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Submission for the Gotham Prize

Dr Chris Reading
BSc, DipAgSc, MB, BS, FRANZCP'

FACNEM

Hypothesis:
threatened m

her cancer is trans-placentally induced by nutritional hormonal deficiencies and


rage

Category: v
Idea type: eti

tlpes of cancer

Examining nuhitional hormonal deficiencies and toxicities at time of threatened miscarriage, a{d comparing them with similar pathologies when cancer presents.
Research

abnorma threatened miscarriage?

Is cancer embryonic
especially d

by low hormones, vitamins and other nutrients affecting vulnerable issue at critical periods of foetal development such as stem cells
to threatened mi scarriage?

er behaves like embryonic tissue, has full telomeres, releases foetal Is this why proteins li CEA, o-foeto-protein, releases placental hormones like HcG, ACTH, growth ho etc and releases angiogenic factors to help new blood vessels develop as i the embryo?
Melanoma receptors

op in moles a type of congenital abnormality. Why do moles have glycoproteins of peanuts?


ns pass across the placenta as the mole was developing in utero and

Did glycop
developed

it

for it? Why?

What aneuploides Why do left

chromosomal changes in bone manow stem cells as trisomy 21 meaning risk for leukaemia etc?
nded women have twice the risk of breast cancer?

in utero and

When and why did women with breast cancer develop accidental fi of Bierman, seen in 25011000 women with breast cancer and 6lr population? What causes the abnormal breast duct patterns to develop in people
cancer?

t pattems

for normal
for breast

What causes the abnormal pituitary/adrenal axis in breast cancer?

In familial breast cancer patients why are they born with skin where p behave like foetal fibroblasts, not adult ones?
What causes cystic ovaries, increasing risk for ovarian cancer?
What causes oesophagal webs, bowel polyps and risk for bowel cancer I

fibroblasts

Is it low 81 in utero that causes a person to be bom with Sydney palmar creases, at risk for leukaemia etc?

li

(2) cancers Thus apart ftom (1) genetic causes of cancer with known oncogenes have been caused by mutations due to prenatal causes where foetal ovary/folli iotic nondamaged in utero resulting in ova being released with a mutation and (3) disjunction in ova resulting in Down's Syndrome and risk for leukaem etc, is the main cause of cancer (4) perinatal or transplancental industion of cancer?
Thus what nutritionallhormonal/toxic disturbances in utero cause cancer cancer cells to develop and flare up cancer later?

lls or pre-

Is the cause of cancer a traumatised stem cell or mutatron rn


abnormality of it or its precursor?

congenital

Does coeliac disease or malabsorption state due to cow's milk/gluteil containing grainllegume and bean sensitivity/intolerance (all of which can cause flatlgut villi etc) result in low nutrients as below?

Nutrients (1) Vitamins (which are coenzymes);

development;
hormones and enzymes; (4) Monosaccharides (blood sugars) that form the 'glyco' part hormones and enzymes; (5) crl3 and co6 essential fatty acids for membranes etc, and (6) Bioflavinoids that help protect breakdown of PGE1 series and second messengers).

for foetal
i

(3) Certain amino acids which form the 'protein' part of glycoproteirls which

are

of

tein

P (first and

and adrenal Thus do nutrient deficiencies across the placenta result in the foetal li fall t n placental cortex releasing less than optimal amounts of DHEA? As levels

oestrogens

all

and TMC is imminent and the foetus is close to death (ie being

aborted).

do stem cellp in the body temporarily release placental hormones/angiogenic factors, cytokines et| to maintain growth and such stress hormones as ACTH to form cortisol, DHEA and $rowth hormone to maintain growth etc?
Is the stem

ll now'programmed'?

congenital abnormality of breast stem cells develop receptors for as oestrogen, progesterone etc and for pesticides with oestrogen-like hormones action oassi g across the placenta, and also develop food lectin receptors ifthey pass across the enta?

Thus does

ed stem cells release CEA etc to help maintain foetal gut. The cancer ifferent membranes and develop special metabolic pathways to survive anoxla as o n at TMC time the mother is anaemic, has blood loss and is in shock (anoxia).
These cells have

Do the low
breast

tamins/hormones cause abnormal pituitary/axis development as seen in and bipolar disorder?

environment' programs the stem cell and switches on oncogenes etc. rful inducers and organizers hold the cancer cells in check and organs develop. F ilure of foetal pancreatic development can cause a choriocarcinoma or

This'mali
However,

placenta to

growing. deficiencies across the placenta mean abnormal protein develops , causing isoenzymes that will not break down protein optimally, ulty in breaking down gluten, u-gliadin, gliadinomorphin, casomorphin tions of cow's milk and legumes/beans etc in the cancer patient? ients have abnormal pancreatic enzymes? Is this why cancer patients food sensitivity/intolerance and prone to autoimmune disease like breast s in ductal cancer etc?

Also could

in the causing di and other


Do cancer
are prone

duct anti

Could nutritional/hormonal deficiencies result in abnormal adrenal cortex and defective st{roid hormones and enzymes such as an isoenzyme of steroid Cl7 C20 lyase? Thi$ is necessary to convert l7-hydroxyprogesterone to DHEA. Can this
enzvme defdct be x-linked?

'-t

,I

Do childrenlat risk to miscarry have difficulty with synthesising DHEA due to I


enzyme deftict and more risk for TMC and cancer?
rti^16

an

Is the low DHEA early in cancer patients due to an isoenzyme defect to In familial cancer is there an isoenzyme defect of steriod Cl7 C 20 I DHEA? In the foetus falling DHEA can cause miscarriage or TMC
Does low pre-natal DHEA cause abnormal release of ova ie a blighted or and does low DHEA just before conception cause meiotic non-di Down's Syndrome with leukaemia risk? In the adult does falling D cancer and switch on oncogenes and mean low glutathione and not switch off IL6, thus flaring up cancer?

DHEA? to form

utated ova,

ion
trigger

and

off

IL2 to

Retum of malignant environment triggers cancer ng grains, As the adult ages the malabsorption state due to cow's milk, gluten con across the legumes/beans etc gets worse and nutrients continue to fall and fewer damaged gut (before it was the placenta). Do falling essential nutrients t form PGE1 cells that series and oAMP and cortisol and falling DHEA mean the programmed 'fear abortion' have their oncogenes etc switched on by the return f the TMC environment?

Also, do food lectins, pesticides etc pass across the gut and do can
receptors for them?

cells have

Do food sensitivities/intolerances cause the release of PGE2 series, TN o, IL6, u-interferon, histamines etc stimulating cancer proliferation?
Future research: What hormones/nutrients are low at TMC and again when cancer flares

ILl,

TL4,

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