The pathophysiology of childhood exposure to elevated levels of Reactive Oxygen Species (ROS)
- "England to offer Covid jab to five to 11-year-olds"
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I will try to stick to the science or I could easily fill this page with expletives at the lies, contradictions and wilful blindness in the following article:
England to offer Covid jab to five to 11-year-olds
16 February 2022, 17:00 GMT
Children aged between five and 11 in England will be offered a low-dose Covid vaccine, the government says.
Official scientific advice concludes the move would help protect the "very small" number of children who become seriously ill with Covid.
Health Secretary Sajid Javid says the rollout will be "non-urgent", with an emphasis on parental choice.
Northern Ireland also said on Wednesday it will be following Wales and Scotland in offering young children the vaccine.
Children are at a much lower risk of becoming severely ill from a Covid infection, so the health benefits of vaccinating them are smaller than in other age-groups. Also, many will have some protection from already having caught the virus.
So the scientists on the Joint Committee on Vaccination and Immunisation, which advises governments across the UK, have been weighing up the evidence for immunising five to 11-year-olds.
It concluded vaccination should go ahead to prevent a "very small number of children from serious illness and hospitalisation" in a future wave of Covid.
Prof Wei Shen Lim, from the JCVI, said: "We're offering this to five to 11-year-olds now in order to future-proof their defences against a future wave of infection."
He suggested parents consider getting their children vaccinated during school holidays to minimise disruption to their education from any flu-like side effects of the jab.
The full guidance says fewer than two children would develop inflamed heart muscle (myocarditis) out of every million vaccinated.
However, it estimates vaccinating one million children would prevent:
98 hospitalisations if the next wave was more severe like previous variants
17 hospitalisations if the next wave was relatively mild, like Omicron
Prof Lim warned other childhood vaccinations include the MMR and HPV campaigns have "fallen behind due to the pandemic" and it was "vital" that Covid jabs did not disrupt these immunisations.
Mr Javid said: "The NHS will prepare to extend this non-urgent offer to all children during April so parents can, if they want, take up the offer to increase protection against potential future waves of Covid-19 as we learn to live with this virus."
He emphasised that children are at low risk from Covid and that the "priority remains for the NHS to offer vaccines and boosters to adults and vulnerable young people" and to catch-up with other childhood immunisation programmes".
The vaccine - which contains just a third of the adult dose - has already been used widely in other countries. The US alone has given it to eight million children in this age group.
However, the JCVCI denied it had been slow to act and said the vaccine had received regulatory approval only in December.
Children aged from five to 11 who have other medical conditions that put them at greater risk are already eligible for the vaccine.
In total, about six million children in the UK in that age group will be offered the jab.
Two 10 microgram doses of the Pfizer/BioNTech vaccine, with at least 12 weeks between each dose, would be administered to those whose parents decide to take up the offer.
The Welsh government announced on Tuesday that it would be offering jabs to children after seeing the JCVI ruling.
It followed reports the committee's announcement was delayed due to a disagreement with the UK government, which says it is "reviewing the JCVI's advice as part of wider decision-making".
Scotland then followed the next day, with First Minister Nicola Sturgeon saying Scottish ministers had received and considered the same JCVI advice and were "content to accept it".
She told parents and carers of children in the five to 11 age group that more information would be given when plans had been finalised.
https://www.bbc.com/news/uk-60406155
Pathology
Where to start? Triple dosing 5+ year olds with a cytotoxic ROS inducing nerve poison that kills tadpoles at 0.1 PPM. Myocarditis and pericarditis we know about. Same with OAS, strokes, thrombosis, neurological disorders and immune suppression.
But what else? Osteoporosis & musculoskeletal disorders, leukemia, glioblastoma and all kinds of carcinoma, encephalitis, fibrosis, diabetes/autoimmune disordersâŚand ROS induced damage at the heart of much of the pathology.
Background:
Reactive oxygen species
Reactive oxygen species (ROS) are highly reactive chemicals formed from O2. Examples of ROS include peroxides, superoxide, hydroxyl radical, singlet oxygen,[1] and alpha-oxygen.
The reduction of molecular oxygen (O2) produces superoxide (â˘Oâ2), which is the precursor to most other reactive oxygen species:[2]
In a biological context, ROS are byproducts of the normal metabolism of oxygen. ROS have roles in cell signaling and homeostasis.[3][4] ROS are intrinsic to cellular functioning, and are present at low and stationary levels in normal cells.[5] In vegetables, ROS are involved in metabolic processes related to photoprotection and tolerance to various types of stress.[6] However, ROS can cause irreversible damage to DNA as they oxidize and modify some cellular components and prevent them from performing their original functions. This suggests that ROS has a dual role; whether they will act as harmful, protective or signaling factors depends on the balance between ROS production and disposal at the right time and place.[7] In other words, oxygen toxicity can arise both from uncontrolled production and from the inefficient elimination of ROS by the antioxidant system. During times of environmental stress (e.g., UV or heat exposure), ROS levels can increase dramatically.[3] This may result in significant damage to cell structures. Cumulatively, this is known as oxidative stress.
More:
https://en.wikipedia.org/wiki/Reactive_oxygen_species
SARS-CoV-2 spike promotes inflammation and apoptosis through autophagy by ROS-suppressed PI3K/AKT/mTOR signaling (2021)
Mechanistically, SCV-2-S inhibited the PI3K/AKT/mTOR pathway by upregulating intracellular reactive oxygen species (ROS) levels, thus promoting the autophagic response.
https://pubmed.ncbi.nlm.nih.gov/34461258/
and this:
Common pathway involved once the free radicals have been generated.
https://doorlesscarp953.substack.com/p/common-pathway-involved-once-the/comments?r=if8oy
I'm was struggling with ROS mediated sequelae in children as I couldnât think of anything approaching this level of reckless endangerment occurring before outside of nuclear accident or cancer therapy designed to kill cells, or perhaps accidentally drinking weedkiller, something like that. It's evil personified.
So what do we have? Accelerated aging as with adults due to damage to mitochondrial RNA and cellular membranes. But aging a 5 year olds tissues isnât the same as aging a middle aged person, who risks cardiovascular disease, joint inflammation, cancers, immunosenescence ie diseases of the elderly, being old before your time.
OK its toxic, but how much exposure? We know from recent studies that spike protein expressing mRNA can remain biologically active in the lymph nodes for at least 2 months. And our kids will get 2 boosters, months apart, followed most likely by a third and then annual follow ups.
So to maintain the fake immunity endpoint of elevated antibody levels for months they will have in consequence elevated ROS levels for months, each year, every year if the drug companies and their well paid sales reps - the hopelessly conflicted âregulatorsâ (!) have their way.
"A Recurring Fountain Of Revenue": FDA Exec Admits Biden Planning Annual Shots, Including Toddlers
Iâve picked a few out here that appear representative. Heredity and epigenetics feature quite strongly as signals. If you are prone to the disorder, are stressed or live an unhealthy lifestyle then ROS exposure can trigger or advance it. Just as with adults.
Oxidative Stress and Immune System Dysfunction in Autism Spectrum Disorders (2020)
Abstract
Autism Spectrum Disorders (ASDs) represent a group of neurodevelopmental disorders associated with social and behavioral impairments. Although dysfunctions in several signaling pathways have been associated with ASDs, very few molecules have been identified as potentially effective drug targets in the clinic. Classically, research in the ASD field has focused on the characterization of pathways involved in neural development and synaptic plasticity, which support the pathogenesis of this group of diseases. More recently, immune system dysfunctions have been observed in ASD. In addition, high levels of reactive oxygen species (ROS), which cause oxidative stress, are present in ASD patients. In this review, we will describe the major alterations in the expression of genes coding for enzymes involved in the ROS scavenging system, in both ASD patients and ASD mouse models. In addition, we will discuss, in the context of the most recent literature, the possibility that oxidative stress, inflammation and immune system dysfunction may be connected to, and altogether support, the pathogenesis and/or severity of ASD. Finally, we will discuss the possibility of novel treatments aimed at counteracting the interplay between ROS and inflammation in people with ASD.
Keywords: ROS, inflammation, ASD, autism, immune system
Full paper:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7247582/
Oxidative Stress and Bronchial Asthma in ChildrenâCauses or Consequences? (2017)
Bronchial asthma is one of the most common chronic inflammatory diseases of the airways. In the pathogenesis of this disease, the interplay among the genes, intrinsic, and extrinsic factors are crucial. Various combinations of the involved factors determine and modify the final clinical phenotype/endotype of asthma. Oxidative stress results from an imbalance between the production of reactive oxygen species and reactive nitrogen species and the capacity of antioxidant defense mechanisms. It was shown that oxidative damage of biomolecules is strongly involved in the asthmatic inflammation. It is evident that asthma is accompanied by oxidative stress in the airways and in the systemic circulation. The oxidative stress is more pronounced during the acute exacerbation or allergen challenge. On the other hand, the genetic variations in the genes for anti-oxidative and pro-oxidative enzymes are variably associated with various asthmatic subtypes. Whether oxidative stress is the consequence of, or the cause for, chronic changes in asthmatic airways is still being discussed. Contribution of oxidative stress to asthma pathology remains at least partially controversial, since antioxidant interventions have proven rather unsuccessful. According to current knowledge, the relationship between oxidative stress and asthmatic inflammation is bidirectional, and genetic predisposition could modify the balance between these two positionsâoxidative stress as a cause for or consequence of asthmatic inflammation.
Full paper:
https://www.frontiersin.org/articles/10.3389/fped.2017.00162/full
Oxidative stress in Duchenne muscular dystrophy: focus on the NRF2 redox pathway (2017)
Abstract
Oxidative stress is involved in the pathogenesis of Duchenne muscular dystrophy (DMD), an X-linked genetic disorder caused by mutations in the dystrophin gene and characterized by progressive, lethal muscle degeneration and chronic inflammation. In this study, we explored the expression and signaling pathway of a master player of the anti-oxidant and anti-inflammatory response, namely NF-E2-related Factor 2, in muscle biopsies of DMD patients. We classified DMD patients in two age groups (Class I, 0â2âyears and Class II, 2â9âyears), in order to evaluate the antioxidant pathway expression during the disease progression. We observed that altered enzymatic antioxidant responses, increased levels of oxidized glutathione and oxidative damage are differently modulated in the two age classes of patients and well correlate with the severity of pathology. Interestingly, we also observed a modulation of relevant markers of the inflammatory response, such as heme oxygenase 1 and Inteleukin-6 (IL-6), suggesting a link between oxidative stress and chronic inflammatory response. Of note, using a transgenic mouse model, we demonstrated that IL-6 overexpression parallels the antioxidant expression profile and the severity of dystrophic muscle observed in DMD patients. This study advances our understanding of the pathogenic mechanisms underlying DMD and defines the critical role of oxidative stress on muscle wasting with clear implications for disease pathogenesis and therapy in human.
Full paper:
https://academic.oup.com/hmg/article/26/14/2781/3792452
Childhood adversity, mental health, and oxidative stress: A pilot study (2019)
Abstract
Childhood adversity is a potent risk factor for mental health conditions via disruptions to stress response systems. Dysregulations in oxidative stress systems have been associated with both childhood adversity and several psychological disorders (e.g., major depressive disorder) in adult populations. However, few studies have examined associations between childhood adversity, oxidative stress, and mental health in pediatric populations. Childhood adversity (Adverse Childhood Events [ACE]), oxidative stress [F2t-isoprostanes (IsoPs)], and mental health pathology were assessed in 50 adolescent females recruited primarily through the Department of Youth Services. Standard ordinary least squares regression models were run co-varying for age, race/ethnicity, adolescent nicotine use, study condition, and parent history of ACEs. Adolescents who reported experiencing four or more ACEs had significantly elevated IsoP levels. Further, internalizing symptom scores across diagnoses were significantly associated with elevated IsoPs, whereas no externalizing symptoms scores, except Attention Deficit Hyperactivity Disorder, were related to altered oxidative stress. Results indicate that IsoPs may be a global marker of childhood adversity and mental health symptomatology, particularly within internalizing symptom domains. A limitation is that body mass index was not collected for this sample. Future studies are needed to replicate and extend these findings in larger, more diverse samples.
A review of epidemiological research found that nearly all mental health disorders start by adolescence [16].
Adolescence is an important period of developmental plasticity and sensitivity when brain development is highly dynamic [17]. Significant pubertal, hormonal, neuroendocrine, and metabolic changes occur during adolescence that may interact with early risk factors (e.g., adversity) and contribute to the onset and progression of mental health pathology. Delineating the mechanisms through which childhood adversity confers risk for emerging mental health problems prior to adulthood is imperative to understanding the etiology and progression of psychiatric illness.
Oxidative stress
Childhood adversity is associated with both physical and mental health outcomes, with limited understanding of the specific mediators of these associations [18]. Metabolic and immune systems have been implicated as potential putative mechanistic pathways underpinning the childhood adversity-health relationship [6, 19, 20]. McEwen and colleagues hypothesized that childhood adversity disrupts development by altering homeostasis through a process termed âallostatic loadâ, which can have targeted effects on mitochondrial function and the production of reactive oxygen species (ROS), as well as systemic effects on brain, immune and metabolic systems [21â23]. Reactive oxygen species refers to a range of molecules and free radicals that derive from molecular oxygen [24]. The majority of ROS are byproducts of cellular metabolism of oxygen that are internally produced by mitochondria, peroxisomes, and cytosolic enzyme systems; however, stress can also externally increase the production of ROS [25]. The dramatic increase in ROS following periods of prolonged stress can be detrimental [26], contributing to redox imbalance which occurs as antioxidant systems are unable to neutralize the effects of the ROS. Altogether, the imbalance between the ROS and antioxidant defenses results in oxidative stress. Oxidative stress has emerged as a candidate homeostatic disruption, with the brain particularly susceptible due to high oxygen consumption [27]. Common measures of oxidative stress include ROS, hydrogen peroxide, sphingolipid and glutathione metabolites, and eicosanoids, such as the family of isoprostanes and catalase activity [28]. Elevated isoprostanes, in particular, have been identified as a gold standard measure of oxidative stress, with the advantage revealing acute elevation in response to pathophysiological states, demonstrated maintenance of elevation over time, and normalized when pathophysiology is resolved [29, 30]. While initially applied in studies of pathogenesis in adults [31â33], more recent studies have demonstrated the capacity to measure elevated isoprostanes in early infancy and throughout childhood related to prematurity, diet and diagnosed disorders [34â38]. Thus, measures of elevated oxidative stress are reflected by isoprostane increases across the lifespan, indicating that the field will benefit from greater inclusion of the isoprostane measure in different contexts.
Full paper:
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0215085
I will finish with multiple sclerosis as childhood MS also correlates with ROS levels.
There are many other degenerative conditions too that can be triggered or made worse by excess ROS exposure as per the above table, but the ones Iâve hi-lighted here will be representative and are every reason not to jab our kids as the risk profile is one sided and itâs all negatives.
Oxidative stress in multiple sclerosis: Central and peripheral mode of action (2015)
Abstract
Accumulating evidence suggests that oxidative stress plays a major role in the pathogenesis of multiple sclerosis (MS). Reactive oxygen species (ROS), which if produced in excess lead to oxidative stress, have been implicated as mediators of demyelination and axonal damage in both MS and its animal models. One of the most studied cell populations in the context of ROS-mediated tissue damage in MS are macrophages and their CNS companion, microglia cells. However, and this aspect is less well appreciated, the extracellular and intracellular redox milieu is integral to many processes underlying T cell activation, proliferation and apoptosis. In this review article we discuss how oxidative stress affects central as well as peripheral aspects of MS and how manipulation of ROS pathways can potentially affect the course of the disease. It is our strong belief that the well-directed shaping of ROS pathways has the potential to ameliorate disease progression in MS.
Keywords: DMF; Neurodegeneration; Neuroprotection; Nrf2.
Related:
Autoantibody Release in Children after Corona Virus mRNA Vaccination: A Risk Factor of Multisystem Inflammatory Syndrome?
https://doorlesscarp953.substack.com/p/autoantibody-release-in-children?r=if8oy
The Diagnostic and Clinical Approach to Pediatric Myocarditis: A Review of the Current Literature
https://doorlesscarp953.substack.com/p/the-diagnostic-and-clinical-approach?r=if8oy
Spike protein (inc vax) induced immunodeficiency & carcinogenesis megathread #8: Original Antigenic Sin: How First Exposure Shapes Lifelong AntiâInfluenza Virus Immune Responses
doorlesscarp953.substack.com/p/spike-protein-inc-vax-induced-immunodeficiency-f8d/comments?r=if8oy
Hat tip to Walter @Parsifaler:
Yes, our kids are at risk of cardiovascular damage too.
Levels of circulating endothelial cells and colony-forming units are influenced by age and dyslipidemia (2012)
Abstract
Background:
The balance between endothelial injury and repair in childhood is poorly understood. We examined this relationship in healthy children, in adults, and in children with familial hypercholesterolemia (FH).
Methods:
Circulating endothelial cells (CECs) were measured as a marker of vascular injury, with vascular repair assessed by counting colony-forming units (CFUs), also known as endothelial progenitor cells.
Results:
CEC number increased with age. Children with FH had elevated CECs as compared with healthy children, with similar levels numerically to those found in healthy adults. CFU numbers were higher in healthy children than either healthy adults or children with FH. Endothelium-dependent vascular function, measured by flow-mediated dilatations, was positively associated with CFU number, even after adjustment for confounding risk variables.
Conclusion:
Levels of CECs increase and CFUs decrease with age. In childhood, before the onset of clinically detectable cardiovascular dysfunction, children with a major risk factor for atherosclerotic disease have levels of these indexes of vascular injury and repair approaching those seen in adults.
Really great work here!!! đ