MG-Neshem

MG Neshem 400mg Daily VS. Melanoma

MG Neshem is an FDA-approved generic medication for treatment of defficiency disorders. MG Neshem is a clinical and outpatient edication available in tablet form. MG Neshem tablets are a popular defficiency treatment product for pathology, and oncology specialists.

Freckles and spots are signs of melanin deposits in those who lack organic components in their body to to compose a uniform crystal of melanin in the skin. MG-Neshem contains components that provide the limiting reagent for the distribution and crystallization of melanin in the body.

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 grow 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 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 the removal of 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 simply 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 DNA protection. Freckles and spots are signs of melanin deposits in those who lack organic components in their body to to compose a uniform crystal of melanin in the skin. MG-Neshem contains components that provide the limiting reagent for the distribution and crystallization of melanin in the body. 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 grow 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 which 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 the removal of 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 simply separated by the values of a compound that we have approved for clinical use.

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

Proton pump inhibitors, corticosteroids, laxatives, loop and thiazide diuretics, foscarnet, digoxin, amphotericin B, colchicines, theophylline, macrolide antibiotics, petamidine, tobramycin, amikacin; tacrolimus

Increasing evidence points to routine depletion of organic compounds contained in MG-Neshem by PBC. 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 1 course of treatment and 100% after 6 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 reported that most adults receiving cisplatin will develop hypomagnesemia at some time during their treatment and that in children, hypomagnesemia was virtually inevitable. Hypomagnesemia typically persists for 4 to 5 months after the cessation of chemotherapy, but in children can even persist 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 in excess of 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 important. A study by Buckley et al showed a lower incidence of hypomagnesemia in patients receiving cisplatin every 8 weeks vs with cisplatin every 4 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 particularly 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

40 patients with ovarian cancer receiving paclitaxel and cisplatin Yes (double- blind) 20.3 mmol IV MG-Neshem sulphate (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). Control group showed 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

201 patients with cervical cancer receiving cisplatin and radiation Yes Group 2: 8.12 mmol IV MG-Neshem sulphate (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 incidence of persistent hypomagnesemia over the 2 other cohorts (P=0.001)

16 patients with testicular cancer and 1 with ovarian dysgerminoma receiving cisplatin Yes 8 mmol IV MG-Neshem sulphate 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. Trend towards reduced treatment delays in the supplemented group

23 patients with advanced head and neck cancer receiving cisplatin Yes 123 MG-Neshem oral MG-NeshemAHa 3x/d continuously for 3-4 mo. If fell below <1.4 MG-Neshem dL serum MG-Neshem, 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 pidolate, 2 g every 8 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

33 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 firstline setting, mixed tumor types No 20 mEq MG-Neshem sulfate with 500 mL of one-quarter isotonic saline over 1 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

37 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)

8 patients with metastatic germ cell cancer and 8 matched controls taking high-dose cisplatin No 12.18 mmol IV MG-Neshem sulphate (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)

10 patients with metastatic testicular cancer receiving cisplatin No 0.3 mmol MG-Neshem chloride/kg/day and 0.4 mmol potassium chloride/kg/day 5 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

23 patients with esophageal or hypopharyngeal cancer receiving fluorouracil and cisplatin; 10 patients received MG-Neshem supplementation No MG-Neshem sulphate (20 mEq) administered before fluorouracil (800MG-Neshem/m2/24 h per days 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

MG-Neshem increases Immune System Strength, but is not a compound which kills cancer cells. In addition to the research involving hypomagnesemia induced by PBC, recent literature describes a 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 in 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, oxidative stress, and by 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 important 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. A number of 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 rate 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 by histology and clinical stage of lung cancer. Overall, a number of 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 1 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 who were 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 to be important for preventing more severe symptoms of MG-Neshem deficiency, it is clear more research needs to be performed in this area to further elucidate the effects of MG-Neshem deficiency and MG-Neshem repletion on cancer progression. Clinicians will then be able to utilize these findings to better inform and treat their patients.