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posted ago by freedomlogic ago by freedomlogic +12 / -1

DISCLAIMER

I am fully aware some of you dont believe in covid, or germs for that matter, this post is not for you.

I however believe that covid is a weaponized cold strain, and the vaccine is the solution to it, for what reason, I can only guess.

https://www.mdpi.com/2227-9059/11/9/2362

https://archive.is/YZ2Co

Among the various aspects under investigation, disruptions in mineral homeostasis have emerged as a critical area of interest. This review aims to provide an overview of the current evidence linking calcium, phosphorus and magnesium abnormalities with COVID-19 infection and explores the potential implications beyond the acute phase of the disease. Beyond the acute phase of COVID-19, evidence suggests a potential impact of these mineral abnormalities on long-term health outcomes. Persistent alterations in calcium, phosphorus and magnesium levels have been linked to increased cardiovascular risk, skeletal complications and metabolic disorders, warranting continuous monitoring and management in post-COVID-19 patients.

Phosphocalcium metabolism plays a crucial role in maintaining the balance of phosphorus and calcium in the body, which is essential for various physiological processes, including bone health, muscle function, nerve transmission and cellular signaling [5]. Any disturbances in this delicate equilibrium can lead to a spectrum of metabolic disorders, with significant implications for an individual’s overall well-being.

This manuscript review aims to provide a comprehensive analysis of the current state of research on phosphocalcium metabolism disorders post-COVID. It will delve into the existing literature to explore the impact of COVID-19 on phosphorus, calcium and parathyroid hormone levels, along with the prevalence and clinical manifestations of these disturbances in recovering individuals [6].

The minerals calcium and phosphorus are essential components in the process of bone mineralization. Both minerals are found in bones and can be dissolved in serum or found intracellularly in soft tissues. Calcium and phosphorus are stored within the bone structure in the form of a crystalline compound known as hydroxyapatite. The presence of soluble calcium and phosphorus in serum is crucial for maintaining homeostasis and facilitating the proper functioning of various systems, including the nervous and muscular systems. Consequently, these levels are tightly regulated by hormones through processes such as intestinal absorption, bone resorption, renal excretion and reabsorption

Phosphorus serves as a structural constituent of bone in the form of hydroxyapatite. Phosphorus primarily serves the crucial role of facilitating cellular energy production and supporting metabolic processes by acting as a constituent of adenosine triphosphate (ATP). The maintenance of serum phosphorus homeostasis is achieved through the ongoing processes of bone mineralization and resorption, which are regulated by a delicate equilibrium between osteoblasts, the cells responsible for bone formation, and osteoclasts, the cells involved in bone reabsorption [2,4].

The regulation of calcium and phosphorus in the body is primarily controlled by three hormones: vitamin D 25(OH), parathyroid hormone (PTH), and fibroblast growth factor 23 (FGF23) [3].

  1. Incidence of Phosphocalcium Metabolism Disorders Related to COVID-19

The literature search revealed 240 studies, 31 of which were ultimately included in this review: 7 articles about hypocalcemia, 12 articles about hypophosphatemia and 12 articles about hypovitaminosis D.

4.2. Hypophosphatemia

There is a suggested association between disturbances in phosphate metabolism and the impact of COVID-19 on the homeostasis of vitamin D, calcium and phosphorus. The prevalence of vitamin D deficiency is high among individuals with severe COVID-19 infection [40]. Povaliaeva et al. recently conducted a study that established an association between abnormal kidney function, abnormal vitamin D metabolism and hypophosphatemia (Table 1) [41]. According to the authors, individuals with severe COVID-19 manifested atypical vitamin D metabolism, increased serum creatinine levels and decreased serum phosphate levels (Figure 4) [41].

Vitamin D insufficiency has been associated with reduced levels of blood calcium and phosphate as a result of renal excretion and impaired absorption in the intestines [42]. The parathyroid hormone (PTH) is known to exhibit several effects in response to low blood calcium levels. It stimulates the reabsorption of calcium in the bones, kidneys and intestines. However, it also leads to an increased loss of phosphate via the kidneys [42]. In relation to this matter, Pal et al. conducted a comparative analysis of blood phosphorus levels between COVID-19 patients and a control group of healthy individuals matched for age, sex and vitamin D status. A study conducted by researchers revealed a decrease in phosphorus levels among individuals diagnosed with COVID-19 [26]. The aforementioned discovery presents a divergence from the previously posited pathways regarding the impact of vitamin D deprivation on disruptions in phosphate metabolism during COVID-19 infection.

There is a notable prevalence of hypophosphatemia among individuals diagnosed with COVID-19 who also have end-stage renal diseases (ESRD) [43].

Mechanisms that are linked to the occurrence of hypophosphatemia in individuals with renal dysfunction have been documented in previous studies [34]. The occurrence of acute kidney injury (AKI) can be attributed to various mechanisms in the context of COVID-19. Prerenal acute kidney injury (AKI) can manifest as a result of profound dehydration and the accumulation of water within the pulmonary interstitial tissue. The predominant etiology of renal dysfunction in individuals afflicted with COVID-19 has been documented as proximal tubulopathies, which can be attributed to either vascular-related factors or direct viral infiltration. This pathophysiological process leads to the subsequent occurrence of electrolyte depletion and subsequent development of additional complications [44].

Malnutrition and the inadequate dietary intake of phosphate-rich foods can lead to hypophosphatemia in COVID-19 patients. During severe illness, especially in hospitalized patients, there might be a reduced oral intake or impaired absorption of essential nutrients, including phosphate. Additionally, COVID-19 patients with concurrent end-stage renal diseases (ESRD) may already have compromised nutrient absorption due to renal dysfunction, further exacerbating the risk of developing hypophosphatemia.

COVID-19 patients, especially those with severe respiratory distress, may experience respiratory alkalosis, a condition characterized by reduced levels of carbon dioxide (CO2) in the blood. This occurs when patients breathe rapidly, leading to CO2 elimination and a shift towards alkalinity. Respiratory alkalosis can cause phosphate to move from the extracellular fluid into the intracellular compartment, resulting in decreased serum phosphate levels.

Both poor nutrition and respiratory alkalosis can act synergistically to contribute to hypophosphatemia in COVID-19 patients with ESRD. Additionally, the combination of these factors with other mechanisms mentioned earlier, such as renal tubulopathies and abnormal vitamin D metabolism, can further compound the phosphate metabolism disturbances in these patients (Figure 5).

4.3. Hypovitaminosis D

The importance of the strong association between VD and COVID-19 emerged during the initial stages of the pandemic, as VD has been widely recognized for its role in modulating both innate and adaptive immune responses [45]. Vitamin D (VD) has been recognized for its antimicrobial properties and ability to inhibit viral activity. It also plays a role in regulating the adaptive immune response by promoting a transition from a pro-inflammatory state to a tolerogenic state. This results in the downregulation of immune responses mediated by T-helper-1 lymphocytes, the inhibition of pro-inflammatory cytokine production and the promotion of regulatory T-cell maturation [46].

Several studies have observed an association between low vitamin D levels and worse COVID-19 outcomes, including an increased risk of severe illness, ICU admission, and mortality [47,48]. Vitamin D has immunomodulatory effects and can influence the expression of genes involved in the immune response. Deficiencies in vitamin D may lead to dysregulated immune responses, increased inflammation and impaired lung function, all of which can contribute to disease severity in COVID-19.

On the other hand, deficiencies in calcium, phosphorus and magnesium may also impact immune function and contribute to an increased susceptibility to viral infections, including COVID-19. These cations are essential for various cellular processes, including immune cell function and cytokine signaling [42]. A deficiency in any of these cations could impair the immune response and potentially compromise the body’s ability to fight off viral infections. COVID-19 itself can disrupt calcium, phosphorus and magnesium homeostasis through multiple mechanisms. The severe inflammatory response triggered by the virus can cause cytokine storm and lead to altered levels of these cations [49]. Additionally, factors like respiratory alkalosis, kidney dysfunction and electrolyte shifts due to fluid imbalances in critically ill patients can further contribute to cation abnormalities.

Vitamin D (VD) has been recognized for its significant involvement in various metabolic pathways related to musculoskeletal health [41]. Previous research has demonstrated that supplementation with VD has been shown to confer advantages in muscle recovery following periods of intense physical activity and tissue damage [31,50]. The studies found that VD levels were able to predict and exert an influence on the duration of illness and the time it took for recovery following an episode of acute severe pneumonia (Table 2). To this day, the role of vitamin D in the occurrence of long COVID has only been examined in a limited number of small-scale studies [51,52,53]. In a recent pilot study involving elderly patients recovering from acute COVID-19, the effectiveness of a six-week therapy with 2000 IU/day of cholecalciferol compared to placebo was examined. The study found that cholecalciferol therapy resulted in a reduction in creatinine kinase values and demonstrated a positive trend in improving overall health and physical well-being [54,55,56,57].

4.4. Hypoparathyroidism (pointing this out because there is no mention of hyper parathyroidism)

4.6. Hypomagnesemia

Magnesium deficiency is another important factor that merits attention in the context of COVID-19 and its impact on phosphocalcium metabolism [42]. Magnesium is a vital cofactor in numerous enzymatic reactions, including those involved in calcium regulation. A deficiency in magnesium can disrupt the balance between calcium and phosphorus levels, potentially contributing to the risk of hypocalcemia in post-COVID-19 patients [83].

Several studies have suggested a possible association between magnesium deficiency and COVID-19 severity [83,84,85,86]. COVID-19 patients with severe symptoms often experience significant inflammation and oxidative stress, leading to increased magnesium loss through urine and sweat. Additionally, the use of certain medications during the treatment of COVID-19, such as diuretics and proton pump inhibitors, can further exacerbate magnesium depletion.

  1. Discussion

The COVID-19 pandemic has not only impacted the respiratory system, but it has demonstrated systemic implications such as modifications in phosphocalcium metabolism. The objective of this review article was to provide a comprehensive summary and critical analysis of the existing research about disorders in phosphocalcium metabolism following COVID-19 [2,26,51]. The review aimed to offer valuable insights into the potential underlying mechanisms and clinical implications associated with these disorders.

The results derived from the examined studies highlight the frequency of phosphocalcium metabolism disorders among individuals in the process of recuperating from COVID-19. Various research studies have documented a variety of disruptions, such as hypophosphatemia, hypocalcemia and secondary hypoparathyroidism [28,50,73]. The results of this study suggest that COVID-19 has the potential to disturb the intricate equilibrium of phosphorus, calcium and parathyroid hormone concentrations within the human body.

Multiple factors contribute to the occurrence of phosphocalcium abnormalities, encompassing the length and intensity of hospitalization, coexisting medical conditions and the occurrence of additional complications like acute respiratory distress syndrome and acute kidney injury (refer to Table 1). There is evidence to suggest that individuals diagnosed with chronic kidney disease or chronic heart disease may be more susceptible to the development of phosphocalcium disorders in the context of COVID-19.

The clinical ramifications of disorders related to phosphocalcium metabolism following a COVID-19 infection are of considerable importance. The presence of hypophosphatemia and hypocalcemia may result in various clinical manifestations, such as muscle weakness, fatigue, bone pain, muscle cramps, tingling sensations and potential cardiac arrhythmias [3,4,26,50].

  1. Conclusions

In summary, this manuscript review highlights the importance of phosphocalcium metabolism disorders in the population recovering from COVID-19. The results underscore the significance of surveillance, interventions and additional investigation in this domain. Healthcare professionals have the potential to enhance the comprehensive care and outcomes of individuals after COVID by addressing these metabolic disturbances.

Lmao, I guess even a broken clock can be right twice a day.

That endocrinologist I seen was a nutter, sees my vitamin d was 42 mmol/l and even lower now and declares thats all it is. Lmao. Prolly a good opportunity to do a real study and learn something but these people are to concerned about protecting arcas taxes in case it does turn out they are responsible.

Speaking of which, some poor immigrant woman here in halifax got caught in a big industrial oven while cleaning it in the bread section at walmart and got roasted to crisp on the night shift. At least thats the rumor, nothing official yet. Its a shame she didnt smoke weed, they could have just blamed it on that!

10,000 dollar fine and a slap on the wrist and its business as usual.