On being your mother’s son

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John Hawks and Tara Smith both have posts on a New York Times article describing the role of events during development on health later in life. A recent article pushed for the development of a framework to describe these kind of effects.

The basic concept is simple: during development (development in utero), the fetus recieves signals that allow it to “predict”, as it were, the environment where it will live. For example, there may be some way to sense whether the environment will be nutrient-poor or nutrient-rich. Based on this information, development proceeds in a way to favor adaptation to the predicted environment. However, if the prediction is wrong, for whatever reason, disease may result later in life. Importantly, the mother acts as the conduit for the environmental information, and may alter it to suit her needs.

The main example given in the article concerns metabolic disease like type II diabetes and obesity. The argument goes like this: due to basic physics, a fetus can’t exceed a certain size (or couldn’t, before the C-section). Thus, in a nutrient-rich environment like we have today, where a fetus would “want” to get much bigger, the mother limits the environmental signal )so as not to have a giant child), leading to a fetus that “predicts” an environment much poorer than what really exists. Once developed, the grown individual is then predisposed to gain weight. The authors put is thusly:

We argue that it is this differential rate of change between the limitations imposed by maternal constraint (which set the fetal prediction) and the reality of the enriched modern postnatal environment that has created the current high incidence of cardiovascular and metabolic disease in humans.

This is a broader framework for what some have called the “thrifty phenotype” hypothesis for the prevelance of type II diabetes, an alternative to the “thrifty genotype” hypothesis.

11 Comments

  1. The graphic shows a slight increase in average adult male height occurring in the last decade or so in the US. Seems like there would have been expected to be a detectable downward trend due to ethnic demographic change.

  2. What’s that about polygenic traits? modern-day epicycles.

  3. Thus, in a nutrient-rich environment like we have today, where a fetus would “want” to get much bigger, the mother limits the environmental signal )so as not to have a giant child), leading to a fetus that “predicts” an environment much poorer than what really exists 
     
    This makes approximately zero sense to me. The basic premise that mother and child have a conflict of interest in terms of optimal baby size is correct, and indeed if you look at a graph that shows the distribution of birthweight versus infant mortality, you see that the modal birthweight is slightly lower than the optimal birthweight from the baby’s perspective (though not by all that much). 
    The nonsensical part is the notion that nutrient countersignaling would be needed to somehow keep the fetal weight down. If oversupply of nutrients were somehow dangerous to maternal survival, a more obvious solution would be to cap the nutrient flow at some agreeable level, not to reduce it to abnormally low levels.

  4. a more obvious solution would be to cap the nutrient flow at some agreeable level, not to reduce it to abnormally low levels 
     
    that’s the point. the levels are only “abnormal” today, as the environment has changed quicker than the mother’s response (which is presumably unde genetic control) can. so the “cap” is set at a level which, in the past, would be agreeable, but in the present is not.  
     
    What’s that about polygenic traits? modern-day epicycles. 
     
    nope.

  5. that is, it’s the difference between the predicted environment and the actual environment that matters. is the prediction is determined by the mother and is under genetic contraint and the actual environment changes rapidly, there’s going to be a problem.

  6. Hmm. So this is just a fancy way of saying that the modern environment is outside the range of environments that occured in the ESS. But in this case why drag maternal signaling into it? You’re supposing that there is some hypothetical signal which would allow the fetus to be adapted to today’s rich environment, but that the mother doesn’t deliver it in order to preserve herself; wouldn’t it be simpler to assume that no such signal exists, because the environment was never encountered before?

  7. Jp, so why then are these “complex, polygenic” diseases so heavily influenced by environmental conditions? 
     
    Do you really think genes influencing sugar metabolism were selected amazingly heavily since 1950? Diseases

  8. Bbartlog: ?So this is just a fancy way of saying that the modern environment is outside the range of environments that occured in the ESS. But in this case why drag maternal signaling into it? You’re supposing that there is some hypothetical signal which would allow the fetus to be adapted to today’s rich environment, but that the mother doesn’t deliver it in order to preserve herself; wouldn’t it be simpler to assume that no such signal exists, because the environment was never encountered before?? 
     
    It might be simpler but it would ignore the existing body of research that shows that there has been an evolutionary conflict between the mother?s womb and the fetal placenta. If you accept the basic model that the fetus has evolved the hormonal ability to trigger maternal changes that favor the fetus and that the mother has evolved the ability to ignore those signals to protect her own health then the question become how is that model responding to the modern nutritional environment.

  9. Fly, offhand, as food becomes more common, that would reduce the cost to the mom of feeding the fetus more, so reduce selective pressure on women. As child/teen/adult starvation becomes rarer the cost of being really big decrease for males. So we should see relaxation of selection in genes that try to resist fetal manipulation.

  10. I’m aware of the research, although the talk of giant babies sort of ignores the fact that the baby has to accommodate its own birth as well. It’s the relevance that I’m questioning. To be specific, I disagree with this: 
     
    leading to a fetus that “predicts” an environment much poorer than what really exists. Once developed, the grown individual is then predisposed to gain weight 
     
    The issue I would have is that, absent countersignaling, the fetus is presumably going to be ‘predicting’ an environment of abundance within the context of the ESS (maternal nutrition provided is at the cap). Due to evolutionary limitations and modern wealth, the actual environment may still be abundant beyond this prediction. But in that case, our tendency to gain weight is just a question of us being adapted to an environment of scarcity *in general*; it has nothing to do with maternal signaling of scarcity and an attendant metabolic adjustment on the part of the fetus. The statement is at best misleading. 
     
    Just to be clear, I believe that prenatal scarcity does result in fetal changes that predispose someone to gain weight later in life. I just don’t think that this ‘scarcity signal’ is sent absent actual conditions of scarcity, so invoking it (rather than more general human adaptations to scarcity) to explain modern diseases of affluence makes no sense.

  11. Rob: ?Fly, offhand, as food becomes more common, that would reduce the cost to the mom of feeding the fetus more, so reduce selective pressure on women.? 
     
    I?m guessing that the placenta-womb interaction is more complicated than just food availability. Growth factors for maturation rate, growth factors for blood vessels, immune suppression factors, fat storage, etc. I?d guess you are right that mother?s fitness cost for feeding the fetus more is lower in modern society. (C-section or artificially induced labor if a baby or multiple babies are too large. Bed rest before labor and recovery after birth that weren?t feasible in harsher times.) Also, as women choose to have fewer babies, the fitness tradeoff between the baby and the mother shifts. I agree that the womb-placenta system will adapt to the modern environment. 
     
    I?m only suggesting that relaxing a constraint should be interpreted using the best model of the placenta-womb system. Thus it is natural to look at maternal signaling by the fetus. (Besides I think it is cool to imagine the tiny fetus hijacking the maternal body to satisfy its own selfish goals.) 
     
    Of course maternal systems independent of the fetus would also adapt, so maternal signaling by the fetus isn?t the whole story. 
     
    Bbartlog: ??maternal signaling of scarcity and an attendant metabolic adjustment on the part of the fetus.? 
     
    Hmmm, I had a different definition of ?maternal signaling? in mind. I was focusing on the womb-placenta interface and the fetal attempt to manipulate the mother by producing hormones and growth factors released into the mother?s tissue for the benefit of the fetus. The modern nutritional environment would change the fitness constraints on this system. 
     
    I see now that you are using ?maternal signaling? to refer to the womb nutritional environment, not just the womb-placenta signaling. So the womb environment could trigger different genetic strategies (predictive adaptive response) such as modified energy metabolism. 
     
    The biological system is complex. I think it is too early to conclude how pre-natal nutrition will affect the offspring?s feeding habits and too early to know the mechanism. But I do find speculation interesting. 
     
    http://jscms.jrn.columbia.edu/cns/2006-02-14/phillips-obesitybabies 
     
    ?Simon Langley-Evans, a professor of biological sciences at the University of Nottingham in England, was the lead researcher in a recent study that found that feeding mice a low-protein diet throughout gestation led to female offspring that were less likely to eat fatty foods. Varying the diet, though, changed the results. 
    ?In the second experiment, we offered low-protein chow only during certain stages of gestation, ? Langley-Evans said, ?and to our horror, we found that the opposite thing happened,? with the offspring actually being more likely to choose fatty foods and become overweight than the mice in the control group. 
    But how does a female mouse?s diet affect her offspring in the first place? Langley-Evans thinks that the low-protein diet affected the development of the hypothalamus in the mouse fetus. The hypothalamus controls the body?s temperature, appetite and sleep cycle and regulates the metabolism. 
    In humans, the hypothalamus begins forming during the first month of pregnancy and is well developed by the end of the first trimester. Langley-Evans hopes that the connection between diet and the development of the hypothalamus in mice might lead to new information about the importance of diet for humans during pregnancy and lead to better education on maternal nutrition.?

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