Clinical Synopsis on Alan Yurko 16.9.97 - 27.11.97


Maternal complications:
Chronic nausea, malnutrition, hypo-vitaminosis, zero wt. gain after wt. loss during pregnancy, gestational diabetes, smoking, constipation, urinary tract infections, strep. B vaginal infection.

Foetal/neonatal complications:
Oligohydramnios, prematurity (birth wt. 5lb 8 oz ), severe prolonged neonatal hypoxia, respiratory distress syndrome, hyperbilirubinaemia with neonatal jaundice, possible hypoplastic kidneys, delayed development.
After discharge at 1/52:
Prolonged jaundice, prolonged Respiratory Distress Syndrome (RDS) with grunting and/or wheezing, apnoeic episodes, constipation.
Vaccinated at 8 weeks but effectively only 3 weeks according to gestational age. Still exhibiting evidence of multi-system impairment including chronic interstitial pneumonitis.
Terminal illness Nov 21-27:
Within 1-2 days of vaccinations, developed high-pitched crying, irritability, fever, diarrhea, at least one epistaxis, altered feeding pattern. Apnoea for about 20 minutes before resuscitation in hospital. On life support for 75 hrs.
Apparent fractured ribs with evidence of some healing.

What is the significance of the following?

1. Very low creatinine from day 3.
2. Constantly increasing platelet count
3. Altered coagulation parameters.
4. Raised WBC
5. What effect would the neonatal heparin have had (250u/250ml at 7.4ml/hr and 4 bottles apparently given from Nov 16th-18th )? Heparin also transfused via radial line 1:1 from the 24th Nov. More importantly still, why was heparin given?
6. Infant had RDS from birth - intubated + surfactant for 3 days.
7. Can perinatal asphyxia and RDS lead to renal failure and would oliguric renal failure lead to metabolic acidosis, hypoproteinaemia and hyperkalaemia?
8. Could the above lead to hypertensive encephalopathy with brain swelling, subarachnoid, subdural or intracranial haemorrhages, especially if compounded by unrecognized but almost inevitable vitamin C deficiency (i.e. acute on chronic scurvy)?
9. Could the maternal state during pregnancy, the perinatal complications, and the microwave heating of nearly all his feeds have made him scorbutic? If so, could this have been the underlying cause of the sub-dural haemorrhage?
10. In view of the prematurity, the continuous medical problems and the sudden deterioration in health, why were both blood histamine and vitamin C levels not performed?
11. In view of the prematurity, the continuous medical problems, should this baby have even been vaccinated on Nov 11th ?
12. Could the thimerosal (over 60mcg) in the vaccines plus the pertussis vaccine have overwhelmed his immune system and used up whatever ascorbate was available?
13. In view of the history of chronic ill-health, would this baby have been a suitable organ donor?
14. In view of the criminal proceedings, why were not all of this baby's organs available for both macroscopic and microscopic examination?
15. Was there any financial gain from the organ harvesting and if so, to whom?

The extensive medical reporting on this infant's history by Drs Buttram and Yazbak, two independent U.S. physicians, does not need repetition as I concur with their findings. However, the above questions need to be addressed as most of the consequences of infant's severely compromised health and death and the subsequent father's prosecution could possibly have been prevented. Furthermore, there could be medico-legal consequences if the most likely correct diagnosis
was indeed unrecognized vitamin C deficiency or infantile scurvy (Barlow's disease), as despite the clinical presentation, no attempts were made to ascertain blood histamine or blood or urine vitamin C levels. The latter could have been readily determined with Ames urine "C-sticks".

According to the currently available literature, between 6 and 15% of the population are suffering from sub-clinical vitamin C deficiency and are scorbutic (<0.2mg/100ml serum) and thus at increased risk of toxicity from pathogen endotoxins (1).

It is also well documented that a number of factors can significantly adversely influence vitamin C levels, including maternal malnutrition and diabetes, infant prematurity, infections, bottle feeding, microwave heating of milk, and vaccinations. The latter can adversely affect vitamin C levels not only by the viral toxins but also due to toxic adjuvants such as thimerosal the mercury preservative, and aluminum, both of which are potent free radical catalysts capable of reducing vitamin C to critical levels. The clinical records indeed reflect this as all of the adverse events are listed in the medical literature as evidence of chronic scurvy.

An in-depth study of the biochemistry and patho-physiology of vitamin C deficiencies was published in a 3-volume textbook in 1989(2) and the author, Professor Clemetson, has also commented on this particular case(3) to quote, "We may have an infant with borderline vitamin C depletion, which on its own would have been relatively innocuous, now becoming more severe as a result of infection or
some other stress; even a common cold or coryza can halve the blood plasma vitamin C concentration in 24 hours. Furthermore, we now know that heavy metals like mercury, copper or even iron ion excess can deplete vitamin C reserves, so we have to wonder about the effects of the mercurial antiseptic thimerosal used in pediatric inoculants. Moreover, it has been shown that the toxins or toxoids of the usual inoculants cause increased blood histamine levels in animals. So we must
consider the effects of all the inoculants given together to an infant already ill or vitamin C depleted; the blood histamine level, the capillary fragility and the likelihood of petechial hemorrhages will be the result of all these factors added together." Notably, this premature and chronically ill infant was simultaneously given polio, DPT, Hib, and Hepatitis B vaccines that included a total of 60 micrograms of thimerosal mercury preservative. In addition, it has since been revealed that the DPT vaccine given to Alan Yurko came from a highly toxic batch (7H81507) with acknowledged deaths. A further quote from Clemetson's textbook would also be applicable: "The latent scorbutic state is often converted into frank scurvy by infections, and under such conditions hemorrhagic phenomena are frequent." (4). The latter would obviously have to include intracranial hemorrhages.

It would be most appropriate if an independent radiologist were to review the bone x-rays and apply the extensive criteria documented in Clemetson's textbook where cases of infantile scurvy in the 1930s are described (5). Scorbutic periostium and bone lesions were frequently mistaken for so-called healing fractures and this would be even more so with the current generation of doctors both generally
unaware of scurvy's clinical signs but keenly aware of SBS.

It is now becoming increasingly evident that significant differences exist between any given individual's ability to cope with toxic metals. Humans are not clones, and individual variability includes an ability to bind to and/or excrete potentially toxic metals by forming metallothionine (MT) proteins. An ability to upregulate MTs following exposures to toxic metals and thus enabling excretion,
can be assessed by determining blood copper-zinc ratios. Notably, high percentages of children who regressed into autism following vaccinations or were diagnosed as having developed ADHD, have been shown to have greatly raised Cu/Zn ratios. Amongst these newer research investigations is apo-lipoprotein E (apo-E) genotyping where the parental genotype determines the inherited homo - or hetero-zygous combinations of apo-E 2, 3, or 4. Six possibilities exist i.e. 2/2, 2/3, 2/4, 3/3, 3/4 and
4/4. The E4 allele due to its chemical structure that has the amino-acid arginine instead of 2 cysteines (as in E2), is unable to bind to and assist the elimination of mercury from the brain (apo-E3 has one cysteine and one arginine molecule and is thus intermediate). Apo-E genotyping therefore becomes relevant in assessing an infant's prospective ability to safely cope with a significant amount of mercury or aluminum in a vaccine. These currently research investigations will eventually become de rigeur due to their clinical relevance to patient safety. However, it would be significant if the parents had either the apo-E4/4 homozygous allele or a 3/4 configuration.

In my opinion, the multiple nutritional and iatrogenic challenges that this neonate had to face prior to and after birth, and the consequent poor resistance and compromised immunity, would have rendered it highly susceptible to severe adverse reactions to the vaccines and their toxic xenobiotic adjuvants. I suspect that these and not SBS, were the most logical underlying causes of the infant's demise.
If this is so, a major miscarriage of justice has been perpetrated.

M.E.Godfrey MD


1. NHANES 111 Survey. FASEB J. 1998
2. Vitamin C vols. 1-3. C. Alan Clemetson 1989 CRC Press Inc. Boca Raton, Florida. ISBN 0-8493-4841-2 (vol.1) -4842-0 (vol.2) -4843-9 (vol.3)
3. Was this baby shaken? Letter to Editor, Townsend Letter for Doctors January 2002.
4. Perla and Marmorston Role of vitamin C in resistance. Arch. Pathol.1937;23:683
5. Clemetson CA. vol.2 p76-79.

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