced blood pressure (Ajayi and Ridder 2007). In high risk patients, such as black Africans, combination therapy is significantly more effective than single drug therapy (Ajayi and Ridder, 2007).

1.5      Management of Hypertension

1.5.1.   Lifestyle Modifications

An  unhealthy  lifestyle  can  cause  hypertension,  so  lifestyle  modifications  are  an essential  component  of hypertensive  management  (Necter  et al., 2003).  A  United States study of factors associated with hypertension control in the general population examined    3077   non-Hispanic    white   participants,    1742    non-Hispanic    black participants  and 1067 Mexican-Americans  participants aged 18 years or older with hypertension. It found that the factors influencing hypertension control were lifestyle modifications, including dietary sodium reduction, weight loss and exercise (He and Mac Gregor, 2002).

1.5.2    Weight Loss

Weight gain causes higher blood pressure and conversely, weight loss causes lower blood pressure. There are strong positive correlations between the degree of adiposity and fasting triglycerides.  Plasma cholesterol is also positively correlated with body mass index, although less strongly than triglycerides (Thompson, 1999).

A study of the long term effects of weight loss and dietary sodium reduction  was undertaken  on  181  men  and  women  aged  30  to  54  years  who  participated  in hypertension prevention trials in Baltimore in 1987-88. All participants had a diastolic blood pressure of 80 to 89 mmHg and systolic blood pressure less than 160 mmHg. Participants were randomly assigned to one of  two  18-month lifestyle modification interventions including a weight loss group and a dietary sodium reduction group – or to a control group. Over a seven year  follow-up, blood pressure was measured by blinded observers using a random-zero sphygmomanometer.  The result showed that the weight  loss  intervention  program  was associated  with a 77% reduction  in the incidence  of  hypertension,  whereas  the  sodium  reduction  program  did  not  reach statistical significance in reducing the incidence of hypertension (He and MacGregor, 2002). A meta-analysis of 25 randomized controlled trials to estimate the effects of weight reduction on blood pressure in 4874 participants showed that systolic blood pressure and diastolic blood pressure could be reduced by between -1.05  and -0.92 mmHg respectively for each kilogram of weight loss (Necter et al., 2003).


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