Low magnesium associated with DNA damage and increased disease risk, study finds

Published: 20-Aug-2024

Low blood magnesium concentration contributes to increased homocysteine levels, which can results in DNA damage and susceptibility to a number of diseases

A study conducted by the University of South Australia has found that low magnesium levels can leave people susceptible to disease and DNA damage.

During the study period, it was observed that low magnesium levels in the blood correlated with the presence of the genotoxic amino acid homocysteine (Hcy). 

The DNA-damaging effects of Hcy have long been known, and aberrant levels of the amino acid can contribute to the development of a range of diseases, including cancers, neurological diseases like Alzheimer's disease and diabetes.

A molecular biologist at the University of South Australia, Dr Permal Deo, claims that a magnesium intake of less than 300mg per day can exhibit this effect — even when accounting for factors such as age, gender and ethnicity.

These results highlight the crucial role magnesium plays in the preservation of human DNA, which was previously unknown.

Varinderpal S. Dhillon, a co-author in this paper and a senior research fellow at the University of South Australia, commented: Magnesium is essential for a vast array of metabolic pathways and its levels — like other micronutrients and minerals — are constantly in flux. Hence, many homeostatic pathways must accommodate these subtle alterations in magnesium availability to preserve cellular functions like ATP production. Ultimately, magnesium deficiency leads to more DNA breaks, an acceleration of telomeric attrition, as well as genomic instability." 

"Although study participants were healthy at the time of sampling, the increased DNA damage in people with low magnesium levels can cause accelerated tissue ageing, making them more susceptible to ageing-related diseases such as Alzheimer's and cancer. Therefore, it is increasingly evident that magnesium plays an important role in protecting against genome damage and telomere attrition as shown in previous reports."

 

Reference

https://link.springer.com/article/10.1007/s00394-024-03449-0

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