Magnesium and Pain

Shin, Hyung-Jin; Na, Hyo Seok; Hwan, Sang

doi:10.3390/nu12082184

Cited by 99 publications

(71 citation statements)

References 118 publications

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“…Following absorption from the upper intestine, they can manage the muscle cells’ response to nerve stimuli through numerous functions [ 274 ]. Even though the tocolytic effect of magnesium has already been proven in vivo and in vitro, the best dosage for treating or preventing dysmenorrhea is not yet clear [ 275 ].…”

Section: Menstrual Disordersmentioning

confidence: 99%

Nutrition in Gynecological Diseases: Current Perspectives

et al. 2021

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Diet and nutrition are fundamental in maintaining the general health of populations, including women’s health. Health status can be affected by nutrient deficiency and vice versa. Gene–nutrient interactions are important contributors to health management and disease prevention. Nutrition can alter gene expression, as well as the susceptibility to diseases, including cancer, through several mechanisms. Gynecological diseases in general are diseases involving the female reproductive system and include benign and malignant tumors, infections, and endocrine diseases. Benign diseases such as uterine fibroids and endometriosis are common, with a negative impact on women’s quality of life, while malignant tumors are among the most common cause of death in the recent years. In this comprehensive review article, a bibliographic search was performed for retrieving information about nutrients and how their deficiencies can be associated with gynecological diseases, namely polycystic ovary syndrome, infertility, uterine fibroids, endometriosis, dysmenorrhea, and infections, as well as cervical, endometrial, and ovarian cancers. Moreover, we discussed the potential beneficial impact of promising natural compounds and dietary supplements on alleviating these significant diseases.

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Section: Menstrual Disordersmentioning

confidence: 99%

Nutrition in Gynecological Diseases: Current Perspectives

et al. 2021

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“…It was also demonstrated that hypermagnesemia reduced headshaking behavior in horses [19]. These actions of Mg have been attributed to its ability to block N-methyl-D-aspartate (NMDA) ionotropic receptors and voltage-dependent calcium channels, reducing neuronal excitability [1,2,21,22]. The inhibitory effect of Mg 2+ over NMDA receptor activity has also been the rationale for its use in acute brain injury, nociception, anesthesia, and behavioral disorders [1][2][3]19,21].…”

Section: Discussionmentioning

confidence: 99%

“…The clinical implications of short-term hypermagnesemia on behavior, cardiovascular function, and neuromuscular activity in horses were recently documented [2,3,19], further demonstrating that Mg is a pleiotropic ion. Magnesium supplementation is recommended for a number of human disorders and is being promoted as a pre-anesthetic to reduce pain [21]. In addition, due to its calcium-channel and NMDA receptor blocking properties and prolonged half-life in horses, MgSO 4 supplementation should be considered for conditions associated with nociception, neuronal hyperexcitability, and energy dysregulation [1,2,21].…”

Section: Plos Onementioning

confidence: 99%

“…Magnesium supplementation is recommended for a number of human disorders and is being promoted as a pre-anesthetic to reduce pain [21]. In addition, due to its calcium-channel and NMDA receptor blocking properties and prolonged half-life in horses, MgSO 4 supplementation should be considered for conditions associated with nociception, neuronal hyperexcitability, and energy dysregulation [1,2,21]. However, it is…”

Section: Plos Onementioning

confidence: 99%

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Effects of intravenous magnesium sulfate on serum calcium-regulating hormones and plasma and urinary electrolytes in healthy horses

et al. 2021

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Intravenous magnesium sulfate (MgSO4) is used in equine practice to treat hypomagnesemia, dysrhythmias, neurological disorders, and calcium dysregulation. MgSO4 is also used as a calming agent in equestrian events. Hypercalcemia affects calcium-regulating hormones, as well as plasma and urinary electrolytes; however, the effect of hypermagnesemia on these variables is unknown. The goal of this study was to investigate the effect of hypermagnesemia on blood parathyroid hormone (PTH), calcitonin (CT), ionized calcium (Ca2+), ionized magnesium (Mg2+), sodium (Na+), potassium (K+), chloride (Cl-) and their urinary fractional excretion (F) after intravenous administration of MgSO4 in healthy horses. Twelve healthy female horses of 4–18 years of age and 432–600 kg of body weight received a single intravenous dose of MgSO4 (60 mg/kg) over 5 minutes, and blood and urine samples were collected at different time points over 360 minutes. Plasma Mg2+ concentrations increased 3.7-fold over baseline values at 5 minutes and remained elevated for 120 minutes (P < 0.05), Ca2+ concentrations decreased from 30–60 minutes (P < 0.05), but Na+, K+ and Cl- concentrations did not change. Serum PTH concentrations dropped initially to rebound and remain elevated from 30 to 60 minutes, while CT concentrations increased at 5 minutes to return to baseline by 10 minutes (P < 0.05). The FMg, FCa, FNa, FK, and FCl increased, while urine osmolality decreased from 30–60 minutes compared baseline (P < 0.05). Short-term experimental hypermagnesemia alters calcium-regulating hormones (PTH, CT), reduces plasma Ca2+ concentrations, and increases the urinary excretion of Mg2+, Ca2+, K+, Na+ and Cl- in healthy horses. This information has clinical implications for the short-term effects of hypermagnesemia on calcium-regulation, electrolytes, and neuromuscular activity, in particular with increasing use of Mg salts to treat horses with various acute and chronic conditions as well as a calming agent in equestrian events.

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“…Nociplastic pain is generally chronic and widespread and is caused by disturbance of central pain processing mechanisms such as elevated excitability of ascending and descending pain facilitatory pathways and/or reduced inhibition of descending anti-nociceptive pathway [14,75,76]. The condition refers to central sensitization in which pain is elicited by innocuous stimuli or different kind of stimuli, resulting in causing central hyperalgesia or allodynia, respectively [77]. The process involves increased activity of the insula, anterior cingulate cortex, and the prefrontal cortex, which becomes active during acute pain sensation as well as of the brain stem nuclei, dorsolateral frontal cortex, and parietal cortex, which do not participate during acute pain sensation [78].…”

Section: Modulation and Nociplastic Painmentioning

confidence: 99%

Co-Players in Chronic Pain: Neuroinflammation and the Tryptophan-Kynurenine Metabolic Pathway

Tanaka¹,

Török²,

Tóth³

et al. 2021

Preprint

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Chronic pain is an unpleasant sensory and emotional experience that persists or recurs more than three months and may extend beyond the expected time of healing. Recently nociplastic pain has been introduced as a descriptor of mechanism of pain, which is due to disturbance of neural processing without actual or potential tissue damage, appearing to replace a concept of psychogenic pain. An interdisciplinary task force of the International Association for the Study of Pain (IASP) compiled a systematic classification of clinical conditions associated with chronic pain, which was published in 2018 and will officially come into effect in 2022 in the 11th revision of the International Statistical Classification of Diseases and Related Health Problems (ICD-11) by the World Health Organization. ICD-11 offers the option for recording the presence of psychological or social factors in chronic pain; however, cognitive, emotional, and social dimensions in the pathogenesis of chronic pain are missing. Earlier pain disorder was defined as a condition with chronic pain associated with psychological factors, but it was replaced with somatic symptom disorder with predominant pain in Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM-5) in 2013. Recently clinical nosology is trending toward highlighting neurological pathology of chronic pain, discounting psychological or social factors in the pathogenesis of pain. This review article discusses components of the pain pathway, the component-based mechanisms of pain, central and peripheral sensitization, roles of chronic inflammation, and the involvement of tryptophan-kynurenine pathway metabolites, exploring participations of psychosocial and behavioral factors in central sensitization of diseases progressing into development of chronic pain, comorbid diseases that commonly present a symptom of chronic pain, and psychiatric disorders that manifest chronic pain without obvious actual or potential tissue damage.

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Magnesium and Pain

Cited by 99 publications

References 118 publications

Nutrition in Gynecological Diseases: Current Perspectives

Nutrition in Gynecological Diseases: Current Perspectives

Effects of intravenous magnesium sulfate on serum calcium-regulating hormones and plasma and urinary electrolytes in healthy horses

Co-Players in Chronic Pain: Neuroinflammation and the Tryptophan-Kynurenine Metabolic Pathway

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