We all know that it's possible to have too much of a good thing. But we don't tend to think of that as applying to nutrients. However, new research has found an association between a beneficial mineral and an increasingly common disease.
For a study published in Neurology, researchers at Erasmus University Medical Center in the Netherlands evaluated nearly 10,000 people who did not have dementia. They conducted blood tests and then followed the participants, whose average age was 65 at the beginning of the study, for the next eight years. Over the course of the study, 823 of the participants developed dementia, 662 of whom were diagnosed with Alzheimer's disease.
When the researchers did the blood work at the beginning of the study, they were looking in particular at the participants' magnesium levels. And when they did, they found something that was very surprising.
They divided the participants into five groups according to their blood magnesium levels. Almost all of them had levels in the normal range (1% were below the range, and only two people had levels above the range). They discovered that even though their levels were "normal" those in the lowest group had an increased risk of dementia. But, here's the surprising thing. So did those in the highest group. Here's how the groups lined up:
- There were 1,771 people in the low group, with 160 developing dementia. That's about 9%.
- There were 1,748 people in the high group, and 179 developed dementia. That amounted to 10%.
- There were 1,387 people in the middle group, and 102 developed dementia. This amounted to 7.3%.
So if you look at the numbers, it's clear the high magnesium group has almost the same risk as those in the middle group. And those in the middle group were 27% less likely to develop dementia than the high magnesium group and 18% less than the low magnesium group. It's pretty clear that a person's magnesium level, even though it's in the so-called normal range, can be an indicator of risk for dementia. But why?
The researchers were quick to point out that this study didn't show that magnesium was causing dementia, only that there was a link between magnesium levels and risk. So, what might the link be? It probably has something to do with faulty mechanisms controlling the balance of blood magnesium levels. Here's how it works.
A simple way to keep your muscles strong as you get older (and it isn't exercise)
This one step can strengthen aging muscles, boost your immune system, and even help you manage your weight.
Click Here To Learn More
Magnesium is incredibly important. It's a cofactor of many enzymes. This means that without enough magnesium around, these enzymes can't work. It's also involved in every single major cellular process including energy metabolism and DNA transcription and protein synthesis. Magnesium also plays an essential role in bone formation and muscle function. I'm telling you all this because you need to know that it's vitally important for the body to tightly regulate our blood magnesium levels. This is why the body has several different systems to control magnesium levels.
Your magnesium levels depend on three organs: the intestines, the bones, and the kidneys. For example, if your magnesium levels were to get too high, your intestines would decrease the absorption of any more magnesium until the levels returned to normal. Your bones would stop the release of magnesium into the bloodstream until the levels became normal. And your kidneys would quickly eliminate the excess magnesium to bring the levels back into balance. Similarly, if your magnesium levels were getting too low, these organ systems would act to increase the levels.
So, the discovery that both high and low levels of blood magnesium are associated with an increased chance of dementia, in all likelihood has to do with abnormalities in the intestinal, bone, and kidney control systems, not with excessive or deficient intakes of magnesium. So, what could cause an abnormality in one or more of these control systems?
A wide spectrum of disorders including type-2 diabetes, hypertension, and hypoparathyroidism, osteoporosis, seizures, and depression can lower magnesium levels by decreasing gastrointestinal absorption and/or increasing the loss of magnesium through the kidneys. Also, remembering that drugs are the third leading cause of death in the United States, it's not surprising that there are a whole host of drugs that can deplete magnesium levels by impairing absorption or by increasing excretion by the kidneys. The list includes diuretics, a great many antibiotics, cetuximab therapy, proton pump inhibitors, immunosuppressive agents, corticosteroids, and certain painkillers.
As was seen in this study, high magnesium levels are extremely uncommon. That's because excessive magnesium intake is almost impossible to achieve and the kidneys are very effective at eliminating too much magnesium. But slightly high levels such as were seen in this study can be caused by the following conditions that affect kidney function: insufficient water intake, depression, undiagnosed low thyroid function, adrenal exhaustion, lithium therapy, and excessive calcium and antacid intake.
So, if you have any of these risk factors that can result in lower or higher magnesium levels, check with your doctor. From the results of this study, it appears that the best blood magnesium level is somewhere in the middle of the range. And one thing else impressed me about this study.
The overall risk of getting dementia was 8.2%. To me, this is way too high! That's almost 10% of the population. So make sure you are in the 90% that don't get dementia. Read my book Bursting With Energy, and be compulsive about following the advice in there. I do, and even though I just turned 71, my brain is still functioning as good as it ever did. And if your memory is already starting to slip, start taking Advanced Memory Formula before it gets any worse.
Yours for better health,
Frank Shallenberger, MD
Jeroen HF, de Baaij JG, et al. Regulation of magnesium balance: lessons learned from human genetic disease. Clinical Kidney Journal, Volume 5, Issue Suppl #1, 1 February 2012, Pages i15-i24.