CDC’s Guidance for Certifying COVID-19 Deaths NOT Accurate — No Virus Testing, Only “Suspected” Cause Required [Video]

 

 

In this revealing interview, Dr. Scott Jensen, explains that the CDC’s present guidelines for determining “COVID-19 deaths” are not evidence-based, and may even have to do with the greater profitability of doing so. His testimony runs directly counter Dr. Fauci, who labeled any criticism of their highly controversial policy “conspiracy theory.”

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Ascorbic acid and iloprost attenuate the lung injury caused by ischemia/reperfusion of the lower extremities.

PMID: 

Ann Vasc Surg. 2006 Jan ;20(1):49-55. PMID: 16378148

Abstract Title: 

Ascorbic acid (vitamin C) and iloprost attenuate the lung injury caused by ischemia/reperfusion of the lower extremities of rats.

Abstract: 

The objectives of this study were to compare the protective effects of ascorbic acid and iloprost on lung injury caused by ischemia reperfusion (I/R) of the lower extremities of rats. Wistar albino rats (n = 34) were divided into five groups. In the I/R group (n = 6), the aorta was cross-clamped for 3 hr, followed by 1 hr of reperfusion. In the vitamin C group (n = 8), animals were pretreated with 100 mg/kg ascorbic acid via the left jugular vein before aortic cross-clamping. In the iloprost group (n = 8), animals were pretreated with 20 ng/(kg x min) iloprost by constant intravenous infusion via the left jugular venous cannula. In the sham group (n = 6), the abdomen was left open at the same period and a juguler venous line was established. In the control group (n = 6), lungs were removed and blood samples taken immediately after sternotomy. No treatment was given in this group. After both lungs were removed, biochemical parameters were measured and histopathological evaluation was made. Although the arterial blood pO2 and HCO3 levels were statistically significantly high in both the vitamin C and iloprost groups compared to the I/R group, plasma malondialdehyde (MDA) levels were significantly low. Meanwhile, the MDA levels in the lung tissue were significantly low in the vitamin C group compared to the I/R group. The MDA level in the lung tissue in the iloprost group was also low compared to the I/R group, but it was not statistically significant. The lungs of the I/R group displayed intense interstitial leukocytic infiltration in histopathological examination compared to the other groups. Pretreatment of animals with iloprost and vitamin C significantly decreased the pulmonary injury characterized by decreased plasma leukocyte sequestration. The results suggest that both vitamin C and iloprost are useful agents for attenuating the lung injury caused by increased oxidative stress and neutrophil accumulation after a period of I/R of the lower extremities.

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A significant association was observed between duration of asthma and plasma vitamin C level.

PMID: 

East Mediterr Health J. 2005 Jan-Mar;11(1-2):87-95. PMID: 16532676

Abstract Title: 

Comparison of plasma and leukocyte vitamin C status between asthmatic and healthy subjects.

Abstract: 

In a case-control study the vitamin C status of 50 adults with chronic controlled asthma was compared with that of 50 randomly selected healthy controls. Vitamin C intake was assessed by 3-day dietary recall, and plasma and leukocyte vitamin C concentrations were measured colorimetrically. A positive significant correlation was found between plasma vitamin C and dietary vitamin C intake. Plasma and leukocyte vitamin C levels were significantly lower in the asthma group. Plasma vitamin C was deficient (

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Vitamin D deficiency and acute lung injury.

PMID: 

Inflamm Allergy Drug Targets. 2013 Aug ;12(4):253-61. PMID: 23782208

Abstract Title: 

Vitamin D deficiency and acute lung injury.

Abstract: 

Acute Lung Injury (ALI) and the more severe form Acute Respiratory Distress Syndrome (ARDS) remain a significant cause of morbidity and mortality in the critically ill patient. It is characterised by a severe inflammatory process resulting in diffuse alveolar damage, influx of neutrophils, macrophages and a protein rich exudate in the alveolar spaces caused by endothelial and epithelial injury. Improvements in outcomes are in part due to restrictive fluid management and protective lung ventilation however successful therapeutic strategies remain elusive with promising therapies failing to translate positively in human studies. The evidence for the role of vitamin D in lung disease is growing – deficiency has been associated with impaired pulmonary function, increased incidence of viral and bacterial infections and inflammatory disease including asthma and COPD. Studies have also reported a high prevalence of vitamin D deficiency in the critically ill and an association with adverse outcomes. Although exact mechanisms are yet to be discerned, vitamin D appears to impact on a variety of inflammatory and structural cells within the lung including macrophages, lymphocytes and epithelial cells. To date there are few directly supportive clinical studies in ALI; this review explores the compelling evidence suggesting arole for vitamin D in ALI and the mechanisms by which it could contribute to pathogenesis.

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Vitamin D deficiency and risk of acute lung injury in severe sepsis and severe trauma.

PMID: 

Ann Intensive Care. 2014 Feb 24 ;4(1):5. Epub 2014 Feb 24. PMID: 24559079

Abstract Title: 

Vitamin D deficiency and risk of acute lung injury in severe sepsis and severe trauma: a case-control study.

Abstract: 

BACKGROUND: The aim of this study was to determine the association between 25-hydroxyvitamin D (25-OHD) levels at the onset of critical illness and the development of acute lung injury/acute respiratory distress syndrome (ALI/ARDS) in patients with sepsis or trauma.METHODS: We performed two nested case-control studies of 478 patients with sepsis and trauma with or without ALI/ARDS admitted to the medical, surgical and trauma ICUs of a tertiary-care center. Cases consisted of patients with either sepsis or trauma and ALI/ARDS; controls consisted of equivalent numbers of matched patients with either sepsis or trauma alone. We measured serum 25-OHD levels the morning after ICU admission and used multivariable regression to assess the relationship between 25-OHD and diagnosis of ALI/ARDS during the first four ICU days, controlling for age, gender, diabetes, smoking status and season.RESULTS: 25-OHD levels did not differ between cases with ALI/ARDS and controls in either the sepsis or trauma cohorts. Using a conditional logistic regression model, sepsis patients during the winter season with higher 25-OHD levels were more likely to develop acute lung injury (odds ratio 1.68, 95% confidence interval of 1.05 to 2.69, P = 0.03). This association did not hold for the trauma cohort in either season. Sepsis and trauma patients had a lower risk of hospital mortality at higher 25-OHD levels but neither relationship reached significance. Higher one-year mortality after trauma was associated with lower 25-OHD levels (HR 0.50, CI 0.35,0.72 P = 0.001).CONCLUSIONS: Serum 25-OHD measured early after admission to intensive care is not associated with the development of acute lung injury, hospital or one-year mortality in critically ill patients with sepsis although lower 25-OHD levels were associated with higher one-year mortality in patients with severe trauma.

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Acute respiratory distress syndrome: Predictors of noninvasive ventilation failure and intensive care unit mortality in clinical practice.

PMID: 

J Crit Care. 2016 Feb ;31(1):26-30. Epub 2015 Oct 30. PMID: 26643859

Abstract Title: 

Acute respiratory distress syndrome: Predictors of noninvasive ventilation failure and intensive care unit mortality in clinical practice.

Abstract: 

PURPOSE: Noninvasive ventilation (NIV) is used as an initial ventilatory support in acute respiratory distress syndrome (ARDS), but its utility is unclear, and persistence in those who do not improve may delay intubation and lead to adverse outcomes. Hence, it becomes imperative to have a clear understanding of selecting patients who will benefit from this modality.METHODS: In this prospective observational study, we included all consecutive adults, over a 3-year period, who fulfilled criteria for ARDS by the Berlin definition. Basic demographics, ventilatory support, intensive care unit course, and outcome were recorded.RESULTS: Of 170 patients, 96 (56.47%) were initially managed with NIV. Noninvasive ventilation failure was seen in 42 (43.75%) of 96, and low baseline PaO2/FIO2, shock, and ARDS severity were associated with NIV failure. Overall intensive care unit mortality was 63 (37.1%) of 170, and high Acute Physiology and Chronic Health Evaluation II score, low PaO2/FIO2, shock, and ARDS severity were associated with increased mortality. Noninvasive ventilation failure and mortality were significantly higher in moderate and severe ARDS.CONCLUSIONS: Noninvasive ventilation maybe useful in selected patients with mild ARDS but should be used with great caution in moderate and severe ARDS, as failure risk is high. In addition, low PaO2/FIO2 and shock are associated with NIV failure. Acute Physiology and Chronic Health Evaluation II score, shock, low PaO2/FIO2, and ARDS severity are associated with increased mortality.

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Vitamin D deficiency is associated with mortality in the medical intensive care unit.

PMID: 

Crit Care. 2011 ;15(6):R292. Epub 2011 Dec 10. PMID: 22152332

Abstract Title: 

Vitamin D deficiency is associated with mortality in the medical intensive care unit.

Abstract: 

INTRODUCTION: The incidence of vitamin D deficiency in critically ill patients has been reported to range from as low as 17% to as high as 79%. Data regarding the relationship between 25-hydroxyvitamin D levels and outcomes in the medical intensive care unit are sparse. The goal of the study was to evaluate the prevalence of 25-hydroxyvitamin D deficiency in the medical intensive care unit and its relationship with outcomes.METHOD: This was a retrospective study in a medical intensive care unit (MICU) at an inner city community hospital. The study period was between October 2009 and February 2010.RESULTS: Of the 932 patients admitted during the study period, 25-hydroxyvitamin D vitamin D (25(OH)D) levels were available in 523 (53%); 86 of them were excluded from the study due to readmission to the intensive care unit. Deficiency was defined as 0 to 19.9 ng/dL 25(OH)D levels, insufficiency as 20 to 29.9 ng/dL, and normal levels as≥30 ng/dL. Of the 437 patients studied, 25(OH)D deficiency was identified in 340 (77.8%), insufficiency in 74 (16.9%), and normal levels in 23 (5.3%) patients. Patients with 25(OH)D deficiency/insufficiency were younger (P = 0.015), were male (P = 0.001), and had kidney disease (P = 0.017) and lower total serum calcium levels (P = 0.003). Hospital mortality was higher in patients with 25(OH)D deficiency (P = 0.01). No differences in ventilator days or length of stay in the MICU were evident among the three groups. Analysis by multiple logistic regression demonstrated that acute physiology and chronic health evaluation (APACHE) IV score ((odds ratio (OR) 1.036; 95% confidence interval (CI) 1.024-1.048, P

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Accumulating evidence suggests that vitamin D deficiency is linked to excess mortality.

PMID: 

Curr Opin Clin Nutr Metab Care. 2009 Nov ;12(6):634-9. PMID: 19710612

Abstract Title: 

Vitamin D deficiency and mortality.

Abstract: 

PURPOSE OF REVIEW: To summarize recent findings on vitamin D deficiency and mortality. The serum concentration of 25-hydroxyvitamin D [25(OH)D], the metabolic precursor of the vitamin D hormone calcitriol, is the standard for assessing vitamin D status. Deficient 25(OH)D concentrations (75 nmol/l), deficient 25(OH)D concentrations are associated with excess mortality in the general population and in patients with increased cardiovascular disease risk. Results support an earlier meta-analysis of controlled trials that were not primarily designed to assess mortality showing a survival benefit of vitamin D supplementation over no supplementation in middle-aged and elderly persons. In patients with advanced chronic diseases such as end-stage heart failure, however, circulating calcitriol predicts mid-term mortality better than 25(OH)D does. Available data indicate that these patients may enter a vicious cycle of low calcitriol, increased inflammation markers, and renal impairment, which may be difficult to escape by simple vitamin D supplementation.SUMMARY: Accumulating evidence suggests that vitamin D deficiency is linked to excess mortality. However, future studies should clarify to which extent vitamin D supplementation can improve survival in the aging population and in specific patient groups.

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Vitamin D prevents experimental lung fibrosis and predicts survival in patients with idiopathic pulmonary fibrosis.

PMID: 

Pulm Pharmacol Ther. 2019 04 ;55:17-24. Epub 2019 Jan 16. PMID: 30659895

Abstract Title: 

Vitamin D prevents experimental lung fibrosis and predicts survival in patients with idiopathic pulmonary fibrosis.

Abstract: 

BACKGROUND: Vitamin D (VitD) is a steroid hormone with cytoprotective and anti-inflammatory properties. Epidemiological studies have suggested a link between VitD deficiency and risk of development of chronic lung diseases. Its role in lung fibrosis is largely unknown. The aim of our study was to investigate the role of VitD in experimental and human lung fibrosis.METHODS: VitD (25-OH-D3, 2 μg/kg) was orally administered from day 3-day 13 following bleomycin-challenge, in 8-10 weeks-old C57/BL6 mice. Mouse Lung Fibroblasts (MLFs) were pre-treated with VitD (2 μM for 24 h) and then stimulated with TGFB1 (10 ng/ml). Serum samples from 93 patients with IPF and other forms of interstitial lung diseases (ILDs) were prospectively collected for VitD measurement.RESULTS: VitD administration prevented bleomycin-induced lung fibrosis, as assessed by reductions in hydroxyproline levels, mRNA levels of col1a1, col3a1 and a-SMA (1.4-, 3.1-, 2.25-, 2.5-fold, respectively) and Masson Trichrome staining compared to the untreated group and these changes were associated with restoration of the bleomycin-induced downregulation of vitamin D-receptor (Vdr) mRNA levels. Pre-treatment with VitD reduced the responsiveness of MLFs to pro-fibrotic stimuli, as indicated by significant decreases of col1a1, col3a1 and a-SMA (3.6-, 4.1- and 2.7-fold, respectively).These changes were associated with restoration of the TGFB1-induced downregulation of vitamin D-receptor (VDR) mRNA levels. VitD treatment deactivated TGFB1-induced Smad3 phosphorylation. Patients with IPF and other forms of ILDs displayed deficient VitD serum concentrations (mean VitD = 18.76 ± 8.36 vs. 18.54 ± 8.39 ng/ml, respectively, p = 0.9). VitD deficiency was correlated with baseline FVC%predicted (r = 0.47, p 

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Vitamin D deficiency is common in severe sepsis.

PMID: 

Crit Care Med. 2017 Feb ;45(2):282-289. PMID: 27632669

Abstract Title: 

Vitamin D Deficiency in Human and Murine Sepsis.

Abstract: 

OBJECTIVES: Vitamin D deficiency has been implicated as a pathogenic factor in sepsis and ICU mortality but causality of these associations has not been demonstrated. To determine whether sepsis and severe sepsis are associated with vitamin D deficiency and to determine whether vitamin D deficiency influences the severity of sepsis.DESIGN, SETTING, AND PATIENTS: Sixty-one patients with sepsis and severe sepsis from two large U.K. hospitals and 20 healthy controls were recruited. Murine models of cecal ligation and puncture and intratracheal lipopolysaccharide were undertaken in normal and vitamin D deficient mice to address the issue of causality.MEASUREMENTS AND MAIN RESULTS: Patients with severe sepsis had significantly lower concentrations of 25-hydroxyvitamin D3 than patients with either mild sepsis or age-matched healthy controls (15.7 vs 49.5 vs 66.5 nmol/L; p = 0.0001). 25-hydroxyvitamin D3 concentrations were significantly lower in patients who had positive microbiologic culture than those who were culture negative (p = 0.0023) as well as those who died within 30 days of hospital admission (p = 0.025). Vitamin D deficiency in murine sepsis was associated with increased peritoneal (p = 0.037), systemic (p = 0.019), and bronchoalveolar lavage (p = 0.011) quantitative bacterial culture. This was associated with reduced local expression of the cathelicidin-related antimicrobial peptide as well as evidence of defective macrophage phagocytosis (p = 0.029). In the intratracheal lipopolysaccharide model, 1,500 IU of intraperitoneal cholecalciferol treatment 6 hours postinjury reduced alveolar inflammation, cellular damage, and hypoxia.CONCLUSIONS: Vitamin D deficiency is common in severe sepsis. This appears to contribute to the development of the condition in clinically relevant murine models and approaches to correct vitamin D deficiency in patients with sepsis should be developed.

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