Low calcium, magnesium levels tied to poorer cognitive performance:
“Interestingly, those with healthy magnesium levels but low calcium levels also performed poorly. However, individuals with low magnesium but healthy calcium levels did not have such pronounced cognitive impairment.”
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adssx
#2
Polish paper published in an MDPI journal, so not the highest quality: The Concurrent Association of Magnesium and Calcium Deficiencies with Cognitive Function in Older Hospitalized Adults 2024
Hypomagnesemia was defined as a serum level of Mg lower than 0.77 mmol/L, while hypocalcemia was defined as a concentration of Ca below 2.2 mmol/L
They don’t give the average Mg and Ca concentrations in each group unfortunately.
For AD and Mg, these papers (not high quality either) suggest an optimal at 0.85 mmol/L:
OTOH, with Dementia with Lewy Bodies have elevated Ca and Mg: CSF Mg and Ca as diagnostic markers for dementia with Lewy bodies 2009: “Patients with DLB had elevated Ca and Mg levels in CSF and Mg levels in plasma as compared to all other groups (p < 0.001). Furthermore, a combination of CSF-Mg and CSF-Ca could distinguish DLB from AD with a sensitivity of 93% and a specificity of 85%.”
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Interestingly, in the US, standard panels don’t measure magnesium, only calcium. Magnesium test is easy to get, but you have to request it - at least that’s the situation at UCLA; I asked my PCP why that is, but he didn’t really have a good answer. In any case I had never previously associated serum levels of calcium and magnesium with dementia. Might these be simply a proxy for diet quality and status? We do know that food intake is strongly affected years prior to f.ex. AD diagnosis, cause and effect notwithstanding. I see a lot of confounders here, including the use of pharmaceuticals in the elderly that affect calcium and magnesium levels, and various morbidities, such as osteoporosis etc.
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adssx
#4
Same in Europe. One issue is that only 1% of magnesium is in the serum so serum magnesium might not be the best indicator of normomagnesia. Some people define deficiency as low as 0.6 mmol/L while others say even 0.85 mmol/L is deficient. 
Some say RBC magnesium is a better indicator but it’s not standardized either.
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LukeMV
#5
I consume about 1g of magnesium per day between food and supplements. I’m a big guy and sweat a ton between working out and daily sauna, so apparently I need more than the 420mg RDA
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JKPrime
#6
This paper also investigated cognitive scores and association with lipid levels and hypertension and mentions that cognitive scores are lower in those with lower lipid levels.
adssx
#7
Yes they also note that those with hypertension scored higher. We don’t know if this is causal.
But Mendelian randomization studies tell us that low LDL is protective for AD and DLB.
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We would know more if we had more data on the folks who do better with hypertension vs those who do not have HBP. What if this is mediated by blood flow to the brain? If you have vascular stenosis and a strong heart, higher BP might be able to push more blood into the brain. We know that a demented brain is a brain that is underfed. If you have stenosis, but a weak heart, you may be normotensive, but your brain is being starved. What is the exercise status? Exercise transiently raises BP - doing so regularly might feed the brain enough, even if you have stenosis, but are normotensive otherwise. Those who don’t get enough blood flow to the brain for whatever reason, severe stenosis, weak heart, but really the whole body, are going to do worse - here HBP might be the lesser evil if it allows better blood flow to the brain.
We do know that HBP in midlife is associated with increased dementia - perhaps HBP in midlife results in damage to blood vessels, also harming the brain, or perhaps HBP is a marker of stiffer blood vessel walls as a result of atherosclerosis, which is also a negative. But HBP with an onset in old age is different, because there hasn’t been decades of vascular damage from midlife HBP, so the compensatory boost in brain blood flow might be a net positive.
We can speculate all day long, but really, without more data on the cohorts it’s very hard to explain the associations.
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