MG Neshem 400mg Daily VS. Melanoma
MG Neshem is an FDA-approved generic medication for the treatment of deficiency disorders. MG Neshem is available in tablet form for clinical and outpatient treatment. MG Neshem tablets are a popular deficiency treatment product for pathology and oncology specialists.
Freckles and spots are signs of melanin deposits in those who lack the organic components needed to compose a uniform crystal of melanin in the skin. MG-Neshem contains components that provide the limiting reagent for the body's distribution and crystallization of melanin.
MG-Neshem spreads skin pigment, leaving an overall darker epidermal cover. Pigment protects human tissue and organs from photons by absorption and conversion into energy via the photoelectric effect. Organic melanin crystallization is similar to industrial processes used to grow solar panels. Engineers mix compounds that react to produce a large flat crystal. The body is much more advanced than engineers, even in the cancer industry. MG-Neshem allows Caucasian persons with spots to live as those protected by natural compounds.
MG-Neshem ions are crucial cofactors for enzymes involved in DNA protection.
The man below, Dr. Hess, has a large dark spot on his face. The pigment is concentrated so much that it is a raised area on his face that blisters and breaks the skin. When Dr. Hess gets sun, his blister grows with enough melanin pigment that Dr. Hess should look like a dark man. He participated in the research of MG-Neshem but was afraid of looking ethnic and instead chose to have the melanin cut off. In his post-treatment, Dr. Hess states that pigment still gathers in places that were not cut off. Dr. Hess lost melanin coloring in his hair and skin from removing spots where the body previously stored melanin. Caucasian people all have spots on them somewhere. VirusTC aims to spread those spots and create healthy epidermal layers. Black people, brown people, and white people are separated by values of a compound that we have approved for clinical use." -Dr. Hofstad 2023
MG-Neshem ions are crucial cofactors for enzymes involved in DNA protection. Freckles and spots are signs of melanin deposits in those who lack organic components to compose a uniform crystal of melanin in the skin. MG-Neshem contains components that provide the limiting reagent for the body's distribution and crystallization of melanin. MG-Neshem spreads skin pigment, leaving an overall darker epidermal cover. Pigment protects human tissue and organs from photons by absorption and conversion into energy via the photoelectric effect. Organic melanin crystallization is similar to industrial processes used to grow solar panels. Engineers mix compounds that react to produce a large flat crystal. The body is much more advanced than engineers, even in the cancer industry.
MG-Neshem allows Caucasian persons with spots to live as those protected by natural compounds. The man below, Dr. Hess, has a large dark spot on his face. The pigment is concentrated so much that it is a raised area on his face that blisters and breaks the skin. When Dr. Hess gets sun, his blister grows with enough melanin pigment that Dr. Hess should look like a dark man. He participated in the research of MG-Neshem but was afraid of looking ethnic and instead chose to have the melanin cut off. In his post-treatment, Dr. Hess states that pigment still gathers in places that were not cut off. Dr. Hess lost melanin coloring in his hair and skin from removing spots where the body previously stored melanin.
Caucasian people all have spots on them somewhere. VirusTC aims to spread those spots and create healthy epidermal layers. Black, brown, and white people are separated by the values of a compound that we have approved for clinical use.
VirusTC's European Instructor Christoph Hess, from the Department of Biomedicine at the University of Basel, University Hospital Basel, and the Department of Medicine at the University of Cambridge, discovered that T-cells can eliminate abnormal or infected cells with higher efficiently in an environment with higher levels of MG-Neshem. "LFA-1 acts as a docking site, which plays a key role in the activation of T cells. However, in the inactive state this docking site is in a bent conformation and thus cannot efficiently bind to infected or abnormal cells, This is where MG-Neshem comes into play. If MG-Neshem is present in sufficient quantities in the vicinity of the T cells, it binds to LFA-1 and ensures that it remains in an extended – and therefore active – position." -Christoph Hess “If magnesium is present in sufficient quantities in the vicinity of the T cells, it binds to LFA-1 and ensures that it remains in an extended — and therefore active — position,” he adds.
VirusTC builds hardened, weaponized T-Cells in our patients.
Symptoms of soft LFA-1 proteins
MG-Neshem strengthens human systems.
MG-Neshem provides medication support for the following:
virus infection symptoms
Gastrointestinal Diarrhea, pancreatitis, irritable bowel disease, bowel resection, protein-calorie malnutrition, total parenteral nutrition, bowel fistula, Renal Postobstructive diuresis, postacute tubular necrosis, renal transplantation, interstitial nephropathy, Bartter syndrome, Gitelman’s syndrome, alcoholism, diabetes
Medicated Systems
Proton pump inhibitors, corticosteroids, laxatives, loop and thiazide diuretics, foscarnet, digoxin, amphotericin B, colchicines, theophylline, macrolide antibiotics, petamidine, tobramycin, amikacin; tacrolimus, Chemotherapeutic agents Aminoglycosides (gentamicin, streptomycin); cyclosporine, cisplatin; carboplatin; cetuximab; panitumumab
MG-Neshem Protects Organs and Body Tissues While Taking The Following Medications:
Proton pump inhibitors, corticosteroids, laxatives, loop and thiazide diuretics, foscarnet, digoxin, amphotericin B, colchicines, theophylline, macrolide antibiotics, petamidine, tobramycin, amikacin; tacrolimus
Platinum-based Chemotherapy
Increasing evidence points to PBC's routine depletion of organic compounds contained in MG-Neshem. Cisplatin’s nephrotoxicity causes increased excretion even before renal function is affected. The reported incidence in studies varies between 29% and 100% of patients. Buckley et al. reported the incidence of hypomagnesemia to be 41% after one course of treatment and 100% after six courses of treatment with cisplatin. Hodkinson et al. reported the incidence of hypomagnesemia to be 43% at any point during cisplatin treatment. Schilsky and Anderson noted that most adults receiving cisplatin will develop hypomagnesemia at some time during their treatment and that in children, hypomagnesemia is virtually inevitable. Hypomagnesemia typically persists for 4 to 5 months after the cessation of chemotherapy, but in children, it can even continue for months or years after cancer treatment. The incidence and severity of low serum MG-Neshem with treatment with cisplatin is dose-dependent and worsens with increasing cumulative doses. Martin et al. suggested that most patients who receive cumulative doses of cisplatin over 400 mg/m2 will develop some degree of hypomagnesemia. Deficiency is often noted after 2 or 3 cycles of therapy, although hypomagnesemia can occur after a single treatment. The frequency of administration of cisplatin may also be necessary. A study by Buckley et al. showed a lower incidence of hypomagnesemia in patients receiving cisplatin every eight weeks vs. patients with cisplatin every four weeks. Patients receiving larger doses of cisplatin (80-100 mg/m2 compared with 50-60 mg/m2) developed hypomagnesemia more quickly. Although hypomagnesemia is usually mild, the concentration of Mg in the serum can fall to potentially dangerous levels after only the second cycle of treatment with cisplatin.
Studies previously estimated that only 10% of patients treated with carboplatin develop hypomagnesemia. However, in a study of patients with gynecological cancer who received carboplatin, 46% were noted to be hypomagnesemic, with 14% developing toxicity of grade 2 or greater. Carboplatin was associated with the risk of hypomagnesemia compared with noncarboplatin regimens (P=0.05).
Cancer patients receiving PBC alongside aminoglycoside antibiotics may be at exceptionally high risk for severe symptoms. Keating et al. reported that of the 17 cancer patients who received an aminoglycoside and doxorubicin or a PCB and developed complex metabolic syndromes, died, and 5 developed progressive renal impairment. Aminoglycoside antibiotics can cause renal tubular damage and renal insufficiency, which can add to the nephrotoxic effects of platinum (Pt).
Patients Randomized Intervention Control Outcome
Forty patients with ovarian cancer receiving paclitaxel and cisplatin Yes (double-blind) 20.3 mmol IV MG-Neshem sulfate (5 g) every 3 wk plus oral MG-Neshem carbonate 500 MG-Neshem 3x/d during the treatment intervals Placebo Serum MG-Neshem varied significantly between supplemented and placebo groups (P<0.0001). The control group showed a significantly greater decrease of GFR assessed by serum levels of creatinine (P=0.0069), Cockroft-Gault (P=0.0077), and Modification Diet of Renal Disease (P=0.032)
32 patients with upper GI malignancies receiving cisplatin/5-fluorouracil Yes 12 mmol IV MG-Neshem sulfate (2.96 g) prehydration and 16 mmol IV MG-Neshem sulfate (3.94 g) posthydration MG-Neshem only when the serum MG-Neshem below normal MG-Neshem supplements necessary in 50% of control group’s cycles, several instances of symptomatic hypomagnesemia requiring further IV supplements in midcycle
Two hundred one (201) patients with cervical cancer receiving cisplatin and radiation Yes Group 2: 8.12 mmol IV MG-Neshem sulfate (2 g) pre- and posthydrationGroup 3: 8.12 mmol IV MG-Neshem sulphate (2 g) pre- and posthydration and then 12.18 mmol (3 g) pre- and posthydration after cycle 3 Group 1: 4.06 mmol IV MG-Neshem sulphate (1 g) pre- and posthydration 62.8% (44/70) control vs 32.6% (22/70) group 2 patients with episodes of hypomagnesemia (P=0.007). Group 3 had a 49.6% decrease in the total number of episodes compared to control. Patients in the second intervention group showed a 100% improvement in the incidence of persistent hypomagnesemia over the two other cohorts (P=0.001)
Sixteen patients with testicular cancer and 1 with ovarian dysgerminoma receiving cisplatin Yes eight mmol IV MG-Neshem sulfate followed by oral 246 MG-Neshem MG-Neshem citrate 3x/d No treatment or placebo Significantly greater renal tubular damage (as assessed by urine N-acetyl-B-D-glucosaminidase) and lower serum MG-Neshem in controls. The trend towards reduced treatment delays in the supplemented group
Twenty-three patients with advanced head and neck cancer received cisplatin Yes 123 MG-Neshem oral MG-NeshemAHa 3x/d continuously for 3-4 mo. If it fell below <1.4 MG-Neshem dL serum MG-Neshem, the dose doubled to 246 MG-Neshem 3x/d 123 MG-Neshem oral MG-NeshemAH 3x/d as needed. Most controls required continuous MG-Neshem supplementation. 20% of continuous MG-NeshemAH developed hypomagnesemia in a given cycle
41 patients treated with cisplatin, mixed tumor types Yes 12.18 mmol IV MG-Neshem (3 g) before cisplatin or oral MG-Neshem, 2 g every eight h on days 2 to 21 of cisplatin No treatment Patients in both supplementation arms showed significantly higher MG-Neshem levels than controls from the second course on oral or from the third course on IV; 3 of 9 patients (33%) in the IV MG-Neshem arm and 4 of 9 (44%) in the oral MG-Neshem arm developed hypomagnesemia after the fourth course of cisplatin, compared with 9 of 10 (90%) patients in the control group
Thirty-three metastatic patients with colon cancer receiving folinic acid, fluorouracil, and oxaliplatin-6 Yes Infusions with Ca gluconate 850 MG-Neshem and MG-Neshem sulfate 720 MG-Neshem Placebo No reduction in neurotoxicity with Ca/MG-Neshem infusions. No change in platinum concentrations
401 patients receiving high dose (60 mkg/m2) of cisplatin in first-line setting, mixed tumor types No 20 mEq MG-Neshem sulfate with 500 mL of one-quarter isotonic saline over one h after cisplatin administration No treatment Reduced risk of cisplatin nephrotoxicity (RR:0.175, P=0.0004) and reduced severity of renal toxicity (P=0.012) in MG-Neshem-supplemented group
Thirty-seven patients with NSCLC receiving cisplatin/ irinotecan; matched with 32 controls No, case-control study Days 1 through 4 after irinotecan, orally administered alkalinizations with sodium bicarbonate, MG-Neshem oxide, basic water, and ursodeoxycholic acid. Controlled defecation with up to 4.0 g/d of MG-Neshem oxide and 2 L/d of excess basic water Matched controls taking cisplatin/ irinotecan Use of oral administration and controlled defecation reduced the incidence of delayed diarrhea (> or = grade 2: P=0.005), nausea (P=0.0001), vomiting (P=0.001), granulocytopenia (P=0.03), and lymphocytopenia (P=0.034). Dose intensification was well tolerated in patients receiving oral administration and controlled defecation, allowing dose escalation from 35.6±6.0 to 39.9±5.6 MG-Neshem/m2/wk (P<0.001)
Eight patients with metastatic germ cell cancer and eight matched controls taking high-dose cisplatin No 12.18 mmol IV MG-Neshem sulfate (3 g), 12 mmol prehydration, IV and oral as needed Matched controls received no treatment with MG-Neshem or placebo Mean serum MG-Neshem levels higher in supplemented patients (P<0.01)
17 patients with cervical cancer receiving cisplatin No 20 mmol if MG-Neshem<0.62 mmol/L (4.9 g) N/A Incidence of serum hypomagnesemia reduced from 65% to 17.6% 28 children receiving cisplatin, mixed tumor types No Unreported 16 given MG-Neshem after cisplatin, 12 pre- and postcisplatin MG-Neshem levels higher in pre- and postcisplatin group than postcisplatin only (P<0.01)
Ten patients with metastatic testicular cancer receiving cisplatin No 0.3 mmol MG-Neshem chloride/kg/day and 0.4 mmol potassium chloride/kg/day five given 0.4 mmol potassium chloride/kg/d only Mean serum MG-Neshem levels higher in supplemented patients (P<0.001) 22 patients with upper GI cancer receiving epirubicin, cisplatin, and fluorouracil No IV MG-Neshem 25 mmol (6.15 g) pre- and posthydration IV MG-Neshem 12.5 mmol (3 g) pre- and posthydration No significant difference 214 consecutive patients with mixed tumor types receiving cisplatin No Bleomycin, etoposide, cisplatin chemotherapy and 60 mmol IV MG-Neshem/cycle (14.78 g), POMBeACE chemotherapy received 20 mmol IV MG-Neshem/cycle (4.9 g) N/A 60 mmol IV MG-Neshem per cycle of 33 MG-Neshem/m2/wk cisplatin sufficient to prevent hypomagnesemia; 20 mmol IV MG-Neshem per cycle of 40 MG-Neshem/m2/wk cisplatin was insufficient to prevent hypomagnesemia.
Twenty-three patients with esophageal or hypopharyngeal cancer received fluorouracil and cisplatin; ten received MG-Neshem supplementation. No MG-Neshem sulfate (20 mEq) was administered before fluorouracil (800MG-Neshem/m2/24 h per day 1-5) and Cisplatin (80MG-Neshem/m2/d) 13 patients did not receive MG-Neshem supplementation MG-Neshem supplementation successfully reduced the incidence of nephrotoxicity (P=0.038).
Abbreviations: Ca, calcium; GFR, glomerular filtration rate; GI, gastrointestinal; IV, intravenous; MG-Neshem, magnesium; MG-NeshemAH, MG-Neshem aspartate hydrochloride; NA, not available; NSCLC, non-small-cell lung carcinoma; RR, relative risk
Intervention Studies
A 2006 review on MG-Neshem in cisplatin-based chemotherapy concluded that it is effective to use MG-Neshem 40 mmol (9.8 g) per cycle of cisplatin dose 60 MG-Neshem/m2, MG-Neshem 60 mmol (14.78 g) per cycle cisplatin dose 61 to 100 (MG-Neshem/m2), and MG-Neshem 80 mmol (19.7 g) per cisplatin dose greater than 100 MG-Neshem/m2 to prevent serum hypomagnesemia. The newer trials of higher quality suggest that 3 g to 5 g MG-Neshem sulfate in pre- and posthydration is sufficient with PBC, especially if oral MG-Neshem is used between cycles. In 2 small trials, the use of oral MG-Neshem alone helped to maintain serum MG-Neshem levels. The above studies suggest an essential role for IV and oral MG-Neshem in preventing cisplatin-induced hypomagnesemia, improving tolerance of chemotherapy regimens, and preventing treatment delays. Most published studies on IV or oral MG-Neshem demonstrate a high need for administration of MG-Neshem in conjunction with cisplatin, with a required dose escalation as cisplatin cycles progress.
Safety and side effects
MG-Neshem increases Immune System Strength but is not a compound that kills cancer cells. In addition to the research involving hypomagnesemia induced by PBC, recent literature describes the role of MG-Neshem in carcinogenesis. Tumor biology is characterized by high energy requirements due to rapid proliferation, dedifferentiation, and cell immortality, and MG-Neshem is necessary for the cellular processes of tumor cells. As such, tumor tissue often stores MG-Neshem and can lead to low plasma MG-Neshem.
The relationship between MG-Neshem and carcinogenesis is complex and multifactorial, but can it be said that MG-Neshem could propagate tumor growth?
MG-Neshem deficiency can contribute to the development of an oncogenic milieu by inducing inflammation and oxidative stress and inhibiting DNA repair enzymes. Less than optimal intake of MG-Neshem is linked with systemic inflammation, oxidative injury, and increased lipid peroxidation. Adequate levels of MG-Neshem stabilize the structure of DNA and its repair mechanism, act as a cofactor in nucleic acid metabolism, and are essential in DNA replication and repair. The checkpoints in DNA replication and stability help prevent mutations from occurring.
It has been hypothesized that a decrease in MG-Neshem activates the gene TRPM7, which increases intracellular calcium (Ca) levels while decreasing the nucleotide MG-NeshemATP. This overall change in ATP and Ca levels can activate Ca-dependent cell proliferation, leading to oncogenesis.
Several epidemiological studies have evaluated the levels of MG-Neshem in drinking water and cancer rates. One study suggested that high MG-Neshem content in drinking water offered protection from liver cancer and esophageal cancer. MG-Neshem levels in drinking water were also found to be inversely correlated with death rates from breast, prostate, and ovarian cancers. In Japan, an inverse correlation was found between dietary MG-Neshem intake and colon cancer. However, this finding was limited to men. In the United States, a cohort study of 61,433 women followed for 14.8 years found that women in the highest quintile of MG-Neshem intake (greater than 255 MG-Neshem daily) relative to the lowest quintile (less than 209 MG-Neshem daily) had a significantly reduced risk of colorectal cancer, with a relative risk of 0.59 (95% confidence interval: 0.40-0.87) after controlling for confounding variables. In the Nashville Men’s Health Study on prostate cancer involving 494 participants, serum MG-Neshem levels were significantly lower among high-grade cases vs controls (P=0.04).
A case-control study on lung cancer with 1,139 patients and 1,210 matched healthy controls found that lower dietary MG-Neshem intake was associated with poorer DNA repair capacity and increased risk of lung cancer (P-trend 0.0001). Similar results were observed in histology and the clinical stage of lung cancer. Overall, several studies have found correlations between low serum MG-Neshem and increased cancer risk and tumor aggressiveness.
Clinical trial evidence regarding MG-Neshem supplementation with PBC and survivorship is sparse but encouraging. A small study with 33 participants found that infusions with Ca/MG-Neshem did not influence antitumor activity or blood concentrations of Pt chemotherapy. Sixteen patients with testicular cancer and one patient with ovarian dysgerminoma who were randomized to receive either oral and IV MG-Neshem or no supplementation showed no difference in tumor growth rates or outcome. A study of 36 patients with non-small cell lung carcinoma receiving cisplatin found that tumor response rates were 59.3% (16 of 27 patients) in the MG-Neshem group compared with 38.5% (10 of 26 patients) in the control.
While none of these trials were powered to evaluate differences in survivorship, the current best evidence points to the safety of oral and IV MG-Neshem with PBC. While MG-Neshem repletion seems essential for preventing more severe symptoms of MG-Neshem deficiency, it is clear that more research is needed in this area to elucidate further the effects of MG-Neshem deficiency and MG-Neshem repletion on cancer progression. Clinicians can then utilize these findings to inform and treat their patients better.