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Do big eggs = sick chicks?

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Veterinary medicine and agricultural biology have a lot to offer the field of evolutionary medicine. (See, for instance, Zoobiquity by Barbara Natterson-Horowitz.) Recently, Fred Madsen sent me a link describing research by Kirk Klasing of UC Davis that highlights those connections.

Here is an excerpt: “The quantitative investment in immune defenses is thought to be under tight evolutionary control because they must be sufficient to thwart pathogens without excessively consuming resources (e.g. nutrients and energy) needed for other important processes or causing immunopathology (Ardia et al., 2010). In poultry production there is concern that the immune system competes for nutrients with tissue growth or egg production. The practical implications are twofold. First, unnecessary or overly robust immune responses may diminish the rate and efficiency of production. Second, that intensive genetic selection of poultry for efficient growth or egg production for many decades may have diminished the immune system and consequently reduced disease resistance.”

In other words, artificial selection by farmers for big eggs = immune compromised chickens. Selection for rapid growth might drive a similar tradeoff.

Klasing goes on to point out that when chicken get sick, the liver ramps up production of acute phase proteins (like C-reactive protein) and this consumes a lot of energy and nutritional resources.  He writes ” The largest source of protective proteins during an immune response is hepatocytes.”

I like the fact that Klasing highlights the immune role of the liver. In clinical medicine, this is often overlooked.

Klasing attempts to quantify the tradeoff between growth and immunity by measuring the use of lysine, which a growth limiting amino acid necessary for protein manufacture that is not stored in the animal.

“We estimate that a robust acute phase immune response against a simulated infection with dead Escherichia coli decreases growth by about 25% but there is no decrease in growth during the subsequent adaptive response. About two-thirds of the growth depression during the acute phase response is due to a decrease in appetite and about a third is due to nutrient diversions or losses related to the immune response.”

In other words, the immune response takes some energy that would otherwise be used in growth – a tradeoff, yes – but the lion’s share of decreased growth happens because animals stop eating.

At the same time, nutrients are diverted from tissues that don’t need them (skeletal muscle) to organs that do (liver and immune cells).

“In the initial stages of an immune response against a novel pathogen, phagocytes are the early responders and release pro-inflammatory cytokines in sufficient amounts that they have endocrine-like effects throughout the body. This cytokine storm induces metabolic changes, including increased protein degradation and insulin resistance, which divert nutrients from skeletal muscle and other tissues so that they become available for the increased demands of the liver and responding leukocytes…”

The same thing happens in our hospitalized patients, contributing to rapid muscle loss and frailty. Although that phenomenon is widely known, its evolutionary underpinnings are opaque to most clinicians.

Read Klasing’s description of his research and watch a video of his presentation here.

Categories: Uncategorized

Joe Alcock

Emergency Physician, Educator, Researcher, interested in the microbiome, evolution, and medicine

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