A little: good. Just a little more: bad

Most clinicians are familiar with the concept that when a little is good, more is often better, but a lot is still reliably toxic. This results in the mindset of there being little chance of doing harm with supplementing a "little," especially when the supplements involved are well-known and relatively popular supplements, widely regarded as being beneficial without question. In the case of calcium, iron, and copper the downside of minimal supplementation could not be more clear-cut. All three of these agents are essential for health, especially inside the cells. Nevertheless, once a relatively low daily intake of these nutrients is exceeded only minimally, toxicity rapidly ensues, with the highest intakes resulting in the greatest toxicity. This is in great contrast with some other nutrients, such as vitamin C, niacin or niacinamide, or vitamin K2, where toxicity is difficult to reach at any degree of intake or supplementation. Many other nutrient supplements, especially minerals, can readily be ingested to the point of toxicity, but the amounts needed are still much more difficult to reach compared to the minimally toxic intakes of calcium, iron, and copper.

Cellular Calcium Excess Underlies Disease

The marketing efforts of the dairy industry over the years have been wildly successful in convincing the public as well as most doctors that high calcium intake by diet (especially dairy), and by extension, supplementation as well, is of clear benefit to general health and for healthy bones as well. Unfortunately, the exact opposite is true, and excess calcium intake is the primary fuel sustaining and even provoking heart disease, cancer, and all chronic degenerative diseases.

Elevated intracellular calcium levels are present in all cells affected by disease processes, and very high levels are present in all malignant cells.

Furthermore, when therapeutic measures are taken to reduce these calcium levels, healthier cells always result. [1]

Several straightforward studies revealed the tremendous toxicity of too much calcium. In a study on 61,433 Swedish women followed for a median of 19 years, those who ingested the most total calcium from both diet and supplementation had an all-cause mortality 250% greater than those with the lowest intakes of calcium. Similarly, the same group with the greatest calcium intake had a more than 200% increase in mortality from coronary artery disease. [2] A meta-analysis of 15 trials also clearly demonstrated an increased risk of myocardial infarction in patients who took calcium supplements. [3]

The Coronary Artery Calcium (CAC) score has been used for over 30 years now to monitor the likelihood of a patient dying of coronary heart disease (myocardial infarction). A higher score indicates an increased chance of cardiac mortality. The CAC score is generated by a CT (computed tomography) scan over the heart. Greater amounts of calcium deposition in the coronary arteries consistently result in higher CAC scores. [4] Therapeutic measures that can increase or decrease this calcium accumulation correlate directly with an increased or decreased chance of cardiac mortality.

Recent research now indicates the CAC score is clearly predictive of all-cause mortality and not just death from coronary artery disease. [5] This indicates that the CAC score also serves as a reliable marker test for indicating the degree of calcium excess throughout the body and not just in the coronary arteries. Having a high amount of calcium deposition in the coronary arteries indicates calcium excess everywhere, even if it is only inside the cells and not as readily detected as calcium deposits. While some excess intracellular calcium can still be present when the CAC score is zero (normal), any positive score assures the presence of such excesses, with higher scores indicating greater excesses and greater degrees of pathology in the body.

Menopause, with its loss of estrogen production in the affected women, contributes directly to increased intracellular calcium levels.[6] Normal estrogen levels are very effective in minimizing cytoplasmic calcium levels as estrogen serves as a calcium channel blocker, limiting calcium uptake into the cells. Consistent with this, it has now been shown that menopause does promote increased CAC scores. [7] Testosterone, the male sex hormone counterpart to estrogen, also serves as a calcium channel blocker throughout the body. [8] This important relationship of increased intracellular calcium levels resulting from decreased sex hormone presence only further underscores the importance of giving some sex hormone support to all older patients, even when the hormone levels are still technically above the lowest levels in the laboratory reference range.

To be clear, the very well-defined relationship between calcium content inside the cells of the body and disease-causing increased intracellular oxidative stress really means only one thing: Never supplement calcium.

Iron and Copper: The Toxic Transition Metal Twins

Why call these two metal twins? Basically, it is because these metals are both prominent promoters of the Fenton reaction inside the cells of the body. All cells contain them, but when these metals increase in concentration by even the most minimal degree, oxidative stress rapidly ramps up. And as increased oxidative stress (where excess biomolecules are in the oxidized, electron-depleted state) is maintained or even further increased, abnormal cell function ("disease") flourishes.

The oxidation stimulated by ionic iron (Fe3+, Fe2+) and ionic copper (Cu2+, Cu1+) remains minimal ("physiological") as long as no significant new intakes of these metals occur, especially when unwittingly supplemented. Most reasonably balanced diets will never supply too much of these metals, although this delicate balance is easily disrupted by the most minimal of supplemental intake.

The Fenton reaction plays a major role in the ability of the body to kill pathogens, pathogen-infected cells, cancer cells, and cells with massively increased intracellular oxidative stress that are on the border of necrosis and/or other forms of cell death like apoptosis. When not properly balanced, it also plays a major role in the chronic toxicity inflicted by supplemental iron and copper intake. Both metals are known as transition metals because they readily shuttle electrons through various metabolic pathways. This ease of electron passage is why iron and copper conduct electricity so well (current is electron flow).

The classic Fenton chemistry is seen in a pathogen-infected cell, especially when provoked by a sufficient administration of vitamin C. While vitamin C has many different immune-supporting and anti-pathogen properties, it is the promotion of Fenton chemistry inside the cell that likely accounts most directly for its infection-resolving properties.

The most virulent of pathogens are the most avid consumers of iron. It is this characteristic that literally allows most pathogens to self-target themselves since this iron excess so strongly fuels the Fenton chemistry metabolism. Of note, some antibiotics owe much of their effectiveness due to their ability to chelate iron, thereby weakening the pathogen as it loses access to new sources of iron for its growth.

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