EFFECT OF DIETARY HABITS, DISEASE PATTERNS AND PSYCHOLOGICAL STRESS ON KNOWN ESSENTIAL HYPERTENSIVE IN RIVERS STATE
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EFFECT OF DIETARY HABITS, DISEASE PATTERNS AND PSYCHOLOGICAL STRESS ON KNOWN ESSENTIAL HYPERTENSIVE IN RIVERS STATE
Effect of dietary habits, disease pattern and psychological stress were investigated 342 essential hypertensive in Rivers State (Nigeria). A total of 121 patients were advice to restrict their dietary salt, 97 complied and their mean blood pressure was significantly lowered (P< 0.01). 74 patients who were on normal salt diet had their BP significantly lowered with no further reduction in salt intake (P<0.05). There was a significant decline in BP of patients who were on high vegetable and fruits intakes and salt restrictions (P< 0.01). Subjects were advice to reduce their fat, carbohydrate and salt intakes had their BP also lowered (P< 0.01). The dietary changes were additives to antihypertensive drugs administered. Hypertension predisposes individuals to multiple disease patterns such as stroke, heart attack, renal failure and headache. Cardiovascular diseases, Renal, adrenal medulla and central nervous diseases predispose to hypertension. Psychological stress exacerbated the course of essential hypertension. Emotional disturbances resulted in an elevated blood pressure above pretreatment levels in hypertensive patients.
TABLE OF CONTENTS
Title Page - - - - - - - - - - i
Declaration - - - - - - - - - ii
Dedication - - - - - - - - - iii
Acknowledgement - - - - - - - - iv
Abstract - - - - - - - - - - v
Table of Contents - - - - - - - - vi
List of Figure and Tables - - - - - - - vii
CHAPTER ONE: INTRODUCTION AND LITERATURE REVIEW
1.1 Definition of Essential Hypertension
1.2 Forms of Essential Hypertension
1.3 Pathogenesis of Essential Hypertension
1.4 Effect of Dietary Habits on Essential Hypertensive Subjects
1.5 Disease Patterns
1.6 Effect of Psychological Stress on Essential Hypertensive
CHAPTER TWO: MATERIALS AND METHODS
CHAPTER THREE: RESULTS
3.1 Age and Sex Distribution of Subjects
3.2 Effect of Dietary Habits on Hypertensive Patients
3.3 Statistical Analysis of Effect of Diet on Blood Pressure
3.4 Disease Pattern of the Hypertensive
3.5 Psychological Stress and Essential Hypertension
LIST OF FIGURES AND TABLES
Figure 1 Bar Chart Effect of Dietary Habits on Blood Pressure
Figure 2 Linear Regression Line Graph
Table 1 Age and Sex Distribution of Patterns
Table 2 Blood Pressure of Hypertensive on Salt Restriction
Table 3 Blood Pressure of Hypertensive on Normal Salt Diet
Table 4 Blood Pressure of Subjects on High Salt Diet
Table 5 Blood Pressure of Subjects on Low Fat, Carbohydrate and Salt Diet
Table 6 Mean BP Changes in Groups A, B, C
Table 7 BP of Subjects on High Fruits and Vegetables and Salt Restriction
Table 8 Statistical Table
Table 9 (a -b) Multiple Compares of Groups A, D, E
Table 10 (a - b) Multiple Compares of Group A, B, C
Table 11 Disease Pattern of the Hypertensive
Table 12 Effect of Psychological Stress on BP
INTRODUCTION AND LITERATURE REVIEW
The effect of dietary habit, disease pattern and psychological stress has been investigated in many essential hypertensive patients. Under high dietary sodium the blood of the hypertensive increases. Low or no sodium intake lowers the blood pressure. Also high dietary potassium lowers the blood pressure of the essential hypertensive. Alcohol and cigarette smoking exacerbate the course of hypertension, so does the excessive intake of calories leading to weight gain. High lipid, cholesterol and lipoprotein intake predisposes the essential hypertensive to cardiovascular diseases.
Also the disease patterns of the hypertensive patient have been investigated. Renal diseases, cardiovascular diseases, endocrine and liver and central nervous diseases are frequently seen in hypertensive subjects. Psychological and environmental influences such as family sizes, depressive illness, socio-economic factors have all been shown to exacerbate the course of hypertension. In this study it is aimed at investigating the effect of dietary habits, disease pattern and psychological stress on the course of hypertension.
1.1 ESSENTIAL HYPERTENSION
In 80% patients with elevated blood pressure, the cause to the hypertension is unknown, and they are said to have essential hypertension or primary hypertension or idiopathic hypertension.
There is a good deal of controversy about where to draw the line between normal and elevated blood pressure (hypertension), particularly in older patients. Yet, if one has to investigate or treat subjects with high blood pressure it is necessary to define the condition and the best solution to this problem would be to relate the definition to the clinical sequelae, and to define hypertension as a level of blood pressure at which demonstrable harm occurs. Unfortunately, no such threshold exists. The World Health Organization (WHO) criteria (fifth korotkoff phase) for use in epidemiological studies are given here.
Normal range Equal to or below 140/90
Hypertensive range and above
Border line or Intermittent
Essential hypertension is symptomless disease in its beginning. When symptoms occur they are either psychoneurotic or consequences of the hypertension and thus similar to those of any other patients of similar age and with hypertension of comparable severity. In the early stage, raised arterial pressure is the only positive finding apart from cardiac hypertrophy, which may be present if the pressure is high enough. In particular the urine, intravenous pyelography, blood and renal function test reveal no abnormalities.
The later symptoms represent the consequences of hypertension on brain, fundi, heart and kidney. Essential hypertension represents those subjects in which the genetic and environmental factors raising arterial pressure are at their most potent. It represents a new kind of disease in which the deviation from the norm is quantitative and not qualitative (Pickering). It should be emphasized that essential hypertension is basically a disease of exclusion – the diagnosis can only be established if a primary cause (such as phaeochromocytoma or renal artery stenosis) has been eliminated.
1.2 FORMS OF ESSENTIAL HYPERTENSION
Usually the range of systolic pressures between 140 and 160 and diastolic pressure between 90 – 100 are taken as indicating “Borderline hypertension” and the values above these as indicating “fixed hypertension”. There seem to be certain physiological difference between “Borderline” and “fixed” essential hypertension. In a proportion of patients of “Borderline” hypertension, the plasma noradrenaline and renin activity are both elevated, also there is elevated cardiac output (C.O.). in “fixed” hypertension, by contrast, peripheral resistance is elevated and there is little evidence of such over activity.
The suggestion has been made that borderline hypertension, maintained by a raised C.O. is the earliest phase of essential hypertension. It has also been postulated that peripheral resistance becomes elevated either by auto regulatory control of tissue perfusion or by hypertrophy.
This term has been used for patients whose arterial pressure is sometimes above and sometimes below, particular dividing line that the observer chooses. The name had led to the supposition that in these patients the arterial pressure is unusually variable, and to the consequent idea that the sympathetic nerve is unusually active. Some authors use this term labile hypertension. Patients with labile hypertension have high cardiac output. It has been supposed that labile hypertension, characterized by the unusually variable pressure and a high C.O. represents the first stage in the development of essential hypertension. So called labile hypertension is a good example of an iatrogenic disease (Pickering).
THE “RENIN SUB-GROUPS”
Plasma renin is low in a minority of patients with essential hypertension. The rise in plasma renin produced by a low salt diet or diuretics is more in essential hypertensive than normotensive. Patients with a relatively low plasma renin activity for their 24 hours urinary sodium are classified as having low renin hypertension, and patients whose renin values are relatively high are classified as having “high renin hypertension”. The dividing lines are however, arbitrary.
There are many patients whose plasma renin values are normal on a sodium intake of 100 – 200m mol/day, and whose plasma renin fails to rise when dietary sodium is reduced to 20 mmols/day. These laragh classifies as having low renin hypertension.
Plasma renin levels are frequently abnormal in essential hypertension. This may be due to: Elevation of renal perfusion pressure suppresses renin secretion, enhanced sympathetic activity, and fluid depletion (caused perhaps by perfusion pressure, natriuretic and diuresis) will increase renin. Arteriolar changes induced by hypertension (e.g. hyaline degeneration, fibroid necrosis) may exert an influence upon the responsiveness of the juxtaglomerular baroreceptor. Antihypertensive medication is also important: Diuretics and vasodilators stimulate renin secretion; beta-blockers, clonidine, reserpine, and methyldopa reduce it.
Patients with low renin hypertension tend to be older, whilst the high renin sub group seems to include patients with sympathetic over activity, patients with malignant hypertension and patients with Reno-vascular or renal disease.
Whilst the changes in plasma renin observed in essential hypertension appear to be secondary, they may still be important either because renin is itself a pathogenic (cause) factor or because it is acting as a marker for a fundamental process.
MALIGNANT (ACCELERATED) HYPERTENSION
The malignant or accelerated phase of hypertension may occur in either essential or secondary hypertension. It is characterized by blurring of vision, mental impairment, Hematuria or haematospermia, severe headache, dyspnea. Other characteristic signs are fundal papilledema, retinopathy, cotton wool spots or hemorrhages, hypertensive encephalopathy and stroke, proteinuria, renal failure.
Sometimes, the first sign of the malignant phase is hematuria or sudden appearance of proteinuria. Occasionally, the urine and renal function are both normal.
THE BENIGH PHASES
The benign phase may occur in any type of hypertension, but is especially common in middle aged or elderly subjects and particularly in those with essential hypertension. The arterial pressure is usually lower than in the malignant phase. Woolly exudates and papilledema are not seen. Most commonly the retina shows no abnormality except varying degree of arterial changes or occasionally a venous thrombosis.
1.3 PATHOGENESS OF ESSENTIAL HYPERTENSION
There is now enough evidence to suggest a probable etiology for essential hypertension. There is no doubt at all from human and animal experiments that when arterial pressure is raised for long enough, the rise tends to persist when the initiating stimuli are removed. A lot of hypothesis has been postulated to explain the pathogenesis of hypertension.
Essential hypertension is seen by some workers as the result purely of environmental influences and by others as a genetically (or dietary) determined disease. The most likely explanation is a combination of both, with genetically predisposed individual being particularly susceptiasle to environmental influences. Numerous studies in different communities have shown a positive correlation between BP and salt intake, but variation in other dietary constituents may be important as well as socio-economic factors.
De Wardener and his colleague have extracted a substance from human urine which when injected intravenously cause a transient natriuretic. Hypertensive patients also have an accelerated natriuretic, when given sodium load. An abnormality of Na-transport has recently been found in the erythrocytes of patients with essential hypertension and more important, the same abnormality has been found in some of their normotensive relatives.
FLUID VOLUME HYPOTHESIS
This sought to explain the genesis of essential hypertension in terms of extracellular fluid expansion and increase in cardiac output. A substantial minority (20 – 30%) of essential hypertensive have low circulating renin level and a depressed renin and aldosterone response to sodium depletion (Harris et al 1967, Crone et al 1972) some workers have suggested that the ECF volume of such patients are higher than other hypertensive patients and that the exchangeable sodium values are significantly higher (Jose et al 1970). This is a case of abnormal sodium metabolism (Schalekamp et al 1974, Swales 1975).
An elevated C.O. has been noted in many young borderline hypertensive subjects and some workers believe that this represents the earliest phase of essential hypertension. This could be due to extracellular fluid expansion, just as the initial rise in C.O. in Gold lath hypertension can be attributed to Na – retention. There is however, no evidence for Na-retention at this stage in essential hypertension. Increased capacitance vessel tone or cardio – sympathetic activity may equally explain the rise C.O.
CELL – SALT HYPOTHESIS
It is proposed that in patients with essential hypertension the cell of the vascular smooth muscle contain an excess of sodium, which causes or enhances vasoconstriction. The blood vessel of hypertensive animals have thick wall that contain more sodium and water than the blood vessel of normal animals. These changes might increase resistance and arterial blood pressure in several ways.
The blood cell of patients with essential hypertension contains an abnormal excess Na and inhibition of the pumps activity transporting Na abnormalities is generalized and that their occurrence in vascular smooth muscles causes vasoconstriction and hypertension.
Poston L, Senell et al (1981) reported a circulating Na-transport inhibitor in essential hypertensive. By incubating a normative white cell with that of impaired essential hypertensive, they observed impediment in Na-transport in the WBC of the normotensive. These result shows that the serums of patient with essential hypertension contain a substance which influences Na- transport, and that is Quailing – like activity. These findings support the hypothesis that the rise in BP in patients with essential hypertension is due to an inhibitor which is continually correcting a tendency for Na retention by kidney.
Most body potassium is within the cell and thus, exchangeable and total body ECF K concentration. The inverse correlation of arterial pressure and plasma K concentration is compatible with the cell salt mechanism, since a fall in ECF K produces vasoconstriction, probably by a mechanism similar with essential hypertension in the blood cells of patients with essential hypertension.
DIETARY SALT HYPOTHESIS
Dietary sodium intake has been implicated in the ethology of essential hypertension. It is proposed that the rise in arterial pressure and the prevalence of hypertension results wholly or partly from increased dietary sodium or decreased potassium intake or both.
The dietary salt hypothesis is being debated. The first hypothesis proposed that a high dietary Na-intake raises blood pressure in most people. It follow, if that is correct, that the blood pressure of people within a population will correlate with their Na-intake and that hypertensive subjects will eat and excrete more Na than normal subjects.
The second hypothesis is that Na-intake is sufficient to raise blood pressure but only in a susceptible minority. Thus, two elements namely susceptibility and sufficient Na are need for BP to rise.
One hypothesis which implicates sodium in an initiating role is that of Dahl and his Co-workers. Dahl developed a strain of rats which developed fixed hypertension upon a salt-supplemented diet, and in which hypertension persisted even when sodium intake was reduced. Support for Dahl has come from one study from New-guinea, where natives consuming a low-salt diet showed a low systolic pressure and virtually no hypertension (Denton et al 1969).
In other different known population compared, that does appear to be correlation between salt intake and hypertension. The prevalence of hypertensive complication is high amongst the Japanese, who have one of the highest dietary sodium intakes known. By contrast, several primitives tribes consume diet extremely low in sodium (< mmol/day) and there is virtually no hypertension.
Among those studies have been the Yanomamo Indians of Brazil, Polynesia and Solomon Islanders. Hypertension and the rise in BP with age were rarely, if ever observed. It is also possible that the high potassium content of this diet may contribute to lowering of blood pressure by enhancing sodium excretion (Louis et al 1971). Watson and Langford (1967) compared sodium excretion in young girls selected randomly from those with highest and those with lower BP in a large population. Over nightly hourly sodium excretion was greater in the high blood pressure group. Miell (1959) observed no relationship between hypertension and salt intake. The Framingham studies also revealed no consistent difference in the salt intake of hypertensive.
Douglas et al (1964) increased the dietary sodium content of partially nephrectomies dogs. Blood volume and sodium space rose transiently and then return to normal. Hypertension persisted, however, until dietary sodium was reduced. Conway (1963) raised the cardiac output and PB of conscious dogs by continuous saline infusion. With long-standing, the C.O. fell again to normal levels, hypertension persisted, however, because of elevated peripheral resistance.
Sodium restriction may be of beneficial advantage, however, there may be possible provocation of fall in GFR, and this is dangerous or even life-threatening in patients with impaired renal function. For patients with good renal function it may be very valuable.
A reduction in the ability of the kidney to excrete sodium at a given arterial pressure leads to Na-retention which raises blood pressure to the point where Na-balance can be restored. A rise in renal arterial pressure urinary Na-excretion. This is the pheromone of pressure natriuretic. A central point of some theory is that pressure natriuretic is reset in essential hypertension, higher pressure being needed to maintain a given Na-excretion. Guyton et al maintain that resetting is a feature of all hypertension.
It can be concluded that two mechanisms operate in essential hypertension. In the early stage of the disease blood pressure is raised by an abnormal process related more closely to K than to sodium. A renal lesion develops later, possibly as a consequence of the hypertension. This lesion is characterized by resetting of pressure natriuretic and is manifest by an abnormal relation between body Na and arterial pressure and by susceptibility to increased dietary sodium.
NEUROGENIC HYPOTHESIS OF ESSENTIAL HYPERTENSION
Essential hypertension could in certain cases be plausibly attributes to volume over load and could have renal origin. In the majority of cases, however, it is primarily initiated by central nervous system, specifically the brain stem (Dickinson).
The disorder is probably not in most cases psychological in origin but represent some changes in function of localized, discrete and bilaterally represented part of the bulbar reticular formation. Stressful life averts prior to illness onset, psychological distress as measured by SCL – 90, and dysthymia as were investigated in patients with essential hypertension by Troubini G. Osti Rated (1980).
They discovered that patients with hypertension were exposed to undesirable life events before disease. The major reason for the involvement of neurogenic disorder is because of demonstrated raised plasma noradrenaline in patients with essential hypertension.
It may follow that due to psychological stress resulting in sympathetic over activity is the earliest stage of essential hypertension. The elevated blood pressure being maintains by structural changes in the resistance vessels. Other studies of mild hypertensive subjects with high renin levels have similar evidence of sympathetic over activity, together with raised plasma noradrenaline levels (Fsler et al 1977). This would suggest that elevation of renin in such patients was secondary to increased sympathetic activity. Psychometric testing of such individual’s demonstrated suppressed hostility compared to other hypertensive subjects.
1.4 EFFECT OF DIETARY HABITS, DISEASE PATTERNS AND PSYCHOLOGICAL STRESS ON THE ESSENTIAL HYPERTENSION
Dietary habits such as dietary sodium, potassium and other electrolytes, alcohol consumption cigarette smoking, energy and fat and other dietary constituents influence the course of hypertension.
EFFECT OF DIETARY ELECTROLYTE SUCH AS SODIUM, POTASSIUM, CALCIUM, CHLORIDE ON HYPERTENSIVES
Many workers have implicated various electrolytes both in the ethology the course of hypertension. The electrolyte that has received most attention in both the genesis and course of hypertension is sodium. Nearly 80 years age, Ambard and Beaugard (1904) showed that salt restriction lowered blood pressure. Other workers Kempner, W et al (1948), murphy R.F. 1950, Walkin DM (1950) have shown that very low level of Na intake, around 10 mmol/day, greatly reduced hypertension, most of their patients had malignant hypertension. Walking et al showed clearly that in patients with serve hypertension and increase in sodium intake from 10 mmol to about 25 – 35 mmol/day would raise the BP towards pre-treatment levels.
Recently, the double blind randomized crossover study by Graham et al 1982 shows that in patients with mild to moderate essential hypertension, sodium restriction, achieved by not adding salt to the food or avoiding foods with large amount of added Na does lower BP. The 6.1% fall in mean BP is in the same range as that produced by a diuretics alone or a beta blocker alone. A long term study of moderate sodium restrictions has suggested that the effect on the BP increases with time (Morgan T. et al 1973). In a more acute study in which both normotensive and hypertensive subjects restricted there sodium intake to 10 mmol/day for 5 days, the hypertensive but not the normotensive subjects had a fall in blood pressure. The fall in blood pressure that occurred was directly related to the severity of BP and inversely related to the activity of the Renin-angiotensin system (Palfrey P.S. et al 1981).
Previous open studies (Parijs J et al, 1973, Morgan T. et al, 1978, Hunt J.C. 1977) have also shown that moderate sodium reduction, reduces blood pressure in those with mild to moderate essential hypertension. However, Parijs et al found that although moderate sodium restriction, reduced 24 hour urinary Na-excretion from 200 – 93 mmol/day, significant fall in BP could only be detected by blood pressure measurement at home. In contrast, Morgan et al, found in their control trial that although salt restriction reduces urinary Na-excretion only from 191 mmol to 159 mmol/day, it reduced BP significantly, Hunts nutritional therapy of essential hypertension includes calories reduction as well as sodium restriction to about 60 mmol/day. He claimed that many patients because normotensive on this regime.
On the other hand both Swales (1980) and Simpson (1979), had remained skeptical of the value of moderate sodium restriction. Again, in recent symposium on nutrition and blood pressure control sponsored by the national kidney foundation, J.H. Laragh, Hilda et al criticized the initiative of dietary restriction on the ground that the cause of essential hypertension is heterogeneity. According to Laragh, those who respond have low serum renin and aldosterone levels. He and his associates found that the serum ionized ca levels in patients with untreated essential hypertension is directly related to plasma renin activity. The patients with below normal renin levels were found to have low serum ionized ca level. They found that low – Na diet produces the highest ionized ca level and the high Na – diet produces substantial reduction in ca levels. On the basis of these and other pre-luminary studies they believed that sodium may mediate the presser action by producing changes in serum and intracellular ca levels. Thus, reduction of Na intake may raise the intracellular ca, casing increase in vascular reactivity.
The finding that within a community individual sodium intake or excretion does not always relate to blood pressure levels (Simpson F.O. et al, 1978) has been used as an argument against the importance of sodium intake in determining blood pressure (Simpson F.O. et al, 1979). However, the range of sodium intake within most communities is quite small and certain individual are more susceptible to the development of high blood pressure. It is not surprising; therefore, that sodium intake and blood pressure are not always related within a community (Graham A. Macgregor 1983).
Epidemiological studies have shown that contact with missionaries led to the introduction of salt amongst the mundurucus Indians of Brazil and this was associated with the appearance of hypertension and rising blood pressure with age. These observations have extrapolated back in time and it has been suggested that man’s vegetarian forbears also had a very low sodium intake. Again, the prevalence of hypertension is high amongst Japanese who have one of the highest dietary sodium intakes known. By contrast, several primitive tribes consume diet extremely low in sodium (1 mmol/day) and there is virtually no hypertension. Furthermore, Nekrasova A et al reported increased salt intake in population in which the spring water has high salt content. This resulted changes in hormonal regulation of essential hypertension with high salt intake (increase of aldosterone in the body, decrease kallikrin excretion, increase in the prostaglandin F.E. ratio, higher plasma renin activity as a response to salt over load) may be responsible for the specific feature of the clinical course of the disease in such patients (sodium and water retention, high total peripheral resistance and high diastolic pressure). Disorder that lead to retention of salt cause hypertension. Modest salt restriction reduces blood pressure in many patients. Reduced salt balance and preventing the compensatory rise in angiotensin II controls blood pressure in most patients. Diuretics which are as effective as sodium restriction in lowering BP can cause adverse metabolic effect. There is already evidence that a high Na-intake reduces the effect of a diuretics on BP (Parijis, 1973), and a reduction in sodium intake would also enhance effect of angiotensin converting enzyme inhibitor on blood pressure.
G.C.M. Watt et al 1983 reported a higher systolic pressure in the offspring with a family history of high blood pressure but found no difference in 24h urinary electrolyte excretion or plasma activity. The high/high mothers and fathers were heavier than the low/low parents by 10.2kg and 4.5kg, respectively, and there is some evidence of an association between body weight and blood pressure in the high/high offspring. They found that in early adult life the offspring of high/high parents have higher systolic pressure than offspring of low/low parents. There are no corresponding difference in urinary electrolyte excretion, sodium – potassium ratio or plasma renin activity. Thus, their study provides strong evidence against the hypothesis that hypertensive have an avidity (greedy) for sodium. However their studies do not rule out the hypothesis that offspring may respond differently to high sodium intake.
Alan J. Silma, et al (1983) observed a significant fall in BP of hypertensive on sodium restriction but argue that the antihypertensive effect of a restricted sodium diet may be related to the increased consultation and monitoring activity of such intervention rather than to the dietary manipulation itself. It should be noted that trials of 4 weeks duration were reported by Parijs et al and Macgregor et al, who found sodium restriction to be of value and also by Watt et al who did not.
Morgan et al reported the fall in BP to be greatest at 2 years. Alan J. et al found no difference in BP reduction caused by placebo or control group and sodium restricted group. This seems to imply that hypotensive effect of restricted sodium may not be sodium reduction per se. They speculate that the fall in BP was a response to increased medical care (weight reduction, increased exercise, reduction of stress by increased relaxation) and involvement per se. For a restricted sodium diet to have had a significant effect on BP reduction, given the observed reduction and confidence interval in the control (Placebo) group, the difference in hypotensive effect between the restricted sodium diet and the normal diet would have had to exceed that observed in previous trials. They, Alan et al (1983) concluded that why they failed to observe difference between the two groups could be that a difference in effect will be noticed after 2 years or it might be that a restricted sodium diet might not as suggested by others have independent hypotensive effect. Since (1) there was no dose response relation in either this trial or other trials between the degree of sodium reduction and fall of BP; (2) the falls in sodium excretion though similar to those in the trial by Morgan et al, were small, making it arguable whether a reduction within this range would be sufficient to cause the observed reduction in BP. However, Morgan et al, found that although salt restriction reduced urinary Na excretion only from 191 to 159 mmol/day, it reduced BP significantly. Puska et al observed no effect of a low sodium diet (they found a hypotensive effect only with a reduction in fat intake).
Nevertheless epidemiological, animal experiment and clinical studies have shown that restriction of dietary sodium lower BP. Samburu soldiers in Kenya were given a daily 16g salt ration, and with this increase in salt intake blood pressure rose (Shaper A.G. et al 1969). An ongoing study of an African rural tribe, some of whom have migrated to cities has shown that the blood pressure is higher in the urban environment and at least part of this rise is related to the increase in urinary sodium and fall in urinary potassium that occurs there (Poulter N. et al 1982). More recent evidence has shown that moderate restriction of Na intake to 70 – 100 mmol/day does cause a fall in blood pressure in patients with mild to moderate essential hypertension and its effect is additive to that of blood pressure lowing drugs. The moderate reduction is sodium intake has approximately the same blood lowering effect as a single antihypertensive drug, such as a diuretic or beta – blockers (G.A. Macgregor 1983).
As well, dietary potassium has received much attention on recent time. The emphasis has been on low sodium/high potassium dietary ratio Stephen J. Smith et al (1982) have shown that moderate potassium supplementation caused a small but significant fall in blood pressure in patients with mild to moderate hypertension and thus could be additive to the effects of moderate sodium restriction. This increase in potassium intake could be achieved with a potassium based salt substitute or a moderate dietary increase in vegetable and fruit consumption. Moderate dietary sodium restriction with dietary potassium supplementation may obviate or reduce the need for drug treatment in some patients with mild to moderate hypertension. Linura O. et al (1981) observed a greater fall in BP with K – supplementation alone in patients with essential hypertension. Their study suggested that the fall in BP that occur with potassium supplementation was related to the resultant loss of sodium and that the fall in BP was greater the higher the sodium intake. Stephen et al however, found that the fall in BP was independent of urinary sodium excretion, suggesting that, even at sodium intakes of between 70 – 100 mmol/day, there is still a in BP with potassium supplementation. It appears that the probable mechanism whereby BP is lowered by potassium is through stimulation of sodium pump (Na+ - K+ - ATP case), inhibited by circulating sodium transport inhibitor in essential hypertension (Overbeck et al 1974; Chen WT 1972; Glynn 1974; Macgregor GA et al 1981).
There is epidemiological evidence that communities which eat small amount of sodium usually eat large amounts of potassium and have a low prevalence of hypertension (Meneely GR et al 1976). Palfrey P.S., Wright P., Goodwin F.J, et al 1981 studied the effect of high potassium low sodium on the hypertensive. They observed a high significant rise, higher than pre-treatment levels in the hypertensive during high sodium diet. But, during the high potassium 1/no sodium diet, BP fall sharply in the hypertensive, much lower than the pre-dietary level.
They also observed a high significant level of noradrenaline in the hypertensive than normotensive. Also during the high sodium diet, the fall in plasma noradrenaline was significant in the hypertensive. During the high potassium/low sodium phase, the plasma aldosterone rose significantly in both hypertensive and normotensive. The concluded that the BP of patients with mild essential hypertension, but not the normotensive subjects is lowered by moderately reduced sodium, and increased potassium – diet.
Epidemiological evidence has indicated that patients with essential hypertension, the BP is dependent on resulting Na: K ration rather than amount of Na ingested. Studies have shown that the unprocessed natural food such as that eaten by primitive population in which hypertension is almost non-existent provides less than 30m Eq (690mg) Na daily and about 200m Eq (7800mg) K, resulting in a Na: K ration of roughly 1:10. Reducing the N – content of a diet decrease the Na: K ratio, keeping the Na – content of the diet but increasing the dietary K will decrease the Na: K ratio. Clinical studies indicate that giving sodium – diet to hypertensive patients, produced an increased BP; whereas, K-salt diet just as regularly produced a decline (ERSH of, BH 1981).
Again, in Randomized double – blind cross – over trial of potassium on blood pressure in mammal subjects, Kay Tee Khaw and Simon Thom (1982), observed a significant fall in systolic and diastolic pressure on potassium diet. These results indicate that, in healthy young Volunteers on a normal unrestricted diet, added potassium can lower mean diastolic blood pressure. A reduction of their BP is evidence for an etiological role of potassium in determining the population as a whole rather than just in hypertensive. Again, this effect was shown on a group with unrestricted salt intake; if dietary potassium affects BP either independently or through lowering the overall sodium/potassium ratio, individuals wanting to lower their BP might find it easier to increase their potassium intake, in the form of fruit and vegetables, than to decrease their sodium intake.
Rose G (1965) Khaw KT et al have estimated that the life-saving benefits achieved by current antihypertensive treatment might equally be achieved by increasing the mean population intake by 20 – 300 mmol potassium dialy. Furthermore, Skrabal, J. Aubock et al (1981) have shown that a moderate reduction of salt intake from 200 to 50 mmol/day over 2 weeks reduced the rise in BP induced by various does of noradrenaline at least by 5mm HG. Also a high potassium intake reduced diastolic BP at least 5mm Hg. A high potassium intake also improves compliance with a low salt regimen, promote sodium loss, prevent rise in plasma catecholamine induced by a low salt diet, and increased the sensitivity of the baron receptor reflex. In all subjects (both hypertensive and normotensive) 2 weeks of a combined low Na/high K intake reduced BP rises induced by mental stress or noradrenaline infusion by 10mm Hg. They thus, suggest that moderate salt restriction combined with a high potassium intake helps to prevent hypertension. Moderate salt restriction or increase in potassium intake led to significant decrease of body weight and concomitant increasing in serum creative and uric acid.
A potassium intake of 80 – 200 mmol/day improves blood pressure regulation; such a diet may be of value in the prevention of hypertension in man. Like sodium restriction, a high K intake alone produced weight loss and increased serum creative, (H. Hortmage et al 1981); these findings indicate a reduction in E.C.F. volume, presumably due to a direct sal-uretic effect of potassium on the kidney. But unlike sodium restriction, a high potassium intake improves baroreceptor function. An increase in potassium intake also prevents the increase in plasma noradrenaline which usually occur after sodium restriction. Again a high potassium intake might help to prevent hypertension by improving compliance with a low salt diet. Food usually consumed with salt is replaced by food, such as fruit and vegetable, which is not generally taken with salt; also the subjects found that the mixture of potassium salts supplied as salt substitute was very acceptable. A moderate increase in potassium intake of around 600mmol/day could be achieved with a potassium – based salt substitute, which could be added either in cooking or at the table, and by a moderate increase in fruit and vegetable consumption.
Studies in which K-excretion has also been measured suggest that within a particular community there is a direct relation between potassium excretion (Holly Jmp et al 1981), the Na/K ratio in the urine (Chen WT 1972), and BP. Plasma potassium within a community has also been found to be inversely related to BP (Overbeck HW et al 1974). K – Intake varies more widely than Na – intake. Vegetarians have a higher K – intake, may have a lower BP, and might be expected to have a longer life expectancy than non – vegetarians. Greater consumption of fresh fruit, vegetables, and cereals is unlikely to be harmful and may carry other benefits from the higher fiber and lower saturated –fat content. Clearly patients with severe renal failure should not increase potassium intake (G.A. Macgregor 1983). Also salt restriction to less than 10 mmol/day might be dangerous in patients not able to conserve sodium (e.g. those with Addison disease or renal failure).
A major reduction in Na intake can be made by stopping the addition of salt to food at the table, and eliminating, or severely reducing salt added in cooking. A further reduction in Na intake can be achieved only by avoiding processed foods. Even Simpson, who has previously been skeptical about the effects of moderate sodium restriction is now worried about the dietary content of salt. Part of the immediate fall in blood pressure with sodium restriction is due to the lack of compensatory rise in angiotensin II with sodium loss (Palfrey PS et al 1981).
Changing the potassium intake is not necessary more expenditure on fresh fruit and vegetables. Steaming vegetables removes less potassium than boiling and it is a useful way of increasing potassium intake. Cheap fruits and vegetables are available and consumption of higher fiber diets are advocated (Morris et al 1977; Kempner et al; G.A. Macgregor et al 1983). Dietary alternation of Na and K intake may obviate the need for drug treatment in many patients with essential hypertension and it might also improve the efficiency of drugs in those patients in whom dietary measures alone are in sufficient.
There has been a lot of debate about the possible role of dietary calcium both in the etiology and the course of hypertension. Some workers believe that hypertension may be associated with a relative state of calcium (ca) depletion and conversely, ca supplement may protect against increase in BP. It has been postulated that low dietary calcium may be a cause of toxemia (Chaudhur). Belizen et al have suggested a mechanism of action for calcium. High ca content in the water supply (hard water) is associated with lower blood pressure (R. Masironic et al 1976). From animal experiments, it has been reported that ca deficient diet can raise BP in the rat and that the BP of spontaneously hypertensive rat can be reduced with dietary calcium supplement (J. Koboyashi 1976).
In a recent symposium on nutrition and BP control sponsored by the National Kidney function; at the symposium, Ma Carron warned that dietary restriction of Na could potentially result in additional reduction in ca intakes. He reported that 46 patients with essential hypertension he studies consumed substantially less ca daily than 44 normotensive (668 and 886mg respectively). Feeding a high ca diet to a normal animal and spontaneously hypertensive rat will reduce the incidence of hypertension and will even lower the BP in the normotensive animals. Ma Carron said that Magnesium’s protective effect is largely against the vascular complications of hypertensions.
Langford and Watson presented data suggesting a negative association between calcium intake and blood pressure. However, Dorst KG et al (1981) reports that in 33 normotensive propends with familial disposition to hypertension and in 18 with no family history of hypertension, the intracellular Na+ and ca2+ activity erythrocytes was higher in the predisposed; intracellularCa2+ activity 84± 3.47 mmol/L in the control group. The result suggests that elevation of intracellular Na+ and Ca2+ development of hypertension.
Again, Hugo Kesteloot and Jozef Geboevs (1982) found a high significant positive slop between serum ca and BP. Bulpitt et al found on association between systolic but not diastolic pressure. Calcium effect is more on the younger subjects than in older subjects. That urinary ca correlated positively with BP in multivariate regression analysis suggests that Ca intake could also be important as a determinant of blood pressure. Urinary Ca excretion depends among other factors on Ca intake and dietary protein (High dietary protein increases renal excretion of Ca), saturated fat and vitamin D.
In subjects with a genetically determined predisposition to the development of hypertension, a high Na-consumption leads to a volume overload, which results in the appearance of natriuretic hormones. This hormone influences membrane permeability, which leads to an increase in intracellular Na and by inhibiting the sodium calcium exchange causes an accumulation of calcium in vascular smooth muscle cells. The increase in intracellular Ca would leads to an increased in contractibility and vascular tone, resulting in an augmented peripheral vascular resistance and consequently in raised blood pressure. This hypothesis is corroborated by the finding of a positive relation between serum Ca and BP and urinary Ca with BP, and the known biological effect of Ca on the heart and circulation points in this direction. Thus, in the role of ca in hypertension, beneficial role of ca antagonist in the treatment of hypertension is demonstrated both experimentally and clinically (Jozef G et al 1982).
Theodore A. Kotcha (1982) reported that the Anion Chloride (cl) may play a pivotal role in the regulations of renin release by Na and in the developmental model of Na-sensitive hypertension. Short and long term administration of sodium bicarbonate in rats failed to suppress plasma renin activity whereas renin was inhibited by both salt and chloride without Na loading. Also plasma renin activity was stimulated by selective chloride depletion. The demonstration that the anion modified both the renin and blood pressure response to salt loading in rats may have substantial clinical applications.
Other electrolytes may be implicated in hypertension. It has been reported that small quantities of cadmium produce sustained blood pressure elevation in dogs and rats (clinical hypertension by J.O. Swales page 60). Some groups in the United States have demonstrated a relationship between clinical hypertension and renal, urinary and plasma cadmium and this element has therefore been incriminated. The effect mg has not been defined in relation to blood pressure.
EFFECTS OF VEGETABLES AND FRUITS ON THE HYPERTENSIVE
Several intervention possibilities have been proposed for the prevention of hypertension including weight reduction, stress management and relaxation and dietary changes.
Several epidemiological studies have suggested blood pressuring lowering effect of vegetarian diet (Sacks FM 1974; Anlolm A.C. et al 1975; Armstrong B. et al 1977; Hainas A.P et al 1980). Rouse L. et al 1982 and Bruce K. et al (1983) reported a blood pressure difference of about 5-6mm Hg systolic and 4-5mm Hg diastolic between vegetarian Advantis and Omnivores. Bruce et al (1983) studied the effect of vegetarian diet on the omnivorous subjects. The diet related fall in BP was independent of initial BP, Age, Sex, Obesity, heart rate, and weight change. BP changes were most evident during the final week of the vegetarian diet period and were reversible within 5 – 6 weeks of returning to an omnivorous diet.
The result of this study and a dietary intervention trial by Sacks et al (1977) suggest that a vegetarian diet may exert a greater effect on systolic than diastolic BP. It has been shown that vegetarians eat more dietary fiber, polyusltreated fat, magnesium, and potassium than omnivorous, significantly less total fat, saturated fats, cholesterol and vitamin B12 and similar quantities of Na, protein and energy (Rosuse L et al 1981). Change in intake of dietary fiber might indirectly modify BP by affecting absorption of important nutrients (Kelsey Jb 1978) or increase in dietary mg 2+ could affect plasma or cellular mg and hence influence cardiac or vascular smooth muscle contraction (Alturas BM et al 1981; Alturas BT et al 1981). The administration of a vegetable diet which is low in total fat and richer in linoleic acid/thus having a higher poly-unsaturated/saturated ratio may modify prostaglandin metabolism so as to increase synthesis of vasodilator or natriuretic prostaglandin (Galli et al 1980, Paoletti R. et al 1981).
Hypertension is an important predisposing factor to the development of stroke, heart attacks and renal failure. Recently Roy M.A. and D.R.R. Williams (1983) postulated that fruits and vegetable consumption could protect against stroke. Changes in eating habits, among them, an increase in intake of vitamin C (Marrjw 1974) and fall in salt intake (Cummins RD, 1983), are known to lower BP. A Pathophysiological explanation for the relation between the consumption of several constituents of fresh fruits and vegetables (particularly vitamin C) and the occurrence of cardiovascular disease (CUD) can be put forward both for hemorrhagic and for the thrombotic stoke. Ross Russell has put forward a hypothesis for the pathogenesis of CVD (1975), Taylor (1976) proposed a role for vitamin C and subsequently Anah (1976) postulated that relative hypokalemia, through an influence on vascular smooth muscle function, might be involved in the immediate precipitation of hemorrhagic episode. Not only are fresh fruits and vegetables the most important source of vitamin C in the diet, they are also rich source of potassium.
The fragility of brain capillaries, arteries and arterioles in hypertensive persons may be related to the adequacy of vitamin C /intake, even above levels necessary to avoid clinical Scurvy, and these may therefore be a relation between the intake of this nutrient and the precipitation of hemorrhagic stroke.
Other nutrients or constituents contained in fresh fruits or vegetables may be important. Low dietary fiber intake has been implicated in the development of hypertension. Dietary fibers lower the serum cholesterol levels, triglycerides and lipoproteins. The incidence of atherosclerosis and hypertension is reduced. Examples of fibers include cereals – oats, maize, wheat, vegetables and fruits, bread, whole grain rice, leguminous seed. Fibers lower BP reduces the risks of both C.V.D and atherosclerosis by reducing plasma cholesterol and fatty substances. Dietary fiber might also indirectly modify BP by affecting absorption of important nutrients (Kelsey et al 1978). Also fiber rich food increase bible salt excretion. A high consumption of starchy carbohydrate food containing their full complement of dietary fiber appears to protect against hypertension. In Kempner, diet for the treatment of hypertension, 40 – 500g/day or rice – rich in fiber was consumed, while fats were reduced. Sugar, if eaten in large quantity also expels other starch foot-rich in fiber from customary diet.
Fresh vegetables and fruits are high in K and low in Na, and evidence is accumulating that Na+/K+ ratio is important in hypertension and hence stroke. Eating fresh fruit and fresh vegetables does indeed reduce hypertension and is also associated with reduced risk of early death from CVD, probably through the vitamin C they contain. Alternation of dietary sodium and K intake may play an important role in containing drug cost especially in poorer countries in the future.
EFFECT OF DIETARY CARBOHYDRATES, FATS AND PROTEIN ON THE HYPERTENSIVE
There is a lot of controversy about the possible effect of carbohydrate in the hypertensive. Several studies indicated an association between the plasma insulin and BP independent of weight; evidences showing a high carbohydrate content diet and hyperinsulinemia; effect of insulin on renal reabsorption of sodium and renal handling of other electrolytes such as ca, K, P04; and effect of insulin carbohydrate intake on sympathetic nervous activity may contribute to diet induced changes in BP (Landsberg L. et al 1981). All these reflect the effect of dietary habit on the hypertensive patients. A positive association was observed for glucose or insulin with body weight, height, obesity indices and serum triglyceride.
It has been found that there is a direct relationship between raised blood sugar and arterial disease. Is calorically feeding of 200g sucrose cause a significant rise in the concentration of plasma triply cerides and thus increase both atherosclerotic risk factors and CVD.
Effect of a glycoside hydrolase inhibitor (BAYg 5421) on BP, fasting blood glucose, fasting insulin and 100g pre-oral sucrose test in 8 obsessed middle-aged men with border line hypertension was investigated. BAYg 5241 caused a significant decrease of plasma insulin after a 100g sucrose tolerance test as compared to placebo. Blood pressure after 4 weeks of treatment with placebo was 135 +- 5.7 systolic and 92 +- 6.6 diastolic mmttg and after 4 weeks of treatment with BHYg 5251 these was no significant difference. There was no change in weight. There is a small but significant fall in BP. Glycoside hydrolase inhibitor causes a fall in insulin level and glucose level. Since the fall in BP is observed in both glucose antagonist and placebo group it seems to imply that the hypotensive effect of restricted glucose may not be due to fall in insulin per se.
Again 212 patients with essential hypertension with over weight of at least 100% in excess of ideal weight were investigated by Evahon H.E. et al (1981). The patients were advice to take balanced low calories (about 1080 Kcel/day as against 2800 Kcal/day); diet containing 83g carbohydrate, 41.5g fat (as against 720g) and 85g protein (as against 65g). They were advice to eat salt freely. 42 patients that complied with the recommendation, decreased in body weight resulted in a significant decrease in BP. In the group receiving no diuretics or any other hypertensive therapy, 82.6% reached normal systolic pressure and 78.3% reached normal diastolic BP, but only 31/38 reached body weight within 10% of ideal body weight.
There had been also a positive correlation between children systolic BP and plasma glucose (Beresm GS et al).
Stamlar J. Farmiiaro, have shown that changes in dietary habits such as low salt intake, moderate weight loss, and reduction in serum cholesterol lower BP. Decrease in BP were sustained, about 10/13 MMHg for hypertensive man, resulting in long-term restoration of normal BP, and about 7/4 MMHg for men with high-normal BP entry, long term improvement in eating and exercise habit yield moderate sustained weight loss and thus preventing HBP in hypertensive prone persons and in controlling established mild hypertension.
Hunt’s nutritional therapy of the essential hypertensive includes calorie reduction as well as sodium restriction to about 60mmol/day. He claimed that patients become normotensive on this regimen. The effect of carbohydrate on BP is not yet clear but it is generally believed that moderate weight reduction through cut in energy intake and exercise help to control hypertension or development of hypertension. High energy intake has therefore been implicated in the development of hypertension, though the evidence is at present sanity and contentious.
DIETARY FAT: More recently, the possible role of fat in the course of hypertension has aroused interest. A controlled randomized trial of the effect of dietary fat on blood pressure was undertaken by PeKKA PUSKA, James M. IACONO et al (1983) in 57 couples in two communities of North Karelia, aged 30 – 50 years. The study groups comprises of (group 1) – a diet low in fat (23% of energy) with high polyunsaturated/saturated (P/S) ratio. Croup II reduced dietary salt intake from 192-77mmol/day and group III (control) – continued the normal diet. In group 1 systolic BP declined from 138.4 to 129.5 MMHg and diastolic BP from 88.9 to 81.3mmHg during the intervention period; the value rose during switch back. The fall was greater among hypertensive than among normotensive subjects. In group II and III the mean blood pressure changed very little during the study.
The finding that BP in the low salt group did not decrease adds to the controversy about the possible role of salt in hypertension. Erkki Vortianen et al (1983) postulated that those people were not sensitive to salt reduction or the possibility that salt reduction at this age is too late, that the intervention should have continued for longer or that the low P/S ratio diet inhibits the possible impact of salt reduction.
The observed fall in BP is reduced fat intake and increase P/S ratio, was quite significant and true reduction. It was not due to reduction in sodium intake or weight reduction because the weight was identical in group I and II. Thus, the BP reduction in low salt diet was a consequence of the dietary fat reduction and increase in P/S ratio. Potassium may play a role in accounting for the fall in BP. The major dietary change was the reduction in saturated fat intake, and increase in P/S ratio and is the most likely reason for the fall in BP.
Their result support the hypothesis that low fat and high P/S ratio diet reduce BP, probably through prostaglandin balance in both normotensive and hypertensive people. Salt intake reduction was ineffective in this trial. Thus, changing dietary fat seems a promising method for the non-pharmacological treatment and prevention of hypertension.
Also Galli et al 1980: Gilli C, 1980; Paoletti R. et al (1981) reported that higher P/S ratio and reduced fat, lowers BP through modification of prostaglandin metabolism so as to increase synthesis of vasodilator or natriuretic prostaglandin.
Change in dietary lipid constituents can alter plasma lipoprotein concentration in various ways. These include a change in the quantity and quality of exogenous input and secondly effect on the synthesis of cholesterol and triglycerides-rich lipoprotein and an alternation of bile acid secretion and of the interestingly output of cholesterol and its metabolites.
High consumption of saturated fatty acid have twice elevating effect on plasma cholesterol as lowering effect of an equal weight of polyunsaturated fatty acid. Fats (fatty acids, cholesterol, and lipoprotein) are implicated in the etiology of atherosclerosis. By accumulating in the intima of blood vessels together with variable amounts of connective tissue, they narrow the Lumen of the blood vessels. The chances of developing hyperlipidemia are reduced if only 35% of energy intake is provided by carbohydrate and if the ratio of polyunsaturated: saturated fat is greater than 1.5. Hypertension, hypercholester-olesterolemia, smoking are risk factors in CVD. A significant correlation was found between weight gain and the indices of angina pectoris and arterial hypertension (NOPPA. H.1980). A modified fat diet should comprise less than 300g cholesterol with polyunsaturated to saturated fatty acid ratio of about 2:0.
Brussaad, J.H. et al 1980 observed the effect of absence of dietary fiber, protein, and fat on health students. All foodstuffs were weighed out individually according to each person’s energy needs. Body weight and Na intake were controlled. Initially BP were about 120/70mmHg. It was observed that both systolic and diastolic BP was lowered during test period in all 4 experiments with almost every diet given in the absence of the other by about 0 – 5mmHg. The general reduction in BP by all food items may be due to weight control and salt restriction. It was also found by Gatti E. et al that BP returned to normal in 201 of 280 obsessed men and women with hypertension given a diet providing 800 or 1000 or 1200 Kcal daily for at least 6 months and was considerably reached in the others without the need for reducing salt intake or intensive treatment with drugs.
Yamori Y. et al reported effect of dietary habit in Japanese farming community. Na, K, Urea Nitrogen (as possible index of total protein intake): Inorganic sulphate (P04: as a possible index of sulphuramino acid intake mainly from animal proteins) and creatine (Cr: were estimated in single spot urine void in the morning by 2,500 subjects). They found there was a significant gradual increase in the prevalence of hypertension and mean arterial pressure with increasing Na: K in the urine. They also found a significant positive correlation in all 120 adult subjects examined between BP and Na. Cr, age and obesity and inverse correlation between BP and K: Cr or 804: Urea. They concluded that dietary factor in hypertension seem to be more important in communities where salt intake is high.
EFFECT OF ALCOHOL, SMOKING AND COFEE ON THE HYPERTENSIVE
J.B. Saunder et al investigated the effect of alcohol on the hypertensive. They reported that high alcohol intake may be responsible for as many as 25 – 30 of cases of essential hypertension in Western countries. But effect of alcohol is not uniform – subjects whose intake is moderate (< 40g/day) do not have high blood pressure than total abstainers. There BP may be lower (Klatsky A.L. Stamiler et al 1977). Results show a linear relationship between the height of blood pressure and alcohol intake from a level of 80g/day. There was no relationship between BP and degree of histological liver damage. They also observed that in most patients’ blood pressure fell to normal after detoxification and remain so far at least a year in those who continued to obtain. However, blood pressure rose in those who started drinking again. Raff DP et al (1967) reported that acute ingestion of alcohol does not affect blood pressure (Raff D.P. et al 1967) but observed a highly significant correlation between hypertension and the severity of the alcohol withdrawal syndrome. Many features of alcohol withdrawal are suggestive of a hyper-adrenergic state (Carlson C et al 1967) and can be controlled by beta adrenergic blocking drugs (Zilm D.H. et al 1975). Other mechanisms may also be involved. Activation of renin angiotensin system may play a role, since renin and aldosterone production are stimulated during recovery phase from acute alcohol ingestion from the salt content of alcohol drinks such as beer (Macleod AM et al 1977), may also be implicated. Arkwright P.D. et al found correlation between alcohol consumption with systolic pressure but not diastolic pressure but not diastolic pressure. An effect of alcohol was observed independent of age, obesity or cigarette smoking. Smoking also increases BP in the hypertensive. However, smoking and alcohol habit were not related.
K.I. Bhghurst and T. Dwyer (1981) found no relationship between alcohol consumption and BP despite a wide range of alcohol intake and fair wield range of BP among 350 non-commissioned soldiers. Three general scheme have been postulated as a possible ways by chich alcohol effect the hypertensive; first that alcohol is contributory to hypertension possibly via effect on the adrenal gland (Gordon and Southern 1977) or a mixture of central and peripheral nerve effects (Sexias 1973) secondly, there is the possibility that hypertension predisposes to alcohol use and thirdly, the possibility has been raised of underlying predisposition (be it genetic or psychological in origin) to both excessive alcohol. Bathurst et al concluded that if there is some underlying common risk factor for hypertension and excessive alcohol usage, then it is expressing itself in alcohol usage, some considerable time before its expression as elevated blood pressure of 44 men aged between 35 – 48 years old with hypertension, 22 had previously taken more than 80g alcohol daily. The alcohol patients showed more hypertrophy of the left ventricle than others (Sceel et al 1980). Taylor KG; Garter TJ have shown that alcohol intake is associated with increased serum triply cerides.
Elliott JM and Simpson F.O. reported that BP of hypertensive patients was accelerated with regular smoking. Hypertensive patients who smoke regularly are more likely to develop the accelerated phase of hypertension than those who do not smoke. A community study on the epidemiology of hypertension in Selanger (Kadiah et al 1980) found no significant difference in hypertensive tea drinkers, coffee drinkers and alcohol drinkers with similar normotensive with respect to BP. However, there was a significant difference between hypertension and cigarette smoking.
Stephen Ereostone and Lawrence (1982) investigated the effect of smoking and coffee consumption on hypertensive after they obtained from caffeine and cigarette overnight. Their mean blood pressure 147/87 mmHg was substantially lower than the value recorded in the clinic (164/102 mmHg) and remained so when they continued to abstain. Smoking 2 cigarettes (3.4mg nicotine) elevates BP by 10/8 mmHg but for only 15 minutes. Drinking coffee (200mg caffeine) elevates BP up to 10/7 mmHg between 2 hours. Cigarette smoking increases BP by an average of 10/8 mmHg (Hines E.A; Roth G.M. 1938; Hofmas et al 1979). Caffeine (250mg) causes a rise in BP of up to 14/10 mmHg lasting for at least 2 – h. Since there is a relationship between the use of coffee and cigarette (Dawber T.R. et al 1974; Gilbert H.M. 1976) and both stimuli apparently elevates BP through adrenergic stimulation (Cryer P.E. et al 1976; Robertson D. et al 1978) cigarette and coffee taking may increase the course of hypertension. Robertson et al have suggested that he use of caffeine and nicotine may increase the prevalence of hypertension in the population and may negate the effect of treatment. However, epidemiological studies failed to demonstrate a positive correlation between BP and smoking habits (Dawber et al 1959; Erikson J. et al 1978) or the amount of coffee consumed (Dauber et al 1974; Bertrand C.A. et al 1978). Most studies (Dawber T.R. Kannel W.B. et al 1978; Karvenen M et al 1959; Reid D.O et al 1966 and Selter C.C. et al 1974) have shown that cigarette smokers have slightly lower BP than non-smokers and that BP tends to rise when smokers give up the habit. On the other hand Frestone and Ramsay (1982) showed that patients with mild hypertension had BP substantially lowered than clinical value when the abstained from caffeine and nicotine overnight and that the BP did not rise when they continued to abstain. However, wine consumption has been claimed to reduce mortality from ischemic heart diseases.
1.5 PATTERNS OF DISEASES IN THE HYPERTENSIVE
It has been known for many ears that raised arterial/pressure reduces expectation of life and that in this respect males fare worse than female (Pickering). In many cases of untreated patients, death were from heart failure (1/3); apoplexy (1/6); uremia (1/6) and diseases not related to hypertension (1/3). Arterial pressure is an important factor in determining the work of the heart, increased load may lead to heart failure. Three quite separate arterial – diseases contributes largely to disability and death in patients with hypertension, namely nodular arteriosclerosis (or atheroma), Charcot-Bouchard aneurysms and fibroid necrosis. Atheroma especially afflicts males and is related to age, serum cholesterol and cigarette smoking in addition to arterial pressure. Charcot Bouchard aneurysms are found over the age of 40 and with moderate to serve hypertension. Fibroid arteriolar necrosis occurs at any age and in either sex.
Nodular arteriosclerosis or atheroma is a disease of big arteries, aorta, femoral, popliteal, renal, carotid coronary and vertebral arteries, and circle of Willis.
The pathophysiology of atheroma is fibrous or fibro-fatty plaque occurring in the intima with atrophy of overlying media (Plague is accumulation of lipid and connective tissue in the intima of blood vessel). Thrombi form on this plague, eventually occlusion of the artery with distal ischemia. The disease in the arteries of the leg produces intermittent claudication and gangrene; in renal arteries; renal infarction of in arteries forming the circle of wills or their main branches. Charcot-Bouchard aneurysm – this is aneurysm (local dilatation) of the small perforating arteries of the brain. This is due to age and arterial pressure. Of stroke, 40% is due to cerebral hemorrhage, 10% - cerebral infarct, 10% subarachnoid hemorrhage, and 5% undifferentiated stroke.
Fibroid necrosis of small arteries and arterioles is as a result of a breakdown of the small arteries and arterioles in response to the strain of a greatly raised intravascular pressure. Kidney, pancreas, adrenal, gut, brain, eye, heart and liver are affected.
Cardiac diseases occurring due to raised arterial pressure include cardiac hypertrophy, left ventricular failure, congestive cardiac failure (ccf) and myocardial infarction. Myocardial infarction and angina pectoris are due to a platelet-leucocyte – fibrin thrombus forming on fibrous fatty intimal plagues in coronary artery. Angina pectoris may be due to similar event where collateral circulation was enough to present infarction or simply due to stenosis of an artery.
Dissecting aneurysm of the aorta occurs with increased frequency in hypertensive patients. Hypertensive neuroretino – path occurs in malignant phase of hypertension. Arteriosclerotic retina path may occur in the benign phase. These are due to raised arterial pressure in the fundus.
Hypertensive encephalopathy results from elevation of BP above the auto-regulatory range. Thus, the focal breakdown of auto-regulation causes areas of vasodilation with associated edema. Renal disease complications such as nephritic syndrome, proteinuria, and hyaline nephrosclerosis are seen in advanced cases of hypertension not as a cause but as a complication through case history.
In their studies, Schneckloth, R.E. Stuart, K.L. et al 1962 found in extended clinical studies of hypertension and hypertensive diseases in a West Indian Nitro population, that 245 subjects of 1,575 presenting with diastolic pressure of 110mmHg or over, who were closely questioned on family history, work status, and the presence of cerebral, retinal cardiac or renal complications, diastolic hypertension could not be related to family history or to work status. Only two subjects had sign of hemiplegia but fundal abnormalities were found in 85% of hypertensive subjects. The prevalence and severity of retina path increased with raising diastolic pressure. Papilledema was present in only one subject. Signs of left ventricular hypertrophy were observed in only 95 subjects. The prevalence of protein-urea increased at age of 30 – 39 years in hypertensive as well as serum creatine.
Again, a hospital study was carried out in University College Hospital, Ibadan (UCH) 1966 – 1968 by Akinkugbe. About 240 cases of hypertension were investigated. In all there were 113 males and 127 female’s patients. 30 of the female subjects suffered from non-toxemic hypertension occurring during pregnancy. The below table shows the disease pattern of hypertension patients:
Male Female Total
Heart Failure 37 19 56
Renal Failure 14 5 19
C.V.A. - Cerebro Vascular
Accident 6 5 11
Encephalopathy 3 - 3
Headache 5 10 15
Dizziness 9 11 20
Palpitations 2 5 7
Insomnia 1 3 4
Depression 4 2 6
Chest Pain 1 - 1
Epistaxis - 1 1
Menorrhagia - 1 1
TOTAL 133 97 210
Hospital Study Model of Presentation of 210 Patients with Hypertension
DATA FROM HIGH BLOOD PRESSURE IN THE AFRICAN BY AKINNKUGBE
Akinkugbe O.O. observed a high incident of left ventricular failure and congestive cardiac failure in both sexes. The early symptoms frequently attributed to hypertension include headache, nervousness, irritability, easy fatigue, dizziness, depression and insomnia. His find of low incidence of headache supported the general impression that patients with moderate hypertension do not as a rule suffer from headache, of the major complications of hypertension, renal failure accounts for 19 (14 male and 5 females). Seven of the 19 patients with renal failure were under the age of 40 years. The cases of cerebra-vascular accident (CVA) seemed almost equally distributed between the 2 sexes (females and 5 female, the majority being in patients between 40 – 60 years of age, the 3 cases of hypertensive encephalopathy occur in males. There was no case of hypertensive retina path reported.
In another study Abrahams D.G. et al (1960) on the systemic BP in a rural West African Community – Ilorin-North of Ibadan, total of 641 subjects (281) males and 360 males were examined. 36 subjects had protein –urea. In 3 instances proteinuria was accompanied by raised BP. General clinical examination showed the presence of hypertensive heart disease; vascular disease in 7 (aortic incompetence 4, mitral value disease 2, and caorctation of the aorta 1). Disease pattern of hypertensions may represent a consequence of hypertension and if right treatment is not instituted may in most cases lead to death.
1.6 EFFECT OF PSYCHOLOGICAL STRESS ON HYPERTENSIVE SUBJECTS
Psychological factors are factors that operate through the mind. It may involve anger, fear, worry, excitement, frustration or hostility, emotion, anxiety, depression. It is psychic rather than organic. The state of the mind influences the state of the body. The evidence so far available suggest that both genetic and environmental (psychology) factor contribute to the genesis and course of essential hypertension. Psychological stress influences the arterial pressure. Emotional stimuli coverage through the hypothalamus on the Cardio Inhibitory Centre (C.I.C) and probably excerpt their effect on heart rate by increasing or decreasing its rate of tonic discharge.
Various types of psychological stimuli increase renin secretion. Plasma renin level increases in mice when they are subjected to psychological stress induced by manipulation of their housing pattern (Vender, Henry Stephen et al 1978). Stresses also increase noradrenaline secretion. All these factors are known to affect BP.
Hollenberg NK, Williams GH et al reported renal vascular endocrine response in essential hypertensive to a mild psychological stimulus. In the 11 of the 15 hypertensive, arterial blood pressure rose transiently by 7mmHg or more on mild stimulation. Moderate increase in heart rates was also more common in the hypertensive (P < 0.01). Renal blood flow in each of the 15 patients with hypertension was sustained. Plasma renin activity (PRA) rose in 14 of 15 patients. Changes in plasma angiotensin II concentration and in plasma aldosterone were in accord with the changes in P.R.A.
Shulte W, Nevs H. and Von eff AW 1981 observed an elevated BP due to emotional stress. The study was carried out on 48 patients with elevated causal BP and 48 normotensive of the same age. During basal condition the BP values of the hypertensive group were within the normal range but markedly higher than in value of the normotensive group. During stress the value between both groups increased because the hypertensive group exhibited a stronger reactivity of blood pressure. There was an interaction between sex and hypertension in that contrast to the hypertensive group, normotensive women had lower BP value at rest and under emotional stress than men. This effect could be found in the hypertensive as well as normotensive.
Patients with uncomplicated form of hypertension exhibit a BP hyperactivity on emotional stress independent of age and sex. Normotensive subjects with a family history of hypertension show regard as important pathogenesis of essential hypertension and its course.
A clinical casuistry study by Cazzulo et al (1980) in relation to family configuration and intra personality showed that hypertensive patient’s personal life with particular emphasis on significant events from an emotional affective point of view (sexual experiences, marriage, work, failure, mourning) particularly problems arising in familial environment, in relationship between son and familial environment, in relationship between son and parents and between parents, are strong factors in the pathogenesis and in course of hypertension.
20 patients suffering from essential hypertension were compared to a control patients without hypertension matched for age, sex (Trombin G. Osti R. et al 1980). Stress life events prior to illness onset, psychological distress as measured by SCL – 90, and alexithymia were investigated. Patients with hypertension were exposed to undesirable life events before disease onset and exhibited alexithymia traits significantly more than the control group.
Perinic G.I. and Santonastoso P observed that anxiety and neurotic distress systems in hypertension always develop after the onset of the hypertension. Psychological stress has been fully implicated in both the genesis and the course of essential hypertension. The psychological stress may be due to defect in noradrenaline uptake. Depressive illness may be due to increased sympathetic nerve firing.
It has been shown by Chendra Petal et al (1975) that if hypertensive patients can follow a suitable programme of relaxation, it is not only possible to reduce the resting BP and anti-hypertensive drug requirement but also the magnitude and duration of the rise in BP associated with every day emotional stress. Evidence in laboratory animals suggests that reduction in proprioception lowers the sympathetic respondents of the hypothalamus and vice vasa (Petal C.H., 1964; Gellham et al 1953). Meditation reduces oxygen consumptions and relaxes the mind and body.