A previously healthy 51-year-old woman presented to the emergency department with a 2-month history of dyspnea. The physical examination was notable for diminished breath sounds at both lung bases and a firm, nontender pelvic mass that appeared to originate from the left ovary. A chest radiograph showed pleural effusions that were greater on the right side than on the left (Panel A). Analysis of a pleural fluid sample revealed a sterile exudate with negative cytologic findings. Computed tomography of the abdomen (Panel B, coronal view) showed a pelvic mass (asterisk) and perihepatic ascites (arrows). The CA-125 level was 1794.0 IU per milliliter (reference value, <35.0). During a subsequent exploratory laparotomy, a left ovarian tumor was found. There were no peritoneal metastases. The solid, smooth tumor was excised (Panel C) and identified on histopathological analysis as a fibroma. Cytologic testing of the ascitic fluid was negative for a malignant condition. A diagnosis of Meigs’ syndrome — the triad of a benign ovarian tumor, ascites, and pleural effusion — was made. Meigs’ syndrome mimics ovarian cancer, but excision of the tumor results in the resolution of ascites and pleural effusion. Radiography was performed 3 weeks after surgery, at which time the patient’s symptoms, effusions, and ascites had abated.
Although the past several years have seen substantial advances in the understanding of molecular and cellular mechanisms regulating sodium, potassium, calcium, bicarbonate, and volume homeostasis in health and disease,1-3 there has been a paucity of clinically relevant information about disorders of magnesium. Around 1980, magnesium was described as the “forgotten electrolyte,”4 even though it was and remains recognized as “nature’s … calcium blocker.”5 Reasons for the apparent lack of appreciation for the clinical significance of magnesium may be due, at least in part, to the lack of information regarding the regulatory processes of this cation at the cellular, tissue, and systems levels.
Although Murphy suggested at the turn of the millennium that it was high time to “unravel … the mysteries of magnesium,”6 her call was heeded only recently, with a growing appreciation of the role of magnesium in clinical medicine. This change has been facilitated by the discovery of magnesium-specific channels and transporters, as well as the characterization of physiological and hormonal processes that regulate magnesium homeostasis.7 This review focuses on recent discoveries in how magnesium functions in the body, concentrating on hypomagnesemia, the most common clinical magnesium disorder. Hypermagnesemia is rare and occurs primarily in patients with kidney disease who are receiving magnesium-retaining drugs.8
Magnesium as Vital for Cell Function and Health
Typically, magnesium exists as the Mg2+ ion. It is present in all cells in all organisms from plants to higher mammals and is indispensable for health and life because it is an essential cofactor for ATP, the cellular source of energy.9 Magnesium is involved in major cellular and physiological processes, primarily through its nucleotide-binding properties and its regulation of enzymatic activity.10 All ATPase reactions require Mg2+–ATP, including those involved in RNA and DNA functions. Magnesium is a cofactor for hundreds of enzymatic reactions in every cell type (Figure 1).10,11 Furthermore, magnesium regulates glucose, lipid, and protein metabolism.12 Magnesium is involved in the control of neuromuscular function, regulation of cardiac rhythm, modulation of vascular tone, hormone secretion, and N-methyl-D-aspartate (NMDA) release in the central nervous system.10 Magnesium is a second messenger involved in intracellular signaling and a regulator of circadian-clock genes, which control circadian rhythm in biologic systems.13,14
FIGURE 1
Magnesium and Cell Function.
KEY POINTS
MAGNESIUM DISORDERS
•
The normal serum magnesium concentration in adults is 1.7 to 2.4 mg per deciliter (0.7 to 1.0 mmol per liter) and is tightly controlled through intestinal absorption, renal excretion, and storage in bone.
•
Hypomagnesemia is present in 3 to 10% of the general population, but its prevalence is increased among persons with type 2 diabetes and hospitalized patients, especially those in the intensive care unit.
•
Hypomagnesemia is usually associated with other electrolyte derangements, including hypocalcemia, hypokalemia, and metabolic alkalosis, and refractory hypokalemia is often responsive to treatment only after the magnesium concentration has been normalized.
•
Patients with hypomagnesemia often present with nonspecific symptoms, such as lethargy, muscle cramps, or muscle weakness, and thus the diagnosis of magnesium deficiency may be overlooked.
•
Many drug classes, such as antibiotics, diuretics, biologic agents, immunosuppressants, proton-pump inhibitors, and chemotherapies, cause renal magnesium loss and hypomagnesemia.
•
In 80% of patients with familial hypomagnesemia, pathogenic variants in genes that encode for magnesium transport pathways have been identified.
Magnesium Transporters and Their Roles
Because of the fundamental nature of magnesium in the regulation of cell function and signaling, intracellular magnesium levels need to be tightly controlled. Magnesium-specific carriers were originally identified in the 1950s in bacteria, fungi, and yeast.15,16 But it was some 50 years later that magnesium-selective transporters were identified as gatekeepers of human magnesium homeostasis.17-19
Among the first magnesium transporters characterized in humans were the transient receptor potential cation channel subfamily M members 6 and 7 (TRPM6 and TRPM7).17-20 TRPM6 is expressed primarily in the colon and distal convoluted tubule of the kidney and is responsible for magnesium reabsorption in the intestine and kidney (Figure 2).10,18 The clinical significance of TRPM6 was first realized when TRPM6 mutations were linked to hypomagnesemia and secondary hypocalcemia (HSH) as well as to other hypomagnesemia-associated syndromes.18 In mice, homozygous deletion of Trpm6 is lethal to the embryo, whereas its heterozygous deletion leads to hypomagnesemia that is refractory to magnesium supplementation.21,22 Unlike TRPM6, TRPM7 is ubiquitously expressed and is essential for cell viability and life itself.21,22 Homozygous Trpm7-knockout mice do not survive the embryonic stage, whereas Trmp7 heterozygotes have hypomagnesemia, blunted growth, and vascular dysfunction.23 Numerous factors that influence TRPM6 and TRPM7 activity have been described as magnesiotropic (involving magnesium regulation), including epidermal growth factor (EGF), fibroblast growth factor 23 (FGF23), uromodulin, adenosine disphosphate (ADP) ribosylation factor–like protein 15, aldosterone, angiotensin II, bradykinin, and insulin.10,24–26
FIGURE 2
Mechanisms of Magnesium Transport in the Kidney.
Other magnesium transporters include solute carrier family 41 members 1, 2, and 3; cyclin and CBS domain divalent metal cation transport mediators 1 through 4 (CNNM1 through CNNM4); and the magnesium-selective mitochondrial RNA splicing protein 2 (MRS2).7,12 MAGT1, originally described as a magnesium transporter, is a facilitator of N-linked protein glycosylation that indirectly influences magnesium transport and homeostasis.27
Coordinated Control of Magnesium Balance
The body contains approximately 25 g of magnesium, with the majority stored in bones and soft tissues (Figure 3A). Magnesium is an intracellular ion and second only to potassium as the most abundant intracellular cation.10 In cells, 90 to 95% of magnesium is bound to ligands (ATP, ADP, citrate, proteins, and nucleic acids). Only 1 to 5% of intracellular magnesium exists as free magnesium. The intracellular concentration of free magnesium is 1.2 to 2.9 mg per deciliter (0.5 to 1.2 mmol per liter), which is similar to the extracellular concentration. In plasma, 30% of the circulating magnesium is bound to proteins, mostly through free fatty acids.28 Therefore, patients with chronically high levels of free fatty acids generally have a lower blood magnesium concentration, and plasma magnesium levels are inversely proportional to the risk of cardiovascular and metabolic diseases.28 Changes in free fatty acids and levels of EGF, insulin, and aldosterone may contribute to variability in blood magnesium levels.10 At a systems level, magnesium is regulated primarily by three organs: the intestine, where dietary magnesium absorption is regulated; the bone, which stores magnesium as hydroxylapatite; and the kidney, which regulates urinary magnesium excretion.10 These systems are integrated and highly coordinated and constitute the intestine–bone–kidney axis responsible for magnesium uptake, exchange, and excretion, respectively. Disturbances in this balance have pathophysiological consequences.
FIGURE 3
Magnesium Homeostasis and Signs and Symptoms of Hypomagnesemia and Therapeutic Approaches.
The Intestine–Bone–Kidney Axis and Magnesium Homeostasis
Dietary sources rich in magnesium include cereals, beans, nuts, and green vegetables (magnesium is the central core of chlorophyll). Of the total dietary magnesium consumed, 30 to 40% is absorbed in the intestine.10 Most absorption occurs in the small intestine through paracellular transport (passage of molecules between cells), which is a passive process and involves tight junctions (complexes that form the intercellular barrier between cells).29 Fine-tuning of magnesium absorption occurs in the large intestine by transcellular mechanisms involving TRPM6 and TRPM7.21,30,31 Genetic inactivation of intestinal TRPM7 causes severe deficiency in magnesium, zinc, and calcium and is incompatible with early postnatal growth and survival.26,31 Intestinal magnesium absorption is influenced by factors such as dietary magnesium, intestinal lumen pH, hormones (estrogen, insulin, EGF, FGF23, and parathyroid hormone [PTH]), and gut microbiota.26,31–34
In the kidney, magnesium reabsorption by the nephron is facilitated by paracellular and transcellular pathways.33Unlike most ions (e.g., sodium and calcium), only a small amount (20%) of magnesium is reabsorbed in the proximal tubule, whereas most magnesium (70%) is taken up by the thick ascending limb of the loop of Henle.10 In the proximal tubule and the thick ascending limb of the loop of Henle, magnesium reabsorption is paracellular, mainly driven by concentration gradients and membrane potential. Claudins 16 and 19 form the magnesium pores in the thick ascending limb of the loop of Henle, whereas claudin 10b contributes to the lumen-positive transepithelial voltage that drives paracellular transport.29 Along the distal convoluted tubule, fine-tuning of transcellular reabsorption of magnesium (5 to 10%) is mediated through apical TRPM6 and TRPM7, which determines the final urinary magnesium excretion.33,35
Magnesium is a key component of bone — 60% of the total magnesium in the body is stored in this compartment. Exchangeable magnesium in bone provides a dynamic reservoir to maintain physiologic plasma concentrations.10 It also contributes to the biologic process of bone formation by influencing activation of osteoblasts and osteoclasts.36 High magnesium intake results in increased bone mineral content, which is important in reducing the risk of bone fractures and osteoporosis during aging.37 Magnesium has a biphasic effect in bone repair. During acute phases of inflammation, magnesium promotes increased expression of TRPM7 in macrophages, magnesium-dependent cytokine production, and a pro-osteogenic immune microenvironment.38 In the later remodeling phases of bone healing, magnesium influences osteogenesis and suppresses hydroxyapatite precipitation. TRPM7 and magnesium are also involved in vascular calcification by influencing phenotypic switching of vascular smooth-muscle cells to an osteogenic phenotype.39
Hypomagnesemia
The normal serum magnesium concentration in adults is 1.7 to 2.4 mg per deciliter (0.7 to 1.0 mmol per liter). Hypomagnesemia is defined as serum magnesium levels below 1.7 mg per deciliter.10,40 Most patients with borderline hypomagnesemia are asymptomatic.41,42 Because patients can present with chronic latent magnesium deficit at serum magnesium levels above 1.5 mg per deciliter (0.6 mmol per liter), it has been suggested to raise the low cutoff point that defines hypomagnesemia.41 However, this level is controversial and awaits further clinical validation.42Hypomagnesemia is present in 3 to 10% of the general population, but its prevalence is increased among persons with type 2 diabetes (10 to 30%) and hospitalized patients (10 to 60%), especially those in the intensive care unit (ICU) (>65%).43 Data from several cohorts indicate that hypomagnesemia is associated with an elevated risk of death from any cause and death from cardiovascular causes.43,44
The Clinical Spectrum of Hypomagnesemia
Hypomagnesemia may result from inadequate dietary intake, increased gastrointestinal loss, reduced renal reabsorption, or redistribution of magnesium from the extracellular to the intracellular space. Patients with hypomagnesemia often present with nonspecific symptoms, such as lethargy, muscle cramps, or muscle weakness (Figure 3B).42 Hypomagnesemia is usually associated with other electrolyte derangements, including hypocalcemia, hypokalemia, and metabolic alkalosis. Consequently, the presence of hypomagnesemia may be overlooked, especially because the serum magnesium level is not routinely measured in most clinical settings. Only in severe cases of hypomagnesemia (serum magnesium level, <1.2 mg per deciliter [0.5 mmol per liter]) do symptoms such as neuromuscular irritability (carpopedal spasm, seizures, and tremors), cardiovascular abnormalities (arrhythmias and vasoconstriction), and metabolic disorders (insulin resistance and chondrocalcinosis) become evident.45 The clinical importance of magnesium is highlighted by findings that low serum magnesium levels are associated with an increased incidence of hospitalization and increased mortality, especially when associated with concurrent hypokalemia.46
Of clinical relevance, less than 1% of the magnesium in the body is in plasma, and hence plasma magnesium is not a reliable marker of the total content in tissues.47 Controlled depletion–repletion studies in metabolic units have shown that even though serum magnesium concentration may be normal, intracellular stores can be depleted.47 Therefore, the use of blood magnesium levels alone, without consideration of dietary magnesium intake and urinary loss, probably underestimates magnesium deficiency in the clinic.48
Hypocalcemia, Hypokalemia, and Hypomagnesemia
Hypokalemia is common in patients with hypomagnesemia.49 Refractory potassium repletion is often linked to magnesium depletion and is corrected only after the magnesium deficit has been normalized.50 Magnesium deficiency amplifies renal potassium loss by promoting potassium secretion in the collecting duct. Decreased intracellular magnesium levels inhibit Na+–K+–ATPase pump activity51 and increase the opening of renal outer medullary potassium (ROMK) channels,50,52 leading to renal potassium loss. The interplay between magnesium and potassium also involves activation of the Na+–Cl− cotransporter (NCC), which promotes sodium reabsorption.52,53 Magnesium deficiency decreases the abundance of NCC through an E3 ubiquitin protein ligase called neuronal precursor cell developmentally down-regulated 4-2 (NEDD4-2) and prevents NCC activation by hypokalemia.54 Sustained NCC down-regulation enhances distal Na+ delivery during states of hypomagnesemia, promoting kaliuresis and hypokalemia.
Hypocalcemia is also frequently linked to hypomagnesemia.18,33 Magnesium deficiency suppresses the release of PTH and decreases renal sensitivity to PTH.55 The decreased PTH level leads to reduced renal reabsorption of calcium, calciuria, and secondary hypocalcemia. Hypocalcemia resulting from hypomagnesemia-induced hypoparathyroidism is refractory to correction until the magnesium concentration is normalized.55
Drug-Induced Hypomagnesemia
Many drug classes, such as antibiotics, diuretics, biologic agents, immunosuppressants, proton-pump inhibitors (PPIs), and chemotherapies, may cause magnesium wasting and hypomagnesemia (Figure 4).56 Long-term use of PPIs causes magnesium deficiency in approximately 20% of patients receiving them, and these effects are dose-dependent.57,58 PPIs reduce intestinal magnesium uptake and are associated with changes in luminal pH and the gut microbiome.58 The reasons why only some patients are prone to PPI-induced hypomagnesemia may relate to the dose and duration of PPI therapy, dietary magnesium intake, cotreatment with other magnesium-losing drugs, and gut microbiome flora. Oral inulin has been reported to improve serum magnesium levels in patients with PPI-induced hypomagnesemia, through increased gastrointestinal absorption.59
FIGURE 4
Drug-Induced Hypomagnesemia.
Most cases of drug-induced hypomagnesemia are explained by renal magnesium wasting. Calcineurin inhibitors, cisplatin, EGF receptor (EGFR) antagonists (e.g., cetuximab and erlotinib), and mammalian target of rapamycin inhibitors cause hypomagnesemia in 20 to 40% of patients receiving them, primarily through reduced TRPM6 and TRPM7 activity in the distal convoluted tubule.59,60
Nondrug Causes of Hypomagnesemia
Hypomagnesemia is the most common electrolyte abnormality associated with chronic alcohol use disorder.61 Underlying mechanisms include decreased magnesium intake in malnourished persons, increased gastrointestinal loss, and magnesuria due to alcohol-induced renal tubular damage.61 The presence of hypomagnesemia in persons with alcohol use disorder is often associated with liver dysfunction and worse prognosis of their liver disease.
Hypomagnesemia is commonly observed in patients with type 2 diabetes mellitus.44,62 Renal magnesium wasting and increased albumin binding in the blood are probably the causes of hypomagnesemia. Insulin activates TRPM6 activity in the distal convoluted tubule.34,62 Consequently, insulin resistance results in decreased renal magnesium reabsorption and increased magnesuria.
Aberrant magnesium homeostasis is also associated with cardiovascular disease.44,63 In the heart, hypomagnesemia confers a predisposition to electrical irritability and arrhythmias, including atrial fibrillation, torsades de pointes, and long QT syndrome.10 In the vascular system, low magnesium levels are associated with endothelial dysfunction, vascular contraction, increased vascular tone, and vascular fibrosis — characteristic features of hypertension.63,64 These vascular effects involve alterations in TRPM7 activity and impaired magnesium influx in vascular cells and are especially evident in hyperaldosteronism.65
Preeclampsia and eclampsia are hypertensive diseases of pregnancy that are characterized by abnormal trophoblast invasion, endothelial dysfunction, and vascular inflammation. Serum magnesium levels may be normal or decreased in both conditions.66 Although the causes of preeclampsia and eclampsia are unknown, intravenous magnesium treatment is beneficial and prevents or lessens complications. The protective effects of magnesium have been attributed to calcium-channel blockade and vasodilation.67 However other factors have been implicated, including decreased levels of fms-like tyrosine kinase 1 and endoglin, reduced oxidative stress, inhibition of brain NMDA receptors, decreased production of proinflammatory mediators, and down-regulation of TRPM6 and TRPM7.67
Autoantibodies against claudin 16 have been identified as a novel cause of hypomagnesemia, hypocalcemia, and tubulointerstitial nephropathy.68 This finding suggests that autoimmunity could be a novel cause of hypomagnesemia.
Hereditary Hypomagnesemia
Identification of pathogenic variants in genes that encode for magnesium transport pathways and their regulators have led to a putative genetic cause of familial hypomagnesemia in approximately 80% of patients (Table S1 in the Supplementary Appendix, available with the full text of this article at NEJM.org). Most genetically based causes of hypomagnesemia affect magnesium reabsorption in the distal convoluted tubule.10,33 Mutations in TRPM6 and TRPM7 subunits lead to HSH.18,69 Hypocalcemia in such patients is explained by hypoparathyroidism, caused by low intracellular magnesium levels in the parathyroid gland, which impair PTH secretion.18,33 Pathogenic variants in EGF and EGFR result in hypomagnesemia and renal magnesium wasting, because of reduced TRPM6 activity.10,60 Pathogenic variants in CNNM2 cause hypomagnesemia, seizures, and cognitive deficiency.70 CNNM2 is expressed in the distal convoluted tubule and regulates basolateral magnesium extrusion, although the molecular mechanism is unclear.17,33,70
Gitelman’s syndrome is primarily a sodium-wasting disorder caused by mutations in the NCC.33,54,71 However, patients with Gitelman’s syndrome present with hypomagnesemia, hypokalemia, and metabolic alkalosis. The cause of hypomagnesemia in this syndrome is elusive, but preclinical data indicate that atrophy of the distal convoluted tubule, which occurs when NCC is defective, may explain reduced magnesium reabsorption.54,71
Pathogenic variants in the mitochondrial transfer RNAs for isoleucine and phenylalanine (MT-TI and MT-TF) are associated with a Gitelman’s syndrome–like phenotype with hypomagnesemia.33,72 These mutations are associated with decreased activity of mitochondrial electron transport chain complex 4. Consequently, impaired cellular ATP production may reduce basolateral Na+–K+–ATPase activity and inhibit the NCC.
NCC activity is regulated by phosphorylation of its intracellular N-terminal domain. A mechanism called the potassium switch may explain how low extracellular potassium results in hyperpolarization of the basolateral membrane and activation of NCC.3,33 Mutations in potassium-switch genes encoding the basolateral potassium channel (KCNJ10 and KCNJ16), chloride channel (CLCNKB and BSND), and the Na+–K+–ATPase complex (ATP1A1 and FXYD2) lead to a phenotype similar to Gitelman’s syndrome, including hypomagnesemia.33,73,74 Patients with mutant HNF1B are prone to renal malformations, kidney cysts, and maturity-onset diabetes of the young (MODY5).74
Mutations in CLDN16 and CLDN19, which encode tight-junction proteins claudin 16 and claudin 19, result in familial hypomagnesemia, hypercalciuria, and nephrocalcinosis.29,75,76 Claudins 16 and 19 form a cation-selective pore that allows the paracellular reabsorption of calcium and magnesium in the thick ascending limb of the loop of Henle.10,29 Clinically, patients carrying pathogenic variants in CLDN19 are distinguished from those with variants in CLDN16 by the presence of ocular defects.75 The main regulators of paracellular divalent cation transport in the thick ascending limb of the loop of Henle are PTH and calcium-sensing receptor. Pathogenic variants in RAS-related GTP binding D (RRAGD) have been identified as a cause of a kidney tubulopathy phenotype reminiscent of the familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC) phenotype combined with dilated cardiomyopathy.77
Evaluating Hypomagnesemia in the Clinic
Measurement of total serum magnesium is the standard approach to determine magnesium status in the clinic. It provides a rapid evaluation of short-term changes in magnesium status but may underestimate the total body content of magnesium.42,47,48 Endogenous factors (hypoalbuminemia) and exogenous factors (hemolyzed specimens and sample-tube anticoagulants [e.g., EDTA]) can influence magnesium measurements and need to be considered when blood results are interpreted. Serum ionized magnesium can also be measured, but the clinical usefulness is unclear.
When hypomagnesemia is diagnosed, the cause is usually apparent from the patient’s history. However, if there is no clear underlying cause, it is important to distinguish between renal and gastrointestinal magnesium losses with the use of specific diagnostic approaches, such as 24-hour magnesium excretion, fractional excretion of magnesium, and the magnesium-loading test.42,47,48
Magnesium Replacement
The feasibility of magnesium replacement is the basis for managing hypomagnesemia. Yet, there are no clear treatment guidelines for hypomagnesemia; thus, approaches depend largely on the presence and severity of clinical manifestations. Mild hypomagnesemia is managed with oral supplements. Many magnesium preparations are available, and they have variable absorption rates. The most effectively absorbed forms are organic salts (magnesium citrate, aspartate, glycinate, gluconate, and lactate) rather than inorganic salts (magnesium chloride, carbonate, and oxide).78 However, a common side effect of oral magnesium supplementation is diarrhea, which poses a challenge for oral replacement.
In resistant cases, adjuvant drug therapies may be necessary. Pharmacologic inhibition of the epithelial sodium channel with amiloride or triamterene in patients with normal renal function increases serum magnesium levels.10,42 Other potential strategies include inhibitors of sodium–glucose cotransporter type 2,79 which increase serum magnesium levels, especially in patients with diabetes. Mechanisms that underlie these effects are unclear, but decreased glomerular filtration and increased renal tubular reabsorption may be important. Parenteral therapy is indicated in patients whose hypomagnesemia is refractory to oral treatment, such as those with short-bowel syndrome, those with tetany or seizures, and those whose condition is hemodynamically unstable with arrhythmias or associated hypokalemia and hypocalcemia.42 PPI-induced hypomagnesemia responds favorably to oral inulin through mechanisms that might involve alterations in gut microbiota.58,59
Magnesium as a Therapeutic Agent
Despite the many conditions in which magnesium has been implicated, there are only a few medical conditions in which magnesium is the therapeutic agent of choice. These include torsades de pointes, acute asthma exacerbations, and preeclampsia or eclampsia (clinical vignettes are provided in the Supplementary Appendix). Patients with torsades de pointes that is refractory to beta-blockers should be treated with magnesium. In severe asthma exacerbations with an inadequate response to intensive initial treatment and in patients with life-threatening asthma, clinical guidelines recommend intravenous magnesium sulfate.42 Nebulized magnesium sulfate when added to inhaled β2-agonists and ipratropium bromide may have additional benefit for lung function and may decrease or shorten hospital admissions. Beneficial effects of magnesium in asthma probably involve calcium-channel blockade in bronchial smooth muscle, resulting in bronchodilation.80
According to international clinical guidelines on the treatment of hypertension in pregnancy, women with eclampsia should receive magnesium sulfate to prevent seizures.81 Women with preeclampsia who have proteinuria and severe hypertension or hypertension with neurologic signs and symptoms should be treated with magnesium sulfate to prevent eclampsia.81 Although these disorders are responsive to magnesium sulfate, the exact mechanisms whereby magnesium mediates clinical benefit are unclear.
Conclusions
Magnesium is a vital but often poorly understood electrolyte in clinical medicine. It is often not measured as part of routine electrolyte screening. Hypomagnesemia is often asymptomatic. Although the exact mechanisms that regulate body magnesium homeostasis are still poorly defined, there have been advances in the understanding of renal magnesium handling. This understanding is attributable largely to gene screening panels and whole-exome sequencing that have identified new genes causing rare forms of inherited hypomagnesemia. Many drugs cause hypomagnesemia. Hypomagnesemia is common in hospitalized patients and is a risk factor for a prolonged ICU stay. Hypomagnesemia should be corrected with magnesium replacement therapy in the form of the organic salt preparation. Although there is still much to be learned about magnesium and its regulation in health and disease, the field has advanced, and clinicians should be more attuned to the importance of magnesium in clinical medicine.
A 3-year-old boy who had been born prematurely was brought to the emergency department with a 1-day history of intermittent abdominal pain, nausea, and vomiting. He had had no bloody stools or contact with persons known to be sick. His vital signs were normal. An abdominal examination was notable for hypoactive bowel sounds and tenderness in the right lower quadrant. Ultrasonography of the right lower abdomen showed a target-sign lesion measuring 1.7 cm by 1.4 cm (Panel A). A longitudinal view of the same lesion showed a 2.4-cm segment of the small intestine telescoping into itself — a finding known as the “sleeve sign” (Panel B). A diagnosis of ileoileal intussusception was made. Intussusception is the most common cause of bowel obstruction in children. In most cases, small-bowel intussusception reduces spontaneously. In this case, the patient’s symptoms and abnormal findings on ultrasonography abated 30 minutes after the initial ultrasound examination. The patient was monitored in the hospital for 1 day. He had no recurrence of abdominal pain and was discharged. Three days after presentation, a follow-up abdominal ultrasound examination was performed, and no mass serving as a pathologic lead point was identified. As in most cases of pediatric small-bowel intussusception, the patient’s episode was considered to be idiopathic.
An inflammatory bone marrow microenvironment contributes to acquired bone marrow failure syndromes. CK0801, an allogeneic T regulatory (Treg) cell therapy product, can potentially interrupt this continuous loop of inflammation and restore hematopoiesis.
METHODS
In this phase 1 dose-escalation study of CK0801 Treg cells, we enrolled patients with bone marrow failure syndromes with suboptimal response to their prior therapy to determine the safety and efficacy of this treatment for bone marrow failure syndromes.
RESULTS
We enrolled nine patients with a median age of 57 years (range, 19 to 74) with an underlying diagnosis of aplastic anemia (n=4), myelofibrosis (n=4), or hypoplastic myelodysplasia (n=1). Patients had a median of three prior therapies for a bone marrow failure syndrome. Starting dose levels of CK0801 were 1 × 106 (n=3), 3 × 106 (n=3), and 10 × 106 (n=3) cells per kg of ideal body weight. No lymphodepletion was administered. CK0801 was administered in the outpatient setting with no infusion reactions, no grade 3 or 4 severe adverse reactions, and no dose-limiting toxicity. At 12 months, CK0801 induced objective responses in three of four patients with myelofibrosis (two had symptom response, one had anemia response, and one had stable disease) and three of four patients with aplastic anemia (three had partial response). Three of four transfusion-dependent patients at baseline achieved transfusion independence. Although the duration of observation was limited at 0.9 to 12 months, there were no observed increases in infections, no transformations to leukemia, and no deaths.
CONCLUSIONS
In previously treated patients, CK0801 demonstrated no dose-limiting toxicity and showed evidence of efficacy, providing proof of concept for targeting inflammation as a therapy for bone marrow failure.
A right-handed adult with a history of an unruptured arteriovenous malformation (AVM) presents with increasing frequency and intensity of partial seizures despite maximum medical management. Magnetic resonance imaging (MRI) (Fig. 1A and 1B) shows a 2 × 4.7 cm AVM in the right frontal lobe just anterior to the motor cortex with deep venous drainage to the right lateral ventricle and deep middle cerebral vein (Spetzler-Martin grade 4). The patient elects for embolization followed by stereotactic radiosurgery (SRS). Partial embolization by SRS is performed, with 16 Gy delivered to the margin of the residual nidus (Fig. 2). Six months post-SRS, the patient is asymptomatic with minimal changes on MRI (Fig. 1C). However, 11 months post-SRS, the patient presents with new-onset severe headaches, multiple seizures, and progressive left-sided weakness. MRI (Fig. 1D) shows more conspicuous AVM flow-voids, substantial vasogenic edema, a 7 mm midline shift, and thrombosis of a large cortical draining vessel.
Fig. 1Magnetic resonance imaging of right frontal lobe. (A) Pretreatment T2 imaging, (B) pretreatment T1 with contrast (C) T2 6 months post-stereotactic radiosurgery (SRS) with mild vasogenic edema surrounding the arteriovenous malformation, (D) T2 11 months post-SRS with substantial vasogenic edema.Fig. 2Stereotactic radiosurgery treatment plan shown as percentages of the prescription dose (16 Gy). V12 Gy = 22.4 mL.
How did the self-expanding supraannular valve compare with the balloon-expandable valve in this trial?
Herrmann et al. conducted a trial in which the self-expanding supraannular valve was compared with the balloon-expandable valve in patients with symptomatic severe aortic stenosis and a small aortic-valve annulus who were undergoing transcatheter aortic-valve replacement (TAVR).
Clinical Pearls
Q: Have the different types of TAVR prostheses been compared in randomized trials?
A: On the basis of multiple prospective randomized trials comparing TAVR with surgery, TAVR has emerged as the dominant treatment method for most patients with symptomatic severe aortic stenosis. Despite differences in their design, hemodynamic characteristics, and implantation techniques, different types of TAVR prostheses have been compared in relatively few randomized trials. In observational studies and randomized trials, the self-expanding supraannular valve has been shown to have better hemodynamic properties than balloon-expandable valves.
Q: What are the post-TAVR risks faced by patients with a small aortic annulus?
A: Patients with a small aortic annulus are an important subgroup of symptomatic patients with aortic stenosis, predominantly women, who undergo TAVR. Patients with a small annulus are at particular risk for high residual gradients and prosthesis–patient mismatch, which are associated with major adverse cardiovascular events, including death, heart failure, and reduced quality of life. Findings from a large national database showed that a mean echocardiographic gradient of greater than 22.5 mm Hg was associated with increased 5-year mortality. Severe prosthesis–patient mismatch after TAVR is also associated with reduced survival. Finally, impaired hemodynamic performance is associated with reduced valve durability.
Morning Report Questions
Q: How did the self-expanding supraanular valve compare with the balloon-expandable valve in this trial?
A: The two powered coprimary end points, both of which were assessed through 12 months, were a clinical outcome composite of death, disabling stroke, or rehospitalization for heart failure and a composite end point of bioprosthetic-valve dysfunction. Among patients who underwent TAVR, a self-expanding supraannular valve was noninferior to a balloon-expandable valve with respect to clinical outcomes and was superior with respect to bioprosthetic-valve dysfunction through 12 months. The Kaplan–Meier estimate of the percentage of patients with a first coprimary end-point was 9.4% in the self-expanding valve group and 10.6% in the balloon-expandable valve group (difference, −1.2 percentage points; 90% CI, −4.9 to 2.5; P<0.001 for noninferiority; hazard ratio, 0.90; 95% CI, 0.56 to 1.43). The Kaplan–Meier estimate of the percentage of patients with bioprosthetic-valve dysfunction through 12 months was 9.4% in the self-expanding valve group and 41.6% in the balloon-expandable valve group (difference, −32.2 percentage points; 95% CI, −38.7 to −25.6; P<0.001).
Q: What were some additional results of this trial?
A: The self-expanding valve was also superior to the balloon-expandable valve with respect to several hypothesis-tested secondary end points: mean gradient, effective orifice area, hemodynamic structural valve dysfunction, and bioprosthetic-valve dysfunction in women through 12 months, as well as moderate or severe prosthesis–patient mismatch at 30 days. No apparent differences in safety outcomes were found between the groups.
Summary: Low-level light therapy aids brain healing in patients with moderate traumatic brain injury (TBI). Using a helmet that emits near-infrared light, researchers observed increased brain connectivity within two weeks of treatment.
While the long-term effects are still unknown, the therapy shows promise for treating various neurological conditions. The study highlights the potential of light therapy as a non-invasive treatment.
Key Facts:
Study Findings: Light therapy increased brain connectivity in TBI patients within two weeks.
Research Method: 38 patients received therapy through a near-infrared light helmet.
Potential Applications: Light therapy could also treat PTSD, depression, and autism.
Source: RSN
Low-level light therapy appears to affect healing in the brains of people who suffered significant brain injuries, according to a study published today in Radiology.
Lights of different wavelengths have been studied for years for their wound-healing properties. Researchers at Massachusetts General Hospital (MGH) conducted low-level light therapy on 38 patients who had suffered moderate traumatic brain injury, an injury to the head serious enough to alter cognition and/or be visible on a brain scan.
Patients who received low-level light therapy showed a greater change in resting-state connectivity in seven brain region pairs during the acute-to-subacute recovery phase compared to the control participants.
Patients received light therapy within 72 hours of their injuries through a helmet that emits near-infrared light.
“The skull is quite transparent to near-infrared light,” said study co-lead author Rajiv Gupta, M.D., Ph.D., from the Department of Radiology at MGH. “Once you put the helmet on, your whole brain is bathing in this light.”
The researchers used an imaging technique called functional MRI to gauge the effects of the light therapy. They focused on the brain’s resting-state functional connectivity, the communication between brain regions that occurs when a person is at rest and not engaged in a specific task.
The researchers compared MRI results during three recovery phases: the acute phase of within one week after injury, the subacute phase of two to three weeks post-injury and the late-subacute phase of three months after injury.
Of the 38 patients in the trial, 21 did not receive light therapy while wearing the helmet. This was done to serve as a control to minimize bias due to patient characteristics and to avoid potential placebo effects.
Patients who received low-level light therapy showed a greater change in resting-state connectivity in seven brain region pairs during the acute-to-subacute recovery phase compared to the control participants.
“There was increased connectivity in those receiving light treatment, primarily within the first two weeks,” said study coauthor Nathaniel Mercaldo, Ph.D., a statistician with MGH.
“We were unable to detect differences in connectivity between the two treatment groups long term, so although the treatment appears to increase the brain connectivity initially, its long-term effects are still to be determined.”
The precise mechanism of the light therapy’s effects on the brain is also still to be determined. Previous research points to the alteration of an enzyme in the cell’s mitochondria (often referred to as the “powerhouse” of a cell), Dr. Gupta said.
This leads to more production of adenosine triphosphate, a molecule that stores and transfers energy in the cells. Light therapy has also been linked with blood vessel dilation and anti-inflammatory effects.
“There is still a lot of work to be done to understand the exact physiological mechanism behind these effects,” said study coauthor Suk-tak Chan, Ph.D., a biomedical engineer at MGH.
While connectivity increased for the light therapy-treated patients during the acute to subacute phases, there was no evidence of a difference in clinical outcomes between the treated and control participants.
Additional studies with larger cohorts of patients and correlative imaging beyond three months may help determine the therapeutic role of light in traumatic brain injury.
The researchers expect the role of light therapy to expand as more study results come in. The 810-nanometer-wavelength light used in the study is already employed in various therapeutic applications. It’s safe, easy to administer and does not require surgery or medications
The helmet’s portability means it can be delivered in settings outside of the hospital. It may have applications in treating many other neurological conditions, according to Dr. Gupta.
“There are lots of disorders of connectivity, mostly in psychiatry, where this intervention may have a role,” he said. “PTSD, depression, autism: these are all promising areas for light therapy.”
A common dietary supplement reduces aggression by 30%
Fish oil supplements containing omega-3 have long been touted as good for heart health. A new study has found they also reduce aggression. Researchers say the safe, common supplements should be used everywhere from the playground to the prison system.
Overt acts of aggression include verbal and physical violence and bullying. Then, there are covert signs like vandalism and property damage, fire-setting, and theft. Both can negatively affect relationships and have legal consequences. It goes without saying that, on many levels, society would be better off if aggressive behaviors were reduced. A new study may have discovered a way of doing that.
The study by researchers from the University of Pennsylvania (Penn) found that commonplace omega-3 supplements reduced aggression, regardless of age or gender.
“I think the time has come to implement omega-3 supplementation to reduce aggression, irrespective of whether the setting is the community, the clinic, or the criminal justice system,” said Adrian Raine, a Penn neurocriminologist and the lead and corresponding author of the study. “Omega-3 is not a magic bullet that is going to solve the problem of violence in society. But can it help? Based on these findings, we firmly believe it can, and we should start to act on the new knowledge we have.
Omega-3 has enjoyed a strange association with violent behavior for a while. Back in 2001, Dr Joseph Hibbeln, a senior clinical investigator at the US National Institutes of Health (NIH), published a study finding a correlation between the consumption of high amounts of fish (a rich source of omega-3) and lower homicide rates. The following year, the University of Oxford in the UK led a study where British prisoners were given nutritional supplements that included vitamins, minerals and essential fatty acids. The researchers found that prisoners given supplements were less violent and antisocial.
In addition to examining the effect of omega-3 supplements on aggression, the researchers in the current study particularly wanted to ascertain whether omega-3 was effective for all forms of aggression. In psychology, a distinction is made between ‘reactive’ aggression, an in-the-moment response to a perceived threat or provocation, and ‘proactive’ aggression, which requires planning.
The researchers conducted a meta-analysis of 29 randomized controlled trials that explicitly measured aggression in people who’d been given omega-3 supplements. They specifically focused on aggressive behavior and not broader traits like anger, which is viewed more as a feeling or emotion, and hostility, which is more of an attitude. Studies where additional nutritional supplements, such as calcium and vitamin D, were included, but the researchers examined them as a potential moderator.
A modest short-term effect linked to omega-3 supplementation, which the researchers say equates to a 30% reduction in aggression, was seen across age, gender, baseline diagnosis, treatment duration and dosage. Notably, omega-3 was found to reduce both reactive and proactive aggression. The researchers were limited to short-term data because only one out of the 19 laboratories conducting the studies followed up with participants after supplementation ended
The researchers explain how they think omega-3 exerts its effects. Previous studies have pointed to aggressive and violent behavior having a cognitive and neurochemical basis. And, omega-3 is known to play a critical role in brain structure and function, including regulating neurotransmitters and gene expression, and reduces brain inflammation.
“As such, given the undeniable fact that omega-3 is pervasively involved in multiple facets of neuronal biology, it is reasonable to believe that omega-3 supplementation could play a causal role in reducing aggression by upregulating brain mechanisms that may be dysfunctional in … individuals, given the assumption that there is, in part, a neurobiological basis to aggression,” said the researchers.
Further studies are needed to assess the long-term effectiveness of omega-3 supplementation on reducing aggression. Other research avenues would be using MRI scans to determine whether omega-3 enhances brain functioning and examining whether genetics affects omega-3 treatment. In the meantime, the researchers say there is little harm in people, including children, taking this widely available, safe and inexpensive dietary supplement.
“At the very least, parents seeking treatment for an aggressive child should know that in addition to any other treatment that their child receives, an extra portion or two of fish each week could also help,” Raine said.
And the researchers say omega-3 should be used in conjunction with existing psychological and psychiatric treatments.
“[W]e would argue that omega-3 supplementation should be considered as an adjunct to other interventions, whether they be psychological (e.g. CBT [cognitive behavioral therapy]) or pharmacological (e.g. [the antipsychotic drug] risperidone) in nature, and that caregivers are informed of the potential benefits of omega-3 supplementation,” the researchers said.
Exercise greatly benefits brain health, improving cognition, mood and reducing the risk of neurodegenerative diseases. Several new studies have demonstrated the profound impact of exercise on various biological systems, further explaining its ability to enhance health and fight disease. In this Special Feature, we explore the most recent research on how exercise can protect brain health as we age.
Recent studies examine the ways in which exercise helps prolong the health span, and maintains brain health with age. Image credit: FG Trade/Getty Images.
Exercise is linked to increased muscle strength, improved heart health, lower blood sugar and numerous other health benefits.
Activities such as running on a treadmill, biking up a steep hill, lifting weights or taking a brisk lunchtime walk offer a wide range of advantages that go beyond enhancing physical appearance or stamina.
Evidence from studies suggests that regular physical activity could boost mood, alleviate stress, and sharpen cognitive function, underscoring the deep connection between body and mind.
However, different people can respond quite differently to various forms of exercise, such as aerobic workouts or strength training.
While it is well-known that regular exercise is crucial for a healthy lifestyle, some older research has suggested that intense exercise might have negative effects.
More recent research, however, showed that elite athletes experienced slightly extended life expectancies over the decades.
Exercise significantly enhances brain health by improving cognition, mood and by reducing the risk of neurodegenerative diseases through promoting neurogenesis and synaptic plasticityTrusted Source.
What does the latest evidence and expert opinion have to say about the ways in which regular physical activity helps maintain brain, as well as general, health as we age?
In a new collaborative effort led by Stanford Medicine, researchers have explored the underlying mechanisms through which exercise promotes overall health, particularly brain health.
By understanding how exercise affects different organs at the molecular level, health care providers could tailor exercise recommendations more effectively.
This knowledge could also pave the way for developing drug therapies that mimic the benefits of exercise for those who are unable to engage in physical activity.
The study — whose findings appear in NatureTrusted Source — involved nearly 10,000 measurements across almost 20 types of tissues to examine the impact of 8 weeks of endurance exercise in lab rats trained to run on tiny treadmills.
Its conclusion reveals remarkable effects of exercise on the immune system, stress response, energy production and metabolism.
The researchers identified significant connections between exercise and molecules and genes that are already known to be involved in numerous human diseases and tissue recovery.
Other recent papers by Stanford Medicine researchers include a report in Nature CommunicationsTrusted Source that explores exercise-induced changes in genes and tissues associated with disease risk, and a paper published in Cell MetabolismTrusted Source, which examines the effects of exercise on mitochondria, the cellular energy producers, in various tissues, in rats.
The Nature study examined the effects of 8 weeks of endurance training on various biological systems, including gene expression (the transcriptome), proteins (the proteome), fats (the lipidome), metabolites (the metabolome), DNA chemical tags (the epigenome) and the immune system.
The researchers conducted analyses on different tissues in rats trained to run increasing distances and compared these with the tissues of sedentary rats.
They focused on mitochondria in the leg muscles, the heart, liver, kidney, white adipose tissue — which accumulates as body fat — as well as lungs, brain, and brown adipose tissue — a metabolically active fat that burns calories.
This comprehensive approach generated hundreds of thousands of results for non-epigenetic changes and over 2 million distinct epigenetic changes in the mitochondria, providing a rich database for future research.
Alongside the primary goal of creating a database, some notable findings emerged. For instance, the expression of mitochondrial genes changed with exercise across different tissues.
Researchers found that training upregulated genes in the mitochondria of skeletal muscle of rats that are downregulated in the mitochondria in the skeletal muscle of individuals with type 2 diabetes.
They also showed that training upregulated genes in the mitochondria in the livers of rats, that are down regulated in people with cirrhosis.
These two findings suggest that endurance training may help improve muscular function in diabetes, as well as boost liver health.
Finally, the researchers identified sex differences in how male and female rats’ tissues responded to exercise.
After 8 weeks, male rats lost about 5% of their body fat, while female rats did not lose a significant amount. However, the female rats maintained their initial fat percentage, whereas sedentary females gained an additional 4% body fat during the study.
The most dynamic difference was in mitochondrial gene expression after exercise in rats was in the adrenal glands.
The study authors propose that differences observed due to exercise are largely due to changes in mitochondrial genetic expression in organs and tissues responsible for maintaining energy balance.
Another study, this time completed by a research group from The University of Queensland in Australia, and published in Aging CellTrusted Source, demonstrated how exercise might deter or decelerate cognitive decline as individuals age.
Researchers examined gene expression in individual brain cells of mice, discovering that exercise profoundly influences gene expression in microglia, the immune cells supporting brain function in the central nervous system.
Specifically, exercise reverted the gene expression patterns of aged microglia to patterns akin to those seen in young microglia.
Experiments depleting microglia demonstrated their necessity for the beneficial effects of exercise on the creation of new neurons in the hippocampus, a brain region vital for memory, learning and emotion.
This study also revealed that providing mice access to a running wheel prevented or reduced the presence of T cells in the hippocampus as they aged.
These immune cells are typically absent in the youthful brain but increase with age.
Co-corresponding author Jana Vukovic, PhD, assistant professor and head of the neuroimmunology and cognition laboratory at The University of Queensland, explained the key findings to Medical News Today.
Vukovic explained that: “[T]he aging process affects all of the different cell types in the brain with the greatest impact on the resident immune cells: microglia. Importantly, exercise reverts the microglial gene profile back to their youthful state.”
Understanding how exercise supports brain health “is a key question for many scientists globally,” Vukovic noted, adding that she and her colleagues “propose that exercise alters the immune landscape in the ageing brain and therefore enables the immune cells to continue to support nerve cell function.”
“The role of microglia beyond being involved in clearance of cellular debris is not very well understood. We know that microglia support birth of new neurons in the hippocampus — a structure important for learning and memory. However, there could be many other mechanisms at play.”
Ryan Glatt, CPT, NBC-HWC, senior brain health coach and director of the FitBrain Program at Pacific Neuroscience Institute in Santa Monica, not involved in these studies, told MNT they “underscore the multifaceted benefits of exercise on brain health, particularly through gene regulation, mitochondrial function, and immune response.”
“They offer valuable insights by merging molecular biology with practical health interventions for aging populations,” he added.
For example, “exercise enhances synaptic plasticity and blood flow while reducing inflammation and increasing the expression of neurotrophic factors like BDNFTrusted Source,” Glatt explained. “These effects can synergistically improve memory, learning, and overall brain health.”
“Exercise can influence gene expression related to brain plasticity, inflammation, and metabolism, while also enhancing mitochondrial function and modulating immune responses. Hormonal changes due to physical activity can also contribute to improved mood and reduced stress.”
Vukovic noted that “there are ongoing studies to optimise exercise programs for elderly; however, Pilates is a good starting point for those who are looking to engage their muscles.”
Glatt agreed, adding that “aerobic exercises like cardiovascular exercise, strength training, and balance exercises are particularly beneficial to brain health, in both shared and unique ways.”
“Activities combining physical and cognitive challenges, like dance or tai chi, can be especially effective for certain aspects of brain health,” Glatt said.
Nevertheless, he cautioned that: “While exercise benefits brain health, individual variability due to genetics and baseline health can affect outcomes. Further research is needed to determine the long-term sustainability and optimal exercise types and intensities for different populations.”
Experts say the new findings add to evidence linking plastics pollution to disease, urge political action to reduce environmental toxins.
That plastic water bottle you regularly drink from could one day decompose into tiny particles that wreak havoc in your brain.
New research shows that nanoplastics—microscopic particles broken down from everyday plastic items—bind to proteins associated with Parkinson’s disease and Lewy body dementia.
These stealthy nanoparticles have already infiltrated our soil, water, and food supply. Now, they may pose the next great toxin threat, fueling a wave of neurodegenerative disease.
Plastic Cups, Utensils Identified as Risk Factors
Polystyrene nanoparticles, commonly found in plastic cups and utensils, bind to alpha-synuclein, a protein linked to Parkinson’s disease and Lewy body dementia, the new study from Duke University’s Nicholas School of the Environment and the Department of Chemistry at Trinity College of Arts and Sciences found. The plastic-protein accumulation was seen in test tubes, cultured neurons, and mouse models.
The most surprising finding was the tight bonds formed between the plastic and protein within neuron lysosomes, according to Andrew West, the study’s principal investigator. Lysosomes are digestive organelles within cells that use enzymes to break down waste materials and cellular debris.
“Our study suggests that the emergence of micro and nanoplastics in the environment might represent a new toxin challenge with respect to Parkinson’s disease risk and progression,” Mr. West said in a statement. This is especially concerning given the expected increase of these contaminants in our water and food, he noted.
Growing evidence indicates that nanoplastics circulate in the air, especially indoors. When inhaled, they can travel from the respiratory tract directly to the blood and brain, increasing cancer risk.
Change Environment Now to Prevent Disease Later: Expert
Our health today is largely a function of our environment in the past, Dr. Ray Dorsey, a professor of neurology at the University of Rochester in New York and author of “Ending Parkinson’s Disease,” told The Epoch Times.
“For example, the risk of lung cancer is a function of our past smoking habits,” he said. “If we want to live lives free of Parkinson’s disease, Alzheimer’s disease, and cancer in the future, we should pay attention to our environment today.”
The Duke study adds to evidence that common toxic pollutants may contribute to Parkinson’s disease, Dr. Dorsey said. While more research is needed, evidence from both laboratory and epidemiological studies suggests our environments are fueling a rise in Parkinson’s incidence.
“Much, if not most” of Parkinson’s cases may be preventable, he said.
Besides reducing our use of plastic, there are other effective precautions that we can take to limit our exposure to this environmental toxin, Dr. Dorsey pointed out. These include the following:
Using carbon filters to protect ourselves from chemicals in the water.
Purchasing organic food.
Thoroughly washing all fruits and vegetables.
Using air purifiers if living in areas with high air pollution.
Parkinson’s-Linked Pollutants, Pesticides Still Legal Despite Risks
Besides nanoplastics, other toxins have been linked to Parkinson’s, including organic pollutants known as polychlorinated biphenyls (PCBs), which were banned in 1979 but are still found in 30 percent of U.S. schools. Researchers have found high concentrations of this pollutant in the brains of deceased people who had Parkinson’s.
“We need to know the full extent of this toxic threat in our classrooms so that we can test for PCBs, remediate it, and inform families that their students may be at risk of exposure to these dangerous chemicals,” Sen. Edward J. Markey (D-Mass.) said in a statement.
Other toxins linked to Parkinson’s in our environment have yet to be removed from use. The Environmental Protection Agency (EPA) has proposed bans on dry cleaning chemicals and pesticides associated with a 500 percent increased risk of Parkinson’s disease, but there has been no action yet.
Toxic Pesticides Harming Health but ‘Political Will’ Lacking
The EPA banned the pesticide chlorpyrifos (CPF) in 2021, but a court reversed that decision in November 2022. Research identifies CPF as a likely Parkinson’s disease risk factor.Another pesticide, paraquat, has allegedly been linked to Parkinson’s by its manufacturer Syngenta’s own research, according to a report by The Guardian. Chinese-owned Syngenta reportedly created a “paraquat SWAT team” to criticize evidence and shift focus to other environmental factors.
“We increasingly know that environmental toxicants from plastics from pesticides are harming our health,” Dr. Dorsey said. “Almost all of these are addressable; the only question is whether we have the political will to do so.”
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