EFFECT OF DIETARY HABITS, DISEASE PATTERNS AND PSYCHOLOGICAL STRESS ON KNOWN ESSENTIAL HYPERTENSIVE IN RIVERS STATE
ATTENTION:
BEFORE YOU READ THE
PROJECT WORK, PLEASE READ THE INFORMATION BELOW. THANK YOU!
TO GET THE FULL
PROJECT FOR THE TOPIC BELOW PLEASE CALL:
08068231953,
08168759420
TO GET MORE PROJECT
TOPICS IN YOUR DEPARTMENT, PLEASE VISIT:
EFFECT OF
DIETARY HABITS, DISEASE PATTERNS AND PSYCHOLOGICAL STRESS ON KNOWN ESSENTIAL
HYPERTENSIVE IN RIVERS STATE
ABSTRACT
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
CHAPTER
FOUR
5.1 Discussion
5.2 Conclusion
References
Appendix
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
CHAPTER
ONE
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
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
BORDELINE
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.
LABILE
HYPERTENSION
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.
KIDNEY-SALT
HYPOTHESIS
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).
DIETARY
POTASSIUM
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.
DIETARY
CALCIUM
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).
DIETARY
CHLORIDE
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
DIETARY
CARBOHYDRATE
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.
AFFILIATE LINKS:
Comments
Post a Comment