Functional Role of Dietary Intervention to Improve the Outcome of COVID-19: A Hypothesis of Work

Authors : Giovanni Messina (1), Rita Polito (1), Vincenzo Monda (2), Luigi Cipolloni (1), Nunzio Di Nunno (3), Giulio Di Mizio (4), Paolo Murabito (5), Marco Carotenuto (6), Antonietta Messina (2), Daniela Pisanelli (1), Anna Valenzano (1), Giuseppe Cibelli (1), Alessia Scarinci (7), Marcellino Monda (2), Francesco Sessa (1)

  1. Department of Clinical and Experimental Medicine, University of Foggia, Italy

2. Department of Experimental Medicine, Section of Human Physiology and Unit of Dietetics and Sports Medicine, Università degli Studi della Campania Naples, Italy

3. Department of History, Society and Studies on Humanity, University of Salento, Lecce Italy

4. Department of Law, Forensic Medicine, Magna Graecia University of Catanzaro, Italy

5. Department of General Surgery and Medical-Surgical Specialties, University of Catania, Italy

6. Department of Mental Health, Physical and Preventive Medicine, Clinic of Child and Adolescent Neuropsychiatry, Università degli Studi della Campania Italy

7. Department of Education Sciences, Psychology and Communication, University of Bari, Italy

Abstract

Background: On the 31 December 2019, the World Health Organization (WHO) was informed of a cluster of cases of pneumonia of unknown origin detected in Wuhan City, Hubei Province, China.

The infection spread first in China and then in the rest of the world, and on the 11th of March, the WHO declared that COVID-19 was a pandemic. Taking into consideration the mortality rate of COVID-19, about 5–7%, and the percentage of positive patients admitted to intensive care units being 9–11%, it should be mandatory to consider and take all necessary measures to contain the COVID-19 infection.

Moreover, given the recent evidence in different hospitals suggesting IL-6 and TNF-α inhibitor drugs as a possible therapy for COVID-19, we aimed to highlight that a dietary intervention could be useful to prevent the infection and/or to ameliorate the outcomes during therapy. Considering that the COVID-19 infection can generate a mild or highly acute respiratory syndrome with a consequent release of pro-inflammatory cytokines, including IL-6 and TNF-α, a dietary regimen modification in order to improve the levels of adiponectin could be very useful both to prevent the infection and to take care of patients, improving their outcomes.

1. Background

On the 31 December 2019, the World Health Organization (WHO) was informed of a cluster of cases of pneumonia of unknown origin detected in Wuhan City, Hubei Province, China. About one month later (on 8 January 2020), the Chinese authorities declared the identification of a new type of coronavirus, informing the WHO a few days later that the outbreak was associated with exposure in a seafood market in Wuhan City.

The infection spread firstly in China and then in the rest of the world, and on the 11th of March, the WHO declared that COVID-19 was a pandemic.Coronaviruses (CoVs) belong to the subfamily Orthocoronavirinae in the family of Coronaviridae in the order Nidovirales, and this subfamily includes α-coronavirus, β-coronavirus, γ-coronavirus, and delta-coronavirus [1].

Coronaviruses primarily cause enzootic infections in birds and mammals and, in the last few decades, have shown to be capable of infecting humans as well [2]. In human infections with highly virulent respiratory viruses—such as avian influenza H5N1, H7N9, Severe Acute Respiratory Syndrome (SARS) coronavirus, and Coronavirus Disease-19 (COVID-19)—immunopathogenesis caused by the overproduction of pro-inflammatory cytokines may play an essential role in disease progression and mortality [3].

Several recent studies have reported that COVID-19 caused the destruction of the pulmonary parenchyma, including interstitial inflammation and extensive consolidation, similarly to the previously reported coronavirus infection [4,5]. During coronavirus infection, it was observed that the lungs increased in weight, with a mild pleural effusion of clear serous fluid, named pulmonary edema, and extensive consolidation [6,7]. In some areas, there was interstitial thickening, with mild-to-moderate fibrosis, but a disproportionately sparse infiltrate of inflammatory cells (mainly histiocytes, including multinucleated forms, and lymphocytes) [8]. A dilatation of the airspaces was observed, as was focal honeycombing fibrosis. An intra-alveolar organization of exudates was described, and the formation of granulation tissues in the small airways and airspaces was reported. These lesions were typically located in the sub-pleural region, and the cellular component mainly consisted of histiocytes, as reported in a previous paper [9]. Xu et al. described in their case report the pathological findings of COVID-19 associated with acute respiratory distress syndrome. At the X-ray investigation, they detected a rapid progression of bilateral pneumonia.

The biopsy samples were taken from the lung; the histological examination showed bilateral diffuse alveolar damage with cellular fibromyxoid exudates [6].Considering that the mortality rate of COVID-19, about 5–7% [10], and the percentage of positive patients admitted to intensive care units being 9–11% [11], it should be mandatory to consider and take all necessary measures intended to contain the viral infection.

A recent study analyzed the data of 150 COVID-19 patients, with the aim of defining the clinical predictors of mortality. The results obtained from this study suggest that COVID-19 mortality might be due to virus-activated “cytokine storm syndrome”, considering that the plasma levels of IL-6 were higher in deceased patients compared to in discharged subjects [12].Considering that a detailed study has not been performed on the immunological response to COVID-19, the only way to discuss this thematic is to refer to previous knowledge about SARS-CoV and MERS-CoV. The first response is obtained through pattern recognition receptors (PRRs) including C-type lectin-like receptors, Toll-like receptors (TLR), NOD-like receptors (NLR), and RIG-I-like receptors (RLR). Moreover, several inflammatory factors are expressed such as IL-6 and TNF-α; moreover, the synthesis of type I interferons (IFNs) is activated, and these exert their actions against virus diffusion, accelerating macrophage phagocytosis [13] (Figure 1).

Figure 1. The main immunological response to COVID-19.

In the light of these considerations and the recent evidence in different hospitals suggesting IL-6 and TNF-α inhibitor drugs as a possible therapy for COVID-19, this review aims to highlight how a dietary intervention could be useful to prevent the infection and/or to ameliorate the outcome during therapy.

2. The Pivotal Role of IL-6 and TNF-α in Lung Infections

The first laboratory report about COVID-19 patients indicated several parameters that were found to be altered in blood samples; for example, D-dimer, neutrophil count, blood urea, and creatinine levels were significantly higher. In the same way, several cytokines such as IL-6 and TNF-α were overexpressed, indicating the immune status of the patients [14].IL-6 represents pro-inflammatory signaling produced by adipose tissue; for this reason, this endocrine cytokine could be important in regulating the host response during acute infection [15].

Several papers have described the essential role of IL-6 in generating a proper immune response during different kinds of viral infection in the pulmonary tract. Others link this cytokine to an exacerbation of viral disease. These latter findings support the hypothesis that IL-6 upregulation during viral infections may promote virus survival and the exacerbation of the clinical disease [16,17].

Indeed, IL-6 has a pleiotropic function, and it is produced in response to tissue damage and infection. In particular, at the pulmonary level, innate and adaptative immune cell proliferation is strongly influenced by this cytokine. After targeting its specific receptor, IL-6 starts a cascade of signaling events mainly associated with the JAK/STAT3 activation pathway, promoting the transcription of multiple downstream genes related to cellular signaling processes, including cytokines, receptors, adaptor proteins, and protein kinase [15].

Furthermore, it has been reported that IL-6 is an essential factor for the survival of mice with a viral infection. This cytokine promotes the optimal regulation of the T-cell response, inflammatory resolution, tissue remodeling promoting lung repair, cell migration, and the phagocytic activities of macrophages, as well as preventing virus-induced apoptosis in lung epithelial cells.

However, experimental scientific evidence also suggests potential adverse consequences that increased levels of IL-6 might have on the cellular immune response against viruses. In this context, different possible mechanisms involving this cytokine might affect viral clearance, ultimately favoring the establishment of a persistent viral state in infected hosts [18,19].

Tumor necrosis factor is a cell-signaling protein (cytokine) involved in systemic inflammation, released predominately from macrophages, but it is also released from a variety of other immune cells. It has been well described that during infection with the influenza virus, the expression of TNF-α in lung epithelial cells was higher, exerting powerful anti-influenza virus activity [20].

In an animal model, it has been demonstrated that TNF-α plays a pivotal role in the development of pulmonary fibrosis. TNF-α signals via two receptors, TNF-RI and TNF-RII; the first receptor (TNF-RI) promotes intracellular signaling involving c-Jun N-terminal kinase (JNK) and nuclear factor (NF)-κB, while the other receptor, TNF-RII, promotes TNF-RI–dependent cell death, without directly inducing apoptosis. Although both receptors are broadly expressed, it is known that the majority of inflammatory signaling is elicited through TNF-RI [21].

In an in vitro model, it has been described that serine/threonine kinases can phosphorylate TNF-RI and its molecules, preventing tyrosine phosphorylation [22,23,24].In patients with COVID-19, the high serum levels of IL-6 and TNF-α are negatively correlated to T cells; contrariwise, it has been demonstrated that T cell levels were restored by reducing IL-6 and TNF-α concentrations [25]. These findings suggested that these cytokines could represent important targets of anti-COVID-19 therapies.

3. Adiponectin Function in Lung Infections

Through the secretion of adipokines, adipose tissue participates in the regulation of several pathophysiological processes in many organs and tissues. Among the adipokines, adiponectin is the most relevant. Adiponectin is one of the most abundant circulating adipocytokines, accounting for 0.01% of total serum protein. Adiponectin is an important regulator of cytokine responses, and this effect is isoform-specific. It is involved in a wide variety of physiological processes, including energy metabolism, inflammation, and vascular physiology. These effects are mediated by two atypical, widely expressed seven-transmembrane receptors, AdipoR1 and AdipoR2 [26]. Adiponectin has beneficial effects in cardiovascular systems and blood vessels, protecting these tissues through the inhibition of pro-inflammatory and hypertrophic responses and stimulation of endothelial cell responses [27].

Adiponectin circulates as three different isoforms (low molecular weight—LMW, medium molecular weight—MMW, and high molecular weight—HMW) [28].Infectious diseases are characterized by an increased production of adiponectin. Several papers suggest that adiponectin may be related to disease activity and/or severity in different conditions such as rheumatoid arthritis, osteoarthritis, and systemic lupus erythematosus. Since adiponectin has been found to display both pro- and anti-inflammatory activities, controversial findings have been observed regarding the role of total adiponectin in systemic autoimmune and inflammatory joint diseases. For this reason, the relative contribution of each adiponectin isoform to the inflammatory response and joint and/or tissue damage requires further study [29].

It is reported that adiponectin is regulated by transcription factors in adipose tissue, such as peroxisome proliferator-activated receptor-γ (PPAR-γ) [30]. During viral infections, it has been reported that the role of the predisposition of hosts is also important, as well as their state of health and nutrition. Indeed, it is well known that white adipose tissue is considered an endocrine source of biologically active substances with local and/or systemic action, called adipokines.

The inappropriate secretion of adipokines seems to participate in the pathogenesis of obesity-related diseases, including endothelial dysfunction, inflammation, and atherosclerosis [31,32,33].The biological function of adipokines in lung diseases seems to be mainly related to the inflammatory process. In particular, the intercorrelation between adipose tissue and the lung has become evident as the involvement of adiponectin has been demonstrated in several lung diseases such as Chronic Obstructive Pulmonary Disease (COPD), emphysema, and cancer [34]. In fact, with specific regard to COPD, a low-grade inflammatory state has been demonstrated [35,36,37].

Moreover, increasing evidence suggests that adiponectin also exerts a crucial role in the vascular endothelium, maintaining vascular homeostasis and protecting against vascular dysfunctions. Altogether, these findings support the anti-inflammatory role of adiponectin in COPD and, in general, in other lung diseases [38].The critical role of adiponectin in the pathophysiological conditions of the lung is also supported by the modulation of AdipoRs with the downregulation of AdipoR2. It has been described that the adiponectin oligomerization state is altered in COPD; moreover, the presence of AdipoR1 and AdipoR2, with a lower expression of AdipoR2 compared to AdipoR1, in lung tissue [39] has been demonstrated. The low expression of AdipoR2 could suggest a specific role of this receptor, mainly implicated in adiponectin’s effects on inflammation and oxidative stress. Mainly, it has been observed that higher levels of adiponectin are associated with a significant and specific increase in HMW adiponectin, representing the most biologically active forms. Thus, HMW adiponectin increases IL-6 secretion in human monocytes and human monocytic leukemia cell lines but does not suppress lipopolysaccharide (LPS)-induced IL-6 secretion. Byn contrast, LMW adiponectin reduces LPS-mediated IL-6 release and also stimulates IL-10 secretion [40].

Furthermore, several in vitro studies have demonstrated that adiponectin in the A549 adenocarcinoma human alveolar basal epithelial cell line has an essential apoptotic effect and also reduces the production of pro-inflammatory cytokines such as TNF-α, blocking NF-κB nuclear translocation [41,42].Indeed, adiponectin can reduce innate and adaptive immune cell proliferation and polarization, also blocking the production of pro-inflammatory cytokines such as TNF-α, IL-2, and IL-6, and enhancing that of anti-inflammatory cytokines such as IL-10, with a decrease in the phosphorylation of AMPK, p38, ERK1/2, and c-JNK [43,44,45,46]. Data from in vitro studies on lung cells were consistent with an anti-inflammatory function of adiponectin, and adiponectin-deficient mouse models developed lung function impairments and systemic inflammation [47].

The possible role of adiponectin in inflammatory pulmonary diseases, such as asthma and chronic obstructive pulmonary disease (COPD), and in critical illnesses has been the subject of recent investigations. Particularly, the HMW isoform has a specific role in pulmonary diseases and critical illnesses, even if its role should be better clarified [48,49].

An interesting study reported that systemic adiponectin concentrations in humans fall during the acute phase of lung infection: particularly, during the early phase, the pro-inflammatory state is generated by the high systemic TNF-α and IL-6 concentrations, with the subsequent inhibition of adiponectin production. Contrariwise, it has been described that the reduction in TNF-α and IL-6 factors generates a corresponding bounce-back in systemic adiponectin concentrations [50].

Although it is still unclear whether the modulation of systemic adiponectin or its signaling pathways has any therapeutic benefit in pulmonary or critical illnesses, it may serve as a novel therapeutic or preventative tool for these illnesses in the future. One obvious pharmaceutical treatment would be the exogenous administration of adiponectin by the inhalational or intravenous route. Although this has been tried in mouse models [51], the problems to be overcome prior to human administration include establishing what the biologically active molecule is and what role post-translational modifications have upon its function, and the associated difficulties in generating biologically active molecules on a large scale.

Considering the difficulty linked to the direct administration of adiponectin, in the last few years, other drugs have been used that indirectly improve adiponectin production. For example, a synthetic ligand of peroxisome proliferator-activated receptors can increase adiponectin mRNA in adipocytes, improving the production and secretion of adiponectin [52,53,54,55]. Moreover, other drugs such as fibrates can increase systemic adiponectin levels by enhancing PPAR-γ activity [56,57]. Another way to improve adiponectin levels is the use of angiotensin converting enzyme inhibitors [58,59,60]. Furthermore, it is possible to stimulate adipocyte differentiation [61] and the activation of PPAR [62].

Finally, it has been described that calcium channel blockers [63] and a central-acting anti-hypertensive agent [64] also increase systemic adiponectin concentrations [65]. The possibility to improve the action of adiponectin through diet is intriguing; it has been described that nutritional interventions may help to regulate systemic adiponectin concentrations. In an animal model, it has been demonstrated that a diet with a high concentration of polyunsaturated fatty acids and supplemented with ω-3 can improve the plasma levels of adiponectin, increasing gene expression [66]. On the other hand, in humans, adiponectin levels are positively associated with a healthy lifestyle and the Mediterranean diet, even if the mechanisms of action are not completely known [66]. Finally, in light of these considerations, in COVID-19 therapy, it could be very useful to combine drug therapy with a specific diet regimen.

4. ω-3 PUFAs and Lung Infections

Another important mediator involved in the immune response and influenced by nutrition are fatty acids, in particular, ω-3 PUFAs [67,68]. In fact, during bacterial and viral infections, they are able to act on immune cells and regulate diverse inflammatory processes. ω-3 PUFAs are known to have anti-inflammatory properties and play an essential role in the resolution of inflammation [69].

In several lung infections, the administration of PUFA can ameliorate the outcome of the patient in acute pneumonia. Sharma et al. reported in their study that the dietary supplementation of ω-3 PUFA can exert an overall beneficial effect against acute pneumonia through the upregulation of the host’s specific and nonspecific immune defenses [70]. ω-3 polyunsaturated fatty acids (PUFA, ω-3-fatty acids), the key components of fish and flaxseed oils, are increasingly consumed by the public because of their potential health benefits and can be used clinically for the treatment of metabolic, cardiac, inflammatory, and autoimmune diseases [71].

However, numerous studies have shown that these compounds are immunoregulatory and immunosuppressive and thus may increase susceptibility to infection. While reports suggest that ω-3 PUFAs may have beneficial effects against extracellular pathogens, few studies have been performed on systemic viral infections in mammals. Jones and Roper described in their study that a diet rich in ω-3 PUFAs did not significantly lower survival of the vaccinia virus infection, at least with short-term (~6 week) feeding in mice [71].

ω-3 PUFAs are metabolized into various mediators possessing anti-inflammatory properties such as resolvins and protectins. It is known that ω-3 PUFAs can reduce NF-κB activation by preventing nuclear p65 NF-κB translocation. Furthermore, ω-3 PUFAs minimize the activation of ERK1/2 MAPK, also reducing COX-2 production. The ω-3 PUFA-derived lipid mediator could markedly attenuate influenza virus replication via the RNA export machinery. In addition, the treatment of protectin D1 with peramivir could completely stop mouse mortality [72].

ω-3 supplementation was previously studied in Acute Respiratory Distress Syndrome (ARDS). Singer and Shapiro suggested that the enteral administration of natural antioxidant substances could improve oxygenation and clinical outcomes in ICU patients [73]. A systematic review performed in 2015 reported a positive effect only for patients suffering from ARDS with high mortality [74]. A more recent meta-analysis highlighted the importance of clinical trials in order to clarify the use of ω-3 fatty acids and antioxidants in patients with ARDS to ascertain the positive effects in order to reduce the lengths of ICU stays and the numbers of days spent on ventilators [75].

Although the role of ω-3 supplementation in ARDS should be better clarified, its pivotal role in reducing reactive oxygen species and pro-inflammatory cytokines, such as TNF-α, IL-1β, IL-6, and IL-8 [76], is well known.Therefore, ω-3 PUFAs, including protectin D1, which is a novel antiviral drug, could be considered for potential interventions for COVID-19.

5. Other Dietary Constituents and Lung Infections

As previously described, other dietary constituents can be used to improve the patients’ outcomes during lung infection, regulating the inflammatory response. Among these, antioxidants play an important role in protecting lung cells against viruses and bacteria. Viral infection leads to an increase in the intrapulmonary oxidative burden. In many diseases, the balance between oxidants and antioxidants (redox balance) is altered, with severe consequences [77].

The pathophysiological mechanisms by which free radicals generate various types of stress—such as oxidative, nitrative, carbonyl, inflammatory, and endoplasmic reticulum stress—lead to lung inflammation and an altered lung immune response. In this scenario, dietary antioxidants may play an important role against lung oxidative stress [77].

Several studies reported the protective role of the antioxidants in lung infection and in lung inflammation [78,79].In particular, vitamin C, polyphenols, and flavonoids can play a protective role in lung infections, being immune modulators and inflammatory mediators. Indeed, as reported by Carr et al., during infection, vitamin C levels may become depleted; for this reason, vitamin C supplementation can attenuate infection. Based on this evidence, these authors suggested a clinical trial with vitamin C infusion for the treatment of severe COVID-19 patients [80].

Among polyphenols, epigallo-catechin 3 gallate (EGCG) is the most potent ingredient in green tea and exhibits antibacterial, antiviral, antioxidative, anticancer, and chemo-preventive activities. Recently, numerous studies have investigated the protective effects of EGCG against asthma and other lung diseases such as COPD and lung pneumonia. EGCG may suppress inflammation and inflammatory cell infiltration into the lungs of asthmatic mice, and may also inhibit epithelial-mesenchymal transition EMT via the PI3K/Akt signaling pathway through upregulating the expression of phosphatase and tensin homolog (PTEN), both in vivo and in vitro [81].

Moreover, flavonoids can be used to attenuate lung injury in mice; it has been reported that they inhibit influenza virus and Toll-like receptor signaling, blocking NF-κB translocation [82].Therefore, as summarized in Table 1, supplementation with vitamin C, flavonoids, and polyphenols can be tested in COVID-19 patients, both in order to prevent viral infection and to improve patients’ outcomes.

Table 1. The principal antioxidants involved in lung infection and the immune-inflammatory response.

6. Discussion and Conclusions

During pulmonary infections, and particularly in COVID-19 patients, intracellular signaling leads to the production of pro-inflammatory cytokines, such as TNF-α and IL-6, which act in concert with chemoattractants, such as CXCL1 and CXCL2, to recruit polymorphonuclear leukocytes (PMNs) to the lungs, killing pathogens but generating fibrosis [83].

Another important consideration during COVID-19 infection is related to the modification of the secretory products of the upper and lower airways, which usually include mucin and pulmonary surfactant. During infection, mucin production is upregulated, with the function of preventing microbes from binding to and infecting epithelial cells [84].

The primary source of phospholipids (PLs) in the lung is pulmonary surfactant, synthesized and released by alveolar epithelial type II cells. The surfactant contains approximately 80–90% PLs, with fatty acid chains that can be oxidized during different challenges in the lung [85]. The oxidation of these PLs in the lung can occur in the setting of an increased oxidative stress situation, such as infection and inflammation [86]. The immune effects of oxidized phospholipids oxPLs during infectious diseases are inevitably dictated by the balance among activation, degradation, and scavenging. It has been shown that oxPLs are generated in the lung during several pulmonary infections, including influenza and avian influenza (H5N1), as well as SARS coronavirus, even if the mechanisms of action are not well known [87,88,89].

As reported by Imai et al., oxPL-induced inflammation is mediated by TLR4 and TRIF, driving an increase in IL-6 production [89]. It is intriguing to consider that oxPL-dependent defects in phagocytosis and ROS generation may lead to an increased susceptibility to respiratory infections [90]. Cholesterol is the major neutral lipid in pulmonary surfactant, in which it is thought to promote the spreading, mobility, and adsorption of surfactant films [91].

As previously documented, modulating adiponectin levels can be considered an important way to reduce cytokines levels; in this way, the adverse effects related to the COVID-19 infection should be attenuated. It is well described in animal models that the consumption of hyperlipidemic diets, rich in saturated fat, reduces the levels of adiponectin, while diets rich in polyunsaturated fatty acids and supplemented with ω-3 PUFA increase adiponectin levels, reducing pro-inflammatory cytokines [66].Innate and adaptive immune responses are influenced not only by oxPLs and cholesterol but also by the fatty acid profiles of tissues in response to pharmacological agents and diet [92].

Several studies performed in animal models demonstrated how ω-3 PUFA uptake into the lung tissue influences outcomes associated with infection, promoting the resolution of inflammation [93]. In another study, ω-3 PUFAs reduced the levels of PMNs and lowered IL-6 levels in lung infections [94]. These positive effects remain controversial; for example, Jones and Roper reported that in their experimental model, no statistically significant differences were found among the diet regimens, with and without ω-3 PUFAs, with respect to the susceptibility of mice to viral infection, morbidity, viral organ titers, recovery time, or mortality [71].

In conclusion, it is well known that general treatments are very important to enhance the host immune response against RNA viral infection. In addition, the immune response has often been shown to be weakened by inadequate nutrition in many model systems as well as in human studies. However, the nutritional status of the host, until recently, has not been considered as a contributing factor to the emergence of viral infectious diseases. The recent reports about the pathogenesis of COVID-19 suggested that one of the most important consequences of this infection is the cytokine storm syndrome [95], which could be strictly linked with coagulopathy, generating acute pulmonary embolism caused by in-situ thrombosis [96,97]. Therefore, a great number of clinical trials are ongoing to define a useful therapy to attenuate cytokine storms [98].For these reasons, an adequate ω-3 PUFA intake may be a valid strategy against viral infection.

Indeed, following the recommended intake of ω-3 PUFA, in the range of 0.5% and 2% of total calories (250 mg/day), may be important to protect against an excessive inflammatory response, also reducing IL-6 levels. This theory found important support in a recent study that demonstrated that ω-3 PUFA-derived lipid mediator protectins can suppress influenza virus replication through a mechanism that blocks the export of viral mRNA. Moreover, Imai demonstrated that this mediator can be used in combination with the antiviral peramivir, even at late time points in infection [99].

Nevertheless, the efficacy of ω-3 PUFAs at the clinical level is under investigation; for example, Hecker et al. described a beneficial effect for a diet regimen with ω-3 PUFAs, describing that the pro-inflammatory cytokine levels decreased after this diet regimen [100]. The suggested positive role in the outcome and prevention of the COVID-19 infection is summarized in Figure 2.

Figure 2. Adiponectin and ω-3 PUFAs reduce the lung inflammation that occurs following coronavirus infection, reducing IL-6 production, ERK1/2, and COX-2 activation and the nuclear translocation of NF-κB.

In addition, adiponectin plays a role in lung diseases and obesity; in the development and progression of lung disease and cancer, a pathogenic role of adiponectin was defined by both in vivo and in vitro studies.

Recently, immunometabolic pathomechanisms have been identified as important factors determining and modulating lung function and disease. Particularly, adiponectin levels have been found to be greater in patients with COPD compared with in control patients, and adiponectin-deficient mice are protected from several lung diseases [101].

Moreover, it has been reported that adherence to the Mediterranean diet was associated with an increase in adiponectin levels, improving cardiovascular system functionality [102], particularly in elderly people [103]. These findings are only apparently contradictory to the first data about the mortality rate from COVID-19 infections in the Mediterranean area (such as in Italy and Spain) [104].

First of all, the data have been referred only to the tested population; moreover, it is well described that the presence of several comorbidities such as hypertension, diabetes, and cardiovascular diseases severely influenced the mortality rate reported in this area [105].

All these comorbidities can be counteracted with a correct dietary regimen. Therefore, both adiponectin and ω-3 PUFAs appear to be attractive biomarkers for monitoring lung disease progression.

Finally, considering that the COVID-19 infection can generate a mild or highly acute respiratory syndrome with a consequent release of pro-inflammatory cytokines, including IL-6 and TNF-α, a modification of the dietary regimen in order to improve the levels of adiponectin could be very useful both to prevent the infection and to take care of the patients, improving their outcomes.

Given the similar pathway of action, it can be hypothesized that adiponectin and ω-3-PUFA could be used as real drugs to reduce inflammation, reducing both IL-6 and TNF-α levels as well as ameliorating the lung damage that occurs following coronavirus infection.

Investigation into Electrons, Oxygen, Nutrition, pH and COVID (or 5G!)

This is a ramble, of the threads of thought which are on my mind. In time this may be edited and streamlined, but presently I feel it paints a picture that may help others. It is clear something deep is happening in the world, bigger than just COVID in my opinion. So it will start with a long article about using H2O2 and wander on from there.

Surviving the Coronavirus Disease, How Hydrogen Peroxide Works

By Paul Ebeling on April 9, 2020

Hydrogen Peroxide Has a Long History of Medical Use

Hydrogen peroxide (H2O2) consists of a water molecule (H2O) with an extra oxygen atom.

The oxygen inactivates viral pathogens by breaking down the viral structure

Additionally, our immune cells produce hydrogen peroxide. This is in part how your immune system kills infected cells. Hydrogen peroxide therapy aids aids immune cells to perform their natural function more effectively.

H202 is on the shelf at the local grocery or drug store for $1.00 a bottle.

The Big Q: Can an inexpensive and easy to administer at-home treatment treat the novel coronavirus, SARS-CoV-2?

The Big A: Dr. Thomas Levy says Yes. The remedy is hydrogen peroxide H202, aerosolized in any standard nebulizer.

It’s worth keeping in mind that while the elderly and those with underlying medical conditions are at increased risk of serious complications and death, the overall mortality rate of COVID-19 is quite low, and very similar to the flu.

A compilation of reported mortality statistics from around the world can be found in the paper,“Likelihood of Survival of Coronavirus Disease 2019,” published in The Lancet Infectious Diseases, 30 March 2020.

For the latest up to the min COVID-19 resources click here.

To perform this treatment, you need but two items: a nebulizer with a face mask that covers your mouth and nose that emits a fine mist, and common household 3% hydrogen peroxide, available at most grocery stores and pharmacies for less than $1.

However, you may choose to purchase the more expensive food grade hydrogen peroxide as it doesn’t have any stabilizers in it. Stabilizers are proprietary and companies do not need to disclose them on the label, but some can be problematic.

Typically food grade peroxide comes in concentrations higher than 3% so if you chose it your will need to dilute it down to 3% to use it.

Viruses are not “alive” they need a live host in which they can infect live cells that then replicate the viral DNA and RNA. Once a cell is infected, newly replicated viruses exit the cell and move on to the next cell to duplicate the process.

So, when they talk about “killing” a virus, they are talking about inactivating them by breaking down their structure. This is why soap works so well. Coronaviruses are held together by a lipid (fatty) coating. Soap, being amphipathic, meaning it can dissolve most molecules dissolves this fat membrane, causing the virus to fall apart and become harmless.

More specifically, the fat-like substances in soap are structurally similar to the lipids found in the virus membrane, so the soap molecules compete with and replace the fats in the membrane. In so doing, the “fatty glue” holding the virus together dissolves.

Hydrogen peroxide works in a similar way. As noted by Dr. Levy, “the way to control any viral infection is not to kill the virus; rather, the infected cells that have been turned into viral factories must be killed.” 

Our immune cells actually produce hydrogen peroxide. This is in part how the immune system kills cells that have been infected with a virus. By killing the infected cell, viral reproduction is stopped. So, hydrogen peroxide therapy is in essence only aiding our immune cells to perform their natural function more effectively.

Hydrogen peroxide is also a Key redox signaling agent.

“At the low physiological levels in the nanomolar range, H2O2 is the major agent signaling through specific protein targets, which engage in metabolic regulation and stress responses to support cellular adaptation to a changing environment and stress …

Recent methodological advances permit the assessment of molecular interactions of specific ROS [reactive oxygen species] molecules with specific targets in redox signaling pathways.

Accordingly, major advances have occurred in understanding the role of these oxidants in physiology and disease, including the nervous, cardiovascular and immune systems, skeletal muscle and metabolic regulation as well as ageing and cancer.

In the past, unspecific elimination of ROS by use of low molecular mass antioxidant compounds was not successful in counteracting disease initiation and progression in clinical trials. However, controlling specific ROS-mediated signaling pathways by selective targeting offers a perspective for a future of more refined redox medicine.”

In short, hydrogen peroxide is a major ROS, but while ROS are typically thought of as “all bad,” this is a gross oversimplification.

As noted: “Steady-state physiological flux of H2O2 to specific protein targets leads to reversible oxidation, thereby altering protein activity, localization and interactions, which contributes to orchestration of various processes in cells and organs, including cell proliferation, differentiation, migration and angiogenesis. This state of low-level H2O2 maintenance and its associated physiological redox signaling is called ‘oxidative eustress.’”

Contrary to oxidative stress or oxidative distress, oxidative eustress denotes an oxidative challenge that has positive or beneficial effects and is essential in redox signaling.

The Studies: What they tells us

The most relevant study is 1 that was done earlier this year in the Journal of Hospital Infection. They studies 0.5% hydrogen peroxide, 6X weaker than the 3% typically used, and found that it killed human coronaviruses and SARS corona viruses and MERS.

Another study, published in the American Journal of Infection Control in Y 2009, assessed the efficacy of vaporized hydrogen peroxide against viruses on various surfaces, finding exposure to hydrogen peroxide vapor at a concentration of 10 parts per million resulted in 99% inactivation after 2.5 mins.

And a Y 2014 study in the Journal of Hospital Infection found hydrogen peroxide vapor eliminated an array of viruses on stainless steel, including human adenovirus 1, transmissible gastroenteritis coronavirus of pigs (TGEV, a SARS-CoV surrogate), avian influenza virus and swine influenza virus.

According to the authors, “Hydrogen peroxide vapor was virucidal against feline calicivirus, adenovirus, TGEV and avian influenza virus at the lowest vaporized volume tested (25 mL).” Vaporized hydrogen peroxide was found to completely inactivate a range of exotic animal viruses in a Y 1997 study as well.

Hydrogen peroxide’s ability to inactivate dangerous infectious viruses has also been highlighted in vaccine science. As noted in a Y 2016 study in the Vaccine journal, 3% hydrogen peroxide completely and irreversibly inactivated the rabies virus within 2 hrs, thus reducing time and cost of the inactivation process required for the making of a rabies vaccine, which contains inactivated rabies virus.

The most convenient to receive H202 is to inhale its mist, using a nebulizer a small, handheld device that converts liquid into a very fine mist.

The microscopic mist, similar to smoke or vapor, can be comfortably inhaled deep into the nostrils, sinuses and lungs. While nebulizers have routinely been used by asthmatics to deliver medication into their lungs, this delivery system affects not only the lungs but your entire body.

As noted in the Y 2002 review article, “Pulmonary Drug Delivery Systems: Recent Developments and Prospects,” “Targeting drug delivery into the lungs has become one of the most important aspects of systemic … drug delivery systems.

In the case of respiratory infections, the nebulizer has the added advantage of delivering the hydrogen peroxide right to the areas most affected by respiratory viruses: the sinuses, throat, bronchial tract and lungs.

Dr. Levy writes: “Effective hydrogen peroxide nebulization quite literally, ‘chops the head off of the snake,’ and the virus present elsewhere in the body can then readily be mopped up when the new virus influx has been terminated,” 

It should be kept in mind that hydrogen peroxide kills pathogens very readily upon contact in an open wound. It should, therefore, be understandable why putting a fine mist of hydrogen peroxide in all the areas of maximal viral replication promptly puts the body on a pathway to rapid healing.”

 Hydrogen Peroxide Protocol

To prevent an infection from taking hold, begin treatment at 1st signs of symptoms. Commercially available 3% hydrogen peroxide is fine for this purpose, and can be used without dilution.

If the undiluted solution stings or burns your nose, you can dilute it up to 50% with pure water. Even lower concentrations can be used, although the antiviral effects will be reduced at lower concentrations.

If already presenting with runny nose or sore throat, Dr. Levy recommends using the nebulizer for 10 to 15 mins 4X a day until the symptoms are relieved. You can also nebulized hydrogen peroxide for prevention and maintenance, which may be advisable during flu season, or while the COVID-19 pandemic is in full swing.

He notes: “As it is a completely non-toxic therapy, nebulization can be administered as often as desired. If done on a daily basis at least once, a very positive impact on bowel and gut function will often be realized as killing the chronic pathogen colonization present in most noses and throats stops the 24/7 swallowing of these pathogens and their associated toxins.

If daily prevention is not a practical option, the effectiveness of this treatment is optimized when somebody sneezes in your face or you finally get off of the plane after a trans-Atlantic flight. Do not wait for initial symptoms. Just nebulize at your 1st opportunity.”

Eat healthy, Be healthy, Live lively

Source:

https://www.livetradingnews.com/surviving-the-coronavirus-disease-how-hydrogen-peroxide-works-172241.html

ChooseLife : In Mid February I ordered and started using a Nebulizer with 1.5% H2O2 – http://chooselife.co.uk/index.php/2020/02/28/bill-munro-vs-the-coronavirus/

The Dr is bullish in his convictions, however there are associated risks to taking H2O2, perhaps mild or moderate, but they should be discussed, to best inform the reader.

Oxidative Stress may lead to the following :

Oxygen is crucial to life; however, when we use oxygen our bodies constantly produce free radicals. Free radicals are chemically unstable molecules or atoms. They also make other molecules or atoms in the body very unstable, thus damaging proteins, cell membranes, and even DNA structure. This is a process which can lead to permanent damage to cells and tissues resulting in infection, mental decline, depressed immunity system, joint disease, and heart disease. Free radicals are also considered to play an important role in the aging process.

Catalase is constantly in battle against the effect of free radicals to the body. It transforms harmful superoxide radicals into hydrogen peroxide which later breaks down into water and oxygen.

https://sciencing.com/role-catalase-5521462.html

The enzyme Catalase is a key buffer for these dangers, Grey hair may be an indication of inhibited (or low) Catalase production, here are Vegetarian/Vegan food sources:

Vegetarian Sources of Catalase

Written by Don Amerman

Catalase — found throughout nature in the cells of organisms that grow in the presence of oxygen — is an enzyme with potent antioxidant properties. The enzyme facilitates the breakdown of hydrogen peroxide into its harmless components — water and oxygen. Without catalase, the hydrogen peroxide that your body produces during the metabolic process would build up to toxic levels. Catalase occurs naturally in a wide array of plant-based foods, ensuring its availability to vegetarians and vegans.

Age-Related Decline in Catalase

The cells in your body can produce catalase as well as other antioxidant enzymes, such as glutathione peroxidase and superoxide dismutase, or SOD. These enzymes help to neutralize free radicals, according to the authors of “Biology: A Human Emphasis.” Free radicals are atoms or molecules with unpaired electrons that are the byproduct of human biological reactions such as metabolism. Scientists cite free radicals as causative factors in disease and aging-related cell damage. As you age, your body gradually produces less catalase, which results in a buildup of free radicals and an increase in the damage they can cause. To help supplement your body’s declining output of catalase, consume foods that are rich in this vital enzyme.

Garlic, Onions and Their Kin

Nutritionists give members of the allium plant family, which encompasses garlic, leeks, onions and shallots, high praise for their antioxidant properties. Among the cellular antioxidants naturally occurring in allium vegetables is catalase. In a study related to the catalase in allium family members, a team of Hungarian and Romanian researchers evaluated the effects of water stress on the level and activity of catalase and other antioxidant enzymes in these plants. They found that allium plants subjected to water deprivation had increased catalase levels and activity, according to an article published in a 2007 issue of “Plant, Soil and Environment.”

Cruciferous Vegetables

Cruciferous vegetables, including broccoli, cabbage, kale and collard and turnip greens, are rich in catalase. Eating plenty of these green leafy vegetables also stimulates your body’s production of catalase. Researchers at Alabama A&M University conducted an animal study to determine what, if any, anticancer effects could be observed in laboratory rats that were fed a diet of these vegetables. As part of this study, they measured the level of catalase in test animals and found that those fed cruciferous vegetables had sharply higher amounts of catalase in their livers than those animals that were not fed these vegetables. Results of this study were published in a 2012 issue of “International Journal of Cancer Research.”

Other Sources

Wheat sprouts contain high levels of catalase, according to a study by molecular biology researchers at Italy’s University of Perugia. In an article published in the July 2004 issue of the “Journal of Clinical Gastroenterology,” they note that the antioxidant activity of catalase and peroxidase in wheat sprouts is extremely strong. Other vegetarian sources of catalase include apricots, avocados, carrots, cherries, cucumbers, parsnips, potatoes, radishes, spinach and zucchini.

https://healthyeating.sfgate.com/vegetarian-sources-catalase-3693.html

ChooseLife : Parallel to this, is the issues reported of bronchial constriction. This would lead to the thinking that Magnesium Sulphate may be a solid companion to H2O2.

Effect of magnesium sulfate on bronchoconstriction in the lung periphery.

Abstract

Magnesium sulfate has been shown to be effective clinically as a bronchodilator, but its mechanism of action is unknown. We used a wedged bronchoscope technique to study the ability of MgSO4 at clinically relevant concentrations to attenuate hypocapnia-, acetylcholine- (ACh), and dry air-induced bronchoconstriction in the canine lung periphery. Control experiments demonstrated that consecutive challenges of either hypocapnia or ACh resulted in greater collateral system resistance (Rcs) after the second challenge compared with the first. Intravenous infusion of MgSO4 diminished the maximum response to a second hypocapnic challenge (Rcs = 1.59 +/- 0.29 cmH2O.ml-1.s prechallenge vs. 1.12 +/- 0.20 postchallenge) but had no effect on either ACh- or dry air-induced bronchoconstriction. Serum magnesium levels before MgSO4 administration were 1.59 +/- 0.04 meq/l and rose to 6.20 +/- 0.13 during the infusion. Previous studies demonstrated that nifedipine, like MgSO4 in this study, attenuates hypocapnia-induced bronchoconstriction in the canine lung periphery but has no effect on ACh- or dry air-induced bronchoconstriction. We conclude that these results are consistent with the idea that, like nifedipine, magnesium acts in the airway as a voltage-sensitive calcium channel blocker.

https://www.ncbi.nlm.nih.gov/pubmed/2501286/

ChooseLife : Magnesium is also an Electron reducing agent, hence it may donate Electron potential to the free Oxygen released as Catalase supports the body to reduce H2O2 into H2O and 0xygen.

This links to this information, as I see this Disease as an Electron Crisis :

From Wikipedia article NADH section 4.2 Role in redox metabolism:

[QUOTE][…] reduced compounds such as glucose and fatty acids are oxidized, thereby releasing energy. This energy is transferred to NAD++ by reduction to NADH, as part of beta oxidationglycolysis, and the citric acid cycle. In eukaryotes the electrons carried by the NADH that is produced in the cytoplasm are transferred into the mitochondrion (to reduce mitochondrial NAD++) by mitochondrial shuttles, such as the malate-aspartate shuttle. The mitochondrial NADH is then oxidized in turn by the electron transport chain, which pumps protons across a membrane and generates ATP through oxidative phosphorylation.[/QUOTE]

From Wikipedia article FADH2:

[QUOTE]FAD can exist in four different redox states, which are the flavin-N(5)-oxidequinonesemiquinone, and hydroquinoneFAD is converted between these states by accepting or donating electrons. FAD, in its fully oxidized form, or quinone form, accepts two electrons and two protons to become FADH22 (hydroquinone form). The semiquinone (FADH) can be formed by either reduction of FAD or oxidation of FADH22 by accepting or donating one electron and one proton, respectively.[/QUOTE]

Chloroquine was shown to inhibit quinone reductase 2 , a structural neighbour of UDP-N-acetylglucosamine 2-epimerases that are involved in the biosynthesis of sialic acids. The sialic acids are acidic monosaccharides found at the extremity of sugar chains present on cell” 

https://www.sciencedirect.com/science/article/pii/S0924857920300881

ChooseLife : This links together the researchers and testing of hydroxychloroquine. Is this not an Electron cascade crisis? Or a pH crisis which manifests into/from Electron deficiency? Whether this is from a Virus, or 5G, the results are the same, the treatments are the same in need… Though the overlap in effects from the Virus and the reported dangers of 5G are startling, to say the least. It is no wonder getting sunlight, or Vitamin D (Protons) is postulated often as a key player in this illness crisis.

This would make sense that Zinc with chloroquine is showing great promise in tests, as Zinc again is an Electron donor, like Magnesium…

Here it is worth also noting that Johanna Budwig contributed huge research and understanding of Electron dynamics, and stated very vigorously that it is Flax Seeds which have the highest level of Electron surplus, she found in her research that taking high levels of Flaxseed Oil, mixed with Quark (1 part Flaxseed Oil, 2 parts Quark, making it water soluble) was the most efficient mechanism possible to re-invogorate the human ‘Electron Cloud’

Interestingly, in her booklet:

Flax Oil As A True Aid Against Arthritis, Heart Infarction, Cancer And Other Diseases

Dr Budwig relayed:

I often take very sick cancer patients away from hospital where they are said to have only a few days left to live, or perhaps only a few hours. This is mostly accompanied by very good results. The very first thing which these patients and their families tell me is that, in the hospital, it was said that they could no longer urinate or produce bowel movements. They suffered from dry coughing without being able to bring up any mucous.


Every- thing was blocked. It greatly encourages them when suddenly, in all these symptoms, the surface-active fats with their wealth of electrons, start reactivating the vital functions and the patient immediately begins to feel better. It is very interesting to ask how this sudden change is possible. It has to do with the reaction patterns, with the character of electrons. I will return to these electrons later. In the last two years I have come to be very fond of them. A friend of my work in Paris wrote to me how wonderful it is that you have discovered the original birthplace of the electrons in seed oils to be the sun. That’s how these connections are made!

ChooseLife : As soon as I heard about COVID, and the chief symptom of dry cough, I though about the Budwig book and that paragraph above shouted at me. Flax (ALA) I knew was a key supportive element, yet at that stage I did not see the larger context.

Further to this, a new to air youtuber – Ava Green, has become viral, after relating her experiences with Diamox and the alignment of it’s usage and the COVID symptoms : Almost High Altitude Sickness

Pulmonary Edema, Diamox (acetylzolamide) increases Urine pH, relieving this issue:

https://www.cureus.com/articles/29004-acetazolamide-nifedipine-and-phosphodiesterase-inhibitors-rationale-for-their-utilization-as-adjunctive-countermeasures-in-the-treatment-of-coronavirus-disease-2019-covid-19

However, Pulmonary Edema is usually characterised as symptomatic of ‘Productive Cough’ or ‘Wet Cough’ not ‘Dry Cough’. Countless reports I have seen suggest quite the opposite, that the pneumonia/illness type is a very sticky mucus laiden lungs when scanned, hence a dry cough.

So, this drug may hold potential, chiefly via the increasing of urine pH, but has a multitude of nasty potential side effects, a diet with 75% fruit and vegetables is shown to raise Urine pH similarly in 3days, without the nasty side effects, in fact the other effects of this shift in diet, if green foods based, are multitude in potential positives. Mental health may be supported with the richer Magnesium this form of eating may bring (Mental Health Reviews – Magnesium).

This form of eating 75% Fruit and Vegetables, with a strong Alkaline influence (lots of leafy greens especially), if coupled with high Flax intake via a Budwig mix, is shown scientifically to elevate Metabolic and Respiratory status away from Acid and towards neutral (the author does not believe an Alkaline state is any more healthful than acidic, it is the balance which gives the reactive force, and allows the body to extract the electromagnetic energies in foods which in turn release their stored nutrients).

Altitude sickness style illness is what this Dr from New York claims he is seeing:

Oxygen Failure? ARDS may be Lung Injury Caused by the ventillators? Something is not right.

This Doctor, who is leading a COVID ICU, does it not sound like the symptoms you may expect to see if the 5G side effects are correct, Oxygen oscillation acceleration making uptake into the bloodstream troublesome, as the spin of Electrons become too fast to bind with Hemoglobin? It certainly seems that way to me. New York is a 5G pilot city, London, Wuhan. The Doctor says the effects are like how he envisages one would encounter if someone without acclimitisation were dropped at the top of Mount Everest…

This reflection, or speculation, of Altitude Sickness, reminded me of when I saw a documentary of Westerners climbing Mount Everest, in the Documentary I was struck that a much older Gurkha was carrying the Westerners very considerable Luggage, yet was able to smoke ceaselessly! This aligns to the statistics that are showing that a disproportionately low number of Smokers are being admitted to Hospital with COVID, are the smokers already attuned to Hypoxia like conditions and their biochemistry has been attuned coping mechanisms, like the Gurkha in Nepal? Of course he was acclimitised, but it was still staggering his body could cope in those conditions, when the younger, very fit, climber was struggling in the lower oxygen environment.

80% of those needing Ventillation in New York are dying, what if this is because 5G is in almost all the Hospitals in New York? Making the Oxygen Electrons spin too fast, forcefully adding more oxygen may only increase this damage, in those with Electron buffering insufficiency needed to take this sped up Oxygen into Hemoglobin? This paper supports this idea:

COVID-19: Attacks the 1-Beta Chain of Hemoglobin and Captures the
Porphyrin to Inhibit Human Heme Metabolism

Abstract
The novel coronavirus pneumonia (COVID-19) is an infectious acute respiratory infection caused by the novel coronavirus. The virus is a positive-strand RNA virus with high homology to bat coronavirus.

In this study, conserved domain analysis, homology modeling, and molecular docking were used to compare the biological roles of certain proteins of the novel coronavirus. The results showed the ORF8 and surface glycoprotein could bind to the porphyrin, respectively. At the same time, orf1ab, ORF10, and ORF3a proteins could coordinate attack the heme on the 1-beta chain of hemoglobin to dissociate the iron to form the porphyrin.

The attack will cause less and less hemoglobin that can carry oxygen and carbon dioxide. The lung cells have extremely intense poisoning and inflammatory due to the inability to exchange carbon dioxide and oxygen frequently, which eventually results in ground-glass-like lung images.

The mechanism also interfered with the normal heme anabolic pathway of the human body, is expected to result in human disease. According to the validation analysis of these finds, chloroquine could prevent orf1ab, ORF3a, and ORF10 to attack the heme to form the porphyrin, and inhibit the binding of ORF8 and surface glycoproteins to porphyrins to a certain extent, effectively relieve the symptoms of respiratory distress. Favipiravir could inhibit the envelope protein and ORF7a protein bind to porphyrin, prevent the virus from entering host cells, and catching free porphyrins. Because the novel coronavirus is dependent on porphyrins, it may originate
from an ancient virus. Therefore, this research is of high value to contemporary biological experiments, disease prevention, and clinical treatment.

ChooseLife :This could be seen as supporting the 5G hypothesis, it does to me, ALARM BELLS ARE RINGING. Chloroquine is suggested again, and links the Electron issue, covered early in this ramble.

This leads me to this research paper:

Cellular Response to Cigarette Smoke and Oxidants

Adapting to Survive

André M. Cantin

Abstract

The gaseous and soluble phases of cigarette smoke are sources of oxidants that contribute to the pathogenesis of chronic obstructive pulmonary disease (COPD). Chronic oxidative stress of cigarette smoking induces mucus secretion and inhibits cystic fibrosis transmembrane conductance regulator function. The increased mucus viscosity renders the airways susceptible to bacterial infections, a hallmark of chronic bronchitis. Furthermore, lungs chronically exposed to the toxic mixture of oxidants in cigarette smoke show signs of endoplasmic reticulum stress, unfolded protein response, altered ceramide metabolism, and apoptosis. Fortunately, the respiratory tract has developed effective adaptive cellular mechanisms to limit oxidant damage. Numerous antioxidant enzymes and glutathione-dependent detoxification systems are increased in healthy smokers. The regulation of the antioxidant response is largely dependent on the nuclear factor erythroid 2–related factor-2 (Nrf2) pathway. However, patients with COPD have defective Nrf2 responses. Novel therapies such as 2-cyano-3,12-dioxooleana-1,9-dien-28-oic acid (CDDO) to correct defective Nrf2-dependent cellular response may hold promise for patients with COPD.

https://www.atsjournals.org/doi/full/10.1513/pats.201001-014AW

ChooseLife : So, we could see the above as suggesting that healthy smokers bodies may be acclimitised to this Hypoxia type state? Like the old Nepalese Smoker being better able to cope not only with thin air, but also smoke constantly in that environment, the similarities seem stark, however the dry unproductive cough symptom is a key differentiator to HAPE symptoms.

Dry Lungs Low Oxygen 70-80% of cases, called Type L not typical of HAPE

This research area, led me to the following research, when checking into Bronchial dilation (debating in my mind if Magnesium Sulphate is contraidicatd by the above video/Doctor):

CT Features of Coronavirus Disease 2019 (COVID-19) Pneumonia in 62 Patients in Wuhan, China

A decreased lymphocyte count and an increased high-sensitivity C-reactive protein level were the most common laboratory findings.


Read More: https://www.ajronline.org/doi/full/10.2214/AJR.20.22975

Omega3 is known to support lymphocyte production :

Effect of ω-3 polyunsaturated fatty acid-supplemented parenteral nutrition on inflammatory and immune function in postoperative patients with gastrointestinal malignancy

A meta-analysis of randomized control trials in China

In this study, lymphocyte count was significantly higher in ω-3 groups than the control groups. Omega-3 PUFAs improve the body’s defense system by the proliferation of lymphocytes, and the meta-analysis result also confirmed that the incidence of infectious complications in ω-3 groups was significantly lower than the control group.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5916652/

This again says to me Metabolic Acidosis is encountered, the Lyposomes/Endosome Cargo carriers and waste removal system appears to become compromised, this is symptomtic of Cellular pH failure, as the lower pH terrain will always result in slower arrival of nutrient cargo as the Endosomes slow, and the waste removal systems slow affecting C-reactive protein as the paper above reports finding most often. Why would Sodium Bicarbonate, Magnesium Hydoxide and the like (high pH substances) not be a first line defence in these dynamics? I cannot understand why not, but a Doctor I am not!

Why does it affect Afro-Carribeans more? We’ve seen that COVID is seen to affect C-reactive protein in a very high number of cases, what if we overlay Omega 3 to this dynamic?

Relationship of Omega-3 Fatty Acids on C-Reactive Protein and Homocysteine in Haitian and African Americans with and without Type 2 Diabetes

Abstract

Background:

Omega-3 fatty acids (n-3) may be protective of cardiovascular risk factors for vulnerable populations. The purpose of this study was to assess the association between n-3 with, C-reactive protein (CRP), and homocysteine (HCY) in Black minorities with and without type 2 diabetes.

Results:

African Americans had higher waist circumferences and C-reactive protein and consumed more calories as compared to Haitian Americans. Omega 3 fatty acid intake per calorie did not differ between these ethnicities, yet African Americans with low n-3 intake were three times more likely to have high C-reactive protein as compared to their counterparts [OR=3. 32 (1. 11, 9. 26) p=0.031].

Conclusions:

Consumption of n-3 may be protective of cardiovascular risk factors such as C-reactive protein and homocysteine for certain ethnicities. Prospective studies are needed to confirm these results.

Source : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6820196/

How about Magnesium, and C-Reactive Protein?

Dietary magnesium and C-reactive protein levels.

CONCLUSIONS:

Most Americans consume magnesium at levels below the RDA. Individuals with intakes below the RDA are more likely to have elevated CRP, which may contribute to cardiovascular disease risk.

https://www.ncbi.nlm.nih.gov/pubmed/15930481

ChooseLife Notes : None of this should be construed as medical advice, or advice at all. this is just my reflections on Biological Ionisation as it relates to our current situation. The science supports that pH is very, very important, I dearly hope readers may understand this and seek to make informed choices. This period has seen a galvanising of my own diet, and my daughters, to ensure if we are infected/injured by the condition classified as COVID19 (et al) our bodies are the least likely to succumb to the worst effects some people suffer sadly.

I wish you all every wellness. May we come through this brighter and with more positive spirit than we had before, my love to you all.

Well Wishes, Rich Fosh

Coronavirus Data and thoughts which led me here = http://chooselife.co.uk/index.php/category/coronavirus/

Gates’ Globalist Vaccine Agenda: A Win-Win for Pharma and Mandatory Vaccination

By Robert F. Kennedy Jr., Chairman, Children’s Health Defense

Vaccines, for Bill Gates, are a strategic philanthropy that feed his many vaccine-related businesses (including Microsoft’s ambition to control a global vaccination ID enterprise) and give him dictatorial control of global health policy.

Gates’ obsession with vaccines seems to be fueled by a conviction to save the world with technology.

Promising his share of $450 million of $1.2 billion to eradicate polio, Gates took control of India’s National Technical Advisory Group on Immunization (NTAGI), which mandated up to 50 doses (Table 1) of polio vaccines through overlapping immunization programs to children before the age of five. Indian doctors blame the Gates campaign for a devastating non-polio acute flaccid paralysis (NPAFP) epidemic that paralyzed 490,000 children beyond expected rates between 2000 and 2017. In 2017, the Indian government dialed back Gates’ vaccine regimen and asked Gates and his vaccine policies to leave India. NPAFP rates dropped precipitously.The most frightening [polio] epidemics in Congo, Afghanistan, and the Philippines are all linked to vaccines.

In 2017, the World Health Organization (WHO) reluctantly admitted that the global explosion in polio is predominantly vaccine strain. The most frightening epidemics in Congo, Afghanistan, and the Philippines, are all linked to vaccines. In fact, by 2018, 70% of global polio cases were vaccine strain.

In 2009, the Gates Foundation funded tests of experimental HPV vaccines, developed by Glaxo Smith Kline (GSK) and Merck, on 23,000 young girls in remote Indian provinces. Approximately 1,200 suffered severe side effects, including autoimmune and fertility disorders. Seven died. Indian government investigations charged that Gates-funded researchers committed pervasive ethical violations: pressuring vulnerable village girls into the trial, bullying parents, forging consent forms, and refusing medical care to the injured girls. The case is now in the country’s Supreme Court.South African newspapers complained, ‘We are guinea pigs for the drug makers.’

In 2010, the Gates Foundation funded a phase 3 trial of GSK’s experimental malaria vaccine, killing 151 African infants and causing serious adverse effects, including paralysis, seizure, and febrile convulsions, to 1,048 of the 5,949 children.

During Gates’ 2002 MenAfriVac campaign in Sub-Saharan Africa, Gates’ operatives forcibly vaccinated thousands of African children against meningitis. Approximately 50 of the 500 children vaccinated developed paralysis. South African newspapers complained, “We are guinea pigs for the drug makers.” Nelson Mandela’s former senior economist, Professor Patrick Bond, describes Gates’ philanthropic practices as “ruthless and immoral.”

In 2010, when Gates committed $10 billion to the WHO, he said  “We must make this the decade of vaccines.” A month later, Gates said in a TED Talk that new vaccines “could reduce population.” And, four years later, in 2014, Kenya’s Catholic Doctors Association accused the WHO of chemically sterilizing millions of unwilling Kenyan women with a  “tetanus” vaccine campaign. Independent labs found a sterility formula in every vaccine tested. After denying the charges, WHO finally admitted it had been developing the sterility vaccines for over a decade.  Similar accusations came from Tanzania, Nicaragua, Mexico, and the Philippines.

A 2017 study (Morgenson et. al. 2017) showed that WHO’s popular DTP vaccine is killing more African children than the diseases it prevents. DTP-vaccinated girls suffered 10x the death rate of children who had not yet received the vaccine. WHO has refused to recall the lethal vaccine, which it forces upon tens of millions of African children annually.[Global public health officials] say he has diverted agency resources to serve his personal philosophy that good health only comes in a syringe.

Global public health advocates around the world accuse Gates of steering WHO’s agenda away from the projects that are proven to curb infectious diseases: clean water, hygiene, nutrition, and economic development. The Gates Foundation spends only about $650 million of its $5 billion dollar budget on these areas. They say he has diverted agency resources to serve his personal philosophy that good health only comes in a syringe.

In addition to using his philanthropy to control WHO, UNICEF, GAVI, and PATH, Gates funds a private pharmaceutical company that manufactures vaccines and is donating $50 million to 12 pharmaceutical companies to speed up development of a coronavirus vaccine. In his recent media appearances, Gates appears confident that the Covid-19 crisis will now give him the opportunity to force his dictatorial vaccine programs on all American children – and adults.

Related :

Chooselife : Would you trust this man, or his form of Philanthropy near your (or your family, friends and society in general) health? No, no I wouldn’t.

pH Vs Coronavirus

Here are some excerpts of a paper on the functioning of Hydroxychloroquine, the drug being touted as a medicine to combat CoronaVirus. It can be seen that it’s major action, supportive of the previous data I’ve presented, is raising pH…

Hydroxychloroquine (HCQ) enters and accumulates in lysosomes along a pH gradientIn lysosomes, hydroxychloroquine inhibits the degradation of cargo derived externally (via endocytosis or phagocytosis) or internally (via the autophagy pathway) in autolysosomes by increasing the pH to prevent the activity of lysosomal enzymes. Inhibition of lysosomal activity can prevent MHC class II-mediated autoantigen presentation. 

Hydroxychloroquine can also accumulate in endosomes and bind to the minor groove of double-stranded DNA. This drug can inhibit Toll-like receptor (TLR) signalling by altering the pH of endosomes (involved in TLR processing) and/or preventing TLR7 and TLR9 from binding their ligands (RNA and DNA, respectively). Hydroxychloroquine can also inhibit the activity of the nucleic acid sensor cyclic GMP-AMP (cGAMP) synthase (cGAS) by interfering with its binding to cytosolic DNA. By preventing TLR signalling and cGAS–stimulator of interferon genes (STING) signalling, hydroxychloroquine can reduce the production of pro-inflammatory cytokines, including type I interferons.

….

As the pH in lysosomes is optimal for lysosomal enzymes involved in hydrolysis, by increasing the pH of endosomal compartments85, chloroquine and hydroxychloroquine might impair the maturation of lysosomes and autophagosomes and inhibit antigen presentation along the lysosomal pathway (Fig. 3).

These processes possibly occur, at least in part, through drug-mediated changes in the pH of autophagosomes and/or lysosomes, which indirectly influence immune activation; however, such a mode of action requires additional validation to aid with future drug development.

https://www.nature.com/articles/s41584-020-0372-x

This is the drug they are saying shows great promise for Coronavirus treatment.

Here is excerpts from a paper just being released, where studies have shown 100% cure rate with CoronaVirus:

He talks about lowering the acidity in the cells…

https://www.covidtrial.io/

From their prelim paper:

Specifically, the CDC research was completed in primate cells using chloroquine’s well known function of elevating endosomal pH. The results show that “We have identified chloroquine as an effective antiviral agent for SARS-CoV in cell culture conditions, as evidenced by its inhibitory effect when the drug was added prior to infection or after the initiation and establishment of infection. The fact that chloroquine exerts an antiviral effect during pre- and postinfection conditions suggest that it is likely to have both prophylactic and therapeutic advantages.

When chloroquine is added after infection, it can rapidly raise the pH and subvert on-going fusion events between virus and endosomes, thus inhibiting the infection. When added after the initiation of infection, it likely affects the endosome-mediated fusion, subsequent virus replication, or assembly and release. Specifically, rapid elevation of endosomal pH and abrogation of virus-endosome fusion may be the primary mechanism by which virus infection is prevented under post-treatment conditions.

Specifically, the virus depends on turning over the host proteins to trigger response for available building blocks to make their own proteins or nucleic acids. They break down due to low PH catalyzed by hydrolysis. 

It is this part of the coronavirus’ replicative path that chloroquine inhibits. Notably, because of its nitrogen structure, chloroquine has the unique ability to get into cells and cross endosomal membranes. Once inside, nitrogens in chloroquine (and quinines in general) prevent acidification by absorbing a high amount of hydrogens that simply then interact with nitrogen and then chloroquine becomes positively charged – an ionic interaction which makes it harder for the endosome to become acidifiedThe result is a buffer that holds it at the higher pH and prevents it from becoming acidic enough to be functional. To summarize, because chloroquine has a multitude of extra nitrogens, once it crosses the membrane and enters an organelle, the organelle is prevented from reaching a lower pH. The organelle’s enzymes cannot work because the donor group will be a hydrogen ion, disabling the hydrolysis required for coronavirus replication. This means that all kinds of events in the cell are incapable of performing optimally, including viral replication.

https://github.com/covidtrial/info/raw/master/An%20Effective%20Treatment%20for%20Coronavirus%20(COVID-19).pdf

Biological Ionisation…

Wonder why I go on and on about pH…

Stunning nobody is talking about Milk Of Magnesia, or other inexpensive pH raising substances…

Related:

Bill Munro Vs The Coronavirus

Bill brought inhalation of H2O2 to the publics attention, he used it 5-6 pumps, 6 or 7x a day. To keep his Oxygen levels high, to keep the Viruses out, which come when Oxygen is down.

This was something I tried many years ago, but didn’t feel a direct or urgent need to do, so put it into my memory locker.

However, after studying this new Viral Epidemic which increasingly surrounds us, I pulled the information back to my short term memory to mix with the pH principles I had been reflecting on.

My daughter has suffered from Chronic Lung Disease as a result of being born at 24weeks gestation, so Oxygen and Viral susceptibility has been something I am used to reflecting deeply upon.

Anyway, the data shows that if you are of a lower pH, this virus group (Corona) is 10x more forceful and you are 10x more susceptible (at a pH of 6 Vs 7), so after ensuring I got my diet plans and supplements into order, I began to reflect over and over how else I can best prepare.

This is when Bill Munro came back to my mind, so I ordered 2x Nasal Vaporiser’s for about £3, and I decided that I would start taking a similar number of rounds of H2O2 as Bill did, but diluted to 1.5% with 50% Distilled water and 50% Food Grade H2O3 at 3%.

The literature for killing the Virus shows that 0.5% H2O2 kills the virus in 1 Minute, so 1.5% should be effective in 20 Seconds or thereabouts. So, to my unqualified mind, this leads me to presume that several rounds of this daily may safeguard me against this threat, if not preventing it from entering my airways entirely, then at least killing it off 5-6 times a day, minimising the intensity of the infection as best I may.

When I have talked of this method to others, peoples minds immediately seem to jump to “you are swallowing bleach”, with a shocked reaction, yet I explain that this is simply water with an extra Oxygen molecule attached, which people regularly treat their teeth with at 7% some 450% stronger than I am using. People seem to not bat an eyelid at using 4.5x stronger bleach for their teeth and vanity, yet to stave of seemingly very harsh virus people react like I am the crazy one!

This method along with Alkalising my terrain via diet and supplements are the best methods I have encountered to protect myself against this horrid viral outbreak.

If the outbreak worsens in the UK, I am intending to upgrade to the full 3%

Thank you Bill.

Coronavirus leads to Lymphopenia in 82% of patients + Nutrition to enhance the body against Lymphopenia

A recent study from the lead scientific advisor on Coronavirus, has found that 82% of those studied with the virus developed Lymphopenia (abnormally low lymphocytes in the blood)

Dr Zhong Nanshan, who discovered the SARS coronavirus in 2003 is the leading advisor in investigating and managing the current coronavirus crisis.

Lymphopenia, which is a condition where a specific white blood cell that is part of the body’s first-line defence against diseases is dramatically reduced.

https://www.medrxiv.org/content/10.1101/2020.02.06.20020974v1

So, it may be very pertinent to look at the known nutritional elements which nourish the bodies own Lymphocyte making capability, as a means of focus should you feel the need to prepare, eat (or supplement) whilst your body is fighting this Virus.

Here is a strong, concise overview of such dietary elements:

Lymphocyte Nutritional Support:

Dietary Guidelines for a Better Lymphocyte Count
You may want to know how to increase lymphocytes naturally. A healthy, nutrient-rich diet can go a long way toward boosting lymphocyte levels. This will provide your immune system with everything it needs to fight off viruses and bacteria that can potentially lead to low lymphocyte levels.

The following is a dietary guideline to follow to help your body improve its lymphocyte count.

  • Eat lots of lean protein: When the body doesn’t get enough protein, this leads to fewer white blood cells. As a result, you can increase lymphocyte production when you eat protein-rich foods such as grass-fed meats like poultry and beef, organic eggs, wild-caught fish and seafood, and legumes.
  • Avoid foods high in trans and saturated fats: These fats thicken lymphocytes; as such, reducing trans and saturated fat consumption can help improve immune system health. Avoid unhealthy fats such as margarine, fried foods, hydrogenated oils, and processed baked goods.
  • Consume healthy fats: Omega-3 fatty acids, on the other hand, will increase your lymphocyte count. Include omega-3 fatty acid foods such as avocado, ground flaxseed, hemp seeds, chia seeds, walnuts, sardines, albacore tuna, white fish, Alaskan salmon, herring, and Atlantic mackerel in your diet.
  • Eat foods high in beta-carotene: Beta-carotene helps boost lymphocyte production. Foods rich in beta-carotene include carrots, sweet potatoes, butternut squash, romaine lettuce, and spinach.
  • Eat zinc-rich foods: Zinc is needed to make lymphocytes. It also increases levels of NK cells and T cells, which strengthens your immune system. Foods high in zinc include oysters, asparagus, collard greens, spinach, broccoli, sesame seeds, and pumpkin seeds.
  • Consume foods high in vitamin C: Vitamin C is known to increase the production of white blood cells such as lymphocytes. Foods high in vitamin C include bell peppers, parsley, kale, oranges, raspberries, tomatoes, and celery.
  • Eat foods loaded with vitamin D: Not getting enough vitamin D can lower lymphocyte levels and weaken your immune system. Foods rich in vitamin D include organic eggs, raw milk, wild-caught salmon, sardines, mackerel, and tuna.
  • Eat foods high in vitamin E: Vitamin E supports production of NK cells and B cells. Foods rich in vitamin E include sunflower seeds, almonds, kale, spinach, olives, asparagus, and collard greens.
  • Eat selenium-rich foods: Selenium helps the body produce more white blood cells. Foods high in selenium include cod, shiitake mushrooms, salmon, tuna, eggs, oats, and broccoli.
  • Eat more garlic: Garlic is known to boost white blood cell production, which increases the number of NK cells. Purchase fresh, powdered, or dried garlic, and use it in your cooking daily.
  • Drink more green tea: Green tea compounds can boost immunity by fighting viruses that deplete white blood cells.
www.doctorshealthpress.com

Source = Low Lymphocyte Count (Lymphocytopenia)

Low lymphocyte count, also known as lymphocytopenia, is a cause for concern because when lymphocytes (a type of white blood cell) are low, the body’s ability to repel infections is weakened.

By Dr. Richard Foxx, MD

ChooseLife : Of Course, I am always focused on the Acid/Alkaline balancing aspects in life, so this is not to discount the strong evidence that initial infectivity and severity it almost certain to be controlled by the hosts pH, if your tissue at the site of infection is below 7 you are much more likely to become infected, if 6 or lower it has been demonstrated in previous strains that the infectivity is 10x higher, Alkaline eating and supplementation is something I am very focused on for me and my family.

THIS SHOULD NOT BE CONSTRUED AS MEDICAL ADVICE.

pH – CoronaVirus and the SO2 Madness

Dear All,

When I first read about the CoronaVirus (2019-nCoV), my immediate reaction was to DuckDuckGo search pH dependency = https://duckduckgo.com/?q=coronavirus+ph+dependency&atb=v121-1&ia=web

This immediately gave me several bits of vital information, to understand the situation from a biological and nutritional perspective. By looking at historical studies, to see some baseline characteristics:

  • In this report, we show that the SARS-CoV S glycoprotein mediates viral entry through pH-dependent endocytosis.  Reference : 1
  • In contrast, influenza and Ebola viruses are prototypes for viruses that utilize a pH-dependent endocytotic pathway (43). To determine the pathway utilized by the SARS-CoV, the pH dependence of the SARS-CoV S-pseudotyped lentiviral vector was analyzed. Addition of ammonium chloride, which prevents acidification of the endosome, caused a dose-dependent reduction in viral entry (Fig. (Fig.1B,1B, left) at concentrations similar to those described for other pH-dependent viral glycoproteins (31143). This effect was also observed with another inhibitor of endosomal acidification, bafilomycin, also in a dose-dependent fashion (Fig. (Fig.1B,1B, right). Reference : 1
  •     The World Health Organization has concluded that SARS is produced by a new virulent strain of coronavirus. Specific research on the possible pH dependency of the SARS virus has not yet been done.  It is well known that coronavirus infectivity is exquisitely sensitive to pH.  For example, the MHV-A59 strain of coronavirus is quite stable at pH 6.0 (acidic) but becomes rapidly and irreversibly inactivated by brief treatment at pH 8.0 (alkaline).  Human coronavirus strain 229E is maximally infective at pH 6.0.  Infection of cells by murine coronavirus A59 at pH 6.0 (acidic) rather than pH 7.0 (neutral) yields a tenfold increase in the infectivity of the virus. Reference : 2
  • Infection of susceptible murine cells with the coronavirus mouse hepatitis virus type 4 (MHV4) results in extensive cell-cell fusion at pHs from 5.5 to 8.5. The endosomotropic weak bases chloroquine and ammonium chloride do not prevent MHV4 infection. In marked contrast, we have selected variants from a neural cell line persistently infected with MHV4 which are entirely dependent on acid pH to fuse host cells and are strongly inhibited by endosomotropic weak bases…  Wild-type S induced cell-cell fusion at neutral pH, whereas variant S required prolonged exposure to acidic pH to induce fusion… These findings demonstrate that the pH dependence of coronavirus fusion is highly variable and that this variability can be determined by as few as three amino acid residues. Reference : 3

So, we can see above, that in most cases (all that I can find), scientific studies are showing multiple variants of CoronaVirus are completely pH driven, in terms of susceptibility (most cases, sadly only pH range 5.5-8.5 tested, maybe scientists could test Magnesium Hydroxide = 10.5, to show if higher pH is protective/preventative) and intensity of infection (seemingly all), though there are variations in pH levels required to neutralise the impacts.

Now, initially I just doubled down on my thoughts on Alkalising my own terrain and looking after my childrens via diet and key suppliments. However, as the stories became more and more alarming, things took a dramatic turn.

Sunday 9th February 2020 Reports emerged of an outrageous happening in China

Using Windy.com it was discovered that rates of Sulphur Dioxide above Wuhan were reading 1351PPB

Now, this alone, suggests strongly that there has been a huge upsurge in burning of organic matter which releases SO2, leading to speculation that high levels of cremation are occurring. The data is contested by some, claims made that this comes from a ‘modelling’ or predictive site, so the numbers cannot be trusted (maybe true, but they are a strong indicator of ‘in the range of’, if not exact in the measurements. This may have some validity, however, another site, https://earth.nullschool.net/ showed similar numbers to https://windy.com even when you look without the forecast running you still get numbers in the potentially fatal zones (just like predicting the weather in general, supercomputers are pretty accurate at the immediate forecast numbers).

When I saw these reports, my mind was not transfixed on whether or not this was exactly accurate, or whether it was due to cremations (if so the numbers would clearly need to be hugely higher to create this phenomena), it was OMG why is the Chinese Authorities allowing huge ammounts of SO2 into the atmosphere in the midst of a pH dependant Viral outbreak?

So, immediately I went to look at the safe limits, remember the models were showing 1,300+ PPB :

  • SO2 is a toxic gas, which is directly harmful to human health. It is heavier than air and has a suffocating odour at an atmospheric concentration of around 500 parts per billion (ppb), at which level it can be fatal.  At lower levels, chest pains, breathing problems, eye irritation and a lowered resistance to heart and lung diseases can be experienced. At 20 ppb or lower there should be no ill effects to a healthy person. The normal atmospheric background concentration of SO2 is generally less than 10 ppb.
  • A secondary effect is the formation of sulphates (and nitrates), in the form of aerosols or very fine airborne particles, which can comprise a significant proportion of the particulate matter and have been linked to increased asthma attacks, heart and lung disease and respiratory problems in susceptible population groups.
  • A third effect can occur further away from the emission source where the sulphur oxides will have converted to acids by aqueous phase reactions in the atmosphere. These acidic aerosols are eventually precipitated as acid rain, snow, sleet or fog but only when they encounter the right meteorological conditions. In the absence of man made pollution rain water would be slightly acidic, around pH 5, due to the presence of carbonic acid from the interaction of water vapour and naturally occurring levels of CO2. Acid rain on the other hand has been measured with pH levels below 3 corresponding to vinegar. 
  • In their 2009 joint proposal to the IMO, the USA and Canada stated that by designating the eastern and western seaboards of North America an Emissions Control Area, as many as 8,300 lives will be saved and over three million people will experience relief from acute respiratory symptoms each year”. Reference : 4

So, we can see above, that rates at or above 500 PPB are considered an immediate threat to life, to many groups in society when all is otherwise well. However, Wuhan and several other regions are showing numbers at this level and 2-3x this level, which is a clear respiratory danger to life, whilst in the midst of another Respiratory crisis in the form of CoronaVirus.

WHAT THE HELL IS GOING ON!!!

The issue over whether this is Cremations, or not, for me is absolutely secondary (though more on this later).

The issue is, who in a sane mind in Chinese Authorities, would authorise or advise scientifically that it was fine to allow the output of huge plumes of SO2, when whole cities are in lockdown, this is INSANE!

Here is few screen grabs, I took last night to show the current predicted Air levels of Sulphur Dioxide:

Then, using https://earth.nullschool.net/ at around 12:30am 11/02/2020 UK Time, the Supercomputer forecasting modeller showed 928/2.62 = 354PPB
Wuhan area, 22 hours later at 21:00 UK Time showing 1272/2.62 = 485 ppb Near Potentially Fatal level
Chongqing region, 22 hours later at 21:00 UK Time showing 924/2.62 = 352 ppb

This is just the craziest thing I have experienced mankind do to itself ever. In the midst of cities being locked down due to a virulent Viral emergency, something in China is causing SO2 levels up to appear 1-3x that which is considered an immediate threat to life, yet we are hearing no warnings from the Chinese authorities or WHO that this is happening.

When I took these readings, multiple other cities were all showing these same high readings, Chongqing was at (or over) 500PPB and others I did not record the names of, again I stress the forecast as not running, this was a ‘prediction’ of the present.

Here is a graphic from the Wuhan Air Quality guidelines, showing the levels and targets to bring this further down, up to 2015:

So, we can see SO2 µg m3 concentrations were recorded at averaging 20µg m3 in 2015 on a downward trend line, now we are seeing 16-17x this level in the midst of a respiratory viral crisis!

As I write this today (12:45pm 11/02/2020) North West (as the wind is blowing) of Wuhan is showing readings between 300-500µg m3. It appears the out-gassing is highest during the nights, very very small mercies!

Lunchtime 11/02/2020 8:50pm Chinese Time (if burning of organic matter is happening during the night, as the modelling forecasts suggest, this may well rise back in the coming hours)

This has left me staggered, how can the Chinese Scientists who advise Government policy, or the WHO, or NATO, not be shouting and screaming about this? Imagine you are in this region, or your loved ones, and they are already at huge threat due to a clearly highly dangerous virus, then you find that the air is being degraded so much as to cause a huge uptick in susceptibility to respiratory illnesses???

It is beyond any reasonable debate, that SO2 gas is an acid forming respiratory threat, it will drive down the pH of the terrain it encounters when in sufficient volume and/or when the host lacks sufficient buffering capability.

So, now we should look at what level of SO2 output huge numbers of cremations may cause, when I was a young man I travelled around South-East Asia, one place which was fascinating was Varanasi. The ancient town famous for being a place an estimated 25,000-30,000 Hindu’s go, to be cremated in the open air Ghats per year.

If we divide the lower number 25,000 x 365 we can say an estimated 65 people per day are being Cremated in Varanasi (to my recollection I recall massively higher numbers), none-the-less, this gives us a really good baseline, to look at the SO2 levels above/around Varanasi… given this daily figure is more than are reportedly dying in any one place daily in China (or anywhere) due to CoronaVirus:

So, we can see that at 6:50pm local time in Varanasi, when the bodies will have chiefly been burning through the day, we have 12PPB = 65 bodies burned a day, straight out into the atmosphere.

So, the above shows fairly conclusively, that if it is bodies being cremated in China, the numbers must be in the range of 2 orders of magnitude higher (100x), to have anything like the outputs we are seeing in China. 650 cremations would speculatively result in 120PPB, 6,500 would conceivably result in 1,200PPB+ as has been recorded (modelled or forecast, as you will). The article on effects of SO2 cited above states that ambient levels will be below 10PPB, so we could say the difference between 10 and 12 is what 65 bodies being cremated is showing as causative, then the numbers start to spiral into much higher orders of magnitude (if a 2 points SO2 rise is shown for 65 cremations, then 65 x 20 = 130, 65 x 200 = 13,000, 1200 x 65 = 78,000!!! The numbers start to look absolutely catastrophic is this is cremation driven)

This is a crude comparison, of course, but what other way can we compare to get an insight of what might be happening to create such huge waves of seemingly deadly gas sweeping across China? Incineration of bedding, medical materials (and such) likely dampens these numbers down, but none the less, something much more dramatic than we are being shown by the Chinese authorities seems to be happening.

This is not meant to be alarmist, this is meant to be prodding around with the scant information people are discovering, to allow us to get some kind of clearer picture.

That there is a two week gestation period, before symptoms show, then if like other viruses of the type, up to an 8-10 week illness/recovery period, means we have another 4-6 weeks to see what the first wave is actually doing to people, I pray we all keep relaying the truth of our experiences, to allow the best outcome for us all.

Wishing you all well

Rich Fosh

References:

  1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC415834/
  2. https://www.meridianinstitute.com/newslet/Vol7-3/7-3.html
  3. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC240014/
  4. https://www.egcsa.com/technical-reference/what-are-the-effects-of-sulphur-oxides-on-human-health-and-ecosystems/
  5. https://earth.nullschool.net/
  6. https://www.windy.com/

Related :

http://chooselife.co.uk/index.php/2019/08/24/ph-the-toxicity-arrow-piercing-modern-society/

CoronaVirus pH

pH-Dependent Entry of Severe Acute Respiratory Syndrome Coronavirus Is Mediated by the Spike Glycoprotein and Enhanced by Dendritic Cell Transfer through DC-SIGN

June 2004

ABSTRACT

The severe acute respiratory syndrome coronavirus (SARS-CoV) synthesizes several putative viral envelope proteins, including the spike (S), membrane (M), and small envelope (E) glycoproteins. Although these proteins likely are essential for viral replication, their specific roles in SARS-CoV entry have not been defined. In this report, we show that the SARS-CoV S glycoprotein mediates viral entry through pH-dependent endocytosis. Further, we define its cellular tropism and demonstrate that virus transmission occurs through cell-mediated transfer by dendritic cells. The S glycoprotein was used successfully to pseudotype replication-defective retroviral and lentiviral vectors that readily infected Vero cells as well as primary pulmonary and renal epithelial cells from human, nonhuman primate, and, to a lesser extent, feline species. The tropism of this reporter virus was similar to that of wild-type, replication-competent SARS-CoV, and binding of purified S to susceptible target cells was demonstrated by flow cytometry. Although myeloid dendritic cells were able to interact with S and to bind virus, these cells could not be infected by SARS-CoV. However, these cells were able to transfer the virus to susceptible target cells through a synapse-like structure. Both cell-mediated infection and direct infection were inhibited by anti-S antisera, indicating that strategies directed toward this gene product are likely to confer a therapeutic benefit for antiviral drugs or the development of a SARS vaccine.

The severe acute respiratory syndrome coronavirus (SARS-CoV) is the likely cause of an acute infectious respiratory disorder identified in highly lethal outbreaks during the past year (1018213240). Infection is characterized by acute flu-like symptoms that progress to a severe febrile respiratory illness with significant mortality. Coronaviruses, comprising a genus of the Coronaviridae family, are enveloped positive-strand RNA viruses. In general, coronaviruses cause respiratory and enteric diseases in humans and domestic animals (1520). Two previously known human coronaviruses caused only mild upper respiratory infections (1520). In contrast, a highly pathogenic, severe respiratory disease is caused by the SARS-CoV, especially in the elderly (44). Coronaviruses can be divided into three serologically distinct groups (15). Phylogenetically, SARS-CoV is not closely related to any of the three groups (26), though it is most similar to the group II coronaviruses (3336).

Although the organization of the SARS-CoV genome is related to that of animal coronaviruses, its genetic sequence is unique, and the structure and function of its gene products are not known. At least 14 open reading frames (ORFs) can be identified in its genome (263436). Among these, the replicase/transcriptase genes are located in the 5′ portion of the genome. At its 3′ end, the four major structural proteins (S, M, N, and E) are made through different subgenomic RNAs. Based on comparison to animal coronaviruses, three structural gene products are predicted to be present on the viral envelope: the spike (S), membrane (M), and small envelope (E) proteins (202634). The structure of the SARS-CoV envelope differs in some respects from that of other enveloped viruses, such as retroviruses and lentiviruses, many of which contain one viral envelope protein.

Envelope or spike proteins from enveloped viruses have been used to pseudotype retroviral and lentiviral vectors for functional and gene transfer studies (29354345); however, whether coronavirus glycoproteins could pseudotype these viruses was unknown. Here we report that replication-defective retroviral (Moloney murine leukemia virus) and lentiviral (human immunodeficiency virus type 1 [HIV-1]) vectors can be pseudotyped with the SARS-CoV S protein, and the properties of S related to entry have been defined. Using these pseudoviruses, we were able to determine the relative contributions of SARS-CoV envelope proteins to viral entry and fusion and to examine the roles of these different viral envelope gene products with respect to entry, cell specificity, and potential inhibition of viral replication.

Pertinent Extract:

In contrast, influenza and Ebola viruses are prototypes for viruses that utilize a pH-dependent endocytotic pathway (43). To determine the pathway utilized by the SARS-CoV, the pH dependence of the SARS-CoV S-pseudotyped lentiviral vector was analyzed. Addition of ammonium chloride, which prevents acidification of the endosome, caused a dose-dependent reduction in viral entry (Fig. (Fig.1B,1B, left) at concentrations similar to those described for other pH-dependent viral glycoproteins (31143). This effect was also observed with another inhibitor of endosomal acidification, bafilomycin, also in a dose-dependent fashion (Fig. (Fig.1B,1B, right).

Full :

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC415834/

Previous research from Meridian Institute Article :

Possible Relevance to SARS


    The World Health Organization has concluded that SARS is produced by a new virulent strain of coronavirus. Specific research on the possible pH dependency of the SARS virus has not yet been done.  It is well known that coronavirus infectivity is exquisitely sensitive to pH.  For example, the MHV-A59 strain of coronavirus is quite stable at pH 6.0 (acidic) but becomes rapidly and irreversibly inactivated by brief treatment at pH 8.0 (alkaline).  Human coronavirus strain 229E is maximally infective at pH 6.0.  Infection of cells by murine coronavirus A59 at pH 6.0 (acidic) rather than pH 7.0 (neutral) yields a tenfold increase in the infectivity of the virus.

  ChooseLife : If the strain of coronavirus responsible for SARS shares the pH characteristics of these other coronaviruses that are pH-dependent, this could be a valuable clue to effective prevention and treatment strategies for this potential epidemic. Perhaps keeping a balanced or slightly alkaline pH environment for the body’s tissues can provide viral protection or enhanced healing for SARS and common viral agents that cause respiratory infections. 

Inter-related to this, is research on MUC5B, which has shown that those of lower pH, are much more prone to having inhibited mucous membrane formation:

“Moreover, we demonstrate that the conformation of these highly entangled linear polymers is sensitive to calcium concentration and changes in pH. In the presence of calcium (Ca2+, 10 mM) at pH 5.0, MUC5B adopted a compact conformation which was lost either upon removal of calcium with EGTA, or by increasing the pH to 7.4. These results suggest a pathway of mucin collapse to enable intracellular packaging and mechanisms driving mucin expansion following secretion. They also point to the importance of the tight control of calcium and pH during different stages of mucin biosynthesis and secretion, and in the generation of correct mucus barrier properties.

ChooseLife Related Thoughts :

The above shows that there are multiple potential protective methodologies in play, some people may feel a glass of cold water with 1/2 teaspoon of Sodium Bicarbonate every two hours on the first day may be effective (outlined at the bottom of this page), this is one method I would consider myself (Arm and Hammer or Bobs Mill being Aluminium free). Also small Sips of highly Alkaline Milk of Magnesia, every hour, may coat the upper respiratory regions fairly well and rapidly bring up the pH, out of the greater danger zones of lower pH < 6.5 (this is my go to for my kids with sniffles or worse), I would likely do this myself for this situation.

Personally I am going to use this outbreak as a good time to bring my own (and childrens) pH up, using methods as above, plus make some Moreless Alkalising Mineral Mixture, which both Alkalises and significantly raises the Calcium levels in the body but in a complexed form (pre-bonded to Molasses or Honey) which does not hamper the Mucous membrane process outlined above, which as shown above in the scientfic literature is exactly what our bodies need to be ready to either repel, or minimise the effects of such threats.

Moreless Alkalising Mix :

http://chooselife.co.uk/index.php/2019/06/13/moreless-alkalising-remineralising-drink/

1918 Flu Prevention : Baking Soda:

https://www.proliberty.com/observer/20091216.htm

“The proven value of Bicarbonate of Soda as a therapeutic agent (from a letter to the Church and Dwight Company):

In 1918 and 1919 while fighting the Flu with the U.S. Public Health Service it was brought to my attention that rarely any one who had been thoroughly alkalinized with bicarbonate of soda contracted the disease, and those who did contract it, if alkalinized early, would invariably have mild attacks. I have since that time treated all cases of Cold, Influenza and LaGripe by first giving generous doses of Bicarbonate of Soda, and in many, many instances within 36 hours the symptoms would have entirely abated.

Further, within my own household, before Women’s Clubs and Parent-Teachers’ Association, I have advocated the use of soda as a preventative for ‘Colds’, with the result that now many reports are coming in stating that those who took ‘Soda’ were not affected, while nearly everyone around them had the ‘Flu’.

…An occasional three-day course of the Bicarbonate of Soda increases the alkalinity of the blood, assists elimination and increases the resisting power of the body to all Infectious Diseases…

Whenever taking a bicarbonate solution internally, the soda should be dissolved in cold water. In the event of a threatened attack we recommend the following treatment: During the first day take six doses of half a teaspoon of Bicarbonate of Soda in a glass of cool water, at about two hour intervals.”

General essay about pH and Toxicity:

http://chooselife.co.uk/index.php/2019/08/24/ph-the-toxicity-arrow-piercing-modern-society/

This should not be construed as Advice, simply reflections of my own thoughts.

Be Well, Rich