I thought it might be good to explain what the calcium channel my son's missing does and why it's messed up.

From my research, which I hope is correct, Calcium is a possitive charged ion and called CA2+. It enters the cell when a receptor senses the cell is negatively charged and needs more calcium. This same sensor also senses when the cell is possitively charged and stops too much CA2+ from entering the cell. If people are missing, or are weak in, the CA2+ gene/receptor (also called a 'voltage gated receptor') & exposed to drugs that cause calcium to load into the cell, the drug will block the receptor from sensing it has too much calcium. This causes the cells to die (called calcium loading apoptosis), leading to lethal arrythmias. There is some postulating (in mice) that the receptor 'sparks' open a perfect amount of times per second to allow calcium into and out of the cell. Mice with defective receptors have 4 times more sparks as normal ones. That this could be what causes calcium imbalances during stress and sensitivity to certain drugs. It kind of makes sense that the cells would load more calcium if they open more often.

Aluminasilicate (a possitively charged metal) can prevent calcium from entering the cell by blocking it in people with defective calcium channels. Apparently, this causes a multitude of diseases (Alzheimer's being one).

Anyone can be given a drug or exposed to a toxin that can mess up a person's genes and make them sensitive (like chlorine by-products, also known as PBC's, that are felt to be responsible for birth defects and Autism). I feel vaccines have this potential, and this could be why 1/3 of all SIDS deaths are reported as potentially being messed up sensors of Calcium, sodium and potassium. Drugs like calcium channel blockers, anasthesia, phen phen, meridia, can cause heart arrhythmia, stroke or heart attack in these people.

Mice exposed to certain chemicals like PBC's in the womb develop the same heart defects as my son.