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On Thu 17 Oct, Camilla Flintermann wrote:
>
I almost forgot one other item - The posting from Patrick J. Martin ( copied
below) gives just about the best explanation that I have seen so far to
explain why too much Carbidopa is bad for you.  Thanks, Patrick.

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Carbidopa is a non-selective inhibitor of decarboxylating enzymes in the
digestive system.  Levodopa(Ldopa) is a large "neutral" amino acid(LNAA) that
can transfer through the blood/brain barrier and convert to dopamine that we
need. This transfer is accomplished by the LNAA receptors in our blood.  Only
about 1% of the Ldopa makes its way into our brain.  The remainder is digested
and utilized elsewhere in our body -- as a source of dopamine at
neurotransmitting sites and as building material for proteins.  Carbidopa's
intended task is to maximize the Ldopa survival in our digestive system until it
is carried by an LNAA receptor to our brain.

Now -- the bad news.  Carbidopa is non-selective and inhibits the
decarboxylation of other LNAA's derived from our digestion of proteins.  These
other "neutral" amino acids include most of our essential amino acids.  Our
digestive system responds by increasing our acid production, and retention.  Our
protein digestion, utilization, and competition for LNAA receptors gets screwed
up, we get barfy, get gastric reflux,  start swinging in the on/off mode, and
starve ourselves to death..

So -- give it some thought -- keep your carbidopa input down to the level YOU
find necessary to fit your pattern of protein types, protein timing, Ldopa
timing, and everday activities.  I find general agreement with the
less-than-100mg/day limit.
Factors that could affect this level are: my weight (150 pounds); my age(70); my
years of parkinsonism(10); my years of carbidopa/Ldopa(7).  Unfortunately, my
need for Ldopa has reached 1000mg/day, so I am headed for troubled waters again.



--
Brian Collins <[log in to unmask]