Can’t drink milk? You’re “normal”!
How mutations cause lactose tolerance in adults
Lactose intolerance was really only recognized in the 1960s, and ranges from about 5% in northern Europe, around 70% for southern Europe, to more than 90% in some African and Asian countries. The aversion to milk among Asians was once mostly regarded in the West as cultural in basis (rather than biological/genetic), with powdered milk often being sent as part of food aid.18
Published: 26 May 2009(GMT+10)
This is the pre-publication version which was subsequently revised to appear in Creation 32(1):12–15.
For many, the mere mention of milk will be enough to invoke memories of nausea, bloating, cramps, diarrhea, and perhaps in some cases, jibes and taunts about “wind” and bad breath. Some will have undergone medical tests that diagnosed the cause as “ Lactose intolerance ”.
Lacking the enzyme lactase, which breaks down the milk sugar lactose (see box), they are unable to digest milk, whereas lactose-tolerant people can. Others, though, might still be unaware that they are “deficient” in lactase, not realizing that drinking milk causes their feelings of nausea, etc.1
For many years, lactose intolerance was regarded as abnormal, and was used by many as evidence of human evolution. As a measure of evolutionary “advancement”, milk-drinking seemed to fit the stereotype perfectly. Pale-skinnned northern Europeans usually retained full intestinal lactase activity into adulthood, in stark contrast to the world’s darker-skinned peoples who are only able to digest milk as infants or young children. Well, that’s the way the story went.
However, “lactose deficiency” in adults is not in fact abnormal, but the norm! Research has shown that the gene for lactase normally switches off as children are weaned. And a genetic mutation that results in lactase production not being switched off accounts for the ability of certain people to drink milk into adulthood.
So there has now been a dramatic change in terminology, with those who cannot digest milk no longer being called “lactase deficient”. Instead, they are now regarded as normal, while those adults who retain the enzymes allowing them to digest milk are called “lactase persistent”.2,3
Furthermore, different mutations can stop lactase production from being switched off after weaning. The mutation that confers lactase persistence in northern Europeans4 is different from the mutation in East Africans who are lactase persistent.5 Researchers have identified three different mutations (in the same stretch of DNA as the European variant) in various African populations in Tanzania, Kenya and the Sudan.6
Evolutionary notions overturned
The findings have overturned previously-held evolutionary notions in dramatic manner. Anyone enamoured with the black-people-are-less-evolved-than-white-people idea must confront the fact that dark-skinned Africans have been shown to have genetic mutations conferring lactase persistence—some of them even had all three of the mutations so far discovered in that region.7
Some of the symptoms of Charles Darwin’s ‘mystery illness’ match those resulting from lactose intolerance.
In that light it’s interesting to make comparative reference to a notable pale-skinned person, namely, Charles Darwin. Some of the symptoms of his “mystery illness”,8 viz. continual “diarrhea, bloating and gas”,9 match those resulting from lactose intolerance!
Another shake-up for evolutionists was the researchers’ assessment that the most common variant arose “as recently as 3,000 to 7,000 years ago”. University of California anthropologist Diane Gifford-Gonzalez says the finding of recent multiple mutations arising independently is changing the way they think about human history: “Until the geneticists contributed to the data, the rest of us always thought about evolution happening very slowly and gradually.”10
This is not the first time, however, that evolutionists have been surprised by the speed of genetic changes.11
However, they still claim it as evolution. “This is the best example of convergent evolution in humans that I’ve ever seen,” said geneticist Joel Hirschhorn, of the Children’s Hospital Boston, Massachusetts.10 But note that these genetic changes are not “evolution” in the uphill molecules-to-milkman sense, as the changes are downhill, i.e., information has been lost (viz., the normal switching-off mechanism of lactase production following weaning).12 Rather, at best this is an example of selection, as Hirschhorn himself went on to acknowledge: “Lactase persistence has always been a textbook example of selection, and now it’ll be a textbook example in a totally different way.”10
It seemingly doesn’t matter what the evidence is—evolutionary theory can be made to do an ‘about-face’ when desired.
Hirschhorn’s comments also highlight two key factors underscoring the creation-evolution issue. First, the extreme flexibility of evolutionary theory. It seemingly doesn’t matter what the evidence is—evolutionary theory can be made to do an “about-face” when desired. Second, the classic “bait-and-switch” tactic of interchanging “evolution” with “selection”. But natural selection is not evolution.13
Another unexpected result of the milk-drinking mutation survey in east Africa was the finding that the Hadza people of Tanzania “show a surprisingly high level of lactase persistence despite having very little to do with cattle”. That led to this evolutionarily-radical suggestion: “One possibility is that, though they are now mainly hunter-gatherers, their ancestors might have been pastoralists.” While that idea goes against the traditional evolutionary order, it is right in line with a biblical perspective. Furthermore, this is not the first time that evolutionists have had to face up to evidence that today’s hunter-gatherer peoples previously practised farming or animal husbandry—contrary to their cherished ideas.14
Being a “mutant” can be advantageous
I find it ironic that a so-called disease [i.e. ‘lactase deficiency’] actually represents the original condition.—University of California geneticist Leena Peltonen
Although the loss of the ability to turn off lactase production following weaning is a loss of information (i.e. a downhill change), the mutation confers some obvious advantages in areas where milk is available. The “cost” of the mutation, i.e., the extra energy needed to continue to produce lactase beyond infancy, would be more than compensated for by being able to safely extract the energy and nutrients in milk.15
So in what time frame could the milk-drinking mutation have arisen? From a biblical perspective, the mutation first arose after the Fall (there were no mutations in the “very good” world described by God in Genesis 1:31). There is no reference to milk-drinking before the Flood (i.e. around 4,500 years ago), but by the time of Abraham, people were certainly consuming dairy products (Genesis 18:8).16 And there are many references to Israel being a land “flowing with milk and honey” (e.g. Leviticus 20:24).17
Adam and Eve, being genetically perfect, would not have had the milk-drinking mutation, therefore, we can presume, did not drink milk. Even the evolutionists acknowledge that man’s original status was indeed “lactose intolerance”. University of California geneticist Leena Peltonen quipped, “I find it ironic that a so-called disease [i.e. ‘lactase deficiency’] actually represents the original condition.”18
So, those of you who are unable to drink milk as adults today without feeling nauseous (or worse) can take heart from being closer in that respect to the originally “physically-perfect” first man and woman than are those of us who are milk-drinking “mutants”!
Lactase and lactose
Most human infants produce ample quantities of lactase for milk digestion. The cells that line the small intestine produce the enzyme lactase, which breaks down lactose, the characteristic disaccharide sugar of milk, into the monosaccharides glucose and galactose. These sugars are easily digested (absorbed) by humans.
However, when lactase is lacking, as it is in most adult humans19 and animals, the lactose cannot be broken down and absorbed in the small intestine. The lactose therefore passes to the large intestine where the resident bacteria ferment it, generating gas—hence the discomfort of nausea/bloating/flatulence experienced by “lactase-deficient” people after drinking milk.
Many “lactose intolerant” people are able to consume some dairy products, such as cheese, without experiencing the debilitating symptoms they get following consumption of milk. That is because there is little lactose in such fermented products, as the bacteria (e.g. lactobacilli) have already fermented most of the lactose in the original milk into lactic acid, with the by-product gas released harmlessly into the atmosphere.
Don’t confuse “lactose intolerance” for milk protein allergy
Some children who are said to be “lactose intolerant” are later found to be able to tolerate milk. However, almost certainly those children were not lactase deficient but rather were allergic to a milk protein (lactoglobulin). This is fairly common in young children—they usually grow out of milk allergies as their gastro-intestinal tract matures. Such children can usually tolerate goat’s milk, which also has lactose, of course, but lacks the cow’s milk proteins that cause the problems. There is even a difference between breeds of cows, it turns out. A person might not tolerate Friesian milk (most commercial pasteurized milk is largely Friesian) but tolerate Guernsey or Jersey milk, for example. Lactose-intolerant persons can often well tolerate natural yoghurt, which has about 2/3 the lactose of milk. Researchers think that this is due to the presence of lots of live fermenting bacteria, which quickly digest the lactose at body temperature, and also contribute lactase.
Sieber, R., Stransky, M. and de Vrese, M., [Lactose intolerance and consumption of milk and milk products—In German], Z. Ernahrungswiss 36(4):375–93, 1997.
- Common symptoms (nausea, cramps, bloating, etc.) normally begin about 30 minutes to two hours after consuming milk or lactose-containing milk products. Some people cannot even have milk in their tea without experiencing constricted breathing. Return to text.
- What is lactose intolerance?, Physicians Committee for Responsible Medicine, <www.pcrm.org/health/Info_on_Veg_Diets/lactose_intolerance.html>, 12 July 2002. Return to text.
- Even “lactase persistent” people mostly tend to produce less of the lactase enzyme as they age, while for many “lactase deficient” people the development of lactose intolerance is a gradual process spread out over as many as 20 years. Maintaining daily (cow’s) milk consumption after weaning is believed by some to prolong lactase production (and hence the ability to drink milk into adulthood), but conclusive evidence is lacking. There is no known treatment that can improve the body’s ability to produce lactase. Return to text.
- Enattah, N. and 5 others, Identification of a variant associated with adult-type hypolactasia, Nature Genetics 30:233–237, 2002. Return to text.
- Mulcare, C. and 8 others, The T Allele of a Single-Nucleotide Polymorphism 13.9 kb Upstream of the Lactase Gene (LCT) (C–13.9kbT) Does Not Predict or Cause the Lactase-Persistence Phenotype in Africans, American Journal of Human Genetics 74(6):1102–1110, 2004. Return to text.
- The 470 individuals tested came from 43 ethnic groups, including the Maasai and the Beja people. The researchers labelled the three SNPs (Single Nucleotide Polymorphisms) as G/C–14010, T/G–13915 and C/G–13907, adding that “These SNPs originated on different haplotype backgrounds from the European C/T–13910 SNP and from each other.” Tishkoff, S.A. and 18 others, Convergent adaptation of human lactase persistence in Africa and Europe, Nature Genetics 39:31–40, 2006. Return to text.
- The findings might also help to explain why people tolerate milk to varying degrees. As one observer put it, the ability to drink milk is “not a qualitative trait that you have or you don’t”. Researchers in this field expect to discover yet more milk-drinking mutation variants. Gibbons, A., There’s more than one way to have your milk and drink it, too, Science 314(5806):1672, 15 December 2006. Return to text.
- Grigg, R., Darwin’s mystery illness, Creation 17(4):28–30, 1995, <creation.com/illness>. Return to text.
- Kevles, B., Home life at Down House, Science 296(5575):1974, 2002. Return to text.
- Check, E., How Africa learned to love the cow, Nature 444(7122):994–996, 21/28 December 2006. Return to text.
- Catchpoole, D. and Wieland, C., Speedy species surprise, Creation 23(2):13–15, 2001, <creation.com/speedy>. Return to text.
- Wieland, C., The evolution train’s a-comin’ (Sorry, a-goin’—in the wrong direction), Creation 24(2):16–19, 2002, <creation.com/train>. Return to text.
- Wieland, C., Muddy waters—Clarifying the confusion about natural selection, Creation 23(3):26–29, 2001, <creation.com/muddy>. Return to text.
- Catchpoole, D., The people that forgot time (and much else, too), Creation 30(3):34–37, 2008, <creation.com/forgot>. Return to text.
- It has also been suggested that people having the mutation might have been better able to survive drought, by being able to drink milk without the risk of diarrhea, which exacerbates dehydration. Ref. 10. Return to text.
- The Bible refers to Abraham taking “curds and milk”. Curds, being a fermented product, would have been very low in lactose, and therefore digestible by virtually everyone. If the milk was fresh milk (and not whey) then it implies that Abraham’s family were able to tolerate lactose as adults, and that Abraham presumed his three guests would also be able to appreciate it, too. Return to text.
- There are many other passages in Scripture referring to milk and milk products such as curds, butter and cheese—e.g. Proverbs 30:33, Isaiah 7:22, 1 Samuel 17:18, 2 Samuel 17:29. Return to text.
- Randerson, J., Too old to take it—Now we know why it’s usually only babies who can stomach milk, New Scientist 173(2326):13, 19 January 2002. Return to text.
- It is has been estimated that over 70% of the world’s population has low lactase with resultant lactose intolerance. Gilat, T., Kuhn, R., Gelman, E. and Mizrahy, O., Lactase deficiency in Jewish communities in Israel, Digestive Diseases 15(10):895–904, 1970. Return to text.