From https://www.health.harvard.edu/staying-healthy/understanding-the-stress-response

Fight or Flight.

As the initial surge of epinephrine subsides, the hypothalamus activates the second component of the stress response system — known as the HPA axis. This network consists of the hypothalamus, the pituitary gland, and the adrenal glands.

The HPA axis relies on a series of hormonal signals to keep the sympathetic nervous system — the “gas pedal” — pressed down. If the brain continues to perceive something as dangerous, the hypothalamus releases corticotropin-releasing hormone (CRH), which travels to the pituitary gland, triggering the release of adrenocorticotropic hormone (ACTH). This hormone travels to the adrenal glands, prompting them to release cortisol. The body thus stays revved up and on high alert.

Many people are unable to find a way to put the brakes on stress. Chronic low-level stress keeps the HPA axis activated, much like a motor that is idling too high for too long. After a while, this has an effect on the body that contributes to the health problems associated with chronic stress.

——-

Is there a DNA effect that makes some people more susceptible to HPA activation (ie. ACTH production)? Or an environmental effect?

Has this been studied?

mollwollfumble said:

From https://www.health.harvard.edu/staying-healthy/understanding-the-stress-response

Fight or Flight.

As the initial surge of epinephrine subsides, the hypothalamus activates the second component of the stress response system — known as the HPA axis. This network consists of the hypothalamus, the pituitary gland, and the adrenal glands.

The HPA axis relies on a series of hormonal signals to keep the sympathetic nervous system — the “gas pedal” — pressed down. If the brain continues to perceive something as dangerous, the hypothalamus releases corticotropin-releasing hormone (CRH), which travels to the pituitary gland, triggering the release of adrenocorticotropic hormone (ACTH). This hormone travels to the adrenal glands, prompting them to release cortisol. The body thus stays revved up and on high alert.

Many people are unable to find a way to put the brakes on stress. Chronic low-level stress keeps the HPA axis activated, much like a motor that is idling too high for too long. After a while, this has an effect on the body that contributes to the health problems associated with chronic stress.

——-

Is there a DNA effect that makes some people more susceptible to HPA activation (ie. ACTH production)? Or an environmental effect?

Has this been studied?

Any connection between HPA (ie. always highly stressed) and manic-depression?

>Chronic low-level stress keeps the HPA axis activated, much like a motor that is idling too high for too long

not a great example, the motor idling, terrible really

I gather what it means is the rest point, or set-point, usual settled equilibrium state, that sort of thing

>Is there a DNA effect that makes some people more susceptible to HPA activation (ie. ACTH production)? Or an environmental effect?

could be neural unfolding too, gestation and onward

of gestation that’s environment I guess, internal environment, mum’s internal environment (excluding the fetus/baby) could be seen as fetus’ external environment, or you could see the fetus as part mum’s internal environment

upregulate was term I was looking for

transition said:

>Is there a DNA effect that makes some people more susceptible to HPA activation (ie. ACTH production)? Or an environmental effect?

could be neural unfolding too, gestation and onward

of gestation that’s environment I guess, internal environment, mum’s internal environment (excluding the fetus/baby) could be seen as fetus’ external environment, or you could see the fetus as part mum’s internal environment

Upregulate was term I was looking for

Some medical articles blame the influence of early childhood traumas on methylation. I don’t trust that unless it’s tested using a reliable animal model. And to get a reliable animal model you’d first have to created a chilled out animal without HPA activation, ie an animal that has a really short duration “fight or flight” response, like most humans. For most humans, “fight or flight” only lasts of order a dozen heartbeats, but what if it lasted for weeks to decades?

reading here..

https://en.wikipedia.org/wiki/Stress_(biology)#General_adaptation_syndrome

The third stage could be either exhaustion or recovery:

– Recovery stage follows when the system’s compensation mechanisms have successfully overcome the stressor effect (or have completely eliminated the factor which caused the stress). The high glucose, fat and amino acid levels in blood prove useful for anabolic reactions, restoration of homeostasis and regeneration of cells. – Exhaustion is the alternative third stage in the GAS model. At this point, all of the body’s resources are eventually depleted and the body is unable to maintain normal function. The initial autonomic nervous system symptoms may reappear (sweating, raised heart rate, etc.). If stage three is extended, long-term damage may result (prolonged vasoconstriction results in ischemia which in turn leads to cell necrosis), as the body’s immune system becomes exhausted, and bodily functions become impaired, resulting in decompensation.

The result can manifest itself in obvious illnesses, such as general trouble with the digestive system (e.g. occult bleeding, melena, constipation/obstipation), diabetes, or even cardiovascular problems (angina pectoris), along with clinical depression and other mental illnesses

this is a really good read..

https://en.wikipedia.org/wiki/Hypothalamic%E2%80%93pituitary%E2%80%93adrenal_axis

transition said:

this is a really good read..

https://en.wikipedia.org/wiki/Hypothalamic%E2%80%93pituitary%E2%80%93adrenal_axis

Prenatal stress

There is evidence that prenatal stress can influence HPA regulation. In animal experiments, exposure to prenatal stress has been shown to cause a hyper-reactive HPA stress response. Rats that have been prenatally stressed have elevated basal levels and abnormal circadian rhythm of corticosterone as adults. Additionally, they require a longer time for their stress hormone levels to return to baseline following exposure to both acute and prolonged stressors. Prenatally stressed animals also show abnormally high blood glucose levels and have fewer glucocorticoid receptors in the hippocampus. In humans, prolonged maternal stress during gestation is associated with mild impairment of intellectual activity and language development in their children, and with behaviour disorders such as attention deficits, schizophrenia, anxiety and depression; self-reported maternal stress is associated with a higher irritability, emotional and attentional problems.

There is growing evidence that prenatal stress can affect HPA regulation in humans. Children who were stressed prenatally may show altered cortisol rhythms. For example, several studies have found an association between maternal depression during pregnancy and childhood cortisol levels. Prenatal stress has also been implicated in a tendency toward depression and short attention span in childhood. There is no clear indication that HPA dysregulation caused by prenatal stress can alter adult behavior.
Early life stress

yes
yes
yes