In 1836, after returning from the Beagle, Charles Darwin wrote “I have had a bad spell. Vomiting every day for eleven days, and some days after every meal.” Darwin suffered for over 40 years from long bouts of vomiting, stomach cramps, headaches, severe tiredness, skin problems and depression. A number of researchers now suggest that he suffered from lactose intolerance (Campbell and Matthews, 2005). His case is a good example of how easily lactose intolerance can be missed.
Lactose is a disaccharide made up from glucose and galactose. It is the primary carbohydrate (sugar) found exclusively in mammalian milk (Heyman, 2006). To obtain energy from lactose, it must be broken down to glucose and galactose by the enzyme lactase. This enzyme is found in the small intestine on the tips of the villi. Glucose and galactose are then readily absorbed into the bloodstream to provide energy. Lactose intolerance occurs when the body produces little or no lactase, or when the lactase it produces doesn’t work. In the absence of lactase, lactose is fermented by bacteria in the large intestine. These bacteria produce hydrogen and a wide range of potential toxins (Matthews et al., 2005).
Lactose intolerance and cow’s milk allergy are often mistakenly confused. Lactose intolerance is caused by a lack of lactase, cow’s milk allergy is an adverse immune reaction to proteins found in milk.
Hippocrates first described lactose intolerance around 400 years BC but the clinical symptoms have become recognised only in the last 50 years (Lomer et al., 2008). Symptoms include diarrhoea, bloated and painful stomach and on some occasions nausea and vomiting. Typically lactose intolerance causes diarrhoea via an osmotic mechanism. However, persistent lactose-induced diarrhoea that lasts long after the lactose has gone may be caused by a signalling mechanism analogous to cholera or enterotoxin (Matthews et al., 2005).
Other symptoms may include muscle and joint pain, headaches, dizziness, lethargy, difficulty with short-term memory, mouth ulcers, allergies (eczema, rhinitis, sinusitis and asthma) cardiac arrhythmia, sore throat, increased frequency of urination, acne and depression (Lomer et al., 2008). The severity of symptoms depends on the level of lactase produced; someone producing moderate levels may experience mild symptoms, whereas a person producing very little or no lactase will suffer more severe symptoms. Even more worrying is that bacterial toxins may play a key role in several other diseases, such as diabetes, rheumatoid arthritis, multiple sclerosis and some cancers (Campbell et al., 2009).
There are three types of lactase deficiency:
- Primary lactase deficiency (adult-type hypolactasia) is the most common form. In most mammals, lactase activity naturally declines at variable rates following weaning until it reaches undetectable levels (Lomer, 2008). Generally the age of onset ranges from 1-20 years (Rasinperä et al., 2004). However, it is not unknown for lactose intolerance to develop in people over 20 (Seppo et al., 2008).
- Secondary (acquired) lactase deficiency is caused by illness, injury or medication. It can result from digestive diseases of the small intestine (such as ulcerative colitis and Crohn’s disease), or intestinal damage caused by infections (such rotavirus and Giardia) (Matthews, 2005). Chemotherapy and long courses of antibiotics can cause lactose intolerance too. This may be temporary, but if caused by a long-term condition, could be permanent.
- Congenital lactase deficiency is an extremely rare disorder of new-borns associated with a complete absence of lactase. Affected infants present with intractable diarrhoea as soon as human milk or lactose-containing formula is introduced. Infants with this condition would not be expected to survive before the 20th century, as no suitable lactose-free formula was available (Heyman, 2006).
For some years, it was thought that lactase persistence in humans was the ‘wild-type’ pattern. It is now widely accepted that in adulthood, lactase deficiency is the normal state for most people (Lomer et al., 2008). A staggering 4,000 million people cannot digest lactose properly (Campbell et al., 2009). In fact, around 70 per cent of the world’s population has primary lactase deficiency (Heyman, 2006; Lomer et al., 2008). It is most prevalent in Asian and African countries with 80-100 per cent frequency. In Northern Europe, prevalence varies between one and 18 per cent (Rasinperä, 2004). The age of onset varies among different ethnic populations. Around 20 per cent of Hispanic, Asian and black children under five show some evidence of lactase deficiency (Heyman, 2006), while low lactase levels are rarely seen in white children under five (Rasinperä, 2004).
The widespread prevalence of lactose intolerance suggests that lactase deficiency is the normal or natural state and that the ability to continue to digest lactose after weaning originates from a genetic mutation that provided a selective advantage to populations using dairy products (Swagerty et al., 2002). This idea is supported by William Durham in his book Coevolution (Durham, 1991). Durham describes milk as baby food not ‘intended’ for adult consumption. He describes how the ability to digest lactose is the exception to the norm and can originally be traced back to a minority of pastoral tribes: the Tutsi and Hutu of Rwanda; the Fulani of West Africa; the Sindhi of North India; the Tuareg of West Africa and some European tribes. People who have retained the normal intolerance of lactose include: Chinese, Japanese, Inuit, native Americans, Australian Aborigines, Iranians, Lebanese and many African tribes including the Zulus, Xhosas and Swazis. These people, generally, do not have a history of pastoralism. As stated in Part One (The Origins of Dairy Farming) lactase persistence only developed around 8,000 years ago. In evolutionary terms, this is very recent history.
A range of tests can be used to diagnose lactose intolerance. The breath hydrogen test is currently considered to be the most cost-effective, noninvasive reliable test (Lomer et al., 2006). However, it involves drinking a lactose solution and can cause severe symptoms, sometimes lasting for days (Matthews, 2005). In rare cases a small bowel biopsy may be used to measure lactase levels. However, this invasive technique is usually used to determine whether the symptoms are caused by another condition, such as coeliac disease. A stool acidity test may be used to check infants for lactose intolerance. This is because large doses of lactose, such as those given in the breath hydrogen test, are dangerous for young children. Also, infants are more likely to develop dehydration caused by diarrhoea. DNA analysis of blood samples could offer a quick and easy to way to diagnose lactose intolerance and may help to differentiate patients with primary and secondary lactase deficiency (Lomer et al., 2008). However, this test is not yet routinely available.
When a dairy exclusion diet appears to fail, lactose intolerance is often mistakenly ruled out (Matthews et al., 2005). This is because lactose is added to many unexpected (non-dairy) foods and may continue producing symptoms in a patient convinced they are on a lactose-free diet. Lactose is used as a browning agent in bread and cakes, it is added to processed meats (sausages and burgers) and even injected into some chicken meat. It is also added to some soft drinks and lagers. Breakfast drinks, powders and slimming products can contain as much lactose as cow’s milk and it is often used in sauces supplied to butchers and restaurants (Matthews et al., 2005). Since 25 November 2005, all pre-packed foods sold in the UK have to show clearly on the label if they contain milk or any of the ingredients of milk.
Treatment depends on how sensitive the patient is to lactose. If they are mildly intolerant, they may be able to tolerate small amounts of some dairy foods. Fermented dairy foods (such as probiotic yoghurt and milk, sour cream, cottage cheese and hard cheeses, such as Edam and Cheddar) contain less lactose than fresh dairy products. Alternatively lactase may be taken in liquid form or capsules before a meal or added to cow’s milk. Low lactose milk is also available in supermarkets but is quite sweet as it contains galactose and glucose from degraded lactose. Other animal milks (such as goat’s milk), are not lactose-free. In fact, the lactose content of goat’s and cow’s milk are very similar; goat’s milk contains 4.4g of lactose per 100g and whole milk contains 4.5g per 100g and semi-skimmed contains 4.7g per 100g (FSA, 2002). Of course, non-dairy products (such as soya, rice and oat milk) are excellent alternatives that do not require any monitoring at all.
Avoiding all lactose means cutting out all dairy foods and checking labels for lactose in bread, chocolate and other processed foods including meats. In addition, lactose is used in some types of medication so the patient should check with their GP or pharmacist (although symptoms of lactose intolerance rarely occur as a result of taking medication containing it).
Although there is no evidence of calcium deficiency in people eating a Chinese or Japanese diet with no lactose (Matthews, 2005), patients cutting out dairy foods may need some help and advice on how to ensure they still get plenty of calcium. This may be important for young children who need calcium for healthy growth and development. There are many excellent non-dairy sources of calcium including non-oxalate dark green leafy vegetables (broccoli, kale, spring greens, cabbage, bok choy and watercress), dried fruits (figs and dates), nuts (almonds and Brazil nuts) and seeds (sesame seeds and tahini, which contains a massive 680 milligrams of calcium per 100 grams) (FSA, 2002). The dairy industry frequently cites the poor absorption of calcium from spinach as an example of how ‘superior’ cow’s milk is as a source of calcium. However, spinach is an unusually poor source of calcium compared to other plant foods as it contains higher levels of oxalate which binds calcium and lowers its availability. Pulses (soya beans, kidney beans, chick peas, baked beans, broad beans, lentils, peas and calcium-set tofu) also provide a good source, as does calcium-fortified soya milk.
Although rarely life-threatening, the symptoms of lactose intolerance can lead to significant discomfort, disrupted quality of life, loss of school attendance and leisure and sports activities and work time, all at a cost to individuals, families and society (Heyman, 2006). The terminology relating to lactose intolerance (as opposed to milk protein allergy) can be confusing. It is therefore crucial to ensure that these problematic terms do not cause diagnostic mistakes and inappropriate treatment (Harrington and Mayberry, 2008).
In conclusion, drinking cow’s milk is neither normal nor natural. The health implications of being the only mammal to consume milk as adults (and not just that, milk from another species too) are becoming clearer in the scientific literature as levels of the so-called diseases of affluence soar. The treatment for lactose intolerance is straightforward: avoid lactose. This means cutting out all dairy foods and checking labels for lactose in bread, chocolate and other processed foods.