User:KaylaT3210/sandbox

General Statement: I will place all of my notes and my bibliography here.

Exogenous causes of maternal stress transfer: substance use: Tobacco and Marijuana (NOT USED)
Maternal smoking during pregnancy is an example of an exogenous cause of increased cortisol. As a result, there is a higher concentration of cortisol found in the fetus if mother smoked at each stage of pregnancy. The use of marijuana in combination with tobacco also causes an increase in cortisol stress. The impacts of such stress can vary based on the sex of the fetus with more noticeable affects found in male versus female fetuses. Glucocorticoids are raised in the mother and lead to higher concentrations of cortisol being transferred across the placental barrier causing alterations of the HPA pathway. These increased cortisol levels can be detected well into early childhood.

Consequences and Long-Term Effects: Obesity (NOTES)
Depression, obesity review paper :

- Determines that there's a powerful effect of behaviors found in the developing fetus that are shaped by fetal/child sex from intrauterine environment*. (Girls were shown to have different sized amygdala in mothers with high cortisol during pregnancy).

- Mothers being obese themselves has significant impact on the shaping of the HPA-axis activity in their fetuses

- Exposure during important neurodevelopmental periods increase risk of metabolisc disorders*. This risk is most present at a later stage of pregnancy. The fetus has a higher chance of obesity, Type 2, adiposity, insulin resistance and poor lipid profile. This impact can be seen as early as six months of age.

Maternal stress and offpsring obesity chances increasing. Sys lit review :

- ObesityReviews suggest that maternal stress transfer is an exogenous factor that predicts potential environments that the fetus will live in.

- Babies born to mothers with high stress have low weight birth children.

- Stressful situations* also increase the likelihood of the mother engaging in risky health practices such as drinking, and poor dietary habits.

- The hypothesis suggested is that excessive glucocorticoids* not only regulate stress in the fetus, they also regulate "food intake, obesity, and energy expenditure in both animals and humans"

- The other hypothesis is that CRH influences the fetus' likelihood of health and disease.

- Specific glucocorticoids* could be related to the increased chance of obesity when combined with a high energy diet: dexamethasone and betamethasone.

- High stress is connected to increase adiposity, but not BMI.

- Could be potentially offset with increased social support to mother. A study based on the Iowa flood, gave further support to mothers, and as a result, less stress was placed on the expecting mother. This support decreased the likelihood of the babies having a lower birthweight.

- There is a direct relationship of a connection between obesity and high maternal stress, however there needs to be more longitudinal studies to further confirm this.

Obesity phenotypes caused by paternal stress

- Paternal stress could cause a higher connection between BMI, higher LDLs, blood pressure and blood sugar

- Little evidence of the connection of LDLs, blood pressure and blood sugar to this high maternal stress, but definite connection between stress and higher BMIs

- Higher chance of cardiovascular disease, hypertension, high cholesterol, type 2 diabetes

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- Both sexes are equally susceptible to this. Age and ethnicity also have no impact as well.

- Found bias in these studies, so results may be inconsistent, only published studies that showed results.

- Children who experience stress themselves increase the likelihood of becoming obese

- nutrition, lifestyle, family history and environment also play an important part.

Intergenerational childhood trauma and obesity risk

The microbiome-gut-brain axis impacting brain development.

Mother's change in microbiome will ultimately change brain development. Example of extra-placental stress transfer that could be monitored

Impact of stress and stress physiology during pregnancy on child metabolic function and obesity risk

Etiology
Obesity later in life is linked to the changes in the HPA-axis activity in the fetus. As mothers experience increased stress, they may begin to participare in risky health behaviors such as poor dietary habits. This increases the chance of obesity in the mother and the fetus. The fetus has an increased chance of obesity as high stress is used to predict the potential environment the fetus lives in. Two specific types of glucocorticoids, dexamethasone and betamethasone, are transferred to the fetus. CRH(cite to page) as well, also influences the fetus' health and disease.This exposure, in addition to a higher energy diet, increase the likelihood of obesity later on in life. This is due to glucocorticoids not only regulating stress in the fetus, but also appetite, obesity and metabolism in animals and humans.

Consequences and Long-Term Effects
Exposure during important neurodevelopment periods increase risk of metabolic disorders including obesity, Type 2 diabetes, adiposity, insulin resistance and poor lipid profile. This risk is most present at a later stage of pregnancy and can be seen as early as six months of age. The likelihood further increases when children experience high levels of stress.

Reversal of consequences (Not used)
Could be potentially offset with increased social support to mother. A study based on the Iowa flood, gave further support to mothers, and as a result, less stress was placed on the expecting mother. This support decreased the likelihood of the babies having a lower birthweight.

Notes for me on my addition
Explain how smoking causes increased cortisol.

Explain what an example of noticeable effect is. What is the most obvious effect that can be seen in male versus female fetuses?

- Also see if there's any information on why it 's more likely to impact male versus female fetuses.

Annotated Bibliography
It has been determined that cortisol from the mother has an impact on the fetus. It transcends the placenta and can impact the hypothalamic-pituitary- adrenal axis(HPAA). This increases the risk of neuropsychiatric, cardiovascular, and metabolic diseases. It is believed that other impactors that are caused by maternal stress are catecholamines, cytokines, serotonin/tryptophan, reactive oxygen-species and the mother's microbiota. (REVIEW-ARTICLE ONLY. PAST 5 YEAR MARK FOR MEDICAL WIKI).

To determine the impact psychosocial stress has on fetal development, sheep were isolated to determine if there was a physiological change. After a period of time, fetuses were found to have a hyperactive HPA from chronic maternal stress. Catecholamines correspond with norepinephrine. Catecholamine endogenously induce norepinephrine as the prior are unable to pass the placental barrier. Overall, HPA-axis is induced earlier in CMS-affected fetuses, and have adaptations to maternal stress while the control did not. (REVIEW-ARTICLE ONLY. Original Article)

Review article on the impact of dysregulated imprinting genes. Some of the factors include maternal psychological stress, assisted reproductive technologies (ART) and chemical exposure. Understanding the cause of imprinted gene dysfunction can  prevent negative human health impacts, including the prevention of disease caused by the dysregulated imprinted genes. (Will include in the wiki article)

Article for the impact of smoking on cortisol levels of mother, thus child. Significant amounts of cortisol determined in fetuses of mother who smoked every stage of pregnancy versus those who hadn't.

Article determines if the mechanism that translate stress from mother to fetus is expressed in higher amounts when mother smokes. Includes the effects of marijuana and tobacco on cortisol levels of the fetus. In addition to data collection during pregnancy, data collection during childhood is used as well. Higher cortisol levels were found in children of those who had exposure to tobacco and marijuana. Paternal marijuana and tobacco use did not cause a significant impact on the fetus.

Review article that confirms the link of smoking and alterations in the HPA pathway of fetuses. It is associated with glucocorticoids. Cortisol has different effects on a the brains of sex-developing fetuses.

Paper attenuates the connection of sex on the impact of cortisol levels, as well as the usage of both tobacco and marijuana having impacted infant cortisol levels