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.

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.

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.

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.

Zinc absorption adapts to zinc supplementation in postmenopausal women.

OBJECTIVE: To determine if human Zn absorption adapts to chronic high Zn intakes. METHODS: Zn absorption was measured at 0, 8, and 16 wk in healthy postmenopausal women who consumed controlled diets with approximately 5 mg Zn from food, supplemented to 14 (n = 6), 32 (n = 3), or 47 (n = 3) mg Zn/d for 22 wk. Zn absorption for 1 day was determined by (65)Zn-labeling of meals and whole body scintillation counting. RESULTS: At wk 0, less Zn was absorbed from diets with 14, compared with 32 or 47 mg/d (4.6, 8.7, and 10.3 mg/d, respectively; pooled SE = 0.9; p < 0.05). These differences were not apparent at wk 8 (5.4, 5.8, 6.4; NS) and became negligible by wk 16 (5.0, 5.0, 5.1; NS). Plasma Zn concentrations were unaffected. The results are consistent with a saturation response model of Zn absorption. CONCLUSION: Within several weeks, postmenopausal women biologically adapted to absorb a relatively uniform amount of 5 mg Zn/d when controlled, Zn-supplemented diets supplied consistent Zn intakes between 14 and 47 mg/d.

Alzheimer's disease as copper deficiency.

Four classes of etiologic agents can produce toxic, hereditary, infectious and deficiency diseases. Recent research on Alzheimer's disease generally addresses pathogenesis related to the first three classes of agents with little emphasis on cause. Low copper and cytochrome oxidase in Alzheimer brain can be attributed to low copper intakes or higher than average nutritional requirements. Experiments with animals deficient in copper involving amyloid, ceruloplasmin, copper transport, cytochrome oxidase, myelination, organ analysis and oxidative defense are consonant. Decreased cognition and increased tau in cerebrospinal fluid in Alzheimer's disease also are associated with low copper status. A high requirement for copper may explain early onset of Alzheimer's disease in Down's syndrome. Copper deficiency is a plausible cause of Alzheimer's disease. This hypothesis should be tested with a lengthy trial of copper supplementation.

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.

Low dietary magnesium increases supraventricular ectopy.

BACKGROUND: Magnesium has been suggested to be beneficial in counteracting all phases of the processes that lead to ischemic heart disease, including terminal events such as arrhythmia and sudden death. OBJECTIVE: We tested the hypothesis that an intake of magnesium considerably below the recommended dietary allowance can produce chemical and physiologic evidence of depletion. DESIGN: Twenty-two postmenopausal women were maintained in a metabolic unit and ate a diet of conventional foods containing less than one-half of or more than the recommended dietary allowance for magnesium (320 mg/d). Dietary assignments were random and double blind in a crossover design. Magnesium concentrations were measured by spectroscopy and ion-specific electrolyte analysis, and Holter electrocardiograms lasting approximate 21 h were recorded. RESULTS: Magnesium concentrations in erythrocytes, serum (total and ultrafilterable), and urine were significantly lower when dietary magnesium was lower. Holter monitors showed a significant increase in both supraventricular and supraventricular plus ventricular beats when the dietary magnesium concentration was low. Hypomagnesemia, hypocalcemia, and hypokalemia were not found. CONCLUSIONS: The magnesium requirement was defined with the use of biochemical and electrophysiologic criteria. The recommended dietary allowance of 320 mg/d seems correct; 130 mg is too little. Persons who live in soft water areas, who use diuretics, or who are predisposed to magnesium loss or ectopic beats may require more dietary magnesium than would others.

Meat diets and fragile bones: inferences about osteoporosis.

Because women supplemented with copper have improved bone density and femurs of rats deficient in copper have decreased mechanical strength, the hypothesis that mice fed meat would have fragile bones was tested. Mice fed sirloin are hypercholesterolemic in comparison to mice fed meat and beef liver because of a relative deficiency of copper compared to zinc. Male, albino, Swiss mice were fed trimmed sirloin or sirloin supplemented with beef liver (3/1 by weight). After 62 days, when hypercholesterolemia was detected, mice were killed and femurs were removed, cleaned and dried. Breaking strength was measured carefully at room temperature. The meat diet produced femurs 23% weaker (8.8 +/- 0.70 N/mg.100 vs 11.4 +/- 0.92, mean +/- SE, p < 0.04) in comparison to meat plus liver. Calcium, copper and phosphorus concentrations were unaffected but zinc was mildly elevated in the weak bones (426 +/- 17.5 pg/g vs 355 +/- 9.23, p < 0.002). These elements generally are unaltered in osteoporotic bones. Because copper deficiency produces osteoporosis in animals and people and because the Western diet often is low in copper, further tests of the hypothesis that diets low in copper contribute to osteoporosis are warranted.