A new school of thought in evolutionary developmental biology, combined with research in the neurobiology of stress, suggest that early exposure to stressful circumstances may be a cause of dyslexia. A balance between epigenetic, stress-induced and cognitive-growth genetic programs modulates the brain's cellular, regional, and network homeostasis. This balance is essential for adaptability to the normative range of everyday stress. However, even mild chronic stress exposition may overactivate the hypothalmic-pituitary-adrenal stress axis, upsetting the homeostatic balance between these programs, and exposing the brain to harmful levels of stress hormones. A protective strategy to sustained disequilibrium precociously advances maturation at the cost of neuroplasticity, which blunts stress axis reactivity but also compromises learning potential in the prefrontal cortex and networks associated with dyslexia. Stress exceeding an individual's range of resilience: (1) reduces levels of TFEB and BDNF, gene regulatory factors prolonging maturation and neuroplasticity; (2) interferes with the insular cortex, amygdala and hippocampus in coordinating afferent visceral signals with cognitive performance; (3) over-recruits the brain's Default Mode network; and (4) amplifies release from the Locus coeruleus/norepinephrine system which impairs the entrainment of oscillations in the lower phonological frequencies of speech. Evidence supporting a stress-growth imbalance is preliminary, but holds promise for reconceptualizing the neurobiology of dyslexia and reducing its prevalence.

进化发育生物学的新思想流派与压力神经生物学的研究相结合，表明早期暴露于压力环境可能是阅读障碍的一个原因。表观遗传、压力诱导和认知生长遗传程序之间的平衡调节大脑的细胞、区域和网络稳态。这种平衡对于适应日常压力的正常范围至关重要。然而，即使是轻微的慢性压力也可能过度激活下丘脑-垂体-肾上腺应激轴，扰乱这些程序之间的稳态平衡，并使大脑暴露在有害水平的应激激素下。持续不平衡的保护策略会以神经可塑性为代价提前成熟，神经可塑性会减弱应激轴反应性，但也会损害前额皮质和与阅读障碍相关的网络的学习潜力。超过个体承受能力的压力：（1）降低 TFEB 和 BDNF 的水平，这些基因调节因子延长成熟和神经可塑性；(2) 干扰岛叶皮质、杏仁核和海马体协调内脏传入信号与认知表现；(3)过度调动大脑的默认模式网络；(4) 放大蓝斑/去甲肾上腺素系统的释放，从而削弱语音较低语音频率中振荡的夹带。支持压力增长失衡的证据还处于初步阶段，但有望重新概念化阅读障碍的神经生物学并降低其患病率。