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Low calcium and low magnesium: both increasing the risk for cognitive decline in a fading world called “aging brain”

Within the nervous system, magnesium acts as a positive regulator of synaptic plasticity. Magnesium also stabilizes neuronal cell membranes and modulates NMDA receptors, which play a vital role in synaptic transmission. Calcium is associated with learning and memory processes and is, therefore, considered crucial for cognitive functions. It is also essential for neurotransmission and neuronal excitability. Magnesium, on the other side, renders neuronal cells less reactive to excitation; it co-works with GABA recetpros and it is naturally ansiolytic and possesses some anti-seizure activities. The risk of magnesium and calcium deficiencies increases with age due to reduced dietary intake, impaired absorption, and chronic diseases. Several studies have reported that higher dietary intake of calcium and magnesium is associated with better cognitive performance in older adults. Cognitive decline is a typical characteristic feature in older adults that is associated with calcium and magnesium deficiencies.

Magnesium deficiency can lead to impaired mitochondrial energy production and reduced antioxidative capacity, which is needed to prevent oxidative stress.  A recent study published in the journal Nutrients explored the role of calcium and magnesium deficiencies in cognitive decline among hospitalized older adults.The study population comprised 1,220 hospitalized adults 60 years of age and older capable of verbally communicating with others. Serum samples were analyzed for calcium and magnesium levels. Based on these assessments, study participants were classified as those with normal serum levels of calcium and magnesium, hypomagnesemia, hypocalcemia, or both hypomagnesemia and hypocalcemia. Cognitive performance was assessed using the Mini-Mental State Examination (MMSE) and Clock-Drawing Test (CDT). The highest cognitive test scores were observed in participants with normal serum calcium and magnesium levels, followed by participants with hypomagnesemia, hypocalcemia, and both.

The study participants with dementia, as defined by MMSE scores below 24, exhibited significantly lower serum levels of both calcium and magnesium. Similarly, participants with poor cognitive performance, as determined by CDT scores below five, exhibited substantially lower calcium levels. After adjusting for potential confounding factors, the analysis revealed inverse associations between calcium and magnesium deficiencies and cognitive test scores. Overall, the presence of stroke, heart failure, atrial fibrillation, and chronic kidney disease was associated with lower cognitive performance, whereas the presence of hypertension and lipid disorders was associated with better cognitive performance. Age had a significant negative impact on cognitive performance while BMI had a positive association. Therefore, both hypomagnesemia and hypocalcemia are associated with reduced cognitive performance in older adults. Previous studies investigating magnesium deficiencies in older populations have provided mixed results.

Although some studies link high dietary magnesium intake with better cognitive performance, other studies have indicated that both low and high magnesium levels are associated with a greater risk of dementia and mild cognitive impairment. The association between magnesium levels and cognitive performance could be bidirectional. Hypomagnesemia may lead to poorer cognitive performance; however, impaired cognitive function due to nutritional deficiencies could also contribute to lower magnesium levels. Skimilarly, numerous studies have also identified an association between hypocalcemia and poor cognitive performance. Study participants with hypertension and lipid disorders exhibited higher cognitive performance. The scientists justify these findings by stating that high levels of total cholesterol and low-density lipoprotein cholesterol in older adults can be linked to a slower rate of cognitive decline, as these lipids are vital for maintaining cellular integrity in the brain.

They do not justify, however, the eventual connection between lipids and minelar metabolism. Cholesterol may be useful for stabilizing cellular membranes and lipid rafts needed for appropriate receptor signaling and neuronal homeostasis. However, high cholesterol is usually associated to membrane stiffness, which may impair membrane protein and ion channels trafficking. As for magnesium, however, there is no direct involvement with lipid metabolism but rather with carbohydrate metabolism but it is known that its deficiency can cause irritability, fatigue and even insomnia. Maintaining sleep is an important factor for brain health and it has been demonstrated for several years that chronic insomnia can increase the risk of cognitive decline due to altered metabolism and turnover of beta-amyloid. Therefore, the neuroprotective actions of magnesium on brain health can be direct, indirect, collaborating with lipid metabolism and are certainly not mutually exclusive.

Calcium metabolism disorders are more complex than those of magnesium, such as the calcium-dependent regulation of transcription factors involved in memory formation (e.g. CREB). Therefore, too little calcium can compromise memory risks; while excess calcium, on the contrary, can kill the neuron as occurs in apoptosis induced by excessive stimulation of the NMDA glutamate receptor (e.g. in cases of epilepsy or outcomes in cerebral stroke). Neuronal calcium homeostasis, then, is crucial in the pathogenesis of dementia, by promoting the accumulation of beta-amyloid and the formation of neurofibrillary tangles, typical hallmarks for Alzheimer disease. Who’s in and who’s out?

  • Edited by Dr. Gianfrancesco Cormaci, PhD, specialist in Clinical Biochemistry.

Scientific references

Kravchenko G, Stephenson SS et al. Nutrients. 2024; 16(21):3756.

Kravchenko G, Korycka-Bloch R et al. Nutrients. 2023; 15(17):3716.

Stephenson SS, Guligowska A et al. Nutrients. 2023; 15(7):1612.

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Dott. Gianfrancesco Cormaci
Dott. Gianfrancesco Cormaci
Laurea in Medicina e Chirurgia nel 1998; specialista in Biochimica Clinica dal 2002; dottorato in Neurobiologia nel 2006; Ex-ricercatore, ha trascorso 5 anni negli USA (2004-2008) alle dipendenze dell' NIH/NIDA e poi della Johns Hopkins University. Guardia medica presso la casa di Cura Sant'Agata a Catania. Medico penitenziario presso CC.SR. Cavadonna (SR) Si occupa di Medicina Preventiva personalizzata e intolleranze alimentari. Detentore di un brevetto per la fabbricazione di sfarinati gluten-free a partire da regolare farina di grano. Responsabile della sezione R&D della CoFood s.r.l. per la ricerca e sviluppo di nuovi prodotti alimentari, inclusi quelli a fini medici speciali.

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