Archive for the ‘Inflammation’ Category

LDN Webinar

https://www.belmarpharmasolutions.com/resources/clinician-resources/clinician-library/the-ldn-book-volume-two/

**Please note this webinar occurred last year; however, they are making it available to all now.  Just go to the link, fill out info. and you will be directed to the Webinar that already took place.**

The LDN Book: Volume Two

October 12, 2020

By: Belmar Pharmacy

Belmar Pharmacy is presenting the launch of Author and Low Dose Naltrexone (LDN) Advocate, Linda Elsegood’s latest book, The LDN Book Volume 2.

Dr. Angela DeRosa, Belmar Pharma Solutions Medical Director and Tracy Crawford, Director of Customer Experience, speak with authors Linda Elsegood, Darin Ingels ND, FAAM, Olga Cortez MD, and Leonard Weinstock MD about their LDN expertise and their contributions to the book.

Also hear from, Samantha Lebsock, PharmD at Belmar Pharmacy – she will share her extensive knowledge of LDN from a compounding pharmacist perspective. 

This webinar is engaging for both practitioners and patients interested in learning more about LDN and how to get their hands on The LDN Book Volume 2 and all it has to offer.

Conversations contain some of the reasons practitioners prescribe LDN, including:

  • Autoimmune
  • Women’s Health
  • Lyme Disease
  • Thyroid
  • Chronic Skin Conditions
  • Gut Health

This webinar is intended for patients and prescribers. If you would like to watch the webinar, please fill out in the top link. You will be re-directed to the recording after the successful completion of the form.

For more on LDN:

Vaccine-Induced Thrombocytopenia With Severe Headache – Why Lyme/MSIDS Patients Should Care

https://www.nejm.org/doi/full/10.1056/NEJMc2112974?

Vaccine-Induced Thrombocytopenia with Severe Headache

To the Editor:

Vaccine-induced immune thrombotic thrombocytopenia (VITT), a serious adverse event after vaccination with ChAdOx1 nCoV-19 (AstraZeneca) or Ad26.COV2.S (Johnson & Johnson–Janssen), is caused by platelet factor 4 (PF4)–dependent, platelet-activating antibodies.1-3 High-dose immune globulins and anticoagulation are the main treatments.4,5 In this report, we present evidence that vaccine-induced thrombocytopenia (VIT) without associated cerebral venous sinus thrombosis (CVST) or other thromboses and with severe headache as the heraldic symptom may precede VITT (“pre-VITT syndrome”).

Eleven patients presented with severe headache in the absence of CVST 5 to 18 days after ChAdOx1 nCoV-19 vaccination.

  • All the patients had thrombocytopenia (low platelets in the blood which can cause hemorrhaging)
  • high d-dimer levels (a test to detect blood clots – a high level indicates clot formation and breakdown in the body)
  • high levels of anti–PF4–heparin IgG antibodies
  • during follow-up, intracranial hemorrhage occurred in three patients (Patients 1, 2, and 3), with radiologic evidence of new CVST in Patients 2 and 3 (Figure 1, and Table S1 in the Supplementary Appendix, available with the full text of this letter at NEJM.org).
  • Only two patients (Patients 2 and 4) were initially admitted with conditions that met the criteria for VITT; both patients had pulmonary embolism, and additional splanchnic vein thrombosis was present in Patient 2.

In Patient 2, anticoagulation treatment had been initiated several days earlier for pulmonary embolism (without diagnosis of VITT) but was stopped after the onset of headache, shortly before CVST developed.

  • In two patients (Patients 1 and 3), peripheral thromboses were eventually identified during follow-up.

Thrombotic complications did not develop in seven of the patients (Patients 5 through 11); all but one of these patients received high-dose immune globulin, glucocorticoids, or therapeutic-dose anticoagulation within 5 days after headache onset. In contrast, in all four patients with subsequent thrombosis (Patients 1 through 4), therapeutic-dose anticoagulation either was not started until 6 to 9 days after headache onset or was stopped prematurely before the development of CVST.

Although the combination of thrombocytopenia and severe headache due to CVST has been recognized as the typical presentation of VITT,1,2 the experience with these 11 patients suggests that VIT with severe headache, elevated d-dimer levels, and strongly positive results on anti–PF4–heparin IgG enzyme-linked immunosorbent assay may precede VITT.

Our findings have immediate implications for clinical practice: in this pre-VITT syndrome, severe headache may not develop as a symptom secondary to CVST but instead may precede CVST by several days, potentially in association with microthrombosis in smaller cortical veins.

Consequently, patients who present with severe headache 5 to 20 days after adenovirus vector vaccination against coronavirus disease 2019 should undergo immediate testing for thrombocytopenia and d-dimer levels and, if available, testing for anti–PF4–heparin IgG antibodies.

When these antibodies are present at high titers, patients are at imminent risk for CVST, and it is likely that this condition can be prevented with immediate treatment, such as with intravenous immune globulin. The decision to initiate therapeutic-dose anticoagulation is a difficult one; the risk of emerging thrombosis, including CVST, has to be balanced against the risk of intracranial hemorrhage on an individual basis (e.g., with consideration of platelet count and fibrinogen levels).

Farid Salih, M.D.
Charité-Universitätsmedizin Berlin, Berlin, Germany

Linda Schönborn, M.D.
Universitätsmedizin Greifswald, Greifswald, Germany

Siegfried Kohler, M.D., Christiana Franke, M.D., Martin Möckel, M.D., Thomas Dörner, M.D., Hans C. Bauknecht, M.D., Christian Pille, M.D., Jan A. Graw, M.D.
Charité-Universitätsmedizin Berlin, Berlin, Germany

Angelika Alonso, M.D.
University Hospital of Mannheim, Mannheim, Germany

Johann Pelz, M.D.
University Hospital of Leipzig, Leipzig, Germany

Hauke Schneider, M.D., Antonios Bayas, M.D., Monika Christ, M.D.
University Hospital of Augsburg, Augsburg, Germany

Joji B. Kuramatsu, M.D.
University Hospital of Erlangen, Erlangen, Germany

Thomas Thiele, M.D., Andreas Greinacher, M.D.
Universitätsmedizin Greifswald, Greifswald, Germany

Matthias Endres, M.D.
Charité-Universitätsmedizin Berlin, Berlin, Germany

Supported by Deutsche Forschungsgemeinschaft project number 374031971–TRR 240 (to Prof. Greinacher) and EXC-2049–390688087 NeuroCure under the German Excellence Strategy (to Prof. Endres) and by the Domagk-Programm of the Universitätsmedizin Greifswald (to Dr. Schönborn).

Disclosure forms provided by the authors are available with the full text of this letter at NEJM.org.

This letter was published on September 15, 2021, at NEJM.org.

Profs. Greinacher and Endres contributed equally to this letter.

___________________

**Comment**

Both Thrombocytopenia and severe headaches are common with Lyme/MSIDS patients.

Therapy for thrombocytopenia requires treatment or removal of the underlying infection, in addition to maintenance of platelet counts and hemostatic function.

Hopefully it’s clear that a Lyme/MSIDS patient getting a COVID shot could be diagnosed with thrombocytopenia that either already exists or worsens after the injection.  Treating the underlying infection is imperative but won’t be considered by mainstream medicine.

For more:

Go here for the latest VAERS data and the mounting list of adverse reactions and deaths.

Cellular Blueprint of MS Lesions

https://www.nih.gov/news-events/news-releases/nih-scientists-build-cellular-blueprint-multiple-sclerosis-lesions

Friday, September 10, 2021

NIH scientists build a cellular blueprint of multiple sclerosis lesions

Study lays the groundwork for potential new therapies for progressive multiple sclerosis.

Chronic lesions with inflamed rims, or “smoldering” plaques, in the brains of people with multiple sclerosis (MS) have been linked to more aggressive and disabling forms of the disease. Using brain tissue from humans, researchers at the National Institutes of Health’s National Institute of Neurological Disorders and Stroke (NINDS) built a detailed cellular map of chronic MS lesions, identifying genes that play a critical role in lesion repair and revealing potential new therapeutic targets for progressive MS. The study was published in Nature.

“We identified a set of cells that appear to be driving some of the chronic inflammation seen in progressive MS,” said Daniel Reich, M.D., Ph.D., senior investigator at NINDS. “These results give us a way to test new therapies that might speed up the brain’s healing process and prevent brain damage that occurs over time.”

Chronic active lesions are characterized by a slow, expanding rim of immune cells called microglia. Microglia normally help protect the brain, but in MS and other neurodegenerative diseases, they can become overactive and secrete toxic molecules that damage nerve cells. Other cells found at the edge of the lesions, such as astrocytes and lymphocytes, may also contribute to ongoing tissue damage. Prior studies suggest that microglia are the main culprits behind lesion expansion, but the exact types of cells found near lesions and their biological mechanisms are elusive.

To better understand MS lesions, Dr. Reich and his colleagues used single-cell RNA sequencing, a powerful technique which enables researchers to catalog gene activity patterns in individual cells, to examine post-mortem brain tissue of five MS patients and three healthy controls. Samples were provided by the Netherlands Brain Bank, Netherlands Institute for Neuroscience, Amsterdam, the Netherlands, and the NINDS Neuroimmunology Clinic.

“Single-cell RNA sequencing technology allows us to do a much deeper dive into the types of cells present in MS lesions,” said Dr. Reich.

By analyzing the gene activity profiles of over 66,000 cells from human brain tissue, researchers created the first comprehensive map of cell types involved in chronic lesions, as well as their gene expression patterns and interactions.

Dr. Reich’s team found a great diversity of cell types in the tissue surrounding chronic active lesions compared to normal tissue, and a high proportion of immune cells and astrocytes at the active edges of those lesions. Microglia comprised 25% of all immune cells present at the lesion edges.

“Our dataset is very rich. The beauty of having such a detailed map is that now we have a better understanding of the entire network of cells involved in smoldering inflammation,” said Martina Absinta, M.D., Ph.D., a former post-doctoral fellow in Dr. Reich’s lab and current adjunct assistant professor at Johns Hopkins University, Baltimore, who led the study.

More detailed analyses revealed that the gene for complement component 1q (C1q), an important and evolutionarily ancient protein of the immune system, was expressed mainly by a subgroup of microglia responsible for driving inflammation, suggesting that it may contribute to lesion progression.

To determine the function of C1q, researchers knocked out the gene in the microglia of mouse models of MS and examined the brain tissue for signs of neuroinflammation. In mice lacking microglial C1q, they found significantly decreased tissue inflammation compared to control animals. Additionally, in another group of animals, blocking C1q reduced iron-containing microglia, revealing a potential new therapeutic avenue to treat chronic brain inflammation in MS and related neurodegenerative diseases.

According to the authors, it’s possible that targeting C1q in human microglia could halt MS lesions in their tracks.

In MS, the immune system attacks myelin, a protective layer that forms around nerve cells in the brain and spinal cord, leading to vision loss, muscle weakness, problems with balance and coordination, fatigue, numbness, and other debilitating symptoms. A subset of people develop progressive MS, resulting in extensive brain tissue damage and disability. Anti-inflammatory medications help patients manage their symptoms by dampening the responses of immune cells in the blood and lymph nodes. But treatments are not as effective for patients with chronic lesions who experience ongoing brain tissue inflammation.

“We have terrific therapies that block new inflammation but nothing to stop the inflammation that’s already there,” said Dr. Reich. “In order to make strides in developing new therapies for progressive MS, we’re going to need to pick apart the cellular and molecular mechanisms one by one.”

In 2019, Dr. Reich and his team reported that damaging, chronic active lesions may be a hallmark of progressive MS. The current study identifies microglia and C1q as promising targets for progressive MS and supports the use of chronically inflamed rim lesions as an MRI biomarker for disease progression.

There is no cure for MS, and no therapies that directly treat chronic active lesions. By gaining a deeper understanding of lesion features, this study may help pave the way toward early clinical trials to test new therapies for this aspect of the disease.

This study was supported in part by the Intramural Research Program at the NINDS.

NINDS is the nation’s leading funder of research on the brain and nervous system. The mission of NINDS is to seek fundamental knowledge about the brain and nervous system and to use that knowledge to reduce the burden of neurological disease.

About the National Institutes of Health (NIH): NIH, the nation’s medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.

NIH…Turning Discovery Into Health®

Myocarditis After COVID-19 mRNA Shots But Just Mask Up & Shut Up

https://www.nejm.org/doi/full/10.1056/NEJMc2109975?

Myocarditis after Covid-19 mRNA Vaccination

This letter was published on August 18, 2021, at NEJM.org.

TO THE EDITOR:

The Centers for Disease Control and Prevention recently reported cases of myocarditis and pericarditis in the United States after coronavirus disease 2019 (Covid-19) messenger RNA (mRNA) vaccination.1 In recently published reports, diagnosis of myocarditis was made with the use of noninvasive imaging and routine laboratory testing.2-5 Here, we report two cases of histologically confirmed myocarditis after Covid-19 mRNA vaccination.

Figure 1. Histopathological Findings from Endomyocardial Biopsy and Autopsy.

Patient 1, a 45-year-old woman without a viral prodrome, presented with dyspnea and dizziness 10 days after BNT162b2 vaccination (first dose). A nasopharyngeal viral panel was negative for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), influenza A and B, enteroviruses, and adenovirus (Table S1 in the Supplementary Appendix, available with the full text of this letter at NEJM.org). A serum polymerase-chain-reaction (PCR) assay and serologic tests showed no evidence of active parvovirus, enterovirus, human immunodeficiency virus, or infection with SARS-CoV-2. At presentation, she had tachycardia; ST-segment depression detected on electrocardiography, which was most prominent in the lateral leads (Fig. S1); and a troponin I level of 6.14 ng per milliliter (reference range, 0 to 0.30). A transthoracic echocardiogram showed severe global left ventricular systolic dysfunction (ejection fraction, 15 to 20%) and normal left ventricular dimensions. Right heart catheterization revealed elevated right- and left-sided filling pressures and a cardiac index of 1.66 liters per minute per square meter of body-surface area as measured by the Fick method. Coronary angiography revealed no obstructive coronary artery disease. An endomyocardial biopsy specimen showed an inflammatory infiltrate predominantly composed of T-cells and macrophages, admixed with eosinophils, B cells, and plasma cells (Figure 1A and Figs. S2 through S4). She received inotropic support, intravenous diuretics, methylprednisolone (1 g daily for 3 days), and, eventually, guideline-directed medical therapy for heart failure (lisinopril, spironolactone, and metoprolol succinate). Seven days after presentation, her ejection fraction was 60%, and she was discharged home.

Patient 2, a 42-year-old man, presented with dyspnea and chest pain 2 weeks after mRNA-1273 vaccination (second dose). He did not report a viral prodrome, and a PCR test was negative for SARS-CoV-2 (Table S1). He had tachycardia and a fever, and his electrocardiogram showed diffuse ST-segment elevation (Fig. S1). A transthoracic echocardiogram showed global biventricular dysfunction (ejection fraction, 15%), normal ventricular dimensions, and left ventricular hypertrophy. Coronary angiography revealed no coronary artery disease. Cardiogenic shock developed in the patient, and he died 3 days after presentation. An autopsy revealed biventricular myocarditis (Figure 1B and Figs. S5 and S6). An inflammatory infiltrate admixed with macrophages, T-cells, eosinophils, and B cells was observed, a finding similar to that in Patient 1.

In these two adult cases of histologically confirmed, fulminant myocarditis that had developed within 2 weeks after Covid-19 vaccination, a direct causal relationship cannot be definitively established because we did not perform testing for viral genomes or autoantibodies in the tissue specimens. However, no other causes were identified by PCR assay or serologic examination.

Amanda K. Verma, M.D.
Kory J. Lavine, M.D., Ph.D.
Chieh-Yu Lin, M.D., Ph.D.
Washington University School of Medicine, St. Louis, MO

________________________

https://www.brighteon.com/b3d87a5a-faea-4341-bab6-0406b9d356f5  4 Min. Video Here

The HighWire with Del Bigtree
Published Aug. 16, 2021

‘MASK UP AND SHUT UP’

Entering the ridiculous, public health officials are now asking people not to talk to stop the Covid virus. Jefferey Jaxen dives into the science behind the latest Covid mitigation suggestion.

__________________

**Comment**

The video is revealing on many fronts:

  • Propaganda is alive and well.
  • The paper “Viral Load of SARS-CoV-2 in Respiratory Aerosols Emitted By COVID-19 Patients While Breathing, Talking, and Singing,” has numerous disclaimers in fine print, namely, that they couldn’t mechanically retrieve and isolate a viable virus from ambient air in the vicinity of patients.  Well, that’s inconvenient.
  • This study demonstrates perfectly the hypocrisy of our corrupt public health ‘authorities’ in that they demand perfectly done randomized, controlled trials on thousands of patients to approve COVID treatments, completely ignoring clinical results, but will accept and propagate poorly done science that pushes their continued fear narrative that lines their pockets. And even when there properly done RCTs they ignore them and then go on a smear campaign to malign them, and implement bandwagon to make the public believe their accepted narrative.
  • This duplicity has been going on in Lyme-land for over 40 years and continues today.  Hopefully people are waking up to it.

What’s Behind This Epidemic of Chronic, Inflammatory Conditions?

https://www.lymedisease.org/kinderlehrer-epigenetics/

What’s behind this epidemic of chronic, inflammatory conditions?

by Daniel A. Kinderlehrer MD

I have witnessed many changes in the over 40 years I’ve been a doctor, including epidemic rises in multiple medical conditions.

I’m not talking about the present pandemic, nor am I referring to the opioid crisis, another devastating epidemic that has taken the lives of over 500,000 Americans. I’m talking about chronic conditions that cause a slow burn and sometimes kill.

Lyme disease is but one example.

But think how things have changed since the beginning of the previous century: heart disease was barely on the radar in 1900, but for over 50 years it has been the number one cause of death in the U.S.1

A whopping 69% of Americans are now overweight, with 36.5% obese,2 directly contributing to the skyrocketing incidence of adult-onset diabetes mellitus.3 When I was in training in the 1970s, I never saw a patient with AODM who was under 40 years old. Now, it is being diagnosed in children.

And then there are the dramatic increases in autism spectrum disorder,4 attention deficit hyperactivity disorder (ADHD),5 autoimmune conditions,6 some types of cancer7 and food allergies.8

Food sensitivities, mental health

Twenty-five years ago, when I had a large environmental medicine practice, most of my patients with food sensitivities reacted to one or more of a half dozen foods: milk, corn, eggs, wheat, citrus, or sugar/yeast. It was easy to put patients on an elimination diet: fish, lamb, vegetables, legumes, potatoes and rice. Now people react to avocados, rice, and anything under the sun.

And, of course, there’s the rise in mental health disorders. Even before the Covid pandemic, the World Health Organization predicted that depression would become the leading cause of death globally.9

According to the CDC, in 2019, 19% of Americans suffered from depression and 7% were moderately to severely affected.10 Among adults, suicidal ideation is increasing. Suicide has become the second leading cause of death in children and adolescents ages 13 to 19—and the leading cause of death among 13 year-olds.11 (Among all Americans, it is the tenth leading cause of death.11)

The role of epigenetics

There are a host of factors that determine the how, where and why illness occurs. These include genetic proclivity, lifestyle, trauma, diet, exposures to microbes and toxins. But here is what is further catapulting these seemingly disparate epidemics: a change in the human condition that we now understand as epigenetics.

While it takes millennia of natural selection to change our genes, specific proteins that turn genes on and off can alter gene expression in a single generation. Epigenetics explains how a change in expression of genes can be passed from one generation to the next without actually changing the DNA. There are literally thousands of conditions that can cause epigenetic changes.

Nutrient deficiencies, for example exacerbated by soil depletion, can activate epigenetic changes that result in neurological issues from mood and behavioral disorders to cognitive dysfunction, and these problems are passed on to subsequent generations.12,13 Epigenetics helps explain why the skyrocketing sugar intake in our diets is causing obesity.14,15

Chemical exposures also have epigenetic consequences. Over the past century, we have been exposed to hundreds of thousands of chemicals that are new to human existence. Pesticides, insecticides, herbicides, and other chemicals all have the potential to modify epigenetic activity.16 Countless agents now ubiquitous in daily life, from air pollution to air fresheners and fabric softeners can negatively impact overall health.17,18

Societal changes

But it is not only diet, nutrition, and exposure to toxic chemicals that have changed in the past century. Another factor which has undergone radical transformation is the social milieu. The social sphere, which used to revolve around communities, has devolved to extended families, then to nuclear families, then single-parent families, and now, tragically at times, to homeless families or solitude.

It is no longer routine for people to go next door to be held by grandma, or move in with aunts and uncles when the going at home gets rough. In essence, safe shelter has disappeared. This lack of safety is compounded for survivors of childhood trauma, who often develop epigenetic abnormalities and thus pass the trauma on to their offspring.19

Intergenerational trauma

That’s right—PTSD can be inherited. A review paper by Rachel Yehuda and Amy Lehrner on intergenerational transmission of trauma and the role of epigenetic mechanisms states:

“There is now converging evidence supporting the idea that offspring are affected by parental trauma exposures occurring before their birth, and possibly even prior to their conception. On the simplest level, the concept of intergenerational trauma acknowledges that exposure to extremely adverse events impacts individuals to such a great extent that their offspring find themselves grappling with their parents’ post‐traumatic state.”20

PTSD is not only a psychological disorder, it triggers increasing dysregulation of an individual’s neurobiology.21

Other social factors also have an enormous impact on health and well-being. Social isolation is a major risk factor for depression.22 The chronic stresses of poverty, racism, homophobia, and misogyny not only make for a bad day, they act on our biochemical pathways impacting immune, hormonal, and neurological function.23

The long-term release of the stress hormone cortisol and of proteins called cytokines (which regulate the body’s immune system response) can cause even more damage. These biochemical messengers, in turn, can result in epigenetic changes that are passed on to future generations.24

We’re not born with a clean slate

Epigenetic transmission means that both physical and emotional traumas are cumulative over generations. Newborns are not born with a clean slate. And these alterations in epigenetics are manifesting in a tsunami that is destabilizing individuals’ core regulatory systems.

Increasingly, people respond as if they have continuous PTSD—their nervous and immune systems going haywire at both real and imagined threats, with all the downstream consequences evident in an increasingly sick population.

Which brings us back to PANS, which I have discussed in the past few articles.

I think we are witnessing an epidemic of autoimmune reactivity to multiple agents in the environment—like foods, viruses, bacteria, and mold. We are clearly seeing it with SARS-CoV-2 (COVID-19). When autoimmune reactivity results in neuroinflammation, it can result in cognitive dysfunction, PANS and a panoply of mental health disorders—for generations to come.

We need to become more cognizant of the cumulative stresses that result in combined mental and physical issues, and address them at their core.

Dr. Daniel Kinderlehrer is an internal medicine physician in Denver, Colorado, with a practice devoted to treating patients with tick-borne illness. He is the author of  Recovery From Lyme Disease: The Integrative Medicine Guide to the Diagnosis and Treatment of Tick-Borne Illness.

References

  1. https://pubmed.ncbi.nlm.nih.gov/24811552/
  2. https://www.healthline.com/health/obesity-facts#1.-More-than-one-third-of-adults-in-the-United-States-are-obese.
  3. https://www.cdc.gov/mmwr/volumes/67/wr/mm6712a2.htm
  4. https://www.statista.com/statistics/676354/autism-rate-among-children-select-countries-worldwide/
  5. https://chadd.org/adhd-weekly/is-there-an-increase-in-adhd/
  6. https://www.immunology.org/news/report-reveals-the-rising-rates-autoimmune-conditions
  7. https://www.forbes.com/sites/williamhaseltine/2020/12/09/cancer-rates-are-on-the-rise-in-adolescents-and-young-adults-new-study-shows/?sh=5d56188c3b7b
  8. https://www.news-medical.net/health/Whats-Driving-the-Recent-Rise-in-Food-Allergies.aspx
  9. Tucci V, Moukaddam N. We are the hollow men: The worldwide epidemic of mental illness, psychiatric and behavioral emergencies, and its impact on patients and providers. J Emerg Trauma Shock. 2017;10(1):4-6. doi:10.4103/0974-2700.199517
  10. https://www.cdc.gov/nchs/products/databriefs/db379.htm
  11. https://webappa.cdc.gov/sasweb/ncipc/leadcause.html
  12. Liu J, Zhao SR, Reyes T. Neurological and Epigenetic Implications of Nutritional Deficiencies on Psychopathology: Conceptualization and Review of Evidence. Qi L, ed. Int J Mol Sci. 2015;16(8):18129-18148.
  13. https://www.scientificamerican.com/article/soil-depletion-and-nutrition-loss/
  14. https://www.tasteofhome.com/article/american-sugar-intake/
  15. Ling C, Rönn T. Epigenetics in Human Obesity and Type 2 Diabetes. Cell Metab. 2019;29(5):1028-1044.
  16. Collotta M1, Bertazzi PA, Bollati V. Epigenetics and pesticides. Toxicology. 2013 May 10;307:35-41.
  17. https://www.sciencedirect.com/science/article/pii/S0360132316304334
  18. https://www.scientificamerican.com/article/greener-laundry/
  19. Matosin N, Cruceanu C, Binder EB. Preclinical and Clinical Evidence of DNA Methylation Changes in Response to Trauma and Chronic Stress. Chronic stress (Thousand Oaks). 2017;1:10.
  20. Yehuda R, Lehrner A. Intergenerational transmission of trauma effects: putative role of epigenetic mechanisms. World Psychiatry. 2018;17(3):243-257.
  21. McFarlane AC. The long-term costs of traumatic stress: intertwined physical and psychological consequences. World Psychiatry. 2010;9(1):3-10.
  22. Bhatti AB, Haq A ul. The Pathophysiology of Perceived Social Isolation: Effects on Health and Mortality. Muacevic A, Adler JR, eds. Cureus. 2017;9(1):e994.
  23. Song H et. al. Association of Stress-Related Disorders With Subsequent Autoimmune Disease. 2018;319(23):2388-2400.
  24. Notterman DA, Mitchell C. Epigenetics and Understanding the Impact of Social Determinants of Health. Pediatr Clinics North Am. 2015;62(5):1227-1240.

____________________

**Comment**

I’ve got news for you: vaccines are also stressors.  They can reactivate latent infections including but not limited to Lyme/MSIDS.  They can also be contaminated with retroviruses, viruses, cancer, parasites, metals, graphene oxide, poly–ethylene glycol (PEG) and ethylene alcohol, and other harmful nanoparticles.  And all gene-based vaccines such as the COVID jabs can be expected to cause blood clotting and bleeding disorders based on their molecular mechanisms of action. Further, the spike protein is a dangerous toxin causing untold damage.

Vaccines have been and are a source of destruction that is being put directly into bodies of millions worldwide. It is the “golden calf” no one wants to talk about, or is censored and bullied if they do, but is THE elephant in the room.