Biology

Stress and homeostasis

‍Stress is defined as a “real or interpreted threat to the physiological or psychological integrity of an individual which results in physiological and/or behavioral responses.”

When we experience stress — like navigating a new environment, starting a new job, running a race, or breaking a leg — our body responds with a complex set of temporary adaptations to return our physiology to a sort of dynamic equilibrium, known as homeostasis. For example, if we didn’t sweat when we ran a race, our body would overheat. Sweating helps cool the body so our temperature stays within a normal range. That’s the stress response working in a healthy way to bring our body back into homeostasis.

Allostasis and allostatic load

‍Our brain and body aren’t merely working to get back to a state of equilibrium. They’re anticipating what it will take to get there. This adaptive reaction to regulate our body’s stress response is called allostasis, and the energy required to accomplish it is called the allostatic load. When the stress response is activated too often, too intensely, or never stops, it can result in allostatic overload. Rather than returning to homeostasis after the stress response has subsided, the body creates a new “set point” for functioning in a chronic state of allostasis. This can put heavy wear and tear on several biological systems.

Toxic stress

The term “toxic stress” is often misunderstood to mean the cause of stress. Technically, the National Academies of Science, Engineering, and Medicine (NASEM) defines toxic stress as “prolonged activation of the stress response systems that can disrupt the development of brain architecture and other organ systems, and increase the risk for stress-related disease and cognitive impairment, well into the adult years… For children, the result is the disruption of the development of brain architecture and other organ systems and an increase in lifelong risk for physical and mental health disorders.”

Children and toxic stress

Children are especially vulnerable to the effects of stress because their brains and bodies are still developing. If they encounter adversity during these crucial years, without the buffer of nurturing relationships and stable environments, it can trigger a toxic stress response and disrupt development of the neuro- endocrine-immune-metabolic and genetic regulatory mechanisms, which can increase the risk for poor health and more challenges later in life.

Critical and sensitive periods of development

There are crucial periods in a child’s life when certain developments occur.

Critical Periods refer to windows of time when specific developmental processes must occur, or the opportunity is lost.

Sensitive Periods are windows of time when particular areas of the brain are especially receptive due to increased neuroplasticity. The window doesn’t close once a sensitive period has passed, but learning does become harder. Learning a language, for example, comes much more easily to children than it does to adults.

When children experience adversity during these critical and sensitive periods, essential biological developments can be skipped or compromised, which can lead to long-term effects in epigenetics, neurophysiology, the endocrine system, immune function, metabolism, and other biological systems.

Outcomes

The more adversity a child experiences without the buffers of caring adults and safe, supportive environments, the more likely they’ll develop a toxic stress response. They’re also more likely to develop ACE-associated health conditions and adopt high-risk coping adaptations earlier and more severely than someone without ACEs.

For children, these conditions and symptoms may be asthma, unexplained aches and pains, headaches, depression, or self-harm. They may also have a higher likelihood of developing learning or behavioral problems and not completing high school.

For adults, ACE-associated health conditions include depression, cardiovascular disease, chronic obstructive pulmonary disease (COPD), liver disease, cancer, diabetes, obesity, cognitive impairments, risky sexual behaviors, early and high-risk substance use, suicidality, and premature mortality.

Having numerous ACEs is also associated with a variety of personal and societal challenges throughout life, including learning, developmental, and behavior problems, high school non-completion, unemployment, low life satisfaction, poverty, and felony charges, many of which may be passed from generation to generation.

Probabilistic versus deterministic

ACEs alone don’t determine someone’s health or future. They are probabilistic and NOT deterministic. ACE-associated risks are influenced by extrinsic factors — like whether nurturing relationships, a safe environment, and a supportive community are present — and biological susceptibility (what we inherit through our ancestry).

Positive experiences

Resilience is our ability to endure or recover from stress, and it’s built on a variety of different levels. Accumulating positive childhood experiences can buffer the brain and body from the effects of toxic stress and help build resilience on biological, social, and emotional levels.

Intergenerational transmission

ACEs and toxic stress can alter the biology and behavior of people in ways that affect the birth and development of their children.

Generational risk

Children born to parents with high ACE scores are more likely to experience a variety of neuropsychiatric, behavioral, and physical health problems.

Prenatal impacts

The effects of toxic stress due to ACEs may impact our ability to conceive, and may increase risk of miscarriage, preterm birth, and low birth weight.

Adversity and Resilience can be passed on through epigenetics

The intergenerational transmission of ACEs isn’t fully determined in childhood. The same pathways that pass on the negative effects of toxic stress can also pass on positive resiliency factors when we as adults with ACEs adopt long-term practices to heal ourselves, and are supported by communities and systems with resources that address our needs.