Lactose intolerance is one example of food intolerance. The term "food intolerance"
denotes a non-immunologic adverse reaction to a food.
In the case of lactose intolerance it is due to an inability to digest significant
amounts of lactose, the predominant sugar of milk. This inability results from a
shortage of the enzyme lactase, which is normally produced by the cells that line
the small intestines. Lactase breaks down milk sugar into simpler forms that can
be absorbed into the blood stream.
Congenital Lactase Deficiency
This is a rare condition (less than 50 cases are known) in which the individual
cannot produce lactase. Watery diarrhoea occurs after breast-feeding or milk ingestion.
Primary (Late-onset) Lactase Deficiency
Lactase levels are high in all mammals following birth. In most mammals, however,
lactase levels decline after the infant is weaned. Man is the only mammal that may
retain lactase activity into adulthood. The gradual lactase disappearance usually
does not begin until the child reaches pre-school age (2-6 years), although it can
also begin at virtually any time later in life. The timing and rate of decline is
The ability of adults to drink milk is known as lactase persistence. Lactase persistence
is mainly confined to northwest Europeans and certain African subpopulations. This
was a survival trait from times of meat famine, when milk was required as a rich
source of protein and the gene for lactase persistence was passed along. These groups
include the Germans and British, who engaged in cattle farming and dairying by the
late first millennium AD.
Primary lactase deficiency is mostly seen in those racial/geographic groups whose
ancestors did not drink milk as a nutrient. Groups that cannot usually digest milk
include people from:
- East & South Asia
- Pacific & Mediterranean Countries
- Native Americans
- Jews & Eskimos
Secondary Lactase Deficiency
This type of lactase deficiency is secondary to a medical problem or use of certain
therapies. For instance, an episode of acute infectious diarrhoea (gastroenteritis)
can leave the patient lactase deficient through damage and temporary loss of the
relatively shallow intestinal villous section of the intestine. While other enzymes
(eg, sucrase and maltase) may be affected, lactase is the earliest to be lost and
the slowest to regenerate. Average recovery time is 4 weeks.
HIV infection can cause lactase deficiency, as do rotavirus and giardiasis.
Drugs, like Neomycin, Kanamycin, tetracycline and Methotrexate can cause villous
atrophy, leading to secondary lactase deficiency.
Alcohol can also inhibit disaccharidases (lactase & others enzymes) and cause
or worsen a lactase deficiency.
It is estimated that 25% of Americans and 75% of adults worldwide
have lactose intolerance.
81% of black adults and 100% of Asian adult have this problem.
Age is predictive of LA. At least 46% of those over 50 have the problem, in contrast
to only 25% of those under the age of 50.
Both affected equally.
Autosomal recessive single gene inheritance. Therefore, having 2 parents with lactose
intolerance virtually guarantees that the children will develop the disorder.
Two main reasons for symptoms.
Undigested lactose acts as an osmotic laxative. This leads to diarrhoea and abdominal
Intestinal bacteria are able to use lactose as a growth substrate. The rapid growth
of intestinal bacteria leads to the production of large volumes of gas. The gas
is responsible for the flatulence, dyspepsia, abdominal distension and stomach rumbling.
Vomiting, which is a common feature of milk allergy, is rare in lactose intolerance.
The age of presentation is usually after two, in contrast with cows milk allergy
that usually manifests during breast-feeding or shortly after weaning.
Often in LA the patient can tolerate small amounts of some dairy products whereas
in milk allergy even traces of any will cause symptoms.
Lactose elimination & lactase supplementation (in the form of tablets or liquid)
will usually differentiate this problem from milk allergy.
Fermentation of lactose produces hydrogen as a by-product. Breath hydrogen excretion
can be measured after a lactose challenge, and compared with baseline.
Treatment of Lactose Intolerance
Since milk allergy can be life-threatening even in trace amount, it is important
to differentiate lactose intolerance (which is not life-threatening) from milk allergy.
Very few people are so lactase deficient that the remedy is total restriction of
dietary lactose. The disorder is often dose-dependent. Many adults with primary
lactose deficiency can drink 100ml 200ml of milk (5g 10g of lactose)
without having symptoms. However, a little too much causes mild symptoms and a great
deal of excess lactose cause severe symptoms.
The severity of symptoms is product-dependent for many patients as well. Skim milk
causes more severe symptoms than whole milk. Chocolate milk may help the condition.
These differences are attributed to the fat content, osmolality and the delayed
gastric emptying augmented by additional ingredients in the different products.
In one study milk with breakfast cereals prevented symptoms completely.
There are several ways of giving lactase.
Yoghurt has lactase activity. Lactase enzymes are available without a prescription.
One form is a liquid to add to milk. A few drops are added to milk, and then after
24 hours in the refrigerator, the lactose is reduced by 70%.
There are also chewable lactase tablets that help people digest solid foods that
Infants and young children can have dairy based lactose-free formulas or non-dairy
formulas like soy.
Cows Milk Allergy (CMA)
Cows milk allergy is one of the commonest food allergies in children, perhaps
because it is usually the first highly allergenic foreign protein encountered by
infants. CMA is a "true allergy" since it is an immunologically-mediated
Between 2% and 7.5% of infants and young children suffer CMA.
Natural History & Prognosis of CMA
Most children will outgrow their milk allergy by age 3 years: 50% by 1 year of age,
70% by 2 years of age, and 85% by 3 years of age.
Unfortunately, in CMA patients, 50% will develop an allergy to other food proteins
(e.g., egg, soy, peanut) and 50-80% will develop an allergy against one or more
inhalant allergens (pollens, house dust mites, cat) before puberty. Milk allergy
is therefore a high risk factor for predicting infants who will develop asthma and
The two main protein fractions of milk are whey (20%) and casein (80%), and an individual
can be allergic to one or both. The casein is the curd that forms when milk goes
sour, and the whey is the watery fraction, which is left after the curd is removed.
The whey fraction contains mainly alpha-lactalbumin and beta-lactoglobulin and is
the most allergenic fraction and therefore causes the most clinical problem. The
whey fraction is altered by heat, and so the whey sensitive person may be able to
tolerate evaporated, boiled or sterilised (Long Life) milk & milk powder.
Casein is heat stable and is the most important allergen in cheese. The harder the
cheese, the more casein is formed. Extensive heating will reduce only, but not eliminate
the allergenicity of casein.
Exposure & Sensitisation to CM
Exposure to CM proteins may occur prenatally, as indicated by the
demonstration of milk-specific IgE antibodies in cord blood.
Recently, specific IgE against individual cows milk protein was demonstrated
in 76% of selected infants in whom CMA later developed. This data indicate that
prenatal sensitisation occurs and may play a role in the pathogenesis of food allergy.
Postnatally, breast fed infants are exposed to CM and other food
proteins ingested by the mother and excreted by the mammary gland. Bovine beta-lactoglobulin
can be detected in the breast milk in 95% of lactating women. Exclusively breast
fed infants in whom CMA develops may react to minute amounts of CM protein in human
milk. Also, sensitisation to foods during exclusive breast-feeding is likely to
result from ingestion of hidden CM protein and possibly from inhalant and skin contact.
The very small amount of cows milk protein in breast milk may induce tolerance
rather than allergic sensitisation and development of allergic disease. On the other
hand, a significant relationship exists between early neonatal exposure to CM formula
feeding and subsequent development of CMA.
With the introduction of CM-based formula into the infants diet, the antigenic
load of CM proteins becomes enormous. Macromolecular absorption is increased in
preterm infants and in newborns and has also been demonstrated in infants with CMA.
Whether increased macromolecular absorption is part of an allergic constitution
or is due to temporal mucosal damage is not clear
Development of Clinical Disease
There is increasing evidence that intrauterine sensitisation to foods as well as
to inhalants may occur. However, such weak intrauterine sensitisation may be a normal
phenomenon as is the well-known weak postnatal IgE response in infants without allergic
disease. Neonatal exposure to "high dose" of foreign protein may be necessary
for the development of allergic disease. Clinical symptoms of CMA may appear during
breast-feeding, but most infants have symptoms shortly after introduction of CMA
formula. Many studies have shown that CMA develops mostly during early infancy and
Clinical Types of Milk Allergic Reactions
Reactions vary from mild hives to life-threatening anaphylaxis.
Reactions can be immediate, following very small quantities of milk or start several
hours or even days after the intake of moderate to large amounts of CM.
Type 1 (Immediate)
Symptoms start within minutes of intake of small volumes of CM. Mainly cause skin
symptoms – eczema or urticaria (hives).
Respiratory – runny nose, cough or wheezing
Gastrointestinal – vomiting and diarrhoea
This is the most serious type as anaphylaxis and death is possible.
Type 2 (Intermediate)
Symptoms start several hours after intake of modest volumes of CM.
Main symptoms are vomiting and Diarrhoea
Type 3 (Delayed)
Symptoms develop after more than 20 hours, or even days after intake of large volumes
Symptoms include, diarrhoea with or without eczema and asthma
There is cross-reactivity among milk from cows, goats and sheep. Only the whey fraction
in goats milk differs from that in cows milk. Goats milk is tolerated
by only 40% of CMA children.
Diagnosis of Milk Allergy
Only the immediate (Type 1) milk reactions that develop after a few minutes are
most likely to give a positive skin prick test or RAST (blood test) to milk.
Skin Prick Tests (SPT)
SPT is especially accurate in the young child with immediate (type 1) reaction.
The skin is pricked through a small drop of milk placed on the forearm. A wheal
and flare reaction after 15 minutes will indicate that the patient is allergic to
The positive predictive accuracies of SPTs are less than 50% compared with DBPCFCs,
whereas negative SPT responses virtually exclude IgE-mediated reactions (negative
predictive accuracy is greater than 95%)
Nearly 60% of milk reactions in the young child are the delayed type (intolerant,
non-immunologic) and therefore unlikely to give positive results.
The diagnosis is then made by the Elimination-Challenge Test. This
should show the relief of symptoms on the removal of milk and the recurrence of
symptoms when re-introduced. This test should never be done at home. It should be
done under the supervision of the doctor and the dietitian.
An open challenge and careful follow-up may be adequate
for practical clinical purpose to diagnose the Type 1 (Immediate) Milk Reactions.
Double-blind Placebo-controlled Food Challenge (DBPCFC)
remains the gold standard for diagnosing milk allergy/intolerance, especially
in the Intermediate & delayed groups.
Milk is applied to the back in a special Finn chamber for 48 hours. A positive response
suggests a delayed hypersensitivity & is useful in intermediate & delayed
In one study of patients with atopic dermatitis, it was demonstrated that Patch
Testing could identify many patients with negative skin prick test and delayed clinical
reactions. Parallel skin testing with combined prick and patch tests can significantly
enhance the accuracy of specific food allergies in patients with atopic dermatitis.
Blood Tests (RAST & CAP RAST)
The CAP RAST is newer & more accurate than the RAST. It tests for milk proteins
as whole, or individual fractions of milk (casein, whey, beta-lactoglobulin).
A recent study with CAP RAST in children with atopic dermatitis showed that the
positive predictive value for milk, if the level is above 32 kuA/l is 95%. Therefore
for results above 32kUA/l a DBPCFC is not warranted.