I am curious about something. People with CFS have been shown to have higher than normal levels of apoptosis (programmed cell death). According to the methylation hypothesis, many genes may not have the appropriate methyl groups to ensure appropriate silencing. So it makes sense to me that the TNF levels would be higher than normal and therefore stimulate apoptosis.......however, what bothers me is that the process of apoptosis relies on caspases, which are cysteine-containing. If cysteines are in short supply due to methylation cycle problems, how do the cells find enough to maintain these high levels of apoptosis? I have not been able to find out how many cysteines are required for the caspases......anyone?