Parasites, stress, and auto-immune hormone connection

Every week, I have foot massage, walk on the beach, eat salads and whole foods and tried to get adequate sleep. I want to avoid chronic inflammation from parasites, effects of high stress hormones and to prevent cancer and other auto-immune disease.  Low stress can mean we work 4 days a week but high stress is working 2 jobs, more than 60 hours a week in our 50s.

It is not so late even in my 50s. I wish to save and do preventive actions now regarding my health than spend all my savings in health care. Health care costs can be avoided if we spend time and money on preventive measures.  Libraries will soon receive the free ebook that I am completing about health and conversations about cancer, parasites, self care and home care.

Connie Dello Buono

Chronic Stress, Cortisol Dysfunction, and Pain: A … – NCBI – NIH

 

 

Cortisol is also a potent anti-inflammatory hormone; it prevents the widespread tissue and nerve damage associated with inflammation. In addition to its paramount role in normal daily function, cortisol is a key player in the stress response.

Missing: parasites ‎| Must include: parasites

Stress & the gut-brain axis: Regulation by the microbiome – NCBI

 

 

The linkage between gut functions on the one hand and emotional and … yeasts, helminth parasites, viruses, and protozoa (Lankelma et al., 2015, Eckburg et al., …. salivary cortisol awakening response in healthy people (Schmidt et al., 2015). ….. Peripheral administration of pro-inflammatory cytokines in rodents induces a …

How stress influences disease: Study reveals inflammation as the …

 

 

Missing: parasites ‎| Must include: parasites

Why Cortisol Is Good for You – Healthy Gut Company

 

https://healthygut.com › Healthy Gut Company › Why Cortisol Is Good for You

 

 

Adrenal Fatigue, Blastocystis hominis, and Cortisol – Dirty Good Co.

 

 

RHR: High Cortisol and Brain Fog | Kresser Institute

 

https://kresserinstitute.com › Kresser Institute › RHR: High Cortisol and Brain Fog

 

Is Stress Damaging Your Gut? – Amy Myers MD

 

 

The Autoimmune Hormone Connection – Dr. Jolene Brighten

 

https://drbrighten.com › Blog › Autoimmune

 

5 Ways to Reduce Inflammation | The Chopra Center

 

 

Step 1 to cancer free: Limit stress that leads to high blood glucose and lipids

Adrenals and liver come to the rescue as blood sugar levels drop.  The endocrine pancreas, liver and adrenal glands work to normalize blood sugar and triglycerides.

Take care of your stress so it will be easier for you to prevent obesity, depression, sugar cravings and nerve pain which may start to happen at around 55 years of age. When we take care of our stress level, we take care of our metabolism , brain , whole body and we then prevent chronic diseases that lead to cancer.

Activities to make you happy

Beach stroll, dancing, watching comedians , laughing , sleeping at nigh, massage , happy and loving friends and relationships , spending time with family and friends , playing with your pets, gardening , singing , praying , deep breathing exercise, meditation

Side effects of chronically elevated cortisol can include:

Anxiety , Autoimmune diseases , Cancer,  Chronic fatigue syndrome , Common Colds , Hormone imbalance , Irritable bowel disease , Thyroid conditions , Weight loss resistance

Needed nutrients

Digestive enzymes, vitamin C (citrus, kiwi, berries, tamarind), vitamin B, L-carnitine, chromium, anti-oxidants, fiber-rich foods (squash, yams, sulfur family of garlic and onions, greens, okra, radish), spearmint, ginger, beets, carrots, all root crops, sprouts, pineapple, papaya , taurine rich foods (breastmilk, sea algae, fish)

Adaptogenic herbs

  1. Eleuthero ginseng
  2. Holy basil
  3. Rodiola rosea
  4. ashwagandha
  5. Astralagus
  6. Sour date
  7. Mimosa pudica
    Extracts of Mimosa pudica are successful in wiping out harmful bacteria and can be useful in antibacterial products
  8. Medicinal mushrooms
    Mushrooms are rich in B vitamins such as riboflavin (B2), folate (B9), thiamine (B1), pantothenic acid (B5), and niacin (B3).
  9. Licorice root
  10. Valerian

 

Cortisol can reduce cravings for those addicted to heroin

LONG TERM CAFFEINE USE WORSENS ALZHEIMER’S SYMPTOMS

Cumulative lifetime stress may accelerate epigenetic aging

Cumulative lifetime stress may accelerate epigenetic aging

Cumulative lifetime stress may accelerate epigenetic aging, an effect that could be driven by glucocorticoid-induced epigenetic changes.

Background:

Chronic psychological stress is associated with accelerated aging and increased risk for aging-related diseases, but the underlying molecular mechanisms are unclear.

Results: We examined the effect of lifetime stressors on a DNA methylation-based age predictor, epigenetic clock.
After controlling for blood cell-type composition and lifestyle parameters, cumulative lifetime stress, but not childhood maltreatment or current stress alone, predicted accelerated epigenetic aging in an urban, African American cohort (n = 392). This effect was primarily driven by personal life stressors, was more pronounced with advancing age, and was blunted in individuals with higher childhood abuse exposure.

Hypothesizing that these epigenetic effects could be mediated by glucocorticoid signaling, we found that a high number (n = 85) of epigenetic clock CpG sites were located within glucocorticoid response elements.

We further examined the functional effects of glucocorticoids on epigenetic clock CpGs in an independent sample with genome-wide DNA methylation (n = 124) and gene expression data (n = 297) before and after exposure to the glucocorticoid receptor
agonist dexamethasone.

Dexamethasone induced dynamic changes in methylation in 31.2 % (110/353) of these
CpGs and transcription in 81.7 % (139/170) of genes neighboring epigenetic clock CpGs. Disease enrichment analysis of these dexamethasone-regulated genes showed enriched association for aging-related diseases, including coronary artery disease, arteriosclerosis, and leukemias.

These findings contribute to our understanding of mechanisms linking
chronic stress with accelerated aging and heightened disease risk.

https://genomebiology.biomedcentral.com/track/pdf/10.1186/s13059-015-0828-5?site=http://genomebiology.biomedcentral.com

Membrane glucocorticoid receptors (mGRs) are a group of receptors which bind and are activated by glucocorticoids such as cortisol and corticosterone, as well as certain exogenous glucocorticoids such as dexamethasone.[1][2][3][4][5] Unlike the classical nuclear glucocorticoid receptor (GR), which mediates its effects via genomicmechanisms, mGRs are cell surface receptors which rapidly alter cell signaling via modulation of intracellular signaling cascades.[2][3] The identities of the mGRs have yet to be fully elucidated,[6] but are thought to include membrane-associated classical GRs[7][8] as well as yet-to-be-characterized G protein-coupled receptors(GPCRs).[1][4][9][10] Rapid effects of dexamethasone were found not be reversed by the GR antagonist mifepristone, indicating additional receptors besides just the classical GR.[11]

mGRs have been implicated in the rapid effects of glucocorticoids in the early central stress response[12][13] via modulating neuronal activity in the hypothalamushippocampusamygdala, and prefrontal cortex, among other areas.[7] In accordance, glucocorticoids are known to affect cognitionstress-adaptive behavior, and neuroendocrine output (e.g., suppression of oxytocin and vasopressin secretion)[4] within minutes.[7] mGRs appear to be partially involved in the anti-inflammatory and immunosuppressant effects of glucocorticoids.[3][5][14] mGRs are present in and appear to regulate many major bodily systems and organs, including the cardiovascularimmuneendocrine, and nervous systemssmooth and skeletal muscle, the liver, and fat tissue.[9] mGRs appear to cooperate with, complement, and synergize with classical nuclear GRs in various ways

 

Gut Microbes May Talk to the Brain Through Cortisol

Gut Microbes May Talk to the Brain Through Cortisol

Summary: Researchers identify a predictive relationship between serotonin, cortisol and fecal microbiota. The study provides additional support for previous findings that implicate gut bacteria in ASD.

Source: University of Illinois.

Gut microbes have been in the news a lot lately. Recent studies show they can influence human health, behavior, and certain neurological disorders, such as autism. But just how do they communicate with the brain? Results from a new University of Illinois study suggest a pathway of communication between certain gut bacteria and brain metabolites, by way of a compound in the blood known as cortisol. And unexpectedly, the finding provides a potential mechanism to explain the characteristics of autism.

“Changes in neurometabolites during infancy can have profound effects on brain development, and it is possible that the microbiome — or collection of bacteria, fungi, and viruses inhabiting our gut — plays a role in this process,” says Austin Mudd, a doctoral student in the Neuroscience Program at U of I. “However, it is unclear which specific gut bacteria are most influential during brain development and what factors, if any, might influence the relationship between the gut and the brain.”

The researchers studied 1-month-old piglets, which are remarkably similar to human infants in terms of their gut and brain development. They first identified the relative abundances of bacteria in the feces and ascending colon contents of the piglets, then quantified concentrations of certain compounds in the blood and in the brain.

“Using the piglet as a translatable animal model for human infants provides a unique opportunity for studying aspects of development which are sometimes more difficult or ethically challenging to collect data on in human infants,” Mudd says. “For example, in this study we wanted to see if we could find bacteria in the feces of pigletsthat might predict concentrations of compounds in the blood and brain, both of which are more difficult to characterize in infants.”

The researchers took a stepwise approach, first identifying predictive relationships between fecal bacteria and brain metabolites. They found that the bacterial genera Bacteroides and Clostridium predicted higher concentrations of myo-inositol, Butyricimonas positively predicted n-acetylaspartate (NAA), and Bacteroides also predicted higher levels of total creatine in the brain. However, when bacteria in the genus Ruminococcus were more abundant in the feces of the piglets, NAA concentrations in the brain were lower.

“These brain metabolites have been found in altered states in individuals diagnosed with autism spectrum disorder (ASD), yet no previous studies have identified specific links between bacterial genera and these particular metabolites,” Mudd notes.

The next step was to determine if these four bacterial genera could predict compounds in the blood. “Blood biomarkers are something we can actually collect from an infant, so it’s a clinically relevant sample. It would be nice to study an infant’s brain directly, but imaging infants is logistically and ethically difficult. We can, however, obtain feces and blood from infants,” says Ryan Dilger, associate professor in the Department of Animal Sciences, Division of Nutritional Sciences, and Neuroscience Program at U of I.

The researchers found predictive relationships between the fecal microbiota and serotonin and cortisol, two compounds in the blood known to be influenced by gut microbiota. Specifically, Bacteroides was associated with higher serotonin levels, while Ruminococcus predicted lower concentrations of both serotonin and cortisol. Clostridium and Butyricimonas were not associated strongly with either compound.

Again, Mudd says, the results supported previous findings related to ASD. “Alterations in serum serotonin and cortisol, as well as fecal Bacteroides and Ruminococcus levels, have been described in ASD individuals.”

Based on their initial analyses, the researchers wanted to know if there was a three-way relationship between Ruminococcus, cortisol, and NAA. To investigate this further, they used a statistical approach known as “mediation analysis,” and found that serum cortisol mediated the relationship between fecal Ruminococcus abundance and brain NAA concentration. In other words, it appears that Ruminococcus communicates with and makes changes to the brain indirectly through cortisol. “This mediation finding is interesting, in that it gives us insight into one way that the gut microbiota may be communicating with the brain. It can be used as a framework for developing future intervention studies which further support this proposed mechanism,” Dilger adds.

Image shows a gut.

“Initially, we set out to characterize relationships between the gut microbiota, blood biomarkers, and brain metabolites. But once we looked at the relationships identified in our study, they kept leading us to independently reported findings in the autism literature. We remain cautious and do not want to overstate our findings without support from clinical intervention trials, but we hypothesize that this could be a contributing factor to autism’s heterogenous symptoms,” Mudd says. Interestingly, in the time since the researchers wrote the paper, other publications have also reported relationships between Ruminococcus and measures of brain development, supporting that this might be a promising area for future research.

Dilger adds, “We admit this approach is limited by only using predictive models. Therefore, the next step is to generate empirical evidence in a clinical setting. So it’s important to state that we’ve only generated a hypothesis here, but it’s exciting to consider the progress that may be made in the future based on our evidence in the pre-clinical pig model.”

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Mudd and Dilger’s co-authors include Kirsten Berding, Mei Wang, and Sharon Donovan from the Division of Nutritional Sciences and the Department of Food Science and Human Nutrition at U of I.

Funding: The study was supported by Mead Johnson Nutrition.

Source: Lauren Quinn – University of Illinois
Image Source: NeuroscienceNews.com image is in hte public domain.
Original Research: Full open access research for “Serum cortisol mediates the relationship between fecal Ruminococcus and brain N-acetylaspartate in the young pig” by Austin T. Mudd, Kirsten Berding, Mei Wang, Sharon M. Donovan & Ryan N. Dilger in Gut Microbes. Published online July 13 2017 doi:10.1080/19490976.2017.1353849

CITE THIS NEUROSCIENCENEWS.COM ARTICLE
University of Illinois “Gut Microbes May Talk to the Brain Through Cortisol.” NeuroscienceNews. NeuroscienceNews, 21 August 2017.
<http://neurosciencenews.com/gut-microbes-cortisol-7338/&gt;.

Abstract

Serum cortisol mediates the relationship between fecal Ruminococcus and brain N-acetylaspartate in the young pig

A dynamic relationship between the gut microbiota and brain is pivotal in neonatal development. Dysbiosis of the microbiome may result in altered neurodevelopment; however, it is unclear which specific members of microbiota are most influential and what factors might mediate the relationship between the gut and the brain. Twenty-four vaginally-derived male piglets were subjected to magnetic resonance spectroscopy at 30 d of age. Ascending colon contents, feces, and blood were collected and analyzed for volatile fatty acids, microbiota relative abundance by 16s rRNA, and serum metabolites, respectively. A mediation analysis was performed to assess the mediatory effect of serum biomarkers on the relationship between microbiota and neurometabolites. Results indicated fecal Ruminococcus and Butyricimonas predicted brain N-acetylaspartate (NAA). Analysis of serum biomarkers indicated Ruminococcus independently predicted serum serotonin and cortisol. A 3-step mediation indicated: i) Ruminococcus negatively predicted NAA, ii) Ruminococcus negatively predicted cortisol, and iii) a significant indirect effect (i.e., the effect of fecal Ruminococcus through cortisol on NAA) was observed and the direct effect became insignificant. Thus, serum cortisol fully mediated the relationship between fecal Ruminococcus and brain NAA. Using magnetic resonance spectroscopy, this study used a statistical mediation analysis and provides a novel perspective into the potential underlying mechanisms through which the microbiota may shape brain development. This is the first study to link Ruminococcus, cortisol, and NAA in vivo, and these findings are substantiated by previous literature indicating these factors may be influential in the etiology of neurodevelopmental disorders.

“Serum cortisol mediates the relationship between fecal Ruminococcus and brain N-acetylaspartate in the young pig” by Austin T. Mudd, Kirsten Berding, Mei Wang, Sharon M. Donovan & Ryan N. Dilger in Gut Microbes. Published online July 13 2017 doi:10.1080/19490976.2017.1353849