Here's a thought that often circles my head while I waste away my work minutes watching milk drip into a glass bottle at an excruciatingly slow rate: acute as well as chronic stress is known to cause serious disruption to the neuronal circuitry involved in learning and memory, and stress hormones are known to pass into breast milk.
Naturally, this knowledge stresses me out.
(Wash, rinse, repeat)
My work life exists with a certain necessary baseline of hyperattentive stress. I need cortisol (and caffeine) to function properly. It's actually the only way I get anything accomplished. Of course, this makes me feel guilty about my stress, which, in turn, causes more stress, and so and so forth until I've totally forgotten what it is that I'm upset about I just know that it feels bad and isn't going away. (Jack can sympathize with my plight right around 20 minutes past bedtime, I'm sure).
As it turns out, I should really relax about the whole thing: my stress may not be such a bad developmental constant for Jack, after all (see abstract below). Stress produces neuronal atrophy. The infant brain undergoes a tremendous amount of synaptic pruning in the early months. It's not crazy to imagine that low levels of maternal stress could act synergistically with synaptic pruning.
Now the real question comes in about how we define "low levels"... shoot, I better hit pubmed again
Maternal corticosterone effects on hypothalamus-pituitary-adrenal axis regulation and behavior of the offspring in rodents
Catalani, A., Alemà, G.S., Cinque, C., Zuena, A.R., Casolini, P.
Neuroscience and Biobehavioral Reviews (2010)
The behavioral and physiological traits of an individual are strongly influenced by early life events. One of the major systems implicated in the responses to environmental manipulations and stress is the hypothalamus-pituitary-adrenal (HPA) axis. Glucocorticoid hormones (cortisol in humans and corticosterone in rodents) represent the final step in the activation of the HPA system and play an important role in the effects induced by the perinatal environment. We demonstrated, in rats with some differences between males and females, that mothers whose drinking water was supplemented with moderate doses of corticosterone throughout the lactation period, give birth to offspring better able to meet the demands of the environment. The progeny of these mothers, as adults, show improved learning capabilities, reduced fearfulness in anxiogenic situations, lower metabotropic glutamate receptors and higher glucocorticoid receptors in the hippocampus with a persistent hyporeactivity of the HPA axis leading to a resistance to ischemic neuronal damage. Other studies performed in mice showed that low doses of corticosterone in the maternal drinking water, which, as in our rat model, may reflect a form of mild environmental stimulation, enhanced the offspring's ability to cope with different situations, while elevated doses, comparable to those elicited by strong stressors, caused developmental disruption. Significantly, adult rats and mice that had been nursed by mothers with a mild hypercorticosteronemia provide an example of how a moderate corticosterone increase mediates the salutary effects of some events occurring early in life. Both maternal and infantile plasma levels of the hormone may play a role in these effects, the first influencing maternal behavior, the second acting directly on the central nervous system of the developing rat. © 2010 Elsevier Ltd. All rights reserved.