The contemporaneous epidemic of chronic, copper deficiency.

The classical deficiency diseases have nearly disappeared from the industrialised world and are thought to be found largely in sub-Saharan Africa and South Asia. More than 80 collected medical articles, mostly from Europe and North America, describe more than 9000 people with low concentrations of copper in organs or tissues or impaired metabolic pathways dependent on copper. More than a dozen articles reveal improved anatomy, chemistry or physiology in more than 1000 patients from supplements containing copper. These criteria are diagnostic of deficiency according to The Oxford Textbook of Medicine. Alzheimer's disease, ischaemic heart disease and osteoporosis receive major emphasis here. However, impaired vision, myelodysplastic syndrome and peripheral neuropathy are mentioned. Copper deficiency probably causes some common, contemporaneous diseases. Advice is provided about opportunities for research. Seemingly authoritative statements concerning the rarity of nutritional deficiency in developed countries are wrong.

Cholesterotropic and cuprotropic chemicals.

A dozen or so chemicals modify both cholesterol and copper metabolism. Ascorbic acid and cadmium, etc., inhibit copper metabolism and raise cholesterol. Calcium and clofibrate, etc., enhance copper and lower cholesterol. Perhaps the doses of dietary cholesterol and fructose in this experiment were too severe to permit fenofibrate to lower cholesterol in a manner similar to clofibrate. © 2020 Society of Chemical Industry.

Calcium can delay age-related macular degeneration via enhanced copper metabolism.

Secondary analyses of data from the Age-Related Eye Disease Study (AREDS) revealed that higher calcium intakes were associated with slower progression to age-related macular degeneration (AMD). Earlier, primary analyses had revealed that a supplement containing copper reduced the odds of developing AMD while lengthening life. Because ocular lesions are being reported increasingly in neuropathy from copper deficiency and because higher dietary calcium can have beneficial effects on copper metabolism, it is hypothesized that the association of calcium intakes with better vision was mediated by improved copper utilization of study participants who were eating too little copper. Nutrition surveys reveal that amounts of copper proved insufficient for men and women in controlled studies are readily available to the general population. Observations on eye anatomy of animals deficient in copper and on decreased retinal superoxide dismutase, an enzyme dependent on copper for activity, in people with AMD support this hypothesis. Eradication of AMD will require new approaches based on hypotheses that fail falsification.

Some bottled water may be salubrious.

Hard drinking water seems protective against cardiovascular disease compared to soft water. Published data on calcium and magnesium in bottled water products were evaluated to determine water hardness. Data on water chemistry of thirty-three products were obtained from the internet and hardness, as calcium carbonate, was calculated. Approximately two thirds of the products were soft according to criteria of the US Geological Survey; only one fifth were very hard. Beer and wine also were found to be very hard. Consumers and suppliers should avoid soft water. Some beneficial, cardiovascular effects of beer and wine may be the result of hard water.

IHD from copper deficiency: a unified theory.

The theory, in brief outline here, implicating deficiency of Cu in the aetiology and pathophysiology of IHD explains more attributes of the disease than any other theory. This theory satisfies several of Hill's criteria of a half-century ago for deducing association between an environmental feature and presence of an illness. Most important is the temporal association between the rise of IHD and the decrease in dietary Cu since the 1930s along with a parallel increase in the supplementation of pregnant women with Fe, a Cu antagonist. There are more than eighty anatomical, chemical and physiological similarities between animals deficient in Cu and individuals with IHD. Few of these similarities have been produced by other dietary manipulations because feeding cholesterol induces Cu deficiency in animals. The most recent of these to be identified is decreased serum dehydroepiandrosterone. Some concomitant aspects of Cu metabolism and utilisation have been identified in other theories about heart disease: fetal programming, homocysteine, and Fe overload.

Myelin and traumatic brain injury: the copper deficiency hypothesis.

Nearly two million people suffer traumatic brain injury in the US each year. These injuries alter adversely the metabolism of myelin, a major lipid material in brain, both in people and in experimental injuries of animals. A newly discovered and severe human neuropathy from copper deficiency provides evidence that some people in the US are malnourished in copper. As it is well known among copper cognoscenti that it is impossible to synthesize myelin if copper nutriture is inadequate, it seems reasonable to assume that repair will be poor in this situation. Copper status of patients should be evaluated and experiments with injured animals should be repeated with graded doses of copper to determine if copper metabolism is important in this illness.