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August 28, 2010

Magnesium Deficiency – A Common Thread Uniting Periodontal Disease, Osteoporosis, Heart Disease, Diabetes, and Other Disorders of Aging

Dentist Numerous studies show that magnesium may be of particular importance for preventing tooth decay and periodontal disease:

Study Link – Higher serum magnesium:calcium ratio may lower periodontitis risk.

Study Link – Magnesium Deficiency is Associated with Periodontal Disease.

At first blush, these findings aren’t overly surprising – magnesium is, after all, an important structural component of teeth and bone. But the unique importance of magnesium for dental health may involve far more than just magnesium’s role as a structural element of mineralized tissue.

Evidence shows that magnesium has the unique ability to reduce inflammation – including the inflammation caused by bacterial toxins. Periodontal disease, of course, is characterized by chronic inflammation resulting from bacteria in the oral cavity. But a similar sort of inflammation is increasingly thought to be a common thread running through all disorders of aging. As magnesium seems to combat inflammation at the most fundamental cellular level, it’s not surprising to see that magnesium may be a first line of defense against not only periodontal disease, but all inflammatory and age–related disorders.

Chronic Inflammation

In recent decades, chronic systemic inflammation has been implicated as a causative factor in the disorders of aging including heart disease, diabetes, osteoporosis, Alzheimer’s disease, and cancer. As they share a common inflammatory basis, some research has begun to link periodontal disease with the development of many other diseases of aging:

Study Link – Periodontal disease and cardiovascular disease.

Quote from the above study:

Previous studies have demonstrated an association between periodontal disease severity and risk of coronary heart disease and stroke. We hypothesize that this association may be due to an underlying inflammatory response trait, which places an individual at high risk for developing both periodontal disease and atherosclerosis.

Study Link - Periodontal disease and diabetes: A two–way street.

Quote from the above study:

While inflammation plays an obvious role in periodontal diseases, evidence in the medical literature also supports the role of inflammation as a major component in the pathogenesis of diabetes and diabetic complications.

Some of the same oral bacteria responsible for periodontal disease have even been found in the arterial plaque characteristic of heart disease:

Study Link – Human Atherosclerotic Plaque Contains Viable Invasive Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis.

Quote from the above study:

This confirms the presence of periodontal pathogens in atherosclerotic lesions, whereby the bacteria could contribute to the vascular pathology either directly through their cytotoxicity or indirectly by inducing or exacerbating inflammation.

It’s unclear whether oral bacteria actually cause the vascular pathology of heart disease, or whether their presence is merely a function of the disorder, itself (damaged or diseased tissue often serves as a perfect breeding ground for bacteria). But in either case, the inflammation caused by various bacteria can be seen as a driving force behind the disorders of aging.

Inflammation and Endotoxin

The inflammation–inducing effects of bacteria are due, in large part, to structural components of bacteria generally known as endotoxins. In extremely stressful situations, the structural barrier of the intestines is often compromised allowing endotoxins from intestinal bacteria to enter the bloodstream. In this manner, the presence of endotoxin in the blood can lead to sepsis – a common occurrence under the stresses of surgery or trauma.

In less extreme situations, low–level endotoxin–induced inflammation may underlie the persistent inflammation associated with chronic disease. But while the intestinal bacteria constitute a well–known source of bacterial endotoxin, as the above studies indicate, oral bacteria associated with periodontal disease may add to the endotoxin burden as well. But, no matter the source, a lack of magnesium is a common thread running through all types of endotoxin–induced inflammation.

Dental Health, Endotoxin, and Diabetes

Studies have found that diabetics are uniquely prone to periodontal disease:

Study Link – Periodontal disease in non–insulin–dependent diabetes mellitus.

Quote from the above study:

Furthermore, diabetes increases the risk of developing periodontal disease in a manner which cannot be explained on the basis of age, sex, and hygiene or other dental measures.

This finding isn’t terribly surprising, considering the studies which indicate that bacterial endotoxin is likely to play a major role in the development of obesity, insulin resistance, and diabetes:

Study Link – Metabolic endotoxemia initiates obesity and insulin resistance.

Quote from the above study:

When metabolic endotoxemia was induced for 4 weeks in mice through continuous subcutaneous infusion of LPS [lipopolysaccharide – an endotoxin] , fasted glycemia and insulinemia and whole–body, liver, and adipose tissue weight gain were increased to a similar extent as in high–fat–fed mice.

As relates to diabetes, one of the actions of endotoxin is to cause the release of an inflammatory cytokine known as tumor necrosis factor alpha (TNF–a). TNF–a is thought to be responsible for the development of insulin resistance as it stimulates the excessive release of fatty acids into the bloodstream. This action serves to elevate blood levels of cholesterol and triglycerides (a common finding in obesity, diabetes, and heart disease), and these elevated blood lipids, then, impair the proper action of insulin and the metabolism of blood glucose.

Study Link – Endotoxin–induced tumor necrosis factor.

We’ve seen elsewhere that magnesium plays an important role in lowering TNF–a, and in keeping blood lipids and blood sugar within healthy ranges. Along these lines, we’ve also seen that magnesium is very likely to be deficient in those with heart disease and diabetes. It turns out that a large part of magnesium’s role in normalizing blood sugar and blood lipids may stem from magnesium’s ability to counter the inflammation produced by endotoxin. Studies have found, for example, that an early event in magnesium deficiency is the increased production of tumor necrosis factor–alpha in response to endotoxin:

Study Link – Enhanced tumor necrosis factor–alpha production following endotoxin challenge in rats is an early event during magnesium deficiency.

Similarly, we find that a lack of magnesium increases the mortality associated with endotoxin stress:

Study Link – Progressive magnesium deficiency increases mortality from endotoxin challenge: protective effects of acute magnesium replacement therapy.

Magnesium, Endotoxin, Inflammation, and Bone

A similar sort of inflammatory picture presents itself in age–related bone loss and osteoporosis – conditions also very much associated with a lack of magnesium.

Endotoxin stress has been shown to stimulate bone resorption, or, the breakdown of bone:

Study Link – Endotoxin: Stimulation of Bone Resorption in Tissue Culture.

And endotoxin has been shown to play a major role in osteoporosis (the study below examined the role of endotoxin in the osteoporosis associated with alcoholism – a condition known to severely compromise magnesium status):

Study Link – Role of endotoxemia in the pathogenesis of alcoholic osteoporosis.

Similar to its role in dental health, magnesium may counter bone loss and osteoporosis not only by acting as a structural component, but also by reducing the level of inflammatory cytokines which trigger the breakdown of bone:

Study Link – Skeletal and Hormonal Effects of Magnesium Deficiency

Quote from the above study:

It is known that cytokines can increase osteoclastic bone resorption. Mg deficiency in the rat and/or mouse results in increased skeletal substance P, which in turn stimulates production of cytokines. With the use of immunohistocytochemistry, we found that Mg deficiency resulted in an increase in substance P, TNF-a and IL1ß.

And, not surprisingly, studies have shown a correlation between the incidence of osteoporosis and periodontal disease:

Study Link – Osteoporosis, the risk of vertebral fracture, and periodontal disease in an elderly group in Mexico City.

Magnesium, Endotoxin, Inflammation, and Preterm Birth.

The relationship between endotoxin stress, inflammation, and a lack of magnesium even extends beyond age–related disorders. Numerous animal studies have shown, for example, that the inflammatory cascade triggered by endotoxin is also able to stimulate preterm birth. Because of these findings, researchers have suggested monitoring infection and endotoxin levels in amniotic fluid as a means to control preterm labor:

Study Link – Assay of bacterial endotoxin (lipopolysaccharide) in human amniotic fluid: potential usefulness in diagnosis and management of preterm labor.

In keeping with this proposed role of infection and inflammation, studies have found that pregnant women with periodontal disease are at greater risk of delivering prematurely, and of bearing children of lower birth weight:

Study Link – Higher Risk of Preterm Birth and Low Birth Weight in Women with Periodontal Disease.

And, yet again, we find that a lack of magnesium may be the common factor uniting these findings. Women with low serum levels of magnesium have been found to be at greater risk of preterm labor:

Study Link – Serum magnesium levels in pregnancy and preterm labor.

Quote from the above study:

Patients in preterm labor have a significantly depressed serum magnesium level… Hypomagnesemia (magnesium 1.4 mg/dl or less) may be a marker for true preterm labor.

Magnesium The link between dental health and other inflammatory disorders may seem, at first, to indict pathogenic bacteria as the causative elements. But it’s now clear that a lack of essential nutrients such as magnesium may be the key factor allowing all sorts of bacteria to gain a foothold throughout the body in the first place. When we foster energetic and resilient cells by giving our bodies the nutrients they need, it’s likely that all manner of inflammatory and degenerative disorders can be rectified without ever taking steps to combat the bacteria directly.



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