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Comment
. 2019 May 15;85(10):789-791.
doi: 10.1016/j.biopsych.2019.03.975.

Do Sensitive Periods Exist for Exposure to Adversity?

Laurel J Gabard-Durnam  1 , Katie A McLaughlin  2
Affiliations
Comment

Do Sensitive Periods Exist for Exposure to Adversity?

Laurel J Gabard-Durnam et al. Biol Psychiatry. .
No abstract available

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Conflict of interest statement

The authors report no biomedical financial interests or potential conflicts of interest.

Figures

Figure 1.
Figure 1.
Conceptual models of environmental influence on neurodevelopment. Numerous models explain how adverse environmental experiences influence brain development. These models differ in their underlying neurobiological mechanisms, involving either experience-expectant or experience-dependent processes. Experience-expectant mechanisms are specific to development. They reflect neural preparation by specific brain substrates to encode particular types of expected experience (green checkmark) during specific windows of heightened neuroplasticity (developmental changes in neuroplasticity levels shown as curves). Critical and sensitive period models rely on experience-expectant neuroplasticity, either solely within one window (critical periods) or with some residual malleability thereafter (sensitive periods). Although most adversities do not represent expected experiences that constitute critical/sensitive period substrates, they may still influence these processes, depending on their timing. (Left panels) Adverse experiences that happen after a critical/sensitive period is completed have relatively little impact on that neural substrate. (Middle panels) Adverse experience occurring before or during critical/sensitive periods may alter their progression (e.g., accelerate or truncate the period). (Right panels) Adversities that involve the deprivation or delay of expected experience directly impact critical/sensitive period encoding of that experience. In contrast, experience-dependent mechanisms reflect neural learning in response to individual experiences. Experience-dependent mechanisms are available throughout life, though the degree of neuroplasticity associated with these mechanisms can vary across development. Dose-response, recency, and accumulation models prioritize different dimensions of experience in terms of quantity and timing. Dose-response models apply to contiguous, graded exposures like environmental toxins and predict that adversity effects scale continuously with the degree or duration of exposure. The recency model tested by Dunn et al. (1) posits that adverse events closest to the present time have the greatest effect on neurodevelopment. The accumulation model they tested posits that the effect of an adversity varies with the number of occurrences over a given window. Alternatively, the cumulative risk model predicts that the effect of experience varies as a function of the number of unique adversities experienced (regardless of timing), rather than the number of occurrences of a single adversity. Biological sensitivity to context models expect the effects of adversity to differ as a function of individual traits like physiology and (epi)genetics (e.g., genetic polymorphisms). No single conceptual model likely accounts for the entire range of complex effects of adversity on neurodevelopment.
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References

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