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NIGEL COCKLE <[log in to unmask]>wrote: <<<<Like a number of others on this list, I have found that protein seriously interferes with the action of Sinemet. I have got around this by avoiding protein during the day and having a more normal meal late at night. I noticed that dairy products seemed to cause most difficulty - milk seems to cause the PD symptoms to appear very rapidly - it seems to be something more than an interference with absorption of sinemet into the blood stream. I have found that I do not get the same problem if I drink soya milk even though, according to the label, soya milk has more protein than cows milk. I have also tried eating Roquefort cheese which is made from sheeps milk and this does not appear to affect the action of sinemet. Am I alone in having these difficulties in digesting cow's milk or is this a common problem? Nigel Cockle 51/12>>>>>>> There is discussion about this quite often - and about human, adults especially, using cow's milk. I have "inherited" some dislike of milk from my mother (before she forgot she did not eat any other than ice cream due to Alzheimer's). I like ice cream and frozen yogurt but do not drink or usemilk with cereal for many years. The yogurt seems less counter to levodopa. The optimum food for calves is not likely the optimum for animals without four stomachs and enzymatic digestion of grasses, et cetera. Perhaps learned enzymes changes/adjustment in babyhood makes milk digestible. Perhaps the residual hormones and enzymes in cow's milk is somehow detrimental to the digestive "mechanisms" of our stomach such that most/more of the levodopa is digestively destroyed. this is before entering the bloodstream where the carbidopa retards conversion to dopamine. I retrieved the following from somewhere on the net: <<<<<<<<L-Dopa (Larodopa) and l-dopa/carbidopa (Sinemet) In order to replenish dopamine in the striatum, the precursor l-dopa must be given because dopamine itself does not cross the blood brain barrier. Only about 1% of l-dopa reaches the CNS where it is taken up by both dopaminergic and noradrenergic neurons. In the former, it is converted by l-amino acid decarboxylase to dopamine, which, in the striatum, serves to restore dopaminergic activity and alleviate the symptoms of PD. Uptake into other dopaminergic neurons and noradrenergic neurons is responsible for some of the CNS toxicity and side effects of the drug discussed below. The other 99% of a dose of l-dopa can be accounted for by conversion to dopamine in the GI tract before absorption (ca. 70%), and uptake into the terminals of sympathetic neurons, where it is converted to norepinephrine. Peripheral dopaminergic and noradrenergic actions also contribute to the side effects and toxicity of the drug, particularly on the cardiovascular system. Fate of systemic l-dopa. A reduction in the dose of l-dopa, increased efficacy, diminished side effects and quicker stabilization can be achieved with the addition of carbidopa to l-dopa (i.e., Synamet). Carbidopa is an l-amino acid decarboxylase inhibitor which does not cross the blood brain barrier. Consequently, peripheral conversion to dopamine (and norepinephrine) is inhibited without affecting the conversion in the CNS. This combination therapy has become the mainstay in the treatment of PD.>>>>>>> Perhaps one of our experts in pharmacy or biology can validate the 70% conversion loss of levodopa? Perhaps some blood plasma absorption data with and without milk or product hasbeen done? SHOULD be done? Another thought is that tyrosine plentifulness may be involved. Maybe the milkcomponents fill up all the transporter molecules that take large amino acids into the blood. ron 1936, dz PD 1984 Ronald F. Vetter <[log in to unmask]> http://www1.ridgecrest.ca.us/~rfvetter/