Magnesium Oil – Transdermal Magnesium

Posts Tagged ‘diabetes’

I have been asked many times about the differences between magnesium chloride and magnesium sulphate, commonly known as Epsom Salts. There is a great article about it written by Dr Mark Sircus, a well-know and recognised researcher of magnesium and its benefits. I quote it here:

“According to Daniel Reid, author of The Tao of Detox, magnesium sulfate, commonly known as Epsom salts, is rapidly excreted through the kidneys and therefore difficult to assimilate. This would explain in part why the effects from Epsom salt baths do not last long and why you need more magnesium sulfate in a bath than magnesium chloride to get similar results. Magnesium chloride is easily assimilated and metabolized in the human body.[1] However, Epsom salts are used specifically by parents of children with autism because of the sulfate, which they are usually deficient in , sulfate is also crucial to the body and is wasted in the urine of autistic children.

For purposes of cellular detoxification and tissue purification, the most effective form of magnesium is magnesium chloride, which has a strong excretory effect on toxins and stagnant energies stuck in the tissues of the body, drawing them out through the pores of the skin. This is a powerful hydrotherapy that draws toxins from the tissues, replenishes the “vital fluid” of the cells and restores cellular magnesium to optimum levels. Magnesium Chloride is environmentally safe, and is used around vegetation and in agriculture. It is not irritating to the skin at lower concentrations, and is less toxic than common table salt.

Magnesium Chloride solution was not only harmless for tissues,
but it had also a great effect over leucocytic activity and
phagocytosis; so it was perfect for external wounds treatment.

Dr. Jean Durlach et al, at the Université P. et M. Curie, Paris, wrote a paper about the relative toxicities between magnesium sulfate and magnesium chloride. They write, “The reason of the toxicity of magnesium pharmacological doses of magnesium using the sulfate anion rather than the chloride anion may perhaps arise from the respective chemical structures of both the two magnesium salts. Chemically, both MgSO4 and MgCl2 are hexa-aqueous complexes. However MgCl2 crystals consist of dianions with magnesium coordinated to the six water molecules as a complex, [Mg(H2O)6]2+ and two independent chloride anions, Cl-. In MgSO4, a seventh water molecule is associated with the sulphate anion, [Mg(H2O)6]2 +[SO4. H2O]. Consequently, the more hydrated MgSO4 molecule may have chemical interactions with paracellular components, rather than with cellular components, presumably potentiating toxic manifestations while reducing therapeutic effect.”

MgSO4 is not always the appropriate salt in clinical therapeutics.
MgCl2 seems the better anion-cation association to be
used in many clinical and pharmacological indications.[2]
Dr. Jean Durlach et al

Magnesium sulfate is a chemical compound containing magnesium and sulfate, with the formula MgSO4. In its hydrated form the pH is 6.0 (5.5 to 7.0). It is often encountered as the heptahydrate, MgSO4·7H2O, commonly called Epsom salts. Anhydrous magnesium sulfate is used as a drying agent. Since the anhydrous form is hygroscopic (readily absorbs water from the air) and therefore harder to weigh accurately, the hydrate is often preferred when preparing solutions, for example in medical preparations. Epsom salts have traditionally been used as a component of bath salts.

References:

[1] http://www.hps-online.com/foodprof14.htm

[2] Magnesium Research. Volume 18, Number 3, 187-92, September 2005, original article”

http://magnesiumforlife.com/product-information/magnesium-chloride-vs-magnesium-sulfate/




WAYS TO REPLENISH MAGNESIUM QUICKLY & KEEP IT HIGH:


Oral supplementation is probably the first one most of us will think of. However, not all of us can absorb oral magnesium efficiently, especially if the digestive system is clogged up with impurities, or is not very efficient – which is true of the majority of the world population over the age of 30. Even when it is healthy, much of magnesium we take orally passes through the body unabsorbed, and if we take too much then even less of it will be absorbed, since it is a laxative.


This makes transdermal magnesium supplementation a much more suitable option for most people. Transderamlly, magnesium gets into the cells – where it is most needed – very quickly.


The most popular ways to supplement magnesium transdermally is a bath, a spray, or a massage. Body spray and massage are most economical ways to do it. Just spray or massage the body with magnesium oil once a day after a bath or a shower. Leave it on for 1 hour, or even overnight if you can, and you should feel the relaxing and tension relieving effects of magnesium very soon.


Transdermally, magnesium can also be administered in baths, foot baths and compresses. For a bath I suggest using magnesium flakes as the more economical way to achieve the best concentration. Use about 500g of magnesium chloride flake in a bath, and 250g in a foot bath. Such procedures are most beneficial before bed time, since deep relaxation resulting from and increase of magnesium in the body will certainly promote sleep.




FAR-INFRARED MAGNESIUM WRAP


This is an amazingly relaxing and therapeutic treatment which I have developed recently. It is aimed at those who are desperately deficient in magnesium and need quick supplementation. The treatment uses far-infrared heat to open up pores and boost circulation not only in the skin, but in deeper body structures. With the pores open and blood flow increased, magnesium stands a better chance to be absorbed quickly and in large quantities.


The treatment is preceded by a massage to stimulate circulation and soften up the tissues. The infrared heat helps open up the cell membranes, which contributes towards magnesium absorption.


Apart from being very therapeutic, the treatment is thoroughly relaxing, thanks to the effects of magnesium and the infrared heat. It promotes detoxification on the cellular level, helps to relieve aches, pains, muscle spasms, arthritis, sleep problems, fatigue, boost immunity, promote relaxation, help relieve water retention and is a really great start to a weight loss programme. People generally lose a lot of water during the treatment which has an added physical effect of feeling lighter afterwards.


One of my customers described the way she felt during the treatment as “wrapped in a soft cocoon”, and another said that it felt “like being in a mother’s womb waiting to be born”.

WHERE CAN I BUY MAGNESIUM PRODUCTS?


To book a MAGNESIUM WRAP IN LONDON or TO BOOK THE TRAINING please email info@medicina-uk.com.

Diabetes is on the rise in the UK and all over the world. Globally, it is estimated that there are 285 million people with diabetes now, and this number is estimated to increase to 438 million cases in 2030. UK is facing a huge increase in a number of diabetic patients. This number has increased from 1.4 million in 1996 to 2.4 million in 2010.

Contrary to popular belief, diabetes is not limited to the Western society. “The highest diabetes prevalence is in North America. Of the total North American cases, 4% are in Canada, 33% are in Mexico, and 62% are in the United States. The largest population of diabetics in 2001 was in India: 56 million people. ” http://www.worldmapper.org/display.php

“Type 2 diabetes is up to six times more common in people of South Asian descent and up
to three times more common among people of African and African-Caribbean origin”. http://www.diabetes.org.uk/Documents/Reports/Diabetes_in_the_UK_2010.pdf

Diabetes mellitus is a condition in which the amount of glucose (sugar) in the blood is too high
because the body cannot use it properly. There are two main types of diabetes – type 1 & type 2. Type 1 diabetes occurs when the body cannot produce insulin. Insulin is a hormone which helps the glucose to be utilised by the cells to produce energy. Without insulin glucose cannot be broken down and stays in the blood causing devastating damage to the body systems. Type 1 diabetes usually develops in childhood, and is often a result of a viral infection of the pancreas.

Type 2 diabetes is the most prevalent (90% of all cases) and develops later in life, normally in people over 40, although nowadays young children and people in their 20s are becoming its victims more and more often. Type 2 diabetes (non-insulin dependent) develops when the body produces insulin but the cells become resistant to it, since insulin fails to open up the body membranes to allow glucose pass into the cell for energy production, so it stays in the blood.

Why is diabetes on the increase?

Diet, exercise and lifestyle are all contributing factors in the rising levels of diabetes.
“Of all serious diseases, Type 2 diabetes has the strongest association with obesity.

Almost two in every three people in the UK are overweight or obese (61.9 per cent of
women and 65.7 per cent of men).

In 2006, almost one in four children in England measured in reception year were overweight
or obese. In Year 6 in England, the rate was nearly one in three.” http://www.diabetes.org.uk/Documents/Reports/Diabetes_in_the_UK_2010.pdf

Multiple research shows that diabetes is closely connected with magnesium deficiency which is primarily caused by sugar overload. How does it happen? When the body is unable to process sugar it leads to formation of toxic products – pyruvic acid and other abnormal sugars – which accumulate in the blood and body organs such as the brain, nervous system, red blood cells, body cells. They interfere with cellular respiration and lead to degeneration of the body tissues.

When sugar is added to the diet it produces a lot of acid which the body needs to neutralise to prevent tissue damage. For this it summons up all the available resources – its alkali-forming minerals, such as potassium, magnesium & calcium. If there is not enough of them available in the blood and body tissues, these minerals can be taken out of the bones and teeth, and this can lead to tooth decay and osteoporosis in the long run.

Magnesium is needed to produce insulin in the body. Insufficient production of insulin results in diabetes. Diabetic sufferers have insufficient magnesium in the body, and this leads to heart & kidney problems, high blood pressure, burning sensation and numbness in the feet, leg ulcers, damage to the eyes, and obesity.

“Diabetes is responsible for over one million amputations each year. It is a major cause of blindness. It is the largest cause of kidney failure in developed countries and is responsible for huge dialysis costs.” Unite For Diabetes, 2006

Supplementation with magnesium, alongside dietary changes, has shown to reduce and even eliminate some, and even all, of these symptoms, by improving insulin response, glucose tolerance and by reducing stickiness of red blood cells. It is irreplaceable in the treatment of peripheral circulation problems associated with diabetes.

Besides, magnesium is a mineral which takes part in a production of energy from ATP – the energy molecule in the cell, and for diabetics it means that energy can be produced from the glucose stored in the muscles and liver. This contributes to sugar control in diabetic patients.

Dietary changes and adjustments and magnesium supplementation, alongside other minerals such as zinc, chromium, copper, selenium & manganese, and B-group vitamins produce remarkable results. They cannot of course reverse the damage caused to the organs and tissues, but can certainly stop further damage.

Transdermal magnesium therapy is one of the easiest and most effective ways to top up magnesium in the body and keep it at an optimal level. Magnesium taken by the body through the skin bypasses digestion which in diabetic sufferers is often compromised, so much of magnesium taken orally simply passes through the body unutilised. Taken into the body through the skin, magnesium bypasses digestion and gets into circulation very quickly. This also allows magnesium chloride to have a local beneficial effect on peripheral circulation and speed up the healing of ulcers.

Application methods for transdermal magnesium therapy:

• Body spray – simply spray all over the body after a bath or a shower, before bed time.
• Massage – massage into the body 2-3 times a week. Thoroughly relaxing.
• Body rub – same as a massage, only done more quickly.
• Foot bath – used daily it will improve circulation in the legs and help heal ulcers, as well as replenish magnesium levels through the feet.
• Bath – use 1-3 times a week. The most luxurious and relaxing experience.
• Compress – use locally, on affected areas, such as legs, joints, etc. Use very warm water for this, 1 part magnesium oil or flake to 3-4 parts of water. Soak a cloth, apply on the area, wrap around with a cling film and then with a warm scarf. Leave on for 1-3 hours or even overnight.

Magnesium oil Bishofit is a great product to use in trandermal magnesium therapy. Magnesium flake from Holland (Zechstein) is another product to use. It is more economical, since it contains no water, and it is easy to make your own magnesium oil – just use 1 part magnesium flake to 1-2 parts of warm mineral water. Dilute and use.

WHERE CAN I BUY MAGNESIUM PRODUCTS?

To book a MAGNESIUM WRAP IN LONDON please email info@medicina-uk.com.

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.

Type 2 diabetes is on track to become one of the major global public health challenges of the 21st century (1). Primary prevention remains the major strategy to control this worldwide epidemic.

Modification of western diet and lifestyles is effective in preventing diabetes in high-risk populations (2). The western diet is characterized by high intake of saturated and trans fats and refined grains and low intakes of whole grains, vegetables, and fiber, resulting in low micronutrient intake (3). Few studies have addressed the association between specific micronutrient components of western diets and diabetes risk.

Magnesium is an important component of many unprocessed foods, such as whole grains, nuts, and green leafy vegetables, and it is largely lost during the processing of some foods (4). The overprocessing of food and adoption of western diets have contributed to the substantially reduced magnesium intake in industrialized countries during the last century.

Hypomagnesemia is a common feature in patients with type 2 diabetes (5). Although diabetes can induce hypomagnesemia, magnesium deficiency has also been proposed as a risk factor for type 2 diabetes (6). Magnesium is a necessary cofactor for several enzymes that play an important role in glucose metabolism (7). Animal studies (8,9) have shown that magnesium deficiency has a negative effect on the post-receptor signaling of insulin. Some short-term metabolic studies (10,11) suggest that magnesium supplementation has a beneficial effect on insulin action and glucose metabolism.

In our previous analyses of dietary factors and diabetes based on limited follow-up (12–14), we found an inverse association between magnesium intake and risk of type 2 diabetes. However, these analyses did not fully control for other confounding factors and were limited in power to evaluate the association in subgroups. Two other prospective studies (15,16) have specifically evaluated this association, with contradictory results. The purpose of this analysis, with longer follow-up and more incident cases, was to prospectively evaluate the association between magnesium intake and risk of type 2 diabetes in two large cohorts of women and men.

RESEARCH DESIGN AND METHODS

The characteristics of the Nurses’ Health Study (NHS) and the Health Professionals’ Follow-up Study (HPFS) have been described elsewhere (17,18). Briefly, the NHS was initiated in 1976, when 121,700 female registered nurses, aged 30–55 years, completed a mailed questionnaire on their medical history and lifestyle characteristics. Every 2 years, follow-up questionnaires have been sent to update information on potential risk factors and identify newly diagnosed cases of diabetes and other chronic diseases. The HPFS began in 1986 when 51,529 U.S. health professionals, aged 40–75 years, answered a detailed questionnaire on lifestyle and medical history. Similar to the NHS, this cohort has been followed through biennial questionnaires. In both cohorts, the response rate to the follow-up questionnaires has exceeded 90%.

Diet was first evaluated in 1980 in the NHS and in 1986 in the HPFS. Repeated dietary assessments have been carried out every 2–4 years. From participants who returned the baseline dietary questionnaire, we excluded those who had >10 blanks in food items or did not satisfy our a priori criteria of plausible daily caloric intake. For this analysis, we also excluded participants who at baseline reported history of diabetes, cardiovascular disease, or cancer. These exclusions left 85,060 women followed over 18 years (1980–1998) and 42,872 men followed over 12 years (1986–1998) for the present analysis.

Magnesium intake

In the NHS, a 61-item semiquantitative food frequency questionnaire (FFQ) was used to collect dietary information in 1980. In 1984, the questionnaire was expanded to 131 items. Similar FFQs were used to update diet in subsequent follow-up in the NHS (1986, 1990, 1994, and 1998) and the HPFS (1986, 1990, 1994, and 1998). In the FFQ, a common unit or portion size for each food was specified and participants were asked how often they had consumed that amount on average during the previous year. The nine responses ranged from “never or less than once per month” to “six or more times per day.” Nutrient intake was computed by multiplying the frequency of consumption of each food by the nutrient content of the specified portions. Composition values for dietary magnesium and other nutrients were obtained from the Harvard University Food Composition Database (22 November 1993), derived from U.S. Department of Agriculture sources (19), and supplemented with manufacturer information. A detailed description of dietary questionnaires and their validity in these cohorts have been published elsewhere (20,21). Correlation coefficients between FFQ and dietary record for magnesium intake were 0.76 in women and 0.66 in men after within-person variation was taken into account.

Use of specific brand and type of multivitamins was ascertained at baseline and updated every 2 years, asking current users about weekly number of multivitamins taken. This information was included in total magnesium intake computation. Questions on separate magnesium supplements were first asked in 1984 in the NHS and in 1986 in the HPFS, with information updated at least every 4 years. Although we did not have information on the exact magnesium content of these supplements, we estimated the content based on the most frequently used magnesium supplements on the market in the year of the questionnaires and used that amount for the calculation of total magnesium intake. In a separate analysis, we examined the association between magnesium supplement use and diabetes risk.

Measurement of nondietary factors

In both cohorts, body weight was self-reported on baseline questionnaires and updated every 2 years. In validation studies, self-reported weights were highly correlated with measured weights (22). In the NHS, to be consistent with the baseline evaluation, we used the cumulative average of hours per week spent in moderate to vigorous activity. In the HPFS, we had detailed information on the hours per week spent in leisure-time physical activities since baseline and through follow-up. We calculated total weekly energy expenditure from physical activity expressed as metabolic equivalents (METs). The validity and reproducibility of the physical activity questionnaires have been previously documented in these cohorts (23,24). Every 2 years, we updated participants’ smoking status (past, current, and number of cigarettes per day if smoking currently). Family history of diabetes (in first-degree relatives) was assessed on multiple occasions in both cohorts. We inquired about physician-diagnosed hypertension and high cholesterol every 2 years; these self-reports were highly accurate compared with medical records in a validation study (25).

Ascertainment of diabetes

On each biennial questionnaire, we asked the participants if and when they had ever been diagnosed with diabetes. To confirm self-reported diagnoses, we mailed a supplementary questionnaire regarding symptoms, diagnostic tests, and therapy. After excluding participants with type 1 and secondary diabetes, the diagnosis of type 2 diabetes was established when at least one of the following criteria was reported in the supplementary questionnaire: 1) at least one classic symptom of type 2 diabetes and elevated plasma glucose (≥140 mg/dl [7.8 mmol/l] fasting or ≥200 mg/dl [11.1 mmol/l] random measure), 2) elevated plasma glucose concentrations on at least two different occasions in the absence of symptoms, or 3) treatment with hypoglycemic therapy (insulin or oral hypoglycemic agents). These criteria accord with those proposed by the National Diabetes Data Group (NDDG). The new guidelines from the American Diabetes Association (ADA) for diagnosing diabetes (fasting plasma glucose ≥126 mg/dl [7.0 mmol/l]) were announced in June 1997 (26) and have been incorporated into the confirmation and documentation of diabetes in subsequent follow-up in both cohorts.

The validity of the method for confirming type 2 diabetes by supplementary questionnaire using the NDDG criteria has been previously documented in these cohorts (27,28). To document the reliability of reports of diabetes in the most recent cycle (1996–1998), an additional validation study was carried out only in the NHS. In this study, we reviewed medical records in two separate groups: women who satisfied NDDG criteria by the supplementary questionnaire and women who satisfied only ADA criteria (fasting plasma glucose between 126 and 139 mg/dl). Medical record review confirmed the diagnosis of diabetes by NDDG criteria in 94 of 95 (98.9%) subjects for the former group. The number of women reporting that they met ADA but not NDDG criteria was small (<5% of cases in this cycle); medical record review confirmed the diagnosis of diabetes by ADA criteria in all but one person, thus confirming its validity using the new criteria.

Statistical analysis

Person-time of follow-up for each participant was computed from the date of return of the baseline questionnaire (1980 for women and 1986 for men) to either the date of diabetes diagnosis, death, or the end of follow-up (January 1998 for HPFS or July 1998 for NHS), whichever occurred first.

In the primary analysis, participants were divided into quintiles of total magnesium intake (including magnesium from multivitamins), and incidence rates were calculated as the number of events divided by total person-time in each quintile. The relative risks (RRs) were computed as the incidence rates of diabetes in each category of magnesium intake divided by the incidence rate in the lowest quintile of intake (reference group).

To reduce within-person variation and best represent the long-term effects of magnesium intake, we calculated the cumulative average intake of magnesium from all the dietary questionnaires available up to the start of each 2-year period (29). For example, for men, to model diabetes incidence in the 1988–1990 period, we used the 1986 magnesium intake and for the 1990–1992 period, we used the average of 1986 and 1990 intakes. We also conducted a secondary analysis using baseline magnesium intake only.

Cox proportional hazards models stratified by age and time period were used in all multivariate analyses to estimate RRs. To control for multiple confounders, we adjusted for history of hypertension and hypercholesterolemia at baseline and biennially updated information on smoking status, BMI (in eight categories), level of physical activity, family history of diabetes (first-degree relatives), and alcohol intake (four categories). We also adjusted for several dietary variables (30), including glycemic load and intakes of cereal fiber, polyunsaturated fat, trans fat, and processed meat, all in quintiles. Finally, we performed stratified analyses according to levels of BMI, physical activity, and family history of diabetes.

All P values were two sided. Tests for trend were conducted using the median value for each quintile of magnesium intake analyzed as a continuous variable in the regression models. Likelihood ratio χ2 was used to assess the significance of the interactions between magnesium intake and the variables used in the stratified models. All analyses were done with SAS version 8.2 (SAS, Cary, NC).

RESULTS

At baseline, compared with those in the lowest quintile of magnesium intake, both women (in 1980) and men (in 1986) with higher intakes of magnesium tended to be leaner, more physically active, and more likely to take multivitamins and magnesium supplements (Table 1). Magnesium intake was positively associated with intakes of fiber and inversely associated with intakes of fat and processed meat. Averaged over the entire follow-up, the median intake (min-max) of magnesium was 290 mg/day (79–1,110 mg/day) in women and 349 mg/day (102–1,593 mg/day) in men.

During a follow-up of 18 years in the NHS (1,456,362 person-years) and 12 years in men (472,730 person-years), we documented 4,085 incident cases of type 2 diabetes in women and 1,333 in men. After adjusting for age and total energy intake (Table 2), we observed a significant inverse association between magnesium intake and risk of type 2 diabetes in both cohorts, with RRs (95% CIs) comparing the top versus bottom quintiles of 0.55 (0.50–0.61) and 0.56 (0.47–0.67) in women and men, respectively. After additional adjustment for BMI, the RRs were somewhat attenuated in both cohorts. However, the RRs were practically unchanged after further adjustment for other nondietary covariates. The RRs remained significant after the addition of dietary variables in the multivariate models. Further adjustment for caffeine slightly attenuated the association between magnesium intake and diabetes risk. The RRs (95% CIs) between extreme quintiles was 0.83 (0.73–0.95) in women and 0.76 (0.61–0.94) in men. Moreover, the adjustment for other minerals, such as calcium, potassium, and phosphorous, did not change the estimate of the association among women (RR comparing extreme quintiles 0.74 [0.63–0.88]), and the inverse association for magnesium was stronger among men (0.62 [0.48–0.81]). Analyses with the single baseline diet assessment instead of updated cumulative average of repeated measurements yielded similar results: 0.79 (0.71–0.88) in women and 0.73 (0.60–0.90) in men. Excluding participants with a history of hypertension or hypercholesterolemia at baseline, using only symptomatic or nonsymptomatic cases as an outcome, or modeling dietary rather than total magnesium intake did not materially change the results. Finally, the inclusion of diuretic use in the final model did not modify our results.

As shown in Table 3, the inverse association was persistent in subgroup analysis according to BMI, physical activity, and family history of diabetes. We did not identify any significant interactions between magnesium intake and these covariates. The inverse association was also similar between drinkers and nondrinkers and between participants with or without hypertension (data not shown).

Finally, we assessed the association between magnesium supplements and risk of type 2 diabetes. The proportion taking magnesium supplements in the entire follow-up period was 3.1% in women and 3.6% in men. There were relatively few cases in the supplement user group (111 in women and 52 in men). We found a significant inverse association in the age-adjusted model only in women (RR 0.82, 95% CI [0.68–0.99] in women and 1.01 [0.76–1.33] in men). However, in the multivariate models, we found no statistical association between use of magnesium supplements and diabetes risk in both women and men: 0.93 (0.77–1.12) and 1.07 (0.81–1.41), respectively. The use of multivitamins was not significantly associated with diabetes risk.
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CONCLUSIONS

In these two large prospective studies, we observed a consistent inverse association between magnesium intake and risk of type 2 diabetes in men and women. This association was independent of other risk factors for type 2 diabetes, including several dietary factors. Moreover, the inverse association with magnesium intake was consistent across different subgroups defined by the main predictors of type 2 diabetes, such as BMI, physical activity, and family history of diabetes.

The prospective design reduces the possibility of recall and selection bias, and the high rate of follow-up reduces bias due to loss to follow-up. Another advantage is that diet was assessed multiple times during follow-up, which not only reduces measurement error (29), but also takes into account changes in eating behaviors.

Our study has several limitations. Given the size of these cohorts, screening for blood glucose was not feasible, thus some cases of diabetes may have been undiagnosed. However, our validation study showed that undiagnosed diabetes was rare in our cohort because the participants are health professionals (31). It is possible that participants with “unhealthy” diets are more likely to be screened for diabetes. However, the analysis using only symptomatic cases did not substantially change our results, arguing against surveillance bias. On the other hand, the diagnostic criteria for type 2 diabetes were changed in 1997 such that lower plasma glucose levels would now be considered diagnostic. If these criteria were used since baseline, some noncases would have been reclassified as cases. However, this would bias the estimates toward the null.

The inverse association between magnesium intake and diabetes risk was observed in all multivariate models, including the main dietary and nondietary risk factors for diabetes. Moreover, the observed association was consistent within different subgroups, which further supports the idea that confounding by these factors was unlikely to explain our results. However, the effects of residual confounding cannot be completely ruled out in observational studies.

Besides earlier analyses within the NHS and HPFS (12–14), which were consistent with our present results, two other large prospective studies have specifically explored the association between magnesium intake and type 2 diabetes risk. Findings in older women (15) were very similar to our results, with an RR comparing extreme quintiles of 0.76 (95% CI 0.62–0.95) in a multivariate model, including whole grain and cereal fiber. In the other study, Kao et al. (16) found an inverse association between serum magnesium levels and type 2 diabetes, but did not find a significant association between dietary magnesium and subsequent incidence of diabetes. Unlike our study, both of the other studies used only single baseline dietary assessment.

Several experimental studies suggest a protective role of magnesium intake against diabetes. Using a rat model of spontaneous type 2 diabetes, Balon et al. (32) demonstrated a significant reduction in the incidence of diabetes after 7 weeks of feeding with a magnesium-rich diet. In humans, some (11,33,34) but not all (35–37) experimental studies have shown benefits of magnesium supplements on glucose metabolism and/or insulin sensitivity. Some of the inconsistencies among these studies can be explained by differences in treatment periods, doses of magnesium, and parameters used to evaluate the effect. Moreover, most of these studies have been conducted on diabetic subjects, in whom the underlying insulin resistance could interfere with magnesium uptake at the cellular level (38). In one study (11), elderly nondiabetic subjects participated in a double-blind, randomized, crossover study comparing magnesium supplements (4.5 g/day) versus placebo during 4 weeks. This study showed a beneficial effect on insulin response to glucose and insulin action. Whether long-term magnesium supplementation decreases the risk for type 2 diabetes in the general population is unclear, and the hypothesis merits testing in clinical trials. In our observational analysis, magnesium supplement use was not significantly associated with diabetes risk in multivariate models. However, the power of our study was limited by the low prevalence of magnesium supplement use in these cohorts.

Several mechanisms, including insulin secretion, binding, and action, have been proposed to explain the effect of intracellular or plasma magnesium on diabetes pathogenesis (6). Intracellular magnesium is a critical cofactor for several enzymes in carbohydrate metabolism, especially those involved in phosphorylation reactions such as tyrosine-kinase. In animal models (9), hypomagnesemia induced by low magnesium intake triggers severe insulin resistance, which was shown to be partially dependent on deficient tyrosine-kinase activity on the post-receptor pathway of insulin in muscle cells. In healthy humans, a study of short-term low magnesium diet (39) showed that it reduced serum and intracellular magnesium and produced insulin resistance, using a minimal model. Consistent with the effect of magnesium on insulin resistance, Fung et al. (40) found an inverse association between magnesium intake and fasting insulin level, a good marker of insulin resistance, in a cross-sectional sample of the NHS.

Higher magnesium intake is likely more beneficial among individuals with some degree of magnesium deficiency. However, there is no generally accepted test for magnesium status. Also, our subgroup analysis suggests that higher magnesium consumption is likely beneficial for all groups, regardless of their BMI, physical activity levels, and hypertension status.

In conclusion, these two large prospective cohorts provide strong and consistent evidence to support an inverse association between magnesium intake and diabetes risk. The effect of magnesium supplementation in general or high-risk populations requires further research, ideally in randomized clinical trials. This study supports the dietary recommendation to increase consumption of major food sources of magnesium, such as whole grains, nuts, and green leafy vegetables.

Acknowledgments

This study was supported in part by National Institutes of Health Grants nos. CA55075, HL35464, CA87969, and DK58845 and by National Institute of Diabetes and Digestive and Kidney Diseases training grant no. DK07703. R.L.-R. is also supported by a scholarship from the Consejo Nacional de Ciencia y Tecnología (CONACyT), Mexico.

1. Ruy Lopez-Ridaura, MD1,
2. Walter C. Willett, MD123,
3. Eric B. Rimm, SCD123,
4. Simin Liu, MD34,
5. Meir J. Stampfer, MD123,
6. JoAnn E. Manson, MD234 and
7. Frank B. Hu, MD123

+ Author Affiliations

1.
1Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts
2.
2Department of Epidemiology, Harvard School of Public Health, Boston, Massachusetts
3.
3Channing Laboratory, Department of Medicine, Harvard Medical School and Brigham and Women’s Hospital, Boston, Massachusetts
4.
4Division of Preventive Medicine, Harvard Medical School and Brigham and Women’s Hospital, Boston, Massachusetts

1. Address correspondence and reprint requests to Ruy Lopez-Ridaura, MD, Department of Nutrition, Harvard School of Public Health, 665 Huntington Ave., Boston, MA 02215. E-mail: rlopez@hsph.harvard.edu

http://care.diabetesjournals.org/content/27/1/134.full

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