A newly published study out of Australia furthers our understanding of why a diet rich in magnesium may reduce the risk of DNA damage, chronic degenerative disorders, and cancer. https://doi.org/10.1073/pnas.0608757103
Magnesium is the 4th most common element in the human body and plays an important role as a cofactor of enzymes required for DNA replication and repair as well as many other life sustaining biochemical mechanisms. More than 600 enzymes require it as a cofactor and almost 200 of them require it to activate critical processes. Therefore, magnesium has been called “The Magnificent Mineral” https://drsobo.com/magnesium-the-magnificent-mineral/
Whole grains, dark green leafy vegetables, dark chocolate, nuts, and beans are all magnesium-rich foods, which help the body produce energy, build teeth and bones, regulate blood pressure, blood sugar, and are crucial for the heart, muscles and kidneys to all work properly. A diet rich in other essential micronutrients working in coordination with magnesium is key to optimal health and wellbeing, and lowers the risk of chronic degenerative disease. [1, 2]. An insufficient intake of magnesium has been shown to increase the risk of many chronic degenerative disorders. Researcher Professor Michael Fenech says, “The next step is to determine the optimal dietary intake of magnesium, either through food or supplements and how this could impact the onset or progression of cancer and other chronic diseases.”
Research associate Molecular Biologist Dr Permal Deo says a low intake of magnesium (less than 300mg per day) can increase the risk of many diseases, but its role in preventing DNA damage is now being more fully studied. “Our study showed a direct correlation between low magnesium levels in blood and increased DNA damage. “Blood levels of magnesium, homocysteine, folate and vitamin B12 were measured, showing an inverse correlation between magnesium and Homocysteine, and a positive correlation between magnesium, folate and vitamin B12. This indicates that sufficiently high magnesium levels in the blood are essential to protect our genes from toxicity caused by homocysteine, which is also increased when folate and vitamin B12 are deficient.” Co-author of the study, Professor Fenech says chronic magnesium deficiency is likely to disrupt the body’s ability to produce energy and power cells, causing accelerated tissue ageing and making people more susceptible to early onset of many diseases.
Its role in preventing DNA damage is a topic of great interest for current researchers. This new study elucidates the mechanisms by which magnesium deficiency whether on its own, or accompanied by a high homocysteine level induces DNA damage. This study involved 172 healthy middle-aged adults of both sexes. Blood levels of magnesium, homocysteine, folate and vitamin B12 were measured at the beginning of the study to assess the impact of these levels.
Study Results and Conclusions
The study data showed that magnesium and the genotoxic amino acid called homocysteine are significantly inversely correlated with each other. The conditions of both low magnesium and high homocysteine might each contribute to negative health effects. Low magnesium levels and high amounts of homocysteine correlate to the levels of markers of DNA damage called micronuclei (MN), and nucleoplasmic bridges NPBs. Levels of Magnesium have been shown to significantly inversely correlate with MN and NPB. Individuals with low magnesium and high Homocysteine exhibited significantly higher frequency of MN and NPBs compared to those with high magnesium and low Homocysteine. This toxic combination of both low magnesium and high homocysteine increases genetic damage beyond the effect of just one these conditions would result in, making people more susceptible to diseases such as Alzheimer’s and Parkinson’s disease, gastrointestinal diseases, and a range of cancers, and diabetes.
Damage to DNA can happen at any stage of life starting from conception to old age. Medical science has uncovered many detrimental effects on development and organ function due to acquired gene mutations [3,4,5]. DNA damage events occur from a variety of exposures and mechanisms [6]. European Journal of Nutrition, 2024; DOI: 10.1007/s00394-024-03449-0
Magnesium being the 4th most abundant mineral present in the human body, is involved as a cofactor in many of the major metabolic and biochemical pathways necessary for our functioning. [7,8,9]. Its functions include strengthening and development of the bones, nerve function, regulating blood sugar and blood pressure [10], protein metabolism, nucleic acid stability (DNA and RNA), and cell proliferation [9]. [13][13, 14]. It has been recently shown that low levels of magnesium are associated with shorter telomere length [15].
Elevated homocysteine is associated with increased risk for neurodegenerative diseases such as dementia, Alzheimer’s and Parkinson’s disease. DNA damage causes cell death of neurons leading to neurological diseases [21,22,23,24]. Homocysteine is elevated by deficiency of folate and vitamin B12 [25] and high homocysteine may increase DNA damage [26]. DNA damage biomarkers such as micronuclei (MN), nucleoplasmic bridges (NPBs) and nuclear buds (NBuds) are cytogenetic anomalies associated with many diseases [28]. It has been shown that nutritional status modifies the extent of DNA damage and DNA integrity [29]. Nutrient deficiency can induce DNA damage because several vitamins and minerals including magnesium play an important role in DNA replication and DNA repair [5, 30, 31].
Magnesium plays a critical role in health and development, and wellbeing, however, its role in prevention of DNA damage has not been studied fully in humans so far. This study tested the hypothesis that magnesium deficiency either on its own or in conjunction with high homocysteine induces DNA damage in humans.
The Effect of Magnesium and Homocysteine on DNA damage biomarkers
Study participants with higher plasma levels of magnesium and low Homocysteine had the lowest frequency of MN. MN frequency was significantly higher in those with low magnesium and high Homocysteine compared to those with high magnesium and low Homocysteine. In this study, plasma magnesium level was independently and inversely associated with DNA damage biomarkers. This indicates that higher magnesium levels in blood may protect the genome from endogenous genotoxic events. Results obtained in the present study shows that people with low magnesium have greater DNA damage markers. Magnesium deficiency leads to more DNA breaks, accelerated telomere attrition and genomic instability [15, 35,36,37 38, 39]. Deficiencies of essential nutrients such as folate, vitamin B6 and B12 leads to significant higher levels of Homocysteine [41,42,43] and these elevated levels (hyperhomocysteinemia) are associated with increased risk for diseases such as cardiovascular diseases, and Alzheimer’s disease [44, 45]. If magnesium concentration is inadequate or deficient, it adversely affects the body’s attempts at DNA repair, resulting in increased DNA damage.
Conclusion
The results from this recent study show that low levels of magnesium can have an adverse cellular impact by increasing the DNA damage rate. Low magnesium interacts with high Homocysteine to increase MN and NPBs which increase the risk of developing neurodegenerative diseases, cancers and accelerated aging. The results also show that an optimal intake of nutrients such as magnesium and B vitamins that lower Homocysteine, are essential for maintaining genome integrity and healthy aging. Further research is needed to determine the optimal dietary intake to achieve healthy cellular concentration of magnesium and other nutrients for the maintenance of optimal genomic integrity. There are different forms of magnesium available for supplementation such as magnesium citrate, magnesium sulphate or magnesium glycinate. Which form(s) are the most beneficial to use to reduce MN and NPBs should be the focus of further study. The study authors conclude the knowledge regarding the DNA protective effects of magnesium should be of benefit to clinicians for patient counselling regarding food and supplementation recommendations, which when properly implemented may impact the onset or progression of the most common disease states causing disability and death in the population at large.
