New Thought

[Guest guest]

This is going to be long. But since enzymes is what this group is

about, here goes. If any of you are interested, email me privately.

Here's a few interesting tidbits. Oregon does ALL the PKU testing for

five states, and Pacific Astoria labs makes the test kits for several

other states. The reference range is set at 4.0 in the five states,

and in any state that uses the Pacific Astoria kit. The PKU testing

labs in Oregon will not (they say it's the law) give out the NUMBER

results to parents. Only to physicians. They don't even post the

numbers to physicians, just " normal " or not. PKU is very hard to

detect in a child older than a couple years, because phenol is normal

and expected in the blood of an older child. People with PKU lack

certain digestive enzymes to handle the phenol. It causes all sorts

of metobolic problems.

Likewise, yeast strains sensitive to Hg are those which have innately

low levels of tyrosine synthesis. Mercury can deplete cellular

tyrosine by binding to the SH-groups of the tyrosine uptake system,

preventing colony growth (Ono et al, 1987), and Hg-depleted tyrosine

would be particularly significant in cells known to accumulate

mercury (e.g., neurons of the CNS, see below). Similarly, disruptions

in tyrosine production in hepatic cells, arising from a genetic

condition called Phenylketonuria (PKU), also results in autism

(Gillberg & , 1992, p.203).

Oregon law (and a number of other states) mandates insurance coverage

for " medical foods. " PKU diets qualify. No identified PKU -- no

insurance outlay. Read about PKU. They KNOW it causes:

Mental retardation

Motor coordination problems

Autism

Agression and destructive outbursts

Screaming is common

Hyperactivity

Seizures

Heart and Circulatory Problems

Wierd Anemias

Short statutre

Also:

60% have small heads

90% are blond haired blue-eyed Ethinicity: Northern European. Ireland

and land have the highest incidence (1/4,000 there, 1/16,000

worldwide) in the world.

Hair testing in PKU kids shows high aluminum and other

eccentricities. If undetected at birth, a baby can appear " normal "

for up to a year. If not treated within that time, the MR

is " permanent. " (Don't believe it! They are doing research on

previously undetected and untreated PKU adults in institutions and

raising their IQ by many points -- ergo, even previously untreated

adults benefit from the low phenol diet and special enzyme

supplements!) The diet can help even permanently MR people with their

behaviors

In Europe they reference mild PKU in the 3.0 range and monitor/treat

those children through dietary modification as well.

" The Guthrie Inhibition Assay is usually used to test for blood

phenylalanine levels. (An assay compares samples from the body to a

reference standard of known concentration to determine the relative

strength of the substance in the samples.) The test uses a special

strain of the bacterium Bacillus subtilis that requires phenylalanine

for growth. The bacterium is grown on the surface of a special medium

that lacks phenylalanine. Paper disks containing blood samples and

testing standards are placed on top of the agar plate, and the

bacteria are allowed to grow. The amount of growth around each disk

is proportional to the amount of phenylalanine in the disk. A second

assay detects high levels of phenylalanine metabolites in the urine.

(These metabolites are the products of phenylalanine when it's broken

down and used by the body.) These metabolites first appear four to

six weeks after birth and are detected by the addition of a few drops

of a 10% ferric chloride solution to a urine sample. If the

metabolites are present, a deep bluish green color develops. Color

development indicates that the patient has PKU. "

Oregon: in 1988, 58+% of newborn screens were submitted incorrectly,

according to the survey. Again, a lengthy read, but full of

interesting stuff. Wonder what the " submitted incorrectly " results

are now.

http://www.google.com/search?

q=cache:dFJ1K_43C_sC:www.aap.org/advocacy/medhome/NBScategorizedcompen

d.pdf+PKU+missed+%22compendium%22 & hl=en & lr=lang_en & ie=ISO-8859-1

Regarding insurance coverage for medical foods:

http://www.law.uh.edu/healthlawperspectives/Managed/990525MedicalFood.

html

Several links about " the subject " and it's metabolism effects, etc.

http://www.oralchelation.com/ingred/lphenyla.htm

Research from Sweden. Lengthy, but worth the read.

http://publications.uu.se/theses/fulltext/91-554-5156-X.pdf

This is from a school of engineering in VA. Look at the molecular

structure:

http://www.egr.vcu.edu/courses/ENGR122S00/lectures/lec22.pdf

From my husband's chemistry handbook:

Phenol (phenyl alcohol, phenyl hydroxide) Check the molecule.

Identical to phenylalanine. a Constituent of NutraSweet:

Incompatible and/or reactive with: calcium hypochlorite, aluminum

choride, acids. Strong oxidizers.

Most PKU Guthrie testing is done with bacillus subtilis. That

bacteria requires phenol to grow. Bacillus subtilis is found in the

top 2 " of soil in warmer climates, usually arid, not northern

climates. Not naturally native to human gut. It must be renewed in

the human gut to continue. Once it eats what it wants to eat, it

starves and dies. Bacillus subtilis eats yeast. Directly responsive

to what is in the gut, less dietary modification required. Produces

many of the enzymes you and others are using to help digest various

carbos. Used extensively in veterinary and animal food products,

especially those containing cereals.

Used commercially to kill fungus in and around plants, in spray

treatments. Kills 'em dead.

This is from American Family Physician:

http://www.aafp.org/afp/991001ap/1462.html

The blood phenylalanine concentration in newborns is normally 0.5 mg

to 1 mg per dL (30 to 60 µmol per L). In general, few infants with

PKU will remain unidentified when a phenylalanine cut-off value of 2

mg per dL (121 µmol per L) in the first 24 hours is used. Not all

states, however, use 2 mg per dL as the cut-off value. Forty states

and jurisdictions use 4 mg per dL (242 µmol per L) as the screening

cut-off value for PKU, six states use 3 mg per dL (182 µmol per L)

and seven states use 2 mg per dL.10 Some newborns without PKU have

transiently elevated phenylalanine levels of more than 6 mg per dL

(363 µmol per L) related to delayed maturation of enzymes required

for amino acid metabolism. Blood phenylalanine levels are generally

slightly lower in breast-fed infants than in bottle-fed infants.

Breast milk contains only 12 to 14 mg of phenylalanine per ounce,

compared with 24 to 28 mg per ounce in formula.

Because PKU is a heterogeneous disorder, phenylalanine levels vary

greatly in infants with the disease. However, treatment is usually

not necessary in infants who persistently demonstrate blood

phenylalanine concentrations of less than 10 mg per dL (605 µmol per

L). Such cases are mild and permit production of phenylalanine

hydroxylase, which converts phenylalanine to tyrosine, as in the

normal person.11 Persons with severe mutations have much higher

phenylalanine levels. To be completely certain of the diagnosis,

follow-up testing is recommended in male infants with initial

phenylalanine levels between 3 and 10 mg per dL and in female infants

with values between 4 and 10 mg per dL.12 Affected females should be

followed through their reproductive years to prevent impaired fetal

neurologic development as a result of maternal PKU.13

And from the National Library of Medicine:

Diamond A. Phenylalanine levels of 6-10 mg/dl may not be as benign as

once thought. Acta Paediatr Suppl 1994 Dec;407:89-91. Available from:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?

cmd=Retrieve & db=PubMed & list_uids=95284443 & dopt=Abstract

To quote:

" Department of Psychology, University of Pennsylvania, Philadelphia

19104-6196, USA.

Results of a longitudinal study of children treated early and

continuously for phenylketonuria (PKU) indicated that those children

whose plasma phenylalanine (Phe) levels were approximately 3-5 times

normal (6-10 mg/dl; levels previously considered safe in the US) were

impaired in cognitive functions dependent on prefrontal cortex. In

particular, the children had difficulty when required to hold

information in the mind and, at the same time, exercise inhibitory

control to resist doing what might be their first inclination. The

deficits were evident in relation to each of several comparison

groups and at all three age ranges (infants, toddlers and young

children). The deficits appeared to be selective in that the same

children who were impaired on the prefrontal cortex tests performed

normally on the control tests. Since most of the control tasks tap

functions dependent on parietal cortex or the medial temporal lobe,

these results suggest that those functions are spared. To investigate

the biological mechanism causing these cognitive deficits, we created

an animal model of early-treated PKU. The results indicated that rats

whose plasma Phe levels were mildly, but chronically, elevated had

cognitive deficits (impaired performance on a behavioral task

dependent on frontal cortex (delayed alternation)) and neurochemical

changes (most notably, reduced dopamine metabolism in frontal cortex).

Kathleen Stokes