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LACTOSE INTOLERANCE IN PORT HARCOURT
ABSTRACT
Plasma glucose
concentration was determined by lactose tolerance test (LTT) in twenty-nine
subjects, among who are twenty one females and eight males, before and after
ingestion of 170g of liquid milk. Although none of the subjects was milk
tolerant but there were remarkable rises and falls in plasma glucose levels at
certain time intervals in some of the categories of subjects. The highest rise
among two regular milk consumers was 2.2 and 2.3 mmo1/l respectively. And a
fall of 2.6mmol/1 registered by a subject among non-milk consumers. The overall
conclusion from the results of this survey points to the fact that lactase
enzyme may be adaptive in nature.
TABLE OF CONTENTS
Title
Page - - - - - - - - - - i
Declaration - - - - - - - - - ii
Dedication - - - - - - - - - iii
Acknowledgement - - - - - - - - iv
Abstract - - - - - - - - - - v
Table
of Contents - - - - - - - - vi
CHAPTER
ONE
Introduction and Literature Review
CHAPTER
TWO
Materials and
Methods
CHAPTER THREE
Results
CHAPTER FOUR
Discussion
and Summary
Reference
Appendix
LIST
OF FIGURES AND TABLES
Table 1: Plasma
Glucose Concentrations (mmo1/1) in all the subjects before and after intake of
170g of milk
Table 2: Plasma
Glucose Concentrations (mmo1/1), before and after intake in subjects who take
milk regularly.
Table 3: Plasma
Glucose Concentrations (mmo1/1), before and after intake in subjects who take
milk occasionally.
Table 4: Plasma
Glucose Concentrations (mmo1/1), before and after intake in subjects who have
symptoms after milk intake.
Table 5: Plasma
Glucose Concentrations (mmo1/1), before and after intake in subjects who have
not had milk for several years.
Figure 1: Mean
Plasma Glucose Concentration (PGC) in 4 different groups of subjects after
ingestion of milk (170g each).
Figure 2: Mean
Plasma Glucose Concentration (PGC) in 4 different groups of subjects after
ingestion of milk (170g each).
CHAPTER
ONE
INTRODUCTION
Lactose
accounts for a tenth of total dietary carbohydrate and is a disaccharide
containing glucose and galactose. It is found only in milk, hence it is
sometimes called milk sugar, and makes up to half the total solids in milk.
Lactose was first identified in 1633 (Guthrie, 1971). It is a reducing
disaccharide with a (1 4) –
B-D-galactosidic linkage to D-glucose.
The structure of
D-glucose and D-galactose pyranose rings differ only in the configuration
around C4; a
point which is important in the metabolism of D-galactose and therefore of
lactose (Montgomery et al, 1974).
Specific mal-digestion
of disaccharides (maltose, isomaltose, sucrose and lactose) results from
deficiency of a specific enzyme that digests the earlier mentioned
disaccharides. Isolated enzyme deficiencies are mainly congenital and with the
exception of lactose enzyme deficiency are rare (Muir, 1980).
The deficiency or
diminished activity of the enzyme lactose results in lactose or milk
intolerance. Lactase is found in the cell membrane of epithelial cells of the
brush border in the small intestines. Here it catalyzes the hydrolysis of
lactose in milk to glucose and galactose, which are absorbed and transported
via the blood in the portal system to the liver. Here galactose is converted to
glucose. Some of the latter is stored as glycogen in the liver while the rest
is transported by the blood to various body tissues.
Failure to hydrolyze
lactose due to lack or reduced activity of lactase in the small intestines
results in un-hydrolyzed lactose in the small intestinal lumen. The osmotic
effect of un-hydrolyzed lactose and the irritation of the bowel by lactic acid
produced due to bacterial action on lactose result in diarrhea as well as
bloating and flatulence (Anderson, 1963). These are the clinical symptoms of
mal-digestion of lactose when the gut is challenged by milk or lactose meal.
LITERATURE
REVIEW
It is reported that
most infants have a high level of the enzyme lactase, but this declines after 2
to 4 years of age (Muir, 1980). Yet a few infants have congenital deficiency,
just as occurs in older children and adults whose condition has persisted since
infancy. This congenital or primary lactase deficiency is believed to be
permanent and resulting from a genetically determined enzyme defect or from the
environment or both (Cook, 1966; Keusch, 1969). It has been suggested that
lactose deficiency is an autosomal recessive supported by Rosenweig et al in
1967, who believe that lactose intolerance is an inherited disorder because of
the striking racial differences in the incidence. They have noticed a 100%
occurrence of a positive family history of milk intolerance in 9 healthy
children. In another survey of 40 healthy adults, they reported that lactase
activity tended to fall into three groups:
i.
A high activity group, with over 7
units per gram of mucosa in which 8 people are milk and lactose tolerant.
ii.
A low activity group, with less than 2
units, in which all 15 people are both lactose and milk intolerant.
iii.
An intermediate activity group,
ranging from 2 to 7 units, in which there are 17 people. Six of whom have milk
and lactose induced symptoms. They suggest that those in the high and low
groups might be homozygous while the intermediate group might be heterozygous
for lactase deficiency.
The prevalence of
congenital lactase deficiency remains disputed, but Sodeman and Sodeman (1974)
noticed that lactose intolerance most frequently affects Negroes, Orientals and
Cypriot Greeks than Caucasians. This was supported by a report that about 90%
of Caucasians of Northern European extraction and 80% of members of two African
tribes, continue to secrete lactase and therefore can tolerate lactose and
milk, but 70% to 80% of older children and adult of other races and ethnic
groups secrete little or no lactase and are therefore lactose and milk
intolerant (Muir, 1980).
The incidence of
lactase deficiency that leads to lactose intolerance can be as low as 16%
(Auriccho et al, 1963) and as high as 89% (Newcomer and McGill, 1966). They
also suggest that racial differences may account for part of the variations.
Lactase deficiency is noted in 30 of 41 Baltimore blacks (Cauatrecasas et al,
1965) and flat lactose tolerance tests in 31 of 35 Bantus in Uganda (Cook,
Kajubi, 1966).
Apart from congenital
etiology of lactose intolerance which is considered rare (Cautrecases et al,
1965), lactose mal-digestion and mal-absorption can be acquired in children and
adults as a result of many factors, these include:
i.
Mucosal abnormalities such as sprue
and occasionally regional enteritis (Kern, Jr. and Struthers, Jr. 1966).
ii.
Gastrojejunostomy (Gryboski et al,
1963).
iii.
Transient infections enteropathies
(Kleijers and Van de Kamer, 1962).
iv.
Giardiasis (Durand and Lamedica, 1962)
v.
Cystic fibrosis (Cozzetto, 1963).
vi.
Adult celiac disease and other
mal-absorption states with blunting of microvilli (Cooke et al, 1963), Pletkin
and Isselbacher, (1964).
Apart from disease states, other
investigators suggest that lactose intolerant syndrome may result from:
i.
Normal spectrum of development in
adult mammal; and
ii.
Secondary to lack of stimulation by
the substrate lactose (Kern, Jr. and Struthers, Jr. 1966).
Mal-nutrition also plays a role in
lactose intolerance especially in cases of advanced Kwashiorkor (Dean, 1957)
and mal-nourished children (Cevini et al, 1962; Careddu et al, 1963; Bardare et
al, 1965; Kerpel-Fronius et al, 1966).
Drug
induced lactose intolerance is significant with several antibiotics. Keating et
al. (1974) associated it with ampicillin therapy. This was also supported by
Tedesco (1975), Beavis, Parsons and Salfield (1976).
Isolated
deficiencies of the various disaccharides have been described but lactase
deficiency is the most frequent and best understood (Sodeman and Sodeman,
1974). Temporary lactase mal-absorption has been shown to occur in children
during bacterial or non-specific diarrheal diseases (Sunshine and Kretchner,
1964; Cevini et al, 1962), and during massive Giardia lamblia infestation
(Durand et al, 1963; Mardio et al, 1963). It is difficult to understand why
lactase enzyme should be singled out for damage but sparing the other three
alpha glycosidases – namely sucrose, maltase and isomaltase. It is even more
difficult to imagine that the defect can be permanent after the under-lying
condition is relieved. But lactase normally has a much lower activity than the
three – glycosidases and a decrease in all enzymes following a non-specific
injury will become manifest primarily by an impaired lactose tolerance. Again,
lactase may be the only enzyme most susceptible to permanent damage (Haemmerli
et al, 1965).
Most
recent studies with rats, rabbits, calves and humans shows that lactase appears
late during gestation, reaches a maximum shortly after birth and falls
gradually to a plateau (Heilskov, 1952; Alvarez 1961; Doell and Kretchmer,
1962). Attempts to prevent the fall after birth, or to increase the adult level
by administering oral or intraperitoneal lactose, have failed (Heilskov, 1952;
Alvarez and Sas, 1961; Doell and Kretchmer, 1962; Forster et al, 1963). Fischer
(1957) however, found that the diarrhea of rats on 25% lactose diet ceased
after prolonged ingestion, and that the total intestinal lactase increased, but
this was balanced by a 50% increase in mucosal weight.
Diarrhea
can invariably be produced by dietary lactose, although the threshold differs
with species and age (Cuatrecases et al, 1965). However absorption can be
improved and diarrhea disappear with prolonged intake in animals (Whitter et
al, 1935; Riggs and Beauty, 1947, Lawrence, 1950; Fischer and Sutton, 1953) and
in human infants (Lamedica et al, 1962). Cuatrecasas et al (1965) have shown
the same effect with human adults. Therefore, adaption to lactose evidently
occurs but it has an enzymatic basis. Girardet et al (1963) suggested that
lactase activity in the gut varies with dietary lactose in adult rats.
Cuatrecasas
et al (1965) demonstrated that lactase is not lost with advancing age. They
support the thesis that lactase deficiency in the adult results from prolonged
milk and lactose that is substrate deprivation. Attempts to improve absorption
ratio or raise lactase activity with short-term dietary measures have so far
failed. So Cuatrecasas et al suggested long-term dietary measure, consisting of
increase intake of milk or lactose for improved tolerance.
Lactase
deficiency or lack which culminates in lactose or milk intolerance may be a
latent condition, but manifest when the gut is challenged with a diet high in
milk or lactose. A previously asymptomatic lactase deficiency may become
evident also when combined with other gastrointestinal diseases mentioned
earlier because of:
i.
An increased lactose load contained in
an ulcer diet.
ii.
Increased rate of gastric emptying
following gastric resecting, or
iii.
Concurrent development of functional
or inflammatory intestinal disease (Sodeman and Sodeman, 1974).
Proposed criteria for diagnosis of
lactase deficiency include:
i.
Diarrhea, borborygmi, cramping
abdominal pain and flatulence after milk or lactose ingestion;
ii.
Absence or diminished lactase activity
in mucosal biopsy specimen.
iii.
A flat lactose tolerance curve –
obtained by serial determination of plasma glucose level at 30 minutes interval
for two hours after milk or lactose intake.
In children, the dosage of lactase is
2g/kg of body weight (Basferd, 1967; Gudmand-Hoyer, 1977). Adult dose is 50mg
lactose – equivalent to 1 liter of milk or 100mg of lactose. A control test may
be performed using 25g glucose and 25g galactose, if the test indicated
mal-absorption.
Patients
with lactase deficiency exhibit a peak rise less than 20mg/d1 (1.1mmo1) of
plasma glucose level. A group in Chicago noticed that a physiological dose of
50mg of lactose did not produce symptoms earlier mentioned, but showed severe
symptoms with 100mg lactose in subjects considered lactase deficient. These
subjects are said to be “clinically norm” but considered “forme fruste” of the
full syndrome (Haemmuli et al, 1965). Peternel (1965) reported that symptoms in
patients with lactase deficit appeared to depend on the ingestion of threshold
quantities of lactose or milk. And that it is common for milk intolerance to be
identified for the first time when the threshold quantities are exceeded. So
manifestations of lactose intolerance appeared to be dose related. In their
interpretation of reports from a Zurich group of investigators – (Auricchio et
al, 1963; Haemmali et al’ 1963; 1964 and 1965) – James et al (1965) suggested
that normal lactase levels are almost always associated with a maximal rise of
at least 20mg (1.1mmol) while deficit levels are usually associated with
sub-stantially smaller increments. For this reason, they disagree with Haemerli
et al. who stated that “a flat glucose curve alone after an oral lactose load
is meaningless.” They are also in disagreement with the implication of Kochler
et al, (1935); Girardet et al, (1963) and Isselbacher et al. (1964) that “flat”
lactose tolerance curves may occur in 25% or more of “normal” adults. They
experience that lactase-deficient state appears to be common enough to account
for high incidence of “flat” curves support their disagreement with the other
investigators.
Investigators
infer that 55% of adults are intolerance to lactose due to the deficiency of
jejunal B-galactosidase and cellobiase, with consequent inability to hydrolyse
dietary lactose.
Evidence
is strong that lactase deficiency may be an acquired trait and also that it may
be an adaptive enzyme, because this deficiency correlates with dietary milk or
lactose deprivation, for there is loss of symptoms with prolonged milk or
lactose intake, but decreased absorption with milk restriction. For instance,
large quantities of milk are consumed in the northern parts of Nigeria with no
apparent ill-effects, for milk is part of their cultural dietary intake;
especially amongst the nomadic communities, whereas the consumption of
relatively smaller quantities of milk in the southern communities of Nigeria
causes symptoms of milk intolerance such as mentioned earlier.
As
far as is known, there is no published work in the incidence of lactose or milk
intolerance in the southern part of Nigeria. The purpose of this work is
therefore to investigate the extent and the pattern of milk (lactose)
intolerance in a community in southern Nigeria.
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