There exists a cultural myth in our society which perpetuates the idea that eating a balanced diet and taking a daily multivitamin will be sufficient to rectify any and all nutritional deficiencies. But because so many people have unquestioningly accepted this myth, many of our most dangerous nutritional deficiencies go fully unsuspected and unrectified.
Perhaps the most pressing of these modern deficiencies is that of magnesium. This all–important mineral is one of the most conspicuous casualties of our industrialized food supply, and neither food fortification nor most nutritional supplements even begin to bridge the magnesium gap. Even worse, many people who take nutritional supplements are laboring under a false sense of security – most never even suspect that their magnesium status is likely to be sub–optimal despite their use of supplements.
But, as we’ve seen in previous blog posts, magnesium deficiency is shockingly common – even amongst those who take supplements. The scientific literature is also teeming with research showing magnesium deficiency to be a common thread running through the most deadly and debilitating disorders of our day, including heart disease, depression, cancer, and diabetes.
Magnesium Deficiency Leads To Inflammation
Inflammation is the non–specific immune activation which occurs in response to any sort of bodily injury. In simplified terms, the proper role of inflammation is to combat the stressful stimuli and to speed tissue healing. We commonly think of inflammation as a response to things like infection or injury – and this sort of acute inflammation often manifests with the characteristic signs of tissue redness, swelling, and pain.
But when factors interfere with tissue healing, the inflammatory response can become chronic – ultimately damaging tissue instead of stimulating its repair. Chronic inflammation often shows no outward symptoms, but has been implicated as an underlying factor in some of the most prevalent degenerative and age–related disorders of modern times.
If tissue healing is compromised by the lack of an essential nutrient, inflammation is almost sure to become chronic until the lack of this nutrient is rectified. For example, magnesium deficiency is well–documented to increase markers of chronic inflammation:
Study Link - Pathobiology of magnesium deficiency: a cytokine/neurogenic inflammation hypothesis.
Quote from the above study:
During the progression of Mg deficiency in a rodent model, we have observed dramatic increases in serum levels of inflammatory cytokines [interleukin–1 (IL–1), interleukin–6 (IL–6), and tumor necrosis factor–alpha (TNF–alpha)] after 3 wk on a Mg–deficient diet.
Chronic Inflammation and Blood Sugar Control
One of the many negative repercussions of chronic inflammation is a lessening of blood sugar control, leading to the forerunner of diabetes known as insulin resistance. Not coincidentally, obese individuals almost universally experience insulin resistance and increased levels of systemic inflammation. A particular marker of systemic inflammation which has been shown to play an important role in insulin resistance is called tumor necrosis factor–alpha (TNF–alpha):
Quote from the above study:
These results indicate a role for TNF–alpha in obesity and particularly in the insulin resistance and diabetes that often accompany obesity.
Tumor necrosis factor–alpha is thought to chronically stimulate the release of fatty acids (from adipocytes, i.e., fat cells) into the bloodstream. This is a major reason why blood lipids (e.g., triglycerides) are often chronically elevated in obese individuals and diabetics. When the bloodstream contains high levels of fat like this, the body tends to preferentially use these fats for fuel. The result is that the metabolism of glucose is hindered and blood sugar tends to rise to abnormally–high levels. In normal–weight people, insulin (which is released in response to carbohydrate ingestion) usually stops fatty acids from being released so that the cells can take up and metabolize the ingested carbohydrates (i.e., glucose). But a high level of inflammation (and tumor necrosis factor–alpha in particular) can override this effect of insulin – the inflammatory signal persists, and causes fatty acids to be continually released into the blood, even though sufficient glucose is present to fuel cells. For the diabetic who finds that even small amounts of ingested carbohydrates elicit a dramatic increase in blood sugar, this sort of inflammation helps to explain why.
In this sense, blood sugar disorders are somewhat akin to a “false alarm.” The inflammatory mediators are evidence that the body perceives something as a threat. As with most bodily threats, the body responds by mobilizing fuel sources from storage (in this case, fatty acids). But these fatty acids aren’t needed for fuel when glucose is present in the blood stream – glucose is a perfectly fine fuel in its own right. So the question to ask in relation to blood sugar disorders is: What is the body perceiving as a threat causing it to mount such an exaggerated inflammatory response?
One possible answer is a lack of magnesium.
Magnesium is among the most fundamental elements involved in all aspects of human physiology. The very currency of cellular energy production for all cells in the body is dependent upon magnesium to function. For this reason, a lack of magnesium is profoundly threatening to the entire body. A magnesium deficiency can elicit a massive increase in almost every conceivable marker of inflammation.
As relates to the discussion of blood–sugar control, elevated levels of tumor necrosis factor–alpha have been directly tied to low levels of magnesium in obese subjects:
Quote from the above study:
Obese subjects exhibited higher serum concentration of TNF–alpha (p = 0.002) and lower serum magnesium levels (p < 0.0001) than lean and overweight subjects… These data shows that low serum magnesium levels and elevated TNF–alpha are related in the obese subjects.
In keeping with this finding, magnesium has also been shown in some studies to lower blood lipids and triglycerides:
Study Link – Can dietary magnesium modulate lipoprotein metabolism?
Quote from the above study:
After 12 weeks, there was a significant decrease in total serum cholesterol (10.7%), low–density–lipoprotein (LDL) cholesterol (10.5%) and triglyceride (10.1%) in [the group receiving magnesium] compared to the values at entry to the study…
And other studies have found that those with the highest intake of magnesium have the lowest risk of developing type–II diabetes:
Study Link – Magnesium intake and risk of type 2 diabetes in men and women.
Quote from the above study:
Our findings suggest a significant inverse association between magnesium intake and diabetes risk.
So we can clearly see a link between a sub–optimal magnesium intake and increased inflammation. This inflammation is likely to be a major factor driving the increase in blood lipids and triglycerides – and the lessening of blood–sugar control – found in diabetics and pre–diabetics. It seems likely that magnesium is a major factor in allowing us to keep our level of inflammation, as well as blood lipids and blood sugar, within healthy ranges.
Ensuring that we consume sufficient magnesium each day is the first step, but other factors are likely to play important roles as well. Some studies have shown that while the serum level of magnesium is a significant indicator of diabetes risk, this level doesn’t always correlate with how much magnesium is actually ingested:
Study Link – Serum and Dietary Magnesium and the Risk for Type 2 Diabetes Mellitus.
Quote from the above study:
Among white participants, low serum magnesium level is a strong, independent predictor of incident type 2 diabetes. That low dietary magnesium intake does not confer risk for type 2 diabetes implies that compartmentalization and renal handling of magnesium may be important in the relationship between low serum magnesium levels and the risk for type 2 diabetes.
There appear to be other factors in the diet or in individuals’ magnesium metabolism which may block the absorption of, or hasten the excretion of, magnesium. We’ll discuss some of these factors in the next Integrated Supplements blog post.
Stay Tuned.








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