Amazoniac
Member
Regarding iron toxicity, especially for the hypopboyd, vit D supplements along with plenty of dairy is a synergistic program to deplete magnesium. And magnesium is required for the functioning of many nutrients that regulate iron, such as vitamin A and Bs for example. Cramps are not reliable unless vit D is coming from supplements, otherwise the body tries to adequate levels in a way that spares magnesium and prevents calcification. Magnesium stores can be very low without any cramp. Vit D supplements in this sense can be used to diagnose this imbalance. Dairy has a calcium and magnesium disparity that ain't good for the weak metabolism, it just can't afford unless supplemental is provided to compensate. Magnesium relieves body odor, same for dropping dairy in some cases, which is also another clue about their interaction with iron.
Based on Travis' articles published this year (still free for now), if dairy constipates you, it's one more aspect to consider because endotoxin enhances iron absorption.
Iron accumulation in tissues of magnesium-deficient rats with dietary iron overload
So, before embarking on aggressive chelation (not an indirect message to you, Regina), it's best to cover the basics.
And regarding copper, it should accumulate where there's excess iron, so it's protective in way. Biounavailable copper perhaps can be interpreted as iron toxicity instead.
Just some opinions.
Based on Travis' articles published this year (still free for now), if dairy constipates you, it's one more aspect to consider because endotoxin enhances iron absorption.
Iron accumulation in tissues of magnesium-deficient rats with dietary iron overload
"Consistent with these findings, magnesium deficiency in experimental animals affected status of thiamin (16), lipids (17), and minerals (18-21). Magnesium deficiency in rats decreased thiamin concentration in liver and kidney and the disappearance of injected radioactive 14C-thiamin from blood (22). Magnesium deficiency caused a decrease in tissue manganese concentrations and liver pyruvate carboxylase activity in rats (23). A decrease in bone calcium concentration and the reciprocal accumulation of calcium in kidney were found in magnesium deficient rats (24). Magnesium deficiency induces hyperlipidemia (25). Utilization of iron is affected by status of other nutrients, such as protein (26), pyridoxine, riboflavin (27), copper (28), or selenium (29). A preliminary study (19) found the accumulation of iron in liver, spleen, and kidney, and the elevated serum iron and percent saturation of iron binding protein of rats fed a magnesium-deficient diet, suggesting inefficient utilization of iron."
"The findings in the present study confirmed that magnesium deficiency affects iron metabolism. Cohlan et al. (38) reported microcytic anemia of the offspring of the magnesium-deficient rats. Tao et al. (39) observed anemia of magnesium-deprived Japanese quail. As was reported in a previous work (19), iron was accumulated in spleen, liver, heart, and muscle of magnesium deficient rats."
"In magnesium deficient rats, saturation of iron binding capacity was markedly decreased by iron deprivation and was extremely elevated by excess dietary iron. These results suggest the impairment of homeostatic control of transport iron in magnesium deficiency."
"These alterations in iron metabolism may imply that dietary magnesium deficiency causes inefficient utilization of iron and that iron overload with magnesium deprivation deteriorates rather than improves iron utilization.
The liver has the dominant role in plasma protein synthesis (46,47) and it represents the major source of plasma transferrin (48). A decrease of total iron binding capacity by magnesium deficiency may reflect general decline of protein synthesis rather than specific reduction of transferrin synthesis in liver because plasma albumin and choline esterase activity were decreased as well. In addition, magnesium deficient rats had an increased glutamate oxalate transaminase, glutamate pyruvate transaminase, and g-glutamate transaminase activities, indicating the impaired liver function."
"Magnesium deficiency with excess dietary iron may be an alternative model of hemochromatosis based on the pure dietary manipulation. Magnesium deficiency is compatible with the abnormalities in iron metabolism of hemochromatosis, i.e., iron deposition in liver, spleen, and other tissues; decreased total iron binding capacity; elevated saturation of iron binding capacity. In addition, magnesium-deficient rats had an increased glutamate oxalate transaminase, glutamate pyruvate transaminase, and 7-glutamate transaminase activities and a decreased plasma total protein, albumin, choline esterase activity, and total iron binding capacity, indicating liver cell damage and impairment of protein synthesis in liver. Magnesium-deficient rats had increased parathyroid hormone in plasma. Goldsmith (74) found the ectopic calcification in magnesium deficient rats. Kimura et al. (24) found a 24% decrease in the bone calcium concentration of magnesium deficient rats using 15% casein-based diet."
"Magnesium-deficient rats had increased calcium and phosphorus levels in kidney, suggesting the deposition of salt containing calcium and phosphorus. In addition, magnesium-deficient rats possessed the low alkaline phosphatase and inorganic phosphorus in plasma, and low magnesium concentration in kidney as well as plasma. Magnesium ion prevents the formation of calcium pyrophosphate crystal from the buffer solution containing calcium and pyrophosphate ions (75). Magnesium is an activator for alkaline phosphatase (76). Alkaline phosphatase possesses pyrophosphatase activity (77,78)."
"Magnesium-deficient rats in this study had the elevated parathyroid hormone concentration in plasma. The possible explanation to account for the rise in plasma parathyroid hormone in magnesium-deficient rats is a negative feedback control on parathyroid hormone secretion by magnesium. Shimada et al. (81) found an increase in plasma parathyroid hormone by low magnesium dialysate changed from normal magnesium dialysate in patients with chronic renal failure. Anast et al. (82) demonstrated an initial rise in plasma parathyroid hormone in magnesium-deficient rats followed by a fall below to normal. The second possibility is that the degradation of parathyroid hormone is secondarily reduced owing to the impaired liver function in magnesium-deficient rats."
"In conclusion, magnesium deficiency may evoke inefficient iron utilization and iron deposition in tissues that is reinforced by oral iron overload. The abnormalities of iron metabolism in magnesium deficiency are resembling the hemochromatotic conditions in the human."
"The findings in the present study confirmed that magnesium deficiency affects iron metabolism. Cohlan et al. (38) reported microcytic anemia of the offspring of the magnesium-deficient rats. Tao et al. (39) observed anemia of magnesium-deprived Japanese quail. As was reported in a previous work (19), iron was accumulated in spleen, liver, heart, and muscle of magnesium deficient rats."
"In magnesium deficient rats, saturation of iron binding capacity was markedly decreased by iron deprivation and was extremely elevated by excess dietary iron. These results suggest the impairment of homeostatic control of transport iron in magnesium deficiency."
"These alterations in iron metabolism may imply that dietary magnesium deficiency causes inefficient utilization of iron and that iron overload with magnesium deprivation deteriorates rather than improves iron utilization.
The liver has the dominant role in plasma protein synthesis (46,47) and it represents the major source of plasma transferrin (48). A decrease of total iron binding capacity by magnesium deficiency may reflect general decline of protein synthesis rather than specific reduction of transferrin synthesis in liver because plasma albumin and choline esterase activity were decreased as well. In addition, magnesium deficient rats had an increased glutamate oxalate transaminase, glutamate pyruvate transaminase, and g-glutamate transaminase activities, indicating the impaired liver function."
"Magnesium deficiency with excess dietary iron may be an alternative model of hemochromatosis based on the pure dietary manipulation. Magnesium deficiency is compatible with the abnormalities in iron metabolism of hemochromatosis, i.e., iron deposition in liver, spleen, and other tissues; decreased total iron binding capacity; elevated saturation of iron binding capacity. In addition, magnesium-deficient rats had an increased glutamate oxalate transaminase, glutamate pyruvate transaminase, and 7-glutamate transaminase activities and a decreased plasma total protein, albumin, choline esterase activity, and total iron binding capacity, indicating liver cell damage and impairment of protein synthesis in liver. Magnesium-deficient rats had increased parathyroid hormone in plasma. Goldsmith (74) found the ectopic calcification in magnesium deficient rats. Kimura et al. (24) found a 24% decrease in the bone calcium concentration of magnesium deficient rats using 15% casein-based diet."
"Magnesium-deficient rats had increased calcium and phosphorus levels in kidney, suggesting the deposition of salt containing calcium and phosphorus. In addition, magnesium-deficient rats possessed the low alkaline phosphatase and inorganic phosphorus in plasma, and low magnesium concentration in kidney as well as plasma. Magnesium ion prevents the formation of calcium pyrophosphate crystal from the buffer solution containing calcium and pyrophosphate ions (75). Magnesium is an activator for alkaline phosphatase (76). Alkaline phosphatase possesses pyrophosphatase activity (77,78)."
"Magnesium-deficient rats in this study had the elevated parathyroid hormone concentration in plasma. The possible explanation to account for the rise in plasma parathyroid hormone in magnesium-deficient rats is a negative feedback control on parathyroid hormone secretion by magnesium. Shimada et al. (81) found an increase in plasma parathyroid hormone by low magnesium dialysate changed from normal magnesium dialysate in patients with chronic renal failure. Anast et al. (82) demonstrated an initial rise in plasma parathyroid hormone in magnesium-deficient rats followed by a fall below to normal. The second possibility is that the degradation of parathyroid hormone is secondarily reduced owing to the impaired liver function in magnesium-deficient rats."
"In conclusion, magnesium deficiency may evoke inefficient iron utilization and iron deposition in tissues that is reinforced by oral iron overload. The abnormalities of iron metabolism in magnesium deficiency are resembling the hemochromatotic conditions in the human."
So, before embarking on aggressive chelation (not an indirect message to you, Regina), it's best to cover the basics.
And regarding copper, it should accumulate where there's excess iron, so it's protective in way. Biounavailable copper perhaps can be interpreted as iron toxicity instead.
Just some opinions.