Got Milk? Image by A. deAlbornoz, Flickr
(Click on the following link to listen to an audio version of this blog …Got milk?
Milk is the maternally produced nutritional fluid that all baby mammals need to consume to stay alive and grow. Think about it: humans, cows, rats, pandas, dolphins, fruit bats and blue whales (and all of the other 64,000 living species of mammals, too) begin life by consuming their mothers’ milk!
Milk is mostly water (87%) with a calorie-rich emulsion of butter fat (mostly triglycerides). It contains lots of proteins (most of which are organized into huge “casein” micelles), salts and minerals (including calcium, phosphate, magnesium, sodium, potassium and chloride), vitamins (A, B6, B12, C, D, K, E, thiamine, niacin, biotin, riboflavin, folates and pantothenic acid), monosaccharides (glucose, galactose) and a milk-specific disaccharide called lactose (which is glucose and galactose bonded together). Lactose, very significantly, is only found in milk and in the myriad of other foods that are derived from milk (and a few surprising human-made products, too!). Lactose represents 40% of the calories in milk. Obviously, the ability to digest lactose is critical to get the full energy yield from milk!
Public Domain
Of the 64,000 species of mammals all but one of them sets aside milk as an exclusive food for its very young individuals. The singular exception is, of course, us. About a third of human population is able to digest lactose well into their adult life stages. That means, of course, that about two thirds of human beings exhibit the standard mammalian life stage response to lactose: “milk is for kids!”
When a young mammal is weaned from nursing and moves on to more “mature” foods, its ability to make the digestive enzyme that break down lactose (“lactase”) decreases and, often, stops altogether. With no lactase, milk becomes a much less desirable food source and can actually begin to have quite negative impacts on the “lactose intolerant” individual.
Lactose. Figure by Yikrazuul. Wikimedia Commons
Lactose intolerance syndrome is also called “lactose malabsorption syndrome.” In this syndrome, the disaccharide lactose in the digesting food cannot be absorbed into the blood stream by the epithelial cells of the small intestine. It must first be broken into its two simple sugars (glucose and galactose) which then can be very rapidly absorbed into the blood. This digestion is carried out by the enzyme “lactase.” Lactase is synthesized by the cells lining the small intestine and is attached to the complex system of microvilli (called the “brush border”) on the free edge of intestinal epithelial cells. If someone lacks lactase, then lactose in the food simply passes through the entire length of the small intestine and then enters the large intestine (the “colon”).
E. coli. USDA, Public Domain
The colon, unlike the small intestine, has a rich community of bacteria. These bacteria (which include Escherichia coli and a number of other bacterial species) have enzyme systems capable of breaking lactose down into its simple sugars. These catabolic pathways, though, generate large amount of gas (hydrogen, carbon dioxide and methane) which can cause colicky spasms and pain in the colon and also can generate flatulence. Further, the presence of high levels of glucose and galactose from the lactose breakdown osmotically pulls water through the colonic epithelium into the forming feces. This results in diarrhea.
It is possible, however, for someone who is completely incapable of synthesizing lactase, to eat lactose-rich foods without experiencing the gas, the colicky pain and the diarrhea of a full-blown lactose intolerance episode. Limiting the amount of lactose ingested and eating the lactose-rich food along with other, non-lactose foods limits the intensity of the lactose fermentation in the colon. Processing, cooking or fermenting the lactose-rich milk can further reduce the total amount of lactose in the resulting foods. Also, apparently, a person’s colonic bacteria can, with continuous, low-level exposure to lactose, become more efficient at digesting lactose (thus producing less gas) and also become able to utilize the generated simple sugars for their energy needs (thus preventing the increase in colonic osmotic tension, and the resultant diarrhea).
Photo by Jjron. Wikimedia Commons
Humans, as a consequence of the Agricultural Revolution that began about 10,000 years ago, suddenly had foods available to them in large and relatively consistent quantities. In many societies these new foods included milk from domesticated animals (cows, sheep, goats, horses, donkeys, camels, water buffalo, reindeer, yaks, etc.). The first group to domesticate these milk producing animals were in present day Turkey about 9,000 years ago. The domestication of these animals and the harvesting of milk for food moved across northern Europe (6,600 years ago) and to England and Ireland (6,000 years ago). This migration was measured by residue analysis of pottery used for food storage and preparation.
A classical evolutionary model ties this increased milk use directly and immediately to the occurrence of and selection for a mutation that caused lactase persistence in the human populations. Recent research, though, questions the timing of this evolutionary model.
People in Northern Europe were widely consuming milk 6,600 year ago. Genetic analysis of their skeletal remains, though, indicate that the mutation for lactase persistence did not become common until 4,000 years ago. So, for 2,600 years, adult Northern Europeans consumed milk even though they were mostly unable to digest the lactose and, presumably, were prone to experience the difficulties of the lactose intolerance syndrome. Further, in modern human societies, many populations consume significant amounts of milk and milk products even though they do not have the lactase persistence mutation!
Isle of Mull cheese. Photo by Huberti. Wikimedia Commons
Presumably, these lactose non-digesters both in the past and in the present developed colonic microflora that tolerated some levels of lactose without triggering a full blown lactose intolerance reaction. Also, quite possibly, these lactase-deficient people primarily consumed processed milk products that were low in lactose (like cheese and butter, for example) or products (like yogurt) to which fermenting, lactase producing bacteria (like Lactobacillus acidophilus) were added.
But, why did this status quo change in Northern Europe 4000 years ago? The new evolutionary model hypothesizes that intestinal diseases crossing over from the increasingly abundant and intimately housed domesticated livestock began to beset Northern Europeans. The key to survival from these afflictions is vigorous rehydration. One fluid source for rehydration is milk, but a lactose-intolerant individual consuming milk when they are already ill with an intestinal disease will have amplified diarrhea that very likely will be fatal! So, starting 4000 years ago, being lactase-persistent was the key for survival.
Again, humans are the only mammals that have lactase persistence past childhood. Humans have manipulated their own evolution by their powerful control over their food supplies. Worldwide the human population is about 67% lactose intolerant. In East Asia, where milk production and consumption was never a major part of the agricultural food chain, about 90% of the population is lactose intolerant. In Northern Europe, though, where milk products and zoonotic diseases were rampant, only about 5% of the population is lactose intolerant.
Many of my students in the past have asked me if humans are still evolving. The answer is “yes” with some qualifications. Lactase persistence is a very good example of a recent, human-evolutionary event, but the selection process for it was brutal and unforgiving. I am not sure that we could tolerate that level of suffering and death in our present day, culturally-based societies.
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