bookmark_borderHeavy Metals In Your Diet

Heavy metals can either be an essential part of your diet or toxic and deadly. For instance, iron is needed for blood; however, men can build up toxic levels of iron as they grow older.

Living organisms require varying amounts of “heavy metals”. Iron, cobalt, copper, manganese, molybdenum, and zinc are required by humans. Excessive levels can be damaging to the organism. Other heavy metals such as mercury, plutonium, and lead are toxic metals and their accumulation over time in the bodies of animals can cause serious illness. Certain elements that are normally toxic are, for certain organisms or under certain conditions, beneficial. Examples include vanadium, tungsten, and even cadmium.

Heavy metal toxicity can result in damaged or reduced mental and central nervous function, lower energy levels, and damage to blood composition, lungs, kidneys, liver, and other vital organs. Long-term exposure may result in slowly progressing physical, muscular, and neurological degenerative processes that mimic Alzheimer’s disease, Parkinson’s disease, muscular dystrophy, and multiple sclerosis. Allergies are not uncommon, and repeated long-term contact with some metals (or their compounds) may cause cancer.
– Wikipedia

Do not eat:

  • Shark
  • Swordfish
  • King Mackerel
  • Tilefish

Nearly all fish and shellfish contain traces of mercury… some fish and shellfish contain higher levels of mercury that may harm an unborn baby or young child’s developing nervous system. The risks from mercury in fish and shellfish depend on the amount of fish and shellfish eaten and the levels of mercury in the fish and shellfish.
– The FDA of the United States of America

Heavy Metals Song from the album Food For Thought

bookmark_borderCopper Connected to Alzheimer’s Disease

Proceedings of the National Academy of Sciences of the United States of America has conducted a study linking the consumption of copper to Alzheimer’s:

Significance
The causes of the sporadic form of Alzheimer’s disease (AD) are unknown. In this study we show that copper (Cu) critically regulates low-density lipoprotein receptor-related protein 1–mediated Aβ clearance across the blood–brain barrier (BBB) in normal mice. Faulty Aβ clearance across the BBB due to increased Cu levels in the aging brain vessels may lead to accumulation of neurotoxic Aβ in brains. In a mouse model of AD low levels of Cu also influences Aβ production and neuroinflammation. Our study suggests that Cu may also increase the severity of AD.

Abstract
Whereas amyloid-β (Aβ) accumulates in the brain of normal animals dosed with low levels of copper (Cu), the mechanism is not completely known. Cu could contribute to Aβ accumulation by altering its clearance and/or its production. Because Cu homeostasis is altered in transgenic mice overexpressing Aβ precursor protein (APP), the objective of this study was to elucidate the mechanism of Cu-induced Aβ accumulation in brains of normal mice and then to explore Cu’s effects in a mouse model of Alzheimer’s disease. In aging mice, accumulation of Cu in brain capillaries was associated with its reduction in low-density lipoprotein receptor-related protein 1 (LRP1), an Aβ transporter, and higher brain Aβ levels. These effects were reproduced by chronic dosing with low levels of Cu via drinking water without changes in Aβ synthesis or degradation. In human brain endothelial cells, Cu, at its normal labile levels, caused LRP1-specific down-regulation by inducing its nitrotyrosination and subsequent proteosomal-dependent degradation due in part to Cu/cellular prion protein/LRP1 interaction. In APPsw/0 mice, Cu not only down-regulated LRP1 in brain capillaries but also increased Aβ production and neuroinflammation because Cu accumulated in brain capillaries and, unlike in control mice, in the parenchyma. Thus, we have demonstrated that Cu’s effect on brain Aβ homeostasis depends on whether it is accumulated in the capillaries or in the parenchyma. These findings should provide unique insights into preventative and/or therapeutic approaches to control neurotoxic Aβ levels in the aging brain.

In a separate study, playing a musical instrument was found to and years to the life of the brain.