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In the age-adjusted model, higher intakes of magnesium were associated with lower fasting mean plasma C-peptide levels (P for trend=0.002) (Table 4).
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Low levels of magnesium are associated with muscle cramps.
Further, while we are unaware of previous studies examining the association between magnesium intake and constipation, we found that a low intake of magnesium was associated with an increasing prevalence of this condition.
After controlling for a series of potential confounding factors, we found that a low intake of water from foods and magnesium was associated with an increasing prevalence of functional constipation.
When these cases were stratified according to gestational age, magnesium was associated with a significant reduction in neonatal demise (OR, 0.67; 95% CI, 0.54 to 0.84; P =.0005).
A possible explanation is that high levels of plasma magnesium are associated with worse clinical outcomes [ 117].
High intakes of retinol equivalents and vitamin B1 were associated with a decreased risk of OAG, whereas a high intake of magnesium was associated with an increased risk.
Our study partly supports these observations, as increasing serum magnesium was associated with lower odds for MS (model 1 and 2).
Potential mechanisms of the inhibitory effects of magnesium in the calcification process are shown in Figure 3. Low serum levels of magnesium are associated with vascular calcification, both in humans and in a number of experimental animal studies [ 53– 53].
Magnesium could protect against vascular calcification via multiple molecular mechanisms, and decreased serum levels of magnesium are associated with vascular calcification, as revealed in both humans and in animal studies [ 1, 25– 27].
Our findings suggest that dietary magnesium is associated with several markers of inflammation and endothelial dysfunction independent of these dietary factors, although we could not completely exclude the possibility of residual confounding.
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