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.
TABLE OF CONTENTS
PAGES
Title Page… … … … … … … … … i
Certification… … … … … … … … ii
Dedication… … … … … … … … … iii
Acknowledgment… … … … … … … … iv
Abstract… … … … … … … … … v
Table of Contents… … … … … … … … vi List of Figures… … … … … … … … viii
List of Tables… … … … … … … … ix
List of Abbreviations… … … … … … … x
CHAPTER ONE: INTRODUCTION
1.1 Sodium …. …. …. …. …. …. …. 3
1.1.1 Source of dietary sodium in the body… … … … 3
1.1.2 Significance of sodium… … … … … … 4
1.1.3 Physiological role of sodium … … … … … 5
1.1.4 Health effect of sodium… … … … … … 5
1.2 Blood pressure … … … … … …. 5
1.2.1 Cardiovascular disease… … … … … … 6
1.2.2 Stroke …. …. …. …. …. …. …. 6
1.3 Risk factors of hypertension …. …. …. …. …. 6
1.3.1 Age and gender …. …. …. …. …. …. 7
1.3.2 Genetics …. …. …. …. …. …. …. 8
1.3.3 Diet and weight …. …. …. …. …. …. 9
1.3.4 Obesity and body mass index …. …. …. … 9
1.3.5 Consumption of food high in sodium …. …… …. 9
1.3.6 Alcohol consumption …. …. …. …. …. 10
1.3.7 Smoking …. ……. ….. …. …. 11
1.3.8 Lack of activity …. ….. ….. ….. …. 12
1.3.9 Co-morbidity ….. ….. ….. …. … 12
1.4 Mediating factors for hypertension… … … … … 12
1.4.1 Economic factor …. ….. …. …. …. 12
1.4.2 Stress and personality …. … …. … ….. …. 13
1.4.3 Hypertension medication ….. …… …… …… …… …. 13
1.4.3.1 Diuretics …. ……. ….. …. ….. ….. …… ….. 14
1.4.3.2 Adrenergic inhibitors … ….. ….. ….. ….. ….. 14
1.4.3.3 Vasodilators …. ……. …… ….. ….. …. …. 15
1.5 Management of hypertension … … … … … 16
1.5.1 Lifestyle modifications… … … … … … 16
1.5.2 Weight loss …. ….. ….. ….. ….. ….. …. 16
1.5.3 Exercise …. …. ….. …. …. …… .. 17
1.5.4 Dietary sodium reduction …. ….. ….. ….. …. 17
1.5.5 Reduction in alcohol intake and smoking ….. …. ….. 18
1.6 Complimentary therapies… … … … … … 19
1.6.1 Foot reflexology… … … … … … … 19
1.6.2 Effect of food reflexology on hypertension… … … 20
1.6.3 Effect on anxiety and pain… … … … … … 21
1.6.4 Foot message… … … … … … … … 24
1.7 Aim and objectives of the Study …. …. …. ….. ….. 27
1.7.1 Aim of the Study …. ….. …. …. …. ….. …… ….. . 27
1.7.2 Specific objectives of the Study …. ….. ….. ….. …… …. 27
CHAPTER TWO: MATERIALS AND METHODS
2.1 Materials … … … … … … … 28
2.1.1 Subjects … … … … … … … 28
2.1.2 Inclusion criteria… … … … … … … 28
2.1.3 Instrument/Equipments… … … … … … 28
2.1.4 Chemicals… … … … … … … … 29
2.2 Methods… … … … … … … … 29
2.2.1 Preparations of Reagents … … … … … 29
2.2.1.1 Sodium Chloride (Concentration) … … … … 29
2.2.1.2 Alkaline Picric Acid … … … … … 29
2.2.1.3 Sulfuric Acid … … … … … … 29
2.2.1.4 Sodium Hydroxide … … … … … … 29
2.2.1.5 Sodium Tungstate (Concentration) … … … … 29
2.2.1.6 Creatinine Standard … … … … … 29
2.2.2 Urine collection … … … … … … 30
2.2.3 Determination of height and blood pressure … … … 30
2.2.4 Determination of Blood pressure… … … … … 30
2.2.5 Determination of obesity… … … … … … 30
2.2.6 Determination of sodium ion concentration in 24 hour urine… 31
2.2.7 Determination of sodium ion concentration in spot urine… … 31
2.2.8 Determination of 24 hour creatinine concentration … … 31
2.2.9 Determination of creatinine concentration in spot urine… … 31
2.2.10 Statistical analysis… … …… … …… … … 32
CHAPTER THREE: RESULTS
3.1 Baseline characteristics of subjects in measured 24 hour
urinary excretion of sodium by sex aged 20-50 years. … … … 33
3.2 Characteristics of subjects in estimated 24 hour
urinary sodium excretion by sex aged 20-50 years… … … ….. 35
3.3 Relationship between measured and estimated
24 hour urinary sodium excretion (T-Test) … … … … 37
3.4 Group characteristics of subjects
in measured and estimated 24hour urinary sodium excretion … 39
3.5 Mean and correlation coefficient of measured and estimated
24 hour urinary sodium of subjects aged 20-50 years … … 41
3.6 Relationship between systolic blood pressure and
24 hour urinary sodium excretion… … … … … … 43
3.7 Relationship between diastolic blood pressure and 24 hour
sodium excretion… … … … … … … … 45
3.8 Relationship between measured 24 hour urinary sodium
excretion and estimated 24 hour urinary sodium excretion… … 47
3.9 Measured and estimated 24 hour urinary sodium excretion
of subjects with varying age ranges … … … … … 49
3.10 Variation of salt (NaCl) excretion with age ranges …. … … 51
CHAPTER FOUR: DISCUSSION
4.1 Discussion… … … … … …… … … 53
4.2 Conclusion… … … … … … … … 54
4.3 Suggestion for further studies …. …. … … … 54
REFERENCES …. …… ….. ….. ….. ….. …… …… ….. 56
APPENDICES …. ……. ……. …… …… …… ….. ….. … 71
LIST OF FIGURES
Figure 1: Relationship between systolic blood pressure and
24 hour urinary Sodium Excretion of subjects… … … … 44
Figure 2: Relationship between diastolic blood pressure and
24 hour Urinary sodium excretion… … … … …. …. 46
Figure 3: Relationship between measured and estimated 24
hour urinary Sodium excretion of subjects… … … … … 48
Figure 4: Measured and estimated 24 hour urinary sodium
excretion of Participant with varying age ranges… … … … 50
Figure 5: Measured and estimated 24 hour urinary excretion
of sodium chloride of subjects with varying age ranges… … … 52
LIST OF TABLES
Table 1: Baseline characteristics of subjects in measured 24
hour urinary sodium excretion in relation to gender aged 20-50 year… … 34
Table 2: Characteristics of participant in estimated 24 hour
urinary sodium excretion in relation to gender aged 20-50 years… … 36
Table 3: Relationship between measured and estimated
24 hour urinary sodium excretion … … …… 38
Table 4: Group characteristics of subjects
in measured and estimated 24 hour sodium excretion… … 40
Table 5: Mean and correlation of measured and estimated
24 hour urinary sodium excretion of subjects aged 20-50 years… 42
LIST OF ABBREVIATIONS
24HUCr 24- hour urinary creatinine
24HUNa 24- hour urinary sodium
AAS Atomic absorption spectrophotometer
ANOVA: Analysis of variance
BMI Body mass index
cm Centimeter
Cr Creatinine
DBP Diastolic blood pressure
EDTA Ethylene diam amine tetraacetic acid
g/day gramm per day
HCl: Hydrochloric acid
Kg Killogram
Kg/m2 Killogram per meter square
L Liter
M Meter
mg/day Milligram per day
Mg/L Milligram per liter
MmHg Millimeter mercury
mmol/day Mil moles per day
NaCl Sodium chloride
nm Nanometer
SBP Systolic blood pressure
SPSS: Statistical package for social solution
WHO: World Health organization
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) .
