This section was compiled by Frank M. Painter, D.C. Send all comments or additions to:Frankp@chiro.org
If there are terms in these articles you don't understand, you can get a definition from the Merriam Webster Medical Dictionary. If you want information about a specific disease, you can access the Merck Manual. You can also search Pub Med for more abstracts on this, or any other health topic.
Dietary surveys suggest that many Americans do not consume magnesium in the recommended amounts. Treatment with diuretics (water pills), some antibiotics, and some medicines used to treat cancer, such as Cisplatin, can increase the loss of magnesium in urine. Other causes of magnesium loss and deficiency include sweating, poorly controlled diabetes and alcohol use. Signs of magnesium deficiency include confusion, disorientation, loss of appetite, depression, muscle contractions and cramps, tingling, numbness, abnormal heart rhythms, coronary spasm, and seizures.
Magnesium Status and Stress: The Vicious Circle Concept Revisited
Nutrients 2020 (Nov 28); 12 (12): pii: E3672
To conclude, while there is good evidence from animal and human studies of the bi-directional link between magnesium and stress, further research is needed to better understand the impact of this correlation and the benefit of magnesium supplementation on general health. Additional studies should apply standard methodologies (e.g., magnesium load test) to evaluate the magnesium status in well-characterized stressed population. These studies would help to demonstrate the increased need of magnesium supplementation during stress periods, and further strengthen our initial hypothesis. Further, in line with the GUTS model, repetitive negative thinking could be considered as a cognitive indicator of stress and evaluated in relation to blood magnesium levels in a cohort of subjects exposed to chronic stress. Given the strong association of stress with mental and physical diseases, these studies are fundamental to further support adequate magnesium dietary needs.
Can Magnesium Cure Migraines?
About 18 million women and some 5 million men in the United States suffer from migraine headaches. Only about a third are satisfied with their treatments, which can range from over-the-counter headache remedies to serotonin receptor antagonists, beta-blockers and calcium antagonists. Many of these prescription drugs come with an array of side effects. But what if a mineral could make a difference for migraine sufferers?
Stress intensifies release of catecholamines and corticosteroids
that increase survival of normal animals when their lives are
threatened. When magnesium (Mg) deficiency exists, stress
paradoxically increases risk of cardiovascular damage including
hypertension, cerebrovascular and coronary constriction and
occlusion, arrhythmias and sudden cardiac death (SCD). In
affluent societies, severe dietary Mg deficiency is uncommon, but
dietary imbalances such as high intakes of fat and/or calcium
(Ca) can intensify Mg inadequacy, especially under conditions of
stress. Adrenergic stimulation of lipolysis can intensify its
deficiency by complexing Mg with liberated fatty acids (FA), A
low Mg/Ca ratio increases release of catecholamines, which lowers
tissue (i.e. myocardial) Mg levels. It also favors excess release
or formation of factors (derived both from FA metabolism and the
endothelium), that are vasoconstrictive and platelet aggregating;
a high Ca/Mg ratio also directly favors blood coagulation, which
is also favored by excess fat and its mobilization during
adrenergic lipolysis. Auto-oxidation of catecholamines yields
free radicals, which explains the enhancement of the protective
effect of Mg by anti-oxidant nutrients against cardiac damage
caused by beta-catecholamines. Thus, stress, whether physical
(i.e. exertion, heat, cold, trauma--accidental or surgical,
burns), or emotional (i.e. pain, anxiety, excitement or
depression) and dyspnea as in asthma increases need for Mg.
Genetic differences in Mg utilization may account for differences
in vulnerability to Mg deficiency and differences in body
responses to stress.
There is an increased requirement for nutrients in normal
pregnancy, not only due to increased demand, but also increased
loss. There is also an increased insulin resistant state during
pregnancy mediated by the placental anti-insulin hormones
estrogen, progesterone, human somatomammotropin; the pituitary
hormone prolactin; and the adrenal hormone, cortisol. If the
maternal pancreas cannot increase production of insulin to
sustain normoglycemia despite these anti-insulin hormones,
gestational diabetes occurs. Gestational diabetes is associated
with excessive nutrient losses due to glycosuria. Specific
nutrient deficiencies of chromium, magnesium, potassium and
pyridoxine may potentiate the tendency towards hyperglycemia in
gestational diabetic women because each of these four
deficiencies causes impairment of pancreatic insulin production.
This review describes the pathophysiology of the hyperglycemia
and the nutrient loss in gestational diabetes and further
postulates the mechanism whereby vitamin/mineral supplementation
may be useful to prevent or ameliorate pregnancy-related glucose
'Magnesium ischaemia' is a term used to denote the functional
impairment of the ATP-dependent sodium/potassium and calcium
pumps in the cell membranes and within the cell itself. The
production of ATP and the functioning of these pumps is
magnesium-dependent and is critically sensitive to acidosis. Zinc
and iron deficiencies may secondarily impair these pumps and thus
contribute to 'magnesium ischaemia' (as does acidosis). This term
is two-dimensional at its simplest; it refers to a functional
magnesium deficiency, whether actual or induced. It is argued
that chronic acidosis is the most common inducing factor. This
simple hypothesis can begin to unify diverse pathophysiologies:
some spontaneous abortions, aspects of Type II and gestational
diabetes and the curious observation that heroin addicts become
diabetic. It can also unify clinical thinking about
pregnancy-induced hypertension, pre-eclampsia/eclampsia and acute
fatty liver of pregnancy, as well as the coagulopathy of
pregnancy. It makes important predictions about perinatal
morbidity and suggests that early supplementation might prevent
much pregnancy-induced disease.
In a placebo controlled, partially double-blinded, clinical
trial, a combination of evening primrose oil and fish oil was
compared to Magnesium Oxide, and to a Placebo in preventing
Pre-Eclampsia of Pregnancy. All were given as nutritional
supplements for six months to a group of primiparous and
multiparous pregnant women. Some of these women had personal or
family histories of hypertension (21%). Only those patients who
received prenatal care at the Central Maternity Hospital for
Luanda were included in the study. Compared to the Placebo group
(29%), the group receiving the mixture of evening primrose oil
and fish oil containing Gamma-linolenic acid (GLA),
Eicosapentaenoic acid (EPA), and Docosahexaenoic acid (DHA) had a
significantly lower incidence of edema (13%, p = 0.004). The
group receiving Magnesium Oxide had statistically significant
fewer subjects who developed hypertension of pregnancy. There
were 3 cases of eclampsia, all in the Placebo group.
Toxemia in pregnancy is characterized by a combination of at
least two of the following clinical symptoms: hypertension,
edema, and proteinuria. In this study the dietary intakes of
young pregnant women attending a Maternal and Infant Care Program
at Tuskegee Institute were evaluated for selected vitamins and
minerals. Women with toxemia were identified, and women without
toxemia served as controls. The toxemia group generally consumed
lesser amounts of vitamins and minerals than the controls.
However, both groups were deficient (less than two-thirds RDA) in
calcium, magnesium, vitamin B6, vitamin B12, and thiamin. Milk,
meat, and grains supplied an appreciable proportion of each
vitamin except vitamin A, which was found primarily in the two
vegetable groups. Meat and grains contained the greatest
quantities of minerals, but milk provided a relatively good
proportion of potassium, calcium, magnesium, and phosphorus.
Anemia was not related to the incidence of toxemia. Women
exhibiting anemia consumed smaller amounts of vitamins studied
than did women without anemia.
Many different treatments have been suggested for the premenstrual syndrome (PMS), including such nutritional supplements as vitamins, minerals and essential fatty acids. There is little agreement about the causes or treatments of the syndrome. The effect of a nutritional supplement, at high and low dosage, on premenstrual symptoms was assessed in a double-blind, placebo-controlled study. Also, the nutritional state of 11 women with PMS was evaluated. There was laboratory evidence of significant deficiencies in vitamin B6 and magnesium; other deficiencies occurred frequently, also. The multivitamin/multimineral supplement was shown to correct some of these deficiencies and, at the appropriate dosage, to improve the symptoms of premenstrual tension.
We measured plasma Cu, Zn and Mg levels in 40 women suffering
from premenstrual tension syndrome (PMTS) and in 20 control
subjects by atomic absorption spectrophotometer. Mean plasma Cu,
Zn and Mg levels, the Zn/Cu ratio were 80.2 plus or minus 6.00
microg/dl, 112.6 plus or minus 8.35 microg/dl, 0.70 plus or minus
0.18 mmol/l, and 1.40 plus or minus 0.10 in the PMTS group; and
77.0 plus or minus 4.50 microg/dl, 117.4 plus or minus 9.50
microg/dl, 0.87 plus or minus 0.10 mmol/l, and 1.51 plus or minus
0.05 in the control group respectively. The mean Mg level and the
Zn/Cu ratio were significantly lower in PMTS patients than in the
control group. Plasma Mg and Zn levels were diminished
significantly during the luteal phase compared to the follicular
phase in PMTS group. Mg deficiency may play a role in the
etiology of PMTS.
Reduced magnesium (Mg) levels have been reported in women
affected by premenstrual syndrome (PMS). To evaluate the effects
of an oral Mg preparation on premenstrual symptoms, we studied,
by a double-blind, randomized design, 32 women (24-39 years old)
with PMS confirmed by the Moos Menstrual Distress Questionnaire.
After 2 months of baseline recording, the subjects were randomly
assigned to placebo or Mg for two cycles. In the next two cycles,
both groups received Mg. Magnesium pyrrolidone carboxylic acid
(360 mg Mg) or placebo was administered three times a day, from
the 15th day of the menstrual cycle to the onset of menstrual
flow. Blood samples for Mg measurement were drawn premenstrually,
during the baseline period, andin the second and fourth months of
treatment. The Menstrual Distress Questionnaire score of the
cluster 'pain' was significantly reduced during the second month
in both groups, whereas Mg treatment significantly affected both
the total Menstrual Distress Questionnaire score and the cluster
'negative affect'. In the second month, the women assigned to
treatment showed a significant increase in Mg in lymphocytes and
polymorphonuclear cells, whereas no changes were observed in
plasma and erythrocytes. These data indicate that Mg
supplementation could represent an effective treatment of
premenstrual symptoms related to mood changes.
Magnesium deficiency may result from reduced dietary intake of
the ion increased losses in sweat, urine or faeces. Stress
potentiates magnesium deficiency, and an increased incidence of
sudden death associated with ischaemic heart disease is found in
some areas in which soil and drinking water lack magnesium.
Furthermore, it has been demonstrated experimentally that
reduction of the plasma magnesium level is associated with
arterial spasm. Careful studies are required to assess the
clinical importance of magnesium and the benefits of magnesium
supplementation in man.
The preventive merits of "nutritional insurance" supplementation
can be considerably broadened if meaningful doses of nutrients
such as mitochondrial "metavitamins" (coenzyme Q, lipoic acid,
carnitine), lipotropes, and key essential fatty acids, are
included in insurance supplements. From the standpoint of
cardiovascular protection, these nutrients, as well as magnesium,
selenium, and GTF-chromium, appear to have particular value.
Sophisticated insurance supplementation would likely have a
favorable impact on many parameters which govern cardiovascular
risk--serum lipid profiles, blood pressure, platelet stability,
glucose tolerance, bioenergetics, action potential
regulation--and as a life-long preventive health strategy might
confer substantial benefit.
The use of magnesium as an antiarrhythmic agent in ventricular and supraventricular arrhythmias is a matter of an increasing but still controversial discussion during recent years. With regard to the well established importance of magnesium in experimental studies for preserving electrical stability and function of myocardial cells and tissue, the use of magnesium for treating one or the other arrhythmia seems to be a valid concept. In addition, magnesium application represents a physiologic approach, and by this, is simple, cost-effective and safe for the patient. However, when one reviews the available data from controlled studies on the antiarrhythmic effects of magnesium, there are only a few types of cardiac arrhythmias, such as torsade de pointes, digitalis-induced ventricular arrhythmias and ventricular arrhythmias occurring in the presence of heart failure or during the perioperative state, in which the antiarrhythmic benefit of magnesium has been shown and/or established. Particularly in patients with one of these types of cardiac arrhythmias, however, it should be realized that preventing the patient from a magnesium deficit is the first, and the application of magnesium the second best strategy to keep the patient free from cardiac arrhythmias.
We demonstrated similar plasma concentrations and urinary losses but lower erythrocyte magnesium concentrations (2.18 +/- 0.04 vs 1.86 +/- 0.03 mmol/L, P less than 0.01) in twelve aged (77.8 +/- 2.1 y) vs 25 young (36.1 +/- 0.4 y), nonobese subjects. Subsequently, aged subjects were enrolled in a double-blind, randomized, crossover study in which placebo (for 4 wk) and chronic magnesium administration (CMA) (4.5 g/d for 4 wk) were provided. At the end of each treatment period an intravenous glucose tolerance test (0.33 g/kg body wt) and a euglycemic glucose clamp with simultaneous [D-3H]glucose infusion and indirect calorimetry were performed. CMA vs placebo significantly increased erythrocyte magnesium concentration and improved insulin response and action. Net increase in erythrocyte magnesium significantly and positively correlated with the decrease in erythrocyte membrane microviscosity and with the net increase in both insulin secretion and action. In aged patients, correction of a low erythrocyte magnesium concentration may allow an improvement of glucose handling.
OBJECTIVE: To examine the association between magnesium intake and risk of type 2 diabetes.
RESEARCH DESIGN AND METHODS: We followed 85,060 women and 42,872 men who had no history of diabetes, cardiovascular disease, or cancer at baseline. Magnesium intake was evaluated using a validated food frequency questionnaire every 2-4 years. After 18 years of follow-up in women and 12 years in men, we documented 4,085 and 1,333 incident cases of type 2 diabetes, respectively.
RESULTS: After adjusting for age, BMI, physical activity, family history of diabetes, smoking, alcohol consumption, and history of hypertension and hypercholesterolemia at baseline, the relative risk (RR) of type 2 diabetes was 0.66 (95% CI 0.60-0.73; P for trend <0.001) in women and 0.67 (0.56-0.80; P for trend <0.001) in men, comparing the highest with the lowest quintile of total magnesium intake. The RRs remained significant after additional adjustment for dietary variables, including glycemic load, polyunsaturated fat, trans fat, cereal fiber, and processed meat in the multivariate models. The inverse association persisted in subgroup analyses according to BMI, physical activity, and family history of diabetes.
CONCLUSIONS: Our findings suggest a significant inverse association between magnesium intake and diabetes risk. This study supports the dietary recommendation to increase consumption of major food sources of magnesium, such as whole grains, nuts, and green leafy vegetables.
This article describes the studies that have been performed evaluating complementary or alternative medical (CAM) therapies for efficacy and some adverse events fibromyalgia (FM). There is no permanent cure for FM; therefore, adequate symptom control should be goal of treatment. Clinicians can choose from a variety of pharmacologic and nonpharmacologic modalities. Unfortunately, controlled studies of most current treatments have failed to demonstrate sustained, clinically significant responses. CAM has gained increasing popularity, particularly among individuals with FM for which traditional medicine has generally been ineffective. Some herbal and nutritional supplements (magnesium, S- adenosylmethionine) and massage therapy have the best evidence for effectiveness with FM. Other CAM therapies such as chlorella, biofeedback, relaxation have either been evaluated in only one randomised controlled trials (RCT) with positive results, in multiple RCTs with mixed results (magnet therapies) or have positive results from studies with methodological flaws (homeopathy, botanical oils, balneotherapy, anthocyanidins and dietary modifications). Another CAM therapy such as chiropractic care has neither well-designed studies nor positive results and is not currently recommended for FM treatment. Once CAM therapies have been better evaluated for safety and long-term efficacy in randomised, placebo-controlled trials, they may prove to be beneficial in treatments for FM. It would then be important to assess studies assessing cost-benefit analyses comparing conventional therapies and CAM.
97 patients (25 per cent males, ages ranging from 14 to 73 years, median 38 years) with complaints of chronic fatigue (chronic fatigue syndrome, fibromyalgia or/and spasmophilia) have been enrolled in a prospective study to evaluate the Mg status and the dietary intake of Mg. An IV loading test (performed following the Ryzen protocol) showed a Mg deficit in 44 patients. After Mg supplementation in 24 patients, the loading test showed a significant decrease (p = 0.0018) in Mg retention. Mean values of serum Mg, red blood cell Mg and magnesuria showed no significant difference between patients with or without Mg deficiency. No association was found between Mg deficiency, CFS or FM. However serum Mg level was significantly lower in the patients with spasmophilia than in the other patients.
Muscle pain has been associated with magnesium (Mg) and selenium (Se) deficiency: magnesium and selenium status were investigated in fibromyalgia (FM). Erythrocyte (E), leucocyte (L) and serum (S) magnesium, serum selenium and zinc, and vitamin B1, B2, A or E status were assessed in 22 patients with fibromyalgia and in 23 age-matched healthy controls. LMg is significantly increased (P < 0.05) and EMg slightly decreased in fibromyalgia. These magnesium abnormalities are associated with previously-reported impairment of thiamin metabolism. Antioxidant status (as well as plasma malondialdehyde) is unchanged in fibromyalgia and serum selenium levels, slightly but not significantly correlated with serum magnesium, is normal.
Among other things, magnesium regulates active calcium transport.
As a result, there has been a growing interest in the role of
magnesium (Mg) in bone metabolism. A group of menopausal women
were given magnesium hydroxide to assess the effects of magnesium
on bone density. At the end of the 2-year study, magnesium
therapy appears to have prevented fractures and resulted in a
significant increase in bone density.