The Evolution of Lactase Persistence: Milk Consumption, Insulin-Like Growth Factor I, and Human Life-History Parameters

Wiley, Andrea S.

doi:10.1086/700768

Cited by 14 publications

(14 citation statements)

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“…This is genetically regulated by a promotor region (the MCM6 gene) upstream from the lactase gene (LCT). In some human populations with histories that included domestication of mammals for milk usage, mutations in the regulatory area that kept lactase production on throughout adulthood were able to spread, presumably as adaptations to milk consumption, although no specific benefits have been adequately demonstrated (Wiley, 2018). Populations with high frequencies of such mutations include those in northern Europe, pastoralist groups in West and East Africa and the Arabian peninsula, and South Asia (especially those living in the northwestern regions of the subcontinent).…”

Section: Examples Of Biological Normalcy In Actionmentioning

confidence: 99%

“…With T.M Bayless and colleagues' work in the 1960s (Bayless & Rosensweig, 1966; 1967, see also Paige et al, 1972) evidence emerged that there was variation in gastrointestinal symptoms upon drinking milk (90% of Black vs. 10% of White individuals in their studies), but importantly no signs of intestinal pathology. The authors speculated that these differences were attributable to varying population histories with milk, and later authors (mostly anthropologists) began to develop evolutionary hypotheses as it became clear that most human populations had high frequencies of LNP and only among some milk‐drinking populations had variant LP alleles spread (Durham, 1991; McCracken, 1971; see also Wiley, 2018 for a contemporary review)…”

Section: Examples Of Biological Normalcy In Actionmentioning

confidence: 99%

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Pearl lecture: Biological normalcy: A new framework for biocultural analysis of human population variation

Wiley

2021

American J Hum Biol

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Biological normalcy is a new analytical framework for understanding the bi‐directional relationships between the biology of populations and cultural norms. Populations are characterized by statistical distributions—that is, measures of central tendency and variance—for biological traits, and these co‐exist in societies with ideas about what constitutes “normal” human bodies, that is, normative views about what bodies “should” be like. While statistical norms may carry no explicit evaluative weight, the question is how they are related to judgments about what is “normal” or “abnormal.” In a 1947 paper, Margaret Mead recognized their potential relationship: “normal…may refer to the statistically usual in the culture—usually without any recognition that this is culturally relative—so that the statistically usual is identified with the basically human….” Despite her observations over 70 years ago, little has been done on this topic, yet such work promises new insights into the relationship between culture and biology, here described at the population level, rather than as individual genetic characteristics. Using examples of sex/gender, race/ethnicity, age, and my work on human variation in the ability to drink milk, I outline the ways in which statistical norms may: influence individuals' perceptions of what is “normal” (Mead's “basically human”); lead to normative judgments about what human biology “should” be (“ethno‐biocentrism”) that are reinforced by biases in discourse about human variation; and potentially feedback to mold the biological characteristics of a population.

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Section: Examples Of Biological Normalcy In Actionmentioning

confidence: 99%

Section: Examples Of Biological Normalcy In Actionmentioning

confidence: 99%

Pearl lecture: Biological normalcy: A new framework for biocultural analysis of human population variation

Wiley

2021

American J Hum Biol

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“…In fact, on the basis of its high concentrations of tryptophan, leucine, glutamine, palmitate and microRNAcontaining exosomes, Melnic [408,409] identifies milk as an evolved food signalling system that activates mTORC1 to mediate macromolecular synthesis, cell growth and development of the newborn mammal. One key issue is that although changing levels of consumption of dairy products in the 19th and 20th centuries may have contributed to secular national trends in height, with such increases associated with decreased overall mortality [2], there may be some negative pleiotropic consequences of milk consumption in terms of increased risk of some non-communicable chronic diseases such as some cancers [410] as a consequence of continuous hyperactivation of mTORC1 [409] and mediated by increased levels of IGF-1.…”

Section: Length/height Growth and Dietary Protein In Older Children Amentioning

confidence: 99%

Interactions between Growth of Muscle and Stature: Mechanisms Involved and Their Nutritional Sensitivity to Dietary Protein: The Protein-Stat Revisited

Millward

2021

Nutrients

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Childhood growth and its sensitivity to dietary protein is reviewed within a Protein-Stat model of growth regulation. The coordination of growth of muscle and stature is a combination of genetic programming, and of two-way mechanical interactions involving the mechanotransduction of muscle growth through stretching by bone length growth, the core Protein-Stat feature, and the strengthening of bone through muscle contraction via the mechanostat. Thus, growth in bone length is the initiating event and this is always observed. Endocrine and cellular mechanisms of growth in stature are reviewed in terms of the growth hormone-insulin like growth factor-1 (GH-IGF-1) and thyroid axes and the sex hormones, which together mediate endochondral ossification in the growth plate and bone lengthening. Cellular mechanisms of muscle growth during development are then reviewed identifying (a) the difficulties posed by the need to maintain its ultrastructure during myofibre hypertrophy within the extracellular matrix and the concept of muscle as concentric “bags” allowing growth to be conceived as bag enlargement and filling, (b) the cellular and molecular mechanisms involved in the mechanotransduction of satellite and mesenchymal stromal cells, to enable both connective tissue remodelling and provision of new myonuclei to aid myofibre hypertrophy and (c) the implications of myofibre hypertrophy for protein turnover within the myonuclear domain. Experimental data from rodent and avian animal models illustrate likely changes in DNA domain size and protein turnover during developmental and stretch-induced muscle growth and between different muscle fibre types. Growth of muscle in male rats during adulthood suggests that “bag enlargement” is achieved mainly through the action of mesenchymal stromal cells. Current understanding of the nutritional regulation of protein deposition in muscle, deriving from experimental studies in animals and human adults, is reviewed, identifying regulation by amino acids, insulin and myofibre volume changes acting to increase both ribosomal capacity and efficiency of muscle protein synthesis via the mechanistic target of rapamycin complex 1 (mTORC1) and the phenomenon of a “bag-full” inhibitory signal has been identified in human skeletal muscle. The final section deals with the nutritional sensitivity of growth of muscle and stature to dietary protein in children. Growth in length/height as a function of dietary protein intake is described in the context of the breastfed child as the normative growth model, and the “Early Protein Hypothesis” linking high protein intakes in infancy to later adiposity. The extensive paediatric studies on serum IGF-1 and child growth are reviewed but their clinical relevance is of limited value for understanding growth regulation; a role in energy metabolism and homeostasis, acting with insulin to mediate adiposity, is probably more important. Information on the influence of dietary protein on muscle mass per se as opposed to lean body mass is limited but suggests that increased protein intake in children is unable to promote muscle growth in excess of that linked to genotypic growth in length/height. One possible exception is milk protein intake, which cohort and cross-cultural studies suggest can increase height and associated muscle growth, although such effects have yet to be demonstrated by randomised controlled trials.

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“…A number of hypotheses have been proposed for the fitness value of LP. Building on the review by Gerbault et al (2011) , as well as more recent work by Wiley (2018) those hypotheses presented to date can summarized as follows:…”

Section: Introductionmentioning

confidence: 99%

“…Milk drinking could have conferred fitness benefits through the mediating role of elevated IGF1 levels on life history traits, such as increased body size and earlier maturation ( Wiley, 2018 ).…”

Section: Introductionmentioning

confidence: 99%

Evolution of Lactase Persistence: Turbo-Charging Adaptation in Growth Under the Selective Pressure of Maternal Mortality?

2021

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The emergence of the capacity to digest milk in some populations represents a landmark in human evolution, linking genetic change with a component of niche construction, namely dairying. Alleles promoting continued activity of the enzyme lactase through the life-course (lactase persistence) evolved in several global regions within the last 7,000 years. In some European regions, these alleles underwent rapid selection and must have profoundly affected fertility or mortality. Elsewhere, alleles spread more locally. However, the functional benefits underlying the rapid spread of lactase persistence remain unclear. Here, we set out the hypothesis that lactase persistence promoted skeletal growth, thereby offering a generic rapid solution to childbirth complications arising from exposure to ecological change, or to new environments through migration. Since reduced maternal growth and greater neonatal size both increase the risk of obstructed labour, any ecological exposure impacting these traits may increase maternal mortality risk. Over many generations, maternal skeletal dimensions could adapt to new ecological conditions through genetic change. However, this adaptive strategy would fail if ecological change was rapid, including through migration into new niches. We propose that the combination of consuming milk and lactase persistence could have reduced maternal mortality by promoting growth of the pelvis after weaning, while high calcium intake would reduce risk of pelvic deformities. Our conceptual framework provides locally relevant hypotheses to explain selection for lactase persistence in different global regions. For any given diet and individual genotype, the combination of lactase persistence and milk consumption would divert more energy to skeletal growth, either increasing pelvic dimensions or buffering them from worsening ecological conditions. The emergence of lactase persistence among dairying populations could have helped early European farmers adapt rapidly to northern latitudes, East African pastoralists adapt to sudden climate shifts to drier environments, and Near Eastern populations counteract secular declines in height associated with early agriculture. In each case, we assume that lactase persistence accelerated the timescale over which maternal skeletal dimensions could change, thus promoting both maternal and offspring survival. Where lactase persistence did not emerge, birth weight was constrained at lower levels, and this contributes to contemporary variability in diabetes risk.

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The Evolution of Lactase Persistence: Milk Consumption, Insulin-Like Growth Factor I, and Human Life-History Parameters

Cited by 14 publications

References 202 publications

Pearl lecture: Biological normalcy: A new framework for biocultural analysis of human population variation

Pearl lecture: Biological normalcy: A new framework for biocultural analysis of human population variation

Interactions between Growth of Muscle and Stature: Mechanisms Involved and Their Nutritional Sensitivity to Dietary Protein: The Protein-Stat Revisited

Evolution of Lactase Persistence: Turbo-Charging Adaptation in Growth Under the Selective Pressure of Maternal Mortality?

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