Que Interesante. (An MTP rondo)
It's essential of course for digestive exzyme preparations (such as AbsorbAid)
to survive stomach acid. However, this won't help if there is too much oxidative
stress in the gut, as this can wipe out many of the key enzymes (such as
DPP-IV). Oxidative stresses often are the cause of the malabsorption or
maldigestion problems..... Sending in more enzymes can havelimited effect in
this case. It's a little bit like Pickett's charge in the Civil War: The new
soldiers are killed off as soon as they enter the fray.We find that zinc therapy
and metallothionein-promotion therapy can be effective in easing oxidative
stress in the G.I. tract and overcoming these problems.Tests for plasma zinc,
serum copper and serum ceruloplasmin can give a good indication of "metal"
oxidative stress. A Cu/Zn ratio greater than 1.20 or an excessive amount of
"unbound" copper..... that is, copper not bound to ceruloplasmin..... are
indicators of excessive free radical metal ions which can suppress or destroy
many digestive enzymes, cause diarrhea, digestive pain, maldigestion,
malabsorption and multiple food sensitivities. The levels will be abnormal in
the presence of toxic overloads of mercury, cadmium, lead, antimony, etc. A hair
analysis for the metals can provide some information also.(March
6, 2003)
Now, as some of you more persistant readers may note, my labs, while not high in Cu, are high in free/unbound Cu [38% free], due to my low ceruloplamin. This is preceisley why I was told that I was prescribed MTP. (author's note---I am taking the stuff 7 days a week now).
As you same adroit readers may recall, maldigestion, digestive pain, multiple food sensitivities and malabsorbtion are the halmarks of my illness. So, apparently, someone in the PTC was listening or else thier shot in the dark appears aimed at the same target, or its all connected anyway. Anyway, I hold out some hope for this MTP. But man oh man, does it taste terrible.
but wait...there is more.
A complication is that blood levels of copper can be very low in persons
who have severe copper overload. The classic example is Wilson's
Disease in which the liver accumulates huge amounts of copper. These same
Wilson's patients usually exhibit very LOW levels of Cu in blood.....also the
exhibit extraordinary low levels of ceruloplasmin. Is essence
their blood contains little copper, but the blood Cu is predominantly in
"unbound" form.
Yup, that is my case. my copper actually shows up a bit low. Not only that, but I have extraordinarily low Cp. That is why I was tested for the above mentioned Wilson's disease. I do not have wilson's, a biopsy confirmed that, but I still have elevated unbound copper and low Cp, a kind of grey middle ground.
Years ago, we mistakingly thought low blood serum or RBC copper levels meant CuWow....you hear that...normal unbound Cu should be 5-20 percent. I am almost twice the amount of the highest safe number.
deficiency..... and in a few cases we cautiously gave Cu supplements in an
attempt to correct the situation. Most of these patients reacted badly to the
Cu. Proper evaluation of copper status requires both serum Cu and serum
ceruloplasmin tests.Hair mineral copper is very valuable for behavior disorders
and ADHD patients, but is of far less clinical value for autism, bipolar, and schizophrenia populations.
Giving supplemental Cu to
patients is a risky business. It should be considered only in those who exhibit
sufficient ceruloplasmin to accomadate between 80 and 95% of the Cu
present. (April 10, 2003)
Selenium deficiency itself could result in a nasty copper elevation.
Metallothionein at the intestinal mucosa and in the liver is the primary agent
which regulates copper in the body. Selenium is needed for efficient
metallothionein functioning.
Carl Pfeiffer of Princeton, NJ tested more
than 25,000 persons for copper & reported that Cu toxicity was common, but
Cu deficiency extremely rare. We have investigated the metal-metabolism of about
20,000 persons & found the same thing. I admit there are theoretical
rationale for expecting copper deficiency, but it rarely actually happens.Hair
analysis ALONE is a very poor way to assess copper status. I say this after (a)
evaluating more than 100,000 hair analyses, (b) developing the first
high-quality hair standards (loaned to NIH and other researchers), and (c)
performing numerous double-blind, controlled experiments involving hair
chemistries. Findings of high Cu levels in hair are compromised by the many
external sources of Cu which cannot be completely removed by washing. Low levels of Cu in hair and/or blood often are coincident with
dangerous overloads of Cu in liver. Hair Cu values can provide
information of clinical significance, but by itselfis not clinically decisive.
Serum Cu indicates the total amount of Cu in serum. Serum ceruloplasmin
indicates the fraction of serum Cu that is bound as ceruloplasmin. A simple
calculation (paying attention to the assay units) yields the numbers for
comparison. Most copper experts agree that the normal or "healthy"
situation is to have about 80 to 95% of the serum Cu present as
ceruloplasmin.A high fraction of "unbound" Cu is a good
indicator of oxidative stress and low metallothionein activity......
and also a warning to NOT to supplement with Cu, even if serum/RBC/hair levels
of copper are low. In addition, one should consider possible environmental
sources of Cu,expecially drinking water and swimming pools/jacuzzis treated with
copper sulfate (to kill algae).(April 11, 2003)The ceruloplasmin analysis
indicates the amount of Cu properly bound to this protein (Should be 80-95% of
total serum Cu). If serum and hair Cu are low, a high proportion of
"unbound" Cu is a warning signal that there might be a Wilson's
Disease-like situation...... Low serum/hair copper, but severe Cu
overload in the liver. In some cases, testing forpossible Wilson's Disease is
indicatedBeen there, done that, enjoyed the biopsy. Thanks coach.
Usually, the question is whether there is a Cu overload. The incidence of true Cu deficiency/depletion is very low. (April 14, 2003)High copper females respond very well to therapy with zinc, B-6, P-5-P, C, E..... However the Zn should be introduced slowly..... for example 25 mg....50 mg.... 75 mg..... and given either at bedtime or after the evening meal. B-6 and P5P should be given before noon. Failure to phase in the Zn slowly would be likely to result in temporary worsening of symptoms over the first few weeks.She should avoid estrogen therapy, drink bottled water, and limit high-Cu foods like chocolate, carob, and shellfish.If her primary imbalance is the Cu overload, very little improvement is likely during the first 3 weeks..... followed by striking improvement thereafter. If the patient is clearly better during the first week, this is probably due to overcoming the pyrrole disorder. In her case, you might geta nice initial improvement which is partial in nature..... followed by a plateau of several weeks before more progress is made. (April 14, 2003)
Several of you have asked me how to gte in contact with me. I prefer to use firstpitchstrike@yahoo.com for correspondance. Yes, its a baseball reference. Suffering from disperceptions is not ALL that I do.