by Julie Albrecht, Consultant Dietitian – Nutritionist A.P.D.
Both children and adults can experience adverse responses to milk. This hypersensitivity may be related to the proteins in the milk, where the individual is allergic or intolerant or they may be intolerant to the lactose component, where the individual has a lactase enzyme deficiency resulting in a lactose intolerance and hence malabsorption of this carbohydrate.
There is a 2 -3 % prevalence of Cow’s Milk Protein Allergy (CMPA) in children, although it is rarely seen in adults, with only 0.7 % of atopic individuals with a positive skin prick test, however these individuals do not experience any adverse response to the consumption of cow’s milk (1). Twenty five percent of individuals with CMPA go on to develop additional food allergies. Fifteen percent of infants will carry this allergy into adulthood (1).
CMPA usually develops in the first year of life and the infant usually develops symptoms before one month of age (1). These reactions can be mediated by IgE and non-IgE immunological responses. The incidence at one year of age is 2.0 – 2.5 % (1). The symptoms of CMPA are usually present after the first or second exposure to CMP or post partum if breast feeding is delayed and an alternative Cow’s Milk (CM) formula is fed to the infant(1). CMP exposure can also occur via skin contact (kissing) and from vapours from cooking, with the latter resulting in an allergic asthma reaction (1). Breast fed infants with CMPA soon present after birth with eczema or proctocolitis or present after exposure to CM based infant formula or after consuming foods that contain CMP (1).
There are two major protein groups in cow’s milk, with casein constituting 80% of the content and the remaining 20 % being whey. Casein is the major milk allergen and consists of five protein fractions, αs1-, αs2-, β-, κ-, and gamma casein (1). The whey fraction contains globular proteins, alpha- lactalbumin and beta-Lactoglobulin, with beta-Lactoglublin being acid-stable and is likely to remain intact after its passage through the gut, and hence has the potential to initiate an allergic reaction (1). Research performed on the milk of other mammalian species, animals who are phytogentically related, including sheep, goat, water buffalo, horse and donkey, reveals that their milk contains similar proteins to cow’s milk, with B-lactoalbumin being present in the milk of all species studied (1). This confers their allergenic potential and hence they are not suitable alternatives for breast milk (1). A2 milk is often considered as another alternative product. A2 milk is produced by cows homozygous for the A2 polymorphic variant (his→pro) at amino acid 67 of the β-casein gene (2). A difference in degradation patterns of the A1 and A2 variants is purported to lead to differences in immunological or pharmacological effects (2). β-casein is one of at least seven proteins in milk(2). The single amino-acid difference in one protein of the A2 milk is not expected to have a significant effect on A2 milk potential to initiate and allergic response, hence A2 milk is contraindicated for individuals with CMPA (2).
Cow’s Milk Protein (CMP), can induce an acute IgE mediated reaction within less than 2 hours after exposure. It can also induce a delayed reaction (> 2hours) which can be either non- IgE or a combination of IgE and non-IgE mediated response (1). The current research data relates that 58% of individuals experience an early reaction and 42% experience a delayed non–IgE mediated response(1).
CMPA usually affects two systems within the body, with 50 – 60 % affecting the Cutaneous System (Skin); 50 – 60% Gastrointestinal System; 20 – 30 % Respiratory Systems. Gastrointestinal Reflux is seen in 16 – 42 % of infants with CMPA (1). Chronic constipation is seen in 3 – 16% of children and in 30 – 55% this is related to CMPA. CMP as a cause of constipation, though for adults is only seen in a small number of individuals (1).
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IgE Mediated |
Reaction |
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Gastrointestinal |
Gastrointestinal anaphylaxis; symptoms include vomiting, pain and or diarrhoea |
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Cutaneous |
Urticaria, angio-oedema, pruritus, morbilliform rashes and flushing |
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Respiratory |
Acute rhinoconjunctivitis, wheezing, coughing and stridor |
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Generalised |
Anaphylaxis |
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Mixed IgE & Non- IgE Mediated |
Reaction |
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Gastrointestinal |
Eosinophilic Oesophagitis, colitis, and/or proctocolitis |
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Cutaneous |
Atopic eczema |
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Respiratory |
Asthma |
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Non Ig E Mediated |
Reaction |
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Gastrointestinal |
Food protein induced enterocolitis, food protein induced protocolitis and food protein induced enteropathy syndrome |
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Cutaneous |
CMP – induced contact dermatitis |
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Respiratory |
Food induced pulmonary haemosiderosis (Heiner’s Syndrome) (rare) – pulmonary haemosiderosis or bleeding in the lower respiratory tract. |
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Mechanisms Uncertain |
Reaction |
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Gastrointestinal |
Constipation, (association remains controversial), intestinal colic, |
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Respiratory |
Excess mucous production - the snuffly child (association remains controversial, but commonly suspected by parents); Heiners Syndrome |
The diagnosis of CMPA encompasses a detailed clinical history, physical examination and dependent on the type of reaction, Skin Prick Testing (SPT) or specific IgE testing (1). These assessments, in conjunction with elimination diet and challenges are the corner stones to management (1). Non-IgE mediated reactions will usually yield negative test results (1). The avoidance of CMP for at least four weeks, along with possibly patch testing are required for diagnosis of non-IgE mediated CMPA (1).
The management of CMPA encompasses the avoidance of CMP and other mammalian milks, which includes all traces of dairy that may be found in manufactured food items. It is important to be aware of the different terminology used to label CMP (1). Breast fed infants can be exposed to CMP via touch and through breast milk, hence it is paramount that the mother avoids all sources of dairy (1). Beta-lactoglobulin can be detected in breast fed babies, however it is generally tolerated by 95% of infants (1). Hypoallergenic, and elemental hypoallergenic formulas are used for Infants unable to receive breast milk (1). These products include Neocate and Elecare. Soy based products are also considered at this time. However, as there is a strong cross-reactivity between CMP and soya protein, soy products are contraindicated (1).
There are a range of alternative milks, however these products have a lower energy and protein density and have lower levels of fat soluble vitamins and minerals (1). Some of these products are supplemented with calcium and or protein enriched. Infants and mothers may require additional supplementation with respect to calcium and vitamin D. The variety of alterative products includes, rice milk, quinoa milk, oat milk, pea milk and nut milk (only if nut milks are tolerated) and coconut milk. There are a range of dairy free margarines spreads, recipes for homemade rice milk ice cream made with rice milk and rice milk cream and coconut cream. There is also a range of dairy free and soy free products produced by companies such as Orgran, Well and Good, Enjoy Life, Probios and Brighter Life foods. A range of products can be purchased on-line at www.allergyassist.com.
The prognosis of CMPA is quite positive. By one year of age there is 45 – 60% remission, 66 – 75 % are in remission by the age of 2 years, 85 – 90 % by the age of 3, 92% between the age of 5 – 10 and 97% by the age of 15 (1).
Lactose Intolerance is not mediated by the immune system. The symptoms of abdominal bloating and diarrhoea are the result of the malabsorption of the CHO-lactose. There are three major types – congenital, primary and secondary lactose intolerance (1). Seventy percent of lactose intolerance occurs over a period of many years and never before the ages of 2 -5 years up until adulthood. In secondary lactose intolerance, there is reduced lactase activity due to illness, viral gastroenteritis, giardiasis and celiac disease, which results in damage to the brush border of the small intestine (1). Lactose can usually be introduced several weeks after maintaining the lactose free diet (1). The diagnosis of lactose intolerance is by breath hydrogen breath test; the measurement of the rise in BGL after the consumption of dairy; to test for the evidence of reducing substances in the stool (1).
Individuals with lactose intolerance experience symptoms of diarrhoea, abdominal bloating and cramping. These symptoms are a result of the malabsorption of lactose which exhibits an osmotic load (1). This increased load increases the rate of intestinal transit time (1). Once, in the colon the lactose is acted upon by bacteria which produce Short Chain Fatty Acid (SC-FA) and gas which is what causes the bloating (1). Research reveals that 24- 27% of individuals with IBS have lactose Intolerance (1).
The management of lactose intolerance is generally through a lactose free diet, encompassing lactose free milk and for the very sensitive individuals the avoidance all products containing dairy. There are a range of lactose free products including milk (Liddel’s and Parmalat milk), yoghurt, chocolate, and dairy free cakes and biscuits. Individuals can also use a lactase enzyme (Lactese), to digest the lactose in milk or a food product.
1. Tanya Wright and Rosan Meyer., Dietary Management of Milk and Eggs -Food Hypersensitivity: diagnosing and managing food allergies and intolerances – edited by Isabel Skypala, Carina Venter; Wiley and Blackwell 2009, Part 2, p 117- 128.
2.William B Smith, Dery Thompson, Margaret Kummerow, Patrick Quinn, Michael S Gold., A2 milk is allergenic., MJA2004;181(10):574.