The Case of Alan Yurko (Florida, USA)
—an introduction and explanation
Revised - Page 2


To Page 1 ||| To Page 3

Povlishock et al, Department of Anatomy, Virginia Commonwealth University, Richmond, Brain Pathol 1995 Oct;5(4):415-26, state:
Traumatic brain injury has long been thought to evoke immediate and irreversible damage to the brain parenchyma and its intrinsic vasculature. In this review we call into question the correctness of this assumption by citing two traumatically related brain parenchymal abnormalities that are the result of progressive, traumatically induced perturbation. In this context, we first consider the pathogenesis of traumatically induced axonal damage to show that it is a delayed consequence of complex axolemmal and/or cytoskeletal changes evoked by the traumatic episode which then lead to cytoskeletal collapse and impairment of axoplasmic transport, ultimately progressing to axonal swelling and disconnection.

Second, we consider the traumatized brain's increased neuronal sensitivity to secondary insult, evidence is provided that it is triggered by the neurotransmitter storm evoked by traumatic brain injury, allowing for sublethal neuro-excitation. Collectively, it is felt that both examples of the brain parenchyma's response to traumatic brain injury show that the resulting pathobiology is much more complex and progressive than previously envisioned, and as such, rejects many of the previous beliefs regarding the pathobiology of traumatic brain injury.

In other words; trauma does not always result in an immediate shearing effect, as claimed by the prosecution. This also leads one to suspect that the so-called 'acceleration/deceleration' mechanism, described by many is not necessarily correct—as far as diffuse axonal injury is concerned.
The foregoing articles demonstrate some vital issues:
• Anoxia can cause axonal injury
• Once the cascade of abnormal biochemical events is initiated it is virtually impossible to reverse the process
• The extreme complexity of the issue
• Reoxygenation ('reperfusion'), which occurs when the circulation is reestablished, often accelerates the cascade instead of stopping it.
• Iron hemostasis (here meaning 'chemical control') when deregulated, that is when iron, which is normally carefully controlled, gets loose, there is an addition to the cascade of abnormal biochemical processes.

It is extraordinary, when the seriousness of charges laid, are considered, that factors such as those just considered are not raised during shaken baby trials. To understand the issue more fully it is necessary to consider what are called 'free radical reactions', the control of these by 'antioxidants' (particularly vitamin C), the role of bacterially produced toxins (endotoxins and exotoxins), the manner by which these toxins damage the endothelium (lining of blood vessels) and utilize reserves of vitamin C.

Francine's prenatal records show that she was treated with antibiotics for a chronic E.coli infection, and she tested positive for E.coli six months postpartum. So it is necessary to describe some of the mechanisms involved in these infections, and the role played by what is known as 'endotoxin'. Endotoxin is formed by so-called 'Gram-negative' bacteria: the best known is E.coli. This organism normally inhabits the gut. It plays an essential role in digestive processes and produces some compounds that are necessary for life. However, under certain conditions it can become invasive and cause illness or death either directly or indirectly through a variety of mechanisms.

Endotoxin is usually stored in the bacterial wall, and only small amounts are released into the environment. It is essential for bacterial reproduction of Gram-negative bacteria and, normally, under strictly controlled conditions, plays an important role in the development of host immune responses. It is released when the bacterial cell wall breaks down so an abnormal amount of Gram-negative bacterial death can result in the release of excessive amounts of endotoxin. Mechanisms involved are complex.
Factors involved in excessive amounts of endotoxin being produced in infants include:
• Failure to exclusively breast-feed
• The administration of antibiotics
• Infections, bacterial and viral
• The administration of vaccines
• Immune disturbances resulting in the 'overgrowth' of 'abnormal' intestinal bacteria.
• The oral administration of excessive amounts of iron
• Events following what is known as 'reperfusion injury'. When body tissue or organs are temporarily deprived of oxygen and nutrients (for example, when a tourniquet is applied for a period to a limb and then released, or the brain is temporarily deprived when respiration ceases for a period). The circulation is reestablished and products, formed in the tissues during the period of anoxia, are released. These products are carried in the blood stream to the gut, where excessive amounts of endotoxin are quickly produced and absorbed into the blood stream. A cascade of abnormal biochemical processes is initiated and a rapid destruction of some body tissues, including parts of the brain, can result.
The problem does not stop there. Endotoxin can:
• Disturb coagulation/bleeding factors
• Damage the endothelial linings of blood vessels and cause hemorrhages
• Utilize vast quantities of vitamin C (vitamin C 'detoxifies' endotoxin.)
• Precipitate any of a multitude of forms of scurvy, which in turn may result in hemorrhage in a variety of organs or tissues
• Specifically 'target' the brain.
• Disturb liver functions

There are several important issues that must be documented first:
Endotoxin can occur in the absence of bacteremia

Danner et al. Critical Care Medicine Department, Warren G. Magnuson Critical Center, National Institutes of Health, Bethesda, Md 20892. Chest 1991 Jan:99(1):169-75. state:
Detectable endotoxin occurred in 43 of 100 patients with septic shock, but only one of ten patients with shock due to nonseptic causes. During septic shock, endotoxemia frequently occurred in the absence of Gram-negative bacteremia.

Endotoxins have a very fast action

Aleo et al, Inhibition of ascorbic acid uptake by endotoxin: evidence of mediation by serum factor(s), Proc Soc Exp Biol Med 1998 May;179(1):128-31. states:
The effect of endotoxin appears to be instantaneous since the inhibition seen in the cells without any preexposure was similar to the cells preexposed to endotoxin for up to 6 hours.

Endotoxin 'inhibits' the uptake of vitamin C

Aleo, in the article just documented states:
Endotoxin inhibited ascorbic acid uptake by fibroblasts in a dose dependent manner

The inhibition of the ascorbic acid transport by endotoxin

Garcia et al, Department of Biochemistry and Molecular Biology 1, Faculty of Chemistry, Universidad Complutense, Madrid, Proc Soc Biol Med 1990 Apr;193(4):280-284, state:
Lipopolysaccharide (endotoxin) of E.coli modifies the ascorbic acid uptake in a calcium-dependent manner. At low calcium concentrations, lipopolysacharide exerts a stimulating effect on ascorbic acid transport and at high concentrations lipopolysaccharide produces a dose-dependent inhibitory effect. This inhibition of the ascorbic acid transport by the endotoxin can alter the ascorbic acid accumulation in the adrenal gland.

Activation of blood coagulation system during endotoxemia

Luscher, Activation of blood coagulation system during endotoxemia. Fortschr Med 1975 Aug 14;93(22-23):1072-6, states:
Endothelial cells are in fact severely affected by endotoxin and may even be removed from the vascular wall, thus making accessible the subendothelial activating factor X11. Thrombin in turn affects the vascular endothelium therefore, once initiated, the process of intravascular activation of coagulation will perpetuate, this the more as platelets in turn will be stimulated into activity.

The microcirculation during endotoxemia

McCusky et al, Department of Cell Biology and Anatomy, College of Medicine, University of Artizona, Tucson 85724-5044, USA, Cardiovasc Res 1996 Oct;32(4):752-63, state:
The initial responses to endotoxemia are detectable in the microcirculation as microvascular inflammatory responses characterized by activation of the endothelium stimulating these cells from their normal anticoagulant state to a procoagulant state with increased adhesiveness for leucocytes and platelets. Concomitantly, arteriolar tone is lost and reactivity to a variety of agonists is modified. Tissue damage subsequently results not only from reduced perfusion of the exchange vessels, but also from injurious substances released from activated, sequestered leucocytes as well as activated endothelial cells, macrophages, and platelets. This is the result of endotoxins inducing activation and interaction of a number of effector cells, cascades, and acute-phase responses, such as the complement, coagulation, bradykinin/kinin, and hematopoietic systems accompanied by the release of a myriad of mediators. These include eicosanoids, cyctokines, adhesion molecules, reactive free radicals, platelet-activating factor, and nitric oxide.

Free radical reactions and endotoxins
Note at this stage the association discussed in the above article.)

Ascorbic acid reduces endotoxin-induced lung injury

Dwenger et al, Institut fur Klinische Biochemie, Medizinische Hochshule Hannover, Germany, Eur J Clin Invest 1994 Apr,24(4):229-35, state
Paired experiments were performed on eight sheep in which they received either endotoxin alone (ET group) or in combination with ascorbic acid (Et plus Asc group). As a result, for the ET=ASC group a general and most significant improvement in the early hypertensive phase and the late permeability phase of cardiorespiratory function was observed in comparison with the ET group.

Endotoxin affects the permeability of the blood-brain barrier and causes activation of the microglia

Mayer, Department of Pharmacology, Chicago College of Osteopathic Medicine, Midwestern University, Downers Grove, Illinois; Medicina (B Aires) 1998;58(4):377-85, states:
Lipopolysaccharide (endotoxin) affects the permeability of the blood-brain barrier and causes activation of brain microglia (cells that are between the neurons).

Brain injury induced by continuous infusion of endotoxin

Tamada, Department of Pathology, National Defense Medical College, Saitama, Japan; No To Shinkei 1993 Jan:45(1):49-56, states:
Hemorrhagic intracerebral lesions, analogous to multiple punctate hemorrhagic necrosis seen in the brain of human disseminated intravascular coagulation (DIC) can be induced in rats by continuous infusion of E.coli endotoxin.

Coagulation disturbances after endotoxin administration

Wyshock et al, Sol Sherry Thrombosis Research Center, Temple University School of Medicine, Philadelphia; Thromb Res 1995 Dec 1;80((5):377-89, state:
Low doses of endotoxin administered to human volunteers stimulate activation of fibrinolytic, contact and coagulation systems.

Activation of clotting factor XI in experimental human endotoxemia

Minnema et al, Centre for Hemostasis, Thrombosis, Atherosclerosis and Inflammation Research, Amsterdam; Blood, 1998 Nov 1;92(9):329-301, state:
These data provide the first evidence for Factor XI activation in low-grade endotoxemia and suggest that FXI is activated independently of FXII.

Endotoxin affects platelets

Stohlawetz et al, Clinic of Blood Group Serology and Transfusion medicine, Transfusion Medicine, Vienna University of Medicine; Thromb Haemost 1999 Apr;81(4):613-7, state:
Low grade endotoxemia induces a rapid fall of platelet counts, which is followed by an early increase in reticulated platelets and plasma thrombpoietin levels but not of glcocalicin levels, Finally, peripheral platelet counts increase several days after endotoxin infusion.

Sheu et al, Graduate Institute of Medical Svciences, Taipei Medical College, Tawain; Eur J Haematol 1999 May;62(5):317-26, state:
Therefore, endotoxin-mediated alteration of platelet function may contribute to bleeding diathesis in endotoxemic patients.

Ascorbic acid modulates in vitro the function of macrophages from mice with endotoxemic shock, and helps to control free radical reactions

Victor et al, Department of Sanimal Physiology, Faculty of Biological Sciences, Complutense University, Madrid; Immunopharmacology 2000 Jan;46(1):89-101, state:
The toxic effects of oxygen radicals (free radicals) produced by immune cells can be controlled to certain degree by endogenous antioxidants because of their scavenger action (a chemical reaction). Antioxidants, such as ascorbic acid, are free radical scavengers and improve the immune response. In the pathogenesis of endotoxic shock the reactive oxygen species produced by phagocytes have been implicated. These data suggest that ascorbic acid can regulate the phagocytic process in endotoxin shock, principally decreasing free radical production and thus it could reduce endotoxic shock severity.

Antibiotics release endotoxin

Holzheimer, Klinik fur Allgemeichirurgie, Martin-Luther-Universitat-Wittenberg, Germany; Infection 1998 Mar-Apr;26(2):77-84, states:
There is clinical evidence for antibiotic-induced endotoxin release.

Rotimi, et al, Department of Microbiology, Faculty of Medicine, Kuwait University; J Chemother 2000 Feb;12(1):40-7,state:
Endotoxin liberation was detected in the filtered broth cultures after exposing the organisms to four different concentrations of the antibiotics. All seven gram-negative bacteria investigated liberated induced cell-free endotoxin.

Ischemia-reperfusion injury causes endotoxemia but not bacterial translocation

Yassin et al, Department of Surgery, Queen's University of Belfast; Br J Surg 1998 Jun;85(6):785-0, state:
It has been suggested that reperfusion of the acutely ischaemic limb alters gut permeability. The effect of lower limb ischaemia-reperfusion on systemic endotoxin and antiendotoxin antibody concentrations and the incidence of bacterial translocations was investigated. These results demonstrate that a remote and isolated ischaemic-reperfusion injury to the lower limb, in the absence of infection or bacterial translocation, causes endotoxaemia.

Yang et al, Burn Center, Postgraduate Medical College, Hospital, Beijing; Chin Med J (Eng) 1997 Feb;110(2):118-124, state:
Tissue reperfusion might induce the production of oxygen free radicals, resulting in lipid peroxidation injury, especially to intestinal mucosa, and resulting in disruption of mucosal barrier function followed by endotoxemia.

Endotoxin targets the brain within specific cellular populations

Lacroix et al, Laboratory of Molecular Endocrinology, CHUL Research Center and Laval University, Quebec; Brain Pathol 1998 Oct;8(4):625-40, state:
These results provide the very first evidence of a direct role of endotoxin on specific cell populations of the central nervous system, which is likely to be responsible for the transcription of proinflammatory cytokines, first within accessible structures from the blood vessels and thereafter through scattered cells.

Endotoxin causes focal necrosis in the brain

Gilles et al, Ann Neurol 1997 Jul;2(1):49-56, state:
Telencephalic white matter of the neonatal kitten frequently contained astrogliosis or focal necrosis (sometimes including the thalamus and the caudate) following a single injection of endotoxin. No evidence for a disseminated intravascular coagulopathy was found. Large hemispheric cavity lesions are not accompanied by neurological deficits in the kitten.

This last reference shows what has been observed in human neonates—that sometimes quite extensive brain trauma is not accompanied by abnormalities in clinical states detected by ordinary neurological examinations.

Vitamin C and E prevent endotoxin induced cell death in human endothelial cells

Haendler et al, department of Internal medicine1V. Johann Wolfgang Goethe University, Frankfurt; Eur J Pharmacol, Dec 19;317(2-3):407-11, state:
The reduction of endotoxin-induced apoptosis (cell death) by vitamin C and E was paralleled by an increase in Bel-2 and a decrease in Bax protein levels. Thus vitamin C and E seem to interfere with the Bel-2 family of apoptosis regulators in human umbilical venous endothelial cells.

Immunological imbalance produces susceptibility to endotoxin

Chedid, Institut Pasteur and Center National de la Recherche Scientifique, Paris; Journal of Infectious Diseases, Vol128, supplement, July 1973, pages S112-S117, states:
It is now well established that, in many cases, immunological imbalance produces susceptibility to endotoxins.

Increased sensitivity to endotoxin can develop suddenly—and be fatal

Braude, Bacterial Endotoxins, Scientific American ?date, states:
Giuseppi Sanarelli of the University of Rome and Gregory Ahwartzman of Mount Sinai Hospital in New York independently found that if they injected a somewhat less than fatal dose of endotoxin into a rabbit and followed this with another 12 to 24 hours later, the second dose led to massive destruction of the kidney tissues. Other investigators - Rene Dubos and Russell Schaedler of the Rockefeller Institute and Herndon F. Douglas and I found that exposure to endotoxin can increase the lethal effect of the toxin, with the result that a smaller dose will kill the animal.

Bacteria in the gut of normal breast-fed infants, bottle-fed infants and infants that are fed in both ways

Iseki, Department of Pediatrics, Fukagawa General Hospital, Hokkaido Igaku Zasshi, 1987 Dec,62(6):895-906, states:
The development of faecal bacterial flora was studied to determine the differences between various types of feeding. Enterobacteria first colonized predominately in neonatal intestine. In the breast-fed group enterobacteria decreased gradually. Bifidobacteria began to increase after 2 or 3 days of life and outnumbered other bacteria. In the bottle-fed group, enterobacteria maintained their high counts despite the increase of bifidobacteria. At 1 and 3 months of age, bifidobacteria were the most prevalent organisms in all feeding groups. However, the numbers of other bacteria such as enterobacteria were significantly greater in the bottle-fed infants. In the breast-fed formula supplemented group, bacterial colonization of the intestine was in the middle range. In addition to the microbiological study, physiochemical properties of faeces and milk (i.e, pH and buffering capacity) were examined to explore their effects on the faecal bacterial flora. Faeces from breast-fed infants had a lower pH. Low buffering capacity of human milk seems to produce an acidic environment in the intestine, which is favourable for the growth of bifidobacteria and unfavourable for the growth of potential pathogenic bacteria. These results suggest that breast feeding is beneficial for protection against intestinal and/or systemic infection.

Golding et al, Unit of Pediatrics and Perinatal Epidemiology, University of Bristol, U.K., Early Hum Dev 1997 Oct 29;949 Suppl:S131-S142, state:
The major health advantage of breast feeding that has been clearly demonstrated remains in the protection of the infant from certain infections in early life.

Failure to exclusively breast feed may set the stage for gastrointestinal disturbances, and/or gastrointestinal or systemic infections, and set the stage for excessive endotoxin production. Francine did not exclusively breast feed.


Neonatal deaths after vaccine administration
The older form of pertussis vaccine contained a variable and uncontrollable amount of endotoxin and many of the serious adverse side effects were attributed directly to this. The acellular vaccine, recently introduced, is safer but not entirely free from problems. Hepatitis B vaccine has its share of problems.

Pertussis toxin by itself (without endotoxin) can cause encephalopathy

Steinman et al, Proc NatlAcad Sci USA 1985 Dec;82(24):8733-6, state:
A mouse model for encephalopathy induced by pertussis immunization has been described; it has features that closely resemble some of the severe reactions, including seizures and shock-like state leading to death, occasionally seen after administration of Bordetella pertussis (whooping cough) vaccine. Two lines of evidence implicate pertussis toxin as the active bacterial component. Purified pertussis toxin plus bovine serum albumin was tested and found to induce the lethal encephalopathy, demonstrating that the toxin was the critical constituent of B. pertussis responsible for encephalopathy.

However one interprets these results the fact is that either or both—pertussis toxin and endotoxin—can cause fatal encephalopathy.

Manette et al, Neonatal deaths After Hepatitis Vaccine, The Vaccine Adverse Reporting System, 1991-1998; Arch Pediatr Adolesc MED/VOL 153. Dec1999, states:
The causes of death reported by the medical examiner at autopsy were SIDS, infections, bronchopneumonia (no causative organisms noted)—and one case of intracerebral hemorrhage.

Slack et al, Department of Paediatrics Royal Hampshire County Hospital, Winchester, Hampshire, U.K; Arch Dis Child Fetal Neonatal Ed, 1999 Jul;81, state:
Four premature infants developed apnoeas severe enough to warrant resuscitation after immunization with diphtheria, pertussis, and tetanus (DPT), and Haemophilis influenza B (Hib). Although apnoeas after immunizations are recognised, they are not well documented. It is time to further research to elucidate the best time to immunize such infants.

Endotoxin can be identified and its concentration measured, after death

Crawley et al, Department of Microbiology, Withington Hospital, West Didsbury, Manchester, U/K; FEMS Immunol Med Microbiol 1999 Aug 1;25(1-2):131-5, state:
Following the development of an animal model which confirmed that endotoxaemia could be detected after death, we studied endotoxin levels in blood and tissue taken at autopsy.

There is a synergistic effect when two toxins are administered at the same time

Drucker et al, Department of Cell and Structural Biology, University of Manchestser; J Clin Pathol 1992 Sept;45(9):799-801, states:
Straphylococcus aureus toxin preparations showed high lethality when tested alone. E.coli toxin preparations showed high lethality except in high dilution. When the same toxin preparations were tested simultaneously in combination, lethality rose to 14 out of 15. Similar findings were observed over a range of toxin dilutions.

This could be an important issue when an infant has an infection (of any sort), because endotoxin could be produced. If a vaccine is administered at that time more endotoxins can be injected. It must be remembered that the older form of pertussis vaccine contains an uncontrollable amount of endotoxin. Even with the so-called 'acellular' pertussis vaccine toxins are present.

Controversy surrounding this vitamin has escalated during the past 40 years and reached a level that often prevents logical discussion. Several facts need to be considered:
• We cannot live without vitamin C
• Requirements vary enormously from one individual to another
• Requirements can vary from day to day according to a host of factors including environmental conditions and the development of infectious diseases.
• Scurvy, although accepted as a 'specific' disease, is found to be, in clinical practice, a combination of several diseases. The mode of presentation can vary enormously and the presenting picture can be complicated by the multitude of precipitating factors, many of which can overwhelm the situation before there is time for the development of classical signs of scurvy.
• Dietary deficiency of vitamin C is one cause.
• Excessive utilization is another cause.
• Precipitating factors can often be identified when suspected cases of scurvy (in one of its many forms) are investigated
• Reasons for excessive utilization are responsible for many of the atypical presentations.
• The brain, because of its extreme dependence on vitamin C can be specifically targeted by problems involving vitamin C utilization when cerebral circulation is disturbed for any reason—including anoxia, or endotoxin damage.
• Free radical reactions, particularly in the brain, initiated by anoxia (that can be universal throughout the body—as seen after a cardiac arrest—or localized in the brain (or a part of the brain) when parts of the cerebral circulation is disrupted, can trigger these reactions.
• Endotoxin can trigger free radical reactions by damaging the endothelium (blood vessel linings) of cerebral blood vessels, then entering the brain tissue where the cascade of reactions accelerates violently
• At the same time the endotoxin-initiated damage utilizes available stores of brain vitamin C, the disruption of the cerebral circulation prevents supplies of vitamin C entering the damaged brain areas, and the cascade of free radical reactions accelerates further. At the same time, vital supplies of oxygen, glucose and other nutrients are prevented from entering the damaged brain tissue and aiding brain tissue recovery. That is one reason for the rapid development of total brain circulation failure, cerebral edema and brain death.
• At the same time brain, retinal, and other intracranial hemorrhages can occur.
• In 'pure' cases of scurvy, vitamin C deficiency can damage the connective tissue of blood vessels and this can result in hemorrhages
• Vitamin C deficiency (excessive utilization has the same effect) can disturb clotting factors.
• The extreme complexity of so-called 'scurvy' is apparent to anyone who seriously studies the disease. The old 'gold standard' where a response to the administration of vitamin C was used as proof for a diagnosis, no longer applies, because many conditions that are obviously not scurvy (such as acute alcoholism) respond to the intravenous administration of large doses of vitamin C. These conditions do, however, demonstrate the complex role that vitamin C plays in human biochemistry.

Vitamin C utilization and requirements

Sherry Lewin, Department of Postgraduate Molecular Biology, North-East London Polytechnic, London, in a book, Vitamin C: Its Molecular Biology and Medical Potential, 1976, Academic Press, ISBN:0 12 446 3509, on page 137, states:
The daily dose of ascorbate intake is dictated by the need to maintain an ascorbate reservoir in the body at a level which can readily meet the demands made upon it The demands under 'normal' conditions and those when the body is exposed to attack differ considerably.
On pages 182-183) Lewin states:
It follows that the variation in vitamin C requirements by different individuals allowing for the various parameters noted, is of the order of a hundred to a thousand-fold. If the 'minimal' ideal antiscurvy-based requirement of ascorbate are in the region of 5 to 20 mg daily, the probable range for the needs of ascorbate extended by a hundred-fold to a thousand-fold is between 0.5 and 20 g. However, if the probability of oxidation and delactonization prior to absorption into the blood is eliminated, the range is likely to lie between very approximate limits of 0.2 to 10 g daily.

These figures do not allow for problems in specific organs or tissues when the blood supply is temporarily restricted, and these figures will be not accepted by most medical authorities. However, they match closely what I have observed clinically over nearly 33 years. It is the increased need for vitamin C, in some circumstances, that initiated my interest in the subject and enabled me to deal successfully with a range of previously fatal conditions. It is not, in the case being considered (Alan Yurko), of critical importance, because there are many aspects of the case for the defense that can be logically argued without it. However, it does help when attempts are made to make some sense of the complex issues involved.

Most authorities state that a figure of between 5 to 60 mg of vitamin C daily (for an adult) is sufficient. No attempt is made, in individuals, to examine biochemical pathways that are dependent on vitamin C. A true scientist would not just assume that all was well. Tests would show if, in some organs, vitamin C was not present in sufficient amounts to allow normal biochemical pathways to function normally or to maximum ability when necessary. This simple and logical approach, for reasons that are difficult to understand, is not followed when vitamin C needs and utilization are considered. It is certainly not good science to state that a particular intake of vitamin C will prevent scurvy and, therefore, that is all that is required.

Levene et al, Laboratory of Cell Biology and Genetics, National Institute of Diabetes, Digestive, and Kidney Diseases, National Institute of Health, Bethesda; Am J Clin Nutr, 1991 Dec;54(6 Suppl):1157S-1162S, state:
Ascorbic acid requirements are based on preventing the deficiency disease scurvy and on urinary excretion of vitamin C. We proposed the first quantitative approach to determining optimal requirements for ascorbic acid and other vitamins, called in situ kinetics. In situ kinetics biochemically is based on the application of Michaelis-Menten reaction kinetics to ascorbic acid-dependent reactions in situ.

Scurvy, despite being supplemented with vitamin C

Hess, page 229,states:
In spite of the fact that it (an infant) had been receiving an antiscorbutic for almost this entire period, it developed scurvy.

A more recent reference is as follows:

Presse Med. 2004 Feb 14;33(3):170-1 states:
Scurvy can occur in hospitalized patients despite vitamin supplementation...A 63-year-old patient who had spent several weeks in intensive care developed an unexplained anemia and ecchymoses [extravasation of blood into the subcutaneous tissues]. Despite daily administration of 130 mg/day of vitamin C since his admission, his ascorbic acid blood levels had collapsed. Administration of 1g/day relieved his symptoms within four weeks.

I would assume that the cause was excessive utilization of Vitamin C, and administration by injection would have resulted in a more rapid response.

Some infants and adults are susceptible to scurvy

Hess, page 229, (a continuation of the previous reference) states:
It was evident that this baby was peculiarly susceptible to scurvy.

Scurvy can be precipitated by infections (through increased utilization)

Hess, page 229, (a continuation of the previous reference) states;
It may be added that the second attack was complicated by nasal diphtheria.
Hess, page 219, states:
This is an instance where latent scurvy was prematurely changed to acute scurvy by an intercurrent infection; an epidemic of grippe precipitated a pseudo-epidemic of scurvy.

Hemorrhage in any part of the body is a striking manifestation of scurvy. This includes the brain, the meninges, spinal cord, and retina.

Hess, page 84, states:
Hemorrhage is such a striking manifestation of scurvy that it is not surprising to find it was regarded by older writers as the pathognomonic sign of scurvy.
Hess, page 92, states:
Hemorrhage may occur into the brain substance, into the cord or the membranes surrounding them. Petechial hemorrhages may or may not occur in cases of scurvy.
Hess, pages 192-193, states:
The skin, mucous membranes and subcutaneous tissues are frequently the sites of hemorrhage. There is a difference of opinion as to how frequently petechial hemorrhages occur in scurvy, particularly as to whether they are encountered early in the disorder. Great variations in this regard may be noted in individuals and in groups of cases occurring at different times. The idiosyncrasy of the individual has to be considered.

This raises, again, the important issue of the variation in the presentation of scurvy—atypical presentations being, more or less, the norm.

Hess, page 105, states:
Retinal hemorrhages were found by Jacobsthal, and by Kitamura.

Miura et al, Rinsho Ketsueki, 1982 Aug;23(8):1235-1240, states:
A case of scurvy with subdural hematoma.

Clemetson, Volume 111, page 223, states:
In a treatise on scurvy, the famous English physician, Willis (1668) mentioned the occurrence of intracranial hemorrhage in the course of the disease. Likewise. Heym (1871) describing his findings at autopsy in eight patients who died of scurvy during the siege of Paris, mentioned one case of hemorrhagic pachymeningitis.

Sutherland (1894) described the findings of recent and old subdural hemorrhages, respectively in two young children who died at 24 and 14 months of age. Both had classical signs of scurvy, with subcutaneous petechiae, ecchymoses, and subperiosteal hemorrhages, but not the spongy bleeding gums which are said to be rare in infancy and early childhood. Another report on 379 cases of infantile scurvy by the American Pediatric Society (1898) ascribed 3 out of 29 deaths to cerebral hemorrhage.

Spinal cord changes are found in some scurvy cases

Hess, page 104, states:
In an infant a 'focal degeneration' of the cord has been described.

Scurvy is not always 'typical'.

Hess, page 183, states:
This is the syndrome which the medical student is taught to carry away to guide him in his every-day practice. It is the acute, florid type, and presents a striking picture, but must not be regarded as the common form of the disorder. If we are to diagnose infantile scurvy early and not overlook its more subtle manifestations, the classical textbook description must be augmented by portrayals of types of the disorder which are less crude and more difficult to recognize.

Coagulation is disturbed in scurvy.

Hess, pages 211-212 states:
A consideration of factors concerned in the coagulability of the blood (Hess's own italics) is of interest. In an investigation (Hess and Fish) it was found that the oxylated plasma (of blood directly from a vain) showed a slightly delayed coagulation time—eight to fourteen minutes. The ' bleeding time' carried out according to the simple method of Duke was slightly increased. Holt reports a case where a child bled to death following incision into an epiphyseal swelling at the lower end of the femur. The number of blood platelets is increased, running parallel, as is usually the case, with the number of red cells.This increase in the blood platelets, recently confirmed by Tobler and by Brandt, is a very exceptional phenomenon, and was not anticipated in connection with a disorder characterized by hemorrhage. The antithrombin content of the plasma is normal.

Note that the platelet counts were significantly raised when baby Alan was admitted after the acute collapse. This is an important issue will be discussed later under the heading of 'coagulation/bleeding disorders'.

Hindriks et al, Department of Haematology, University Hospital Utrecht, The Netherlands, Thromb Haemost 1991 Oct 1;66(4):505-509, states:
We conclude that ascorbic acid feeding had a significant effect on endogenous deposited matrix of smooth muscle calls and fibroblasts, and that the changed composition had profound effects on platelet interaction with these matrices.

Sushkevich et al, Vopr Pitan 1969 Sep-Oct 28:5 23-7, state:
The significance of changes in the functional properties of blood platelets, factor XIII activity and fibrin clot quality in the pathogenesis of hemorrhagic diathesis secondary to experimental vitamin C deficiency.

There will be further discussion of this in the section dealing with coagulation/bleeding disorders. Infantile scurvy has changed in its presentation, and to an extent, in its nature since Hess wrote his book, because of several reasons:
• The use of antibiotics - that release endotoxin
• The widespread use of vaccines that act, in some infants, like infections, increasing the need for vitamin C and precipitating scurvy
• Pollution of the environment, which increases the need for vitamin C that plays an essential role in detoxification systems.

I have been informed by Francine Yurko that all the baby bottles of milk were heated in a microwave. I researched the possible effects of this on the Vitamin C content and found that this did not substantially affect the levels. However, 'hot spots' can be formed in the milk, and these can scald the mouth, gullet, and stomach. Francine was not given this information.

If a nightmare of complexities ever existed in medicine, its cause was the extreme complexity and variability of coagulation/bleeding factors. That is; the causes of spontaneous hemorrhages. Coagulation/bleeding factors are:
• Complex in the extreme
• Poorly understood, despite availability of an enormous array of knowledge.
• Interact with one another in an extremely complex manner
• The clinical history of the patient is of equal importance, and sometimes of greater importance, than the array of special tests available.

Rock et al, New Concepts In Coagulation, Crit Rev Lab Sci 1997 Oct;34(5):475-501, state:
The process of blood coagulation is a complex and incompletely understood process. Now the challenge of the future is to better elucidate the interactions of these components.

Sallah et al, Division of Hematology and Oncology, East Carolina University School of Medicine, Greenville, North Carolina, Postgrad Med 1998 Apr; 103(4):209-210, state:
A single optimal screening laboratory test for hemostasis would evaluate vascular, platelet, coagulation and fibrinolytic functions. Unfortunately, such a test does not exist. The key factor in determining the presence of a bleeding diathesis is obtaining a detailed patient history.

Dr. Jean McPherson, Senior Lecturer in Medicine, University of Newcastle (Australia) Visiting Hematologist, John Hunter Hospital, in a paper supported by the Australian Commonwealth of Health (ISSN 1036-9630), states:
The practice of routine coagulation tests (APTT, PT) without a bleeding time, prior to invasive diagnostic procedures or surgery is often justified as 'covering oneself' in case the patient bleeds. On this basis, tests with a low sensitivity and specificity are done at the expense of a simple clinical assessment.

In the case of Alan Yurko a number of useful tests were done but the principle expressed in the above references still applies. Furthermore, there is a problem when one attempts to interrupt the test results.

Factor XIII - a coagulation/bleeding factor

Problems involving this factor need to be considered in every so-called 'shaken baby' case. Already considered under 'endotoxin' is the relationship between coagulation/bleeding abnormalities, Factor XIII, platelet properties, fibrin quality and vitamin C deficiency. This illustrates clearly how complex the issue is.

Dr. Kovar, Chelsea & Westminister Hospital, London, in a report filed for the 'Australian nanny' (Louise Sullivan) case in London 1998, states:
Factor XIII consists of two subunits: Subunits A and B. Only the subunit A is enzymatically active and acts on ? and ?-chains of fibrin by crosslinking the ?-chains to so-called ?-dimere and the ?-chain to ?-chain polymerisation respectively. This reaction is dependent on the activity of FXIII, which ranges in the normal human beings between 70 and 130%.

Reduced activity of FXIII occurs congenitally and is acquired (in several disorders by reduced synthesis or increased consumption). Acquired FXIII deficiency occurs more often than generally expected in patients suffering from infectious disorders including some virus infections.

Professor Samuel J. Machin, in a report filed in the 'Australian Nanny' (Louise Sullivan, case in London (Dec. 1998), States:
Similarly as Factor XIII is synthesized mainly in the liver (there is also evidence that the a subunit may be synthesized in platelets and the placenta) one also has to consider if the patient has any degree of liver pathology, which could cause deficient synthesis of the protein involved. Therefore when assessing a specific abnormality in coagulation mechanism it is also standard practice to perform liver function tests at the same time. Similarly if a child had any form of acute viral or bacterial illness with associated pyrexia, such an acute illness may have caused increased consumption of Factor XIII activity and may also be due to the generalized effect of such a septicaemic illness to have potentially increased the risks of a child developing a bleeding episode.

On the plasma sent to my laboratory on 20th April 1998 the first test which we performed was an immunological laurall rocket assay which uses specific antibodies against the subunit a and the subunit s. This test showed a partial deficiency. Further tests at that time were not performed as we were not provided with sufficient plasma. A further plasma sample was sent, and an overall functional Factor XIII activity assay was performed by photometric determination. The test on this sample confirmed that the patient had overall deficiency of Factor XIII.

Problems with Factor XIII are not a critical issue in the defense of the Yurko case. However, existence of a problem here cannot be ruled out. Note the abnormal liver function tests which could reflect endotoxin damage. The problem in this case is that specific tests for Factor XIII were not complete so there is no way of knowing if a temporary (acquired) problem existed.

D-dimer and 'consumptive coagulopathy.

D-dimer is a fibrin degradation product and is used as a 'marker' for ongoing fibrinolysis, the activation of fibrinolysis and the severity of the hypercoagulable state. There are, however, some problems in measurement.

Matsuo et al, Hyogo Prefectural Awaji Hospital, Sumoto, Japan, Semin Thromb Hemost 2000;26(1):101-7, state:
The reactivity to cross-linked fibrin degradation products produced during fibrin degradation differs depending on the kind of antibody used against D-dimer. In patients with disseminated intravascular coagulation or earthquake-induced mental and physical stress and in patients with percutaneous transluminal coronary angioplasty, all of which are associated with acute fibrin formation and degradation, some discrepancies between two methods of D-dimer detection, automated latex agglutination assay (LPIA) and enzyme-linked immunosorbent assay (Stago), were found.

No discrepancies in persistent fibrin formation and degradation were found among the healthy elderly, patients with lacunar stroke, and patients with coronary artery disease, almost all of whom had levels under 5.0 microg/mL, as determined by both methods. Although the clinical utility of D-dimer can be achieved by their detection with specific antibodies, measurement of D-dimer as high molecular-weight fragments may be useful to determine whether patients will undergo further fibrin degradation. When intermediate products of the degradation need to be assessed, D-dimer level measurement by LPISA may serve as a suitable marker for ongoing fibrinolysis.

There is a difference in hemostatic/coagulation factors between trauma and sepsis.

Boldt et al, Departmant of Anesthesiology and Intensive Care Medicine Klinikum der Stadt Ludwigshafen, Germany, Crit Care Med 2000 Feb;28(2):445-50, state:
Fifteen patients with severe trauma, 15 sepsis patients secondary to major surgery, and 15 neurosurgery patients (cancer surgery) were studied. Standard coagulation data and molecular markers of coagulation activation and finrinolytic activity (soluble thrombomodulin, protein C, free protein S, thrombin/antithrombin III complex, plasmin=alpha 2-antiplasmin complex, tissue plasmogen activator, platelet factor 4, beta-thromboglobulin) were measured from arterial blood on the day of admission to the intensive care unit (trauma/neurosurgery patients) or on the day of diagnosis of sepsis (baseline value) and serially during the next five days.

Antithrombin III, fibrinogen, and platelet counts were highest in neurosurgery patients but without significant differences between sepsis and trauma patients. Thrombin/antithrombin III complexes increased in sepsis patients but decrease in trauma and neurosurgery p[atients. Tissue plasminogen activator increased in sepsis patients and remained almost unchanged in the other two groups. Soluble thrombomodulin plasma concentration increased significantly in the sepsis group, while it remained elevated in the trauma and was almost normal in the neurosurgery patients. Protein C and free protein S remained decreased only in the sepsis group.

CONCLUSIONS: Alterations of the hemoistatic network were seen in all three groups of critically ill patients. Hemostasis normalized in the neurosurgery patients and post traumatic hypercoagulability recovered within the study period. By contrast, monitoring of molecular markers of the coagulation process demonstrated abnormal hemostasis in the sepsis patients during the entire study period indicating ongoing coagulation disorders in fibrinolysis in these patients.

It is reasonable to assume that sepsis includes endotoxemia. This study demonstrates:
• The complexity of the issue
• That the so-called 'standard' coagulation profiles do not provide sufficient information (as already discussed).
• The lack of information (about these complex coagulation disorders) when so-called 'shaken baby cases are investigated.
• This lack of information denies the defense a potentially powerful weapon, which makes the trial very undemocratic.

I am uncertain reading the Yurko case notes what method was used to determine the D-dimer level, so I cannot assess the full significance of the result, except to state that it was raised >8.00. Normal range quoted is ?0.4) and represents a state of coagulopathy. It is unfortunate that the level of D-dimer did not reveal how far it was above 8.00. In SIDS cases (and there is no need to become involved here in a debate about the significance of this, except to state that there is some evidence that endotoxin is involved in the genesis of SIDS) levels have been found to be extraordinarily high.

Goldwater, et al, The Medical Journal of Australia, Vol 153 July 2, 1990, state:
To our knowledge there have been no published investigations into why babies who have died of SIDS have liquid blood. Cross-linked fibrin degradation products (XLFOPs) were measured using the D-Di test which utilizes a monoclonal antibody directed against the fibrin degradation product, D-dimer molecule.The mean XLFOP level for SIDS sera was 1792 mg/l and for control sera was 56.6. The high levels seen in sera from SIDS cases most probably reflect a massive consumptive coagulopathy.

The pathogenetic mechanism underlying this is uncertain, but it is possible that in some cases it may be related to bacterial toxaemia. This would concur with our finding that toxigenic E.coli are isolated from the intestinal contents more often than from age-matched controls who have died from established causes or from live age and contemporaneously matched babies' faecal samples. Furthermore, intravascular coagulation is known to occur in other conditions caused by E.coli verotoxins, including the haemolytic uraemic syndrome, the pathogenesis of which involves platelet aggregation in vitro, and endothelial damage could contribute to the common pathological findings in SIDS.

Note, obviously, the extraordinarily high levels of D-dimer found. If such levels existed (and they may have existed) in the Yurko case, at least some evidence assisting the defense would have been forthcoming.

Liver function abnormalities and endotoxin.

My interest in this began more than forty years ago when I observed, in some infants, that sudden unexpected death was associated, before death, with liver tenderness. In severe cases, there was obvious liver pain. Autopsies sometimes revealed yellowish patches on the surface and in the body of the livers, surrounded sometimes by red areas. Reports on liver sections were non-specific—a degree of fatty change and some cellular swelling. The changes were not considered to be the cause of death. Years later I was able to associate these liver changes to endotoxin.

In severe cases the liver pain was sufficient to create acute discomfort. Breathing, typically, would be 'grunting' an observation that I have made many times. How did I know that the grunting (in these cases) was due to liver pain? When I administered Vitamin C by injection the grunting ceased quickly and liver tenderness disappeared.
Liver function tests with Alan Yurko were distinctly abnormal. It is certainly possible, indeed probable, that this was due to endotoxin. Other causes, such as viral hepatitis, were not looked for.

Lund et al, Ugeskr Laeger 1998 Nov;160(46):6632-7, state:
Shaken baby. A combination of subdural haematomas and retinal haemorrhages with minimal or no trauma and no coagulopathy is almost pathognomonic of the syndrome.

Note that they state that 'no coagulopathy' is a factor. This, in most cases is never considered.

The earliest suggestion that a coagulopathy may have existed can be found in the Florida Hospital, Emergency Department, notes, dated 11/2/98:
Presenting complaint: Constipation, dry blood in nose (mother) noticed streaks of dried blood - nose and spit (?'spat') up streaks of bright red blood.

This could, of course, be interpreted in various ways. However, the existence of a coagulopathy cannot be excluded. Taken in conjunction with the history, since birth, what is known about coagulopathys/endotoxin/vitamin C utilization, this is highly significant. Certainly, it cannot be ignored. At the very least it is a powerful piece of evidence supporting the defense—a positive detail that clearly fits the 'hypothesis' I have generated.

Next, there is the presence of many of the factors that are known to 'trigger' coagulation/bleeding disorders. These revolve around endotoxin formation.
• Infection, following birth and later
• Antibiotics administered after birth and again later
• Failure to exclusively breast-feed
• The administration of vaccines

Next, there is the 'detail' of the rib and acromion 'pathology', wrongly reported as 'fractures'. At the very least, a differential diagnosis should have been considered in the radiologist's report; and that differential diagnosis should have included 'infantile scurvy'. Had the report been worded in such a fashion, other signs of infantile scurvy and its causes may have been investigated. Obviously, this was not done, and, once again, a critical piece of evidence for the defense was not made available. This is a characteristic feature of most 'shaken baby' trials. For reasons I cannot understand, this feature, instead of aiding the defense, is used as a weapon by the prosecution—indirectly of course—but it has tremendous influence on the outcome.

Next, there are the results of coagulation tests that were performed. In scurvy, the bleeding time may be normal or increased. It is necessary to comment further on this phenomenon. The complexity of the issue is extreme. Variables, including the presence or absence of endotoxin, can render the interpretation of results difficult. And, what is found on clinical examination and with the aid of special investigations may vary, from time to time, in a particular patient.

Capillary fragility can in some cases be demonstrated in cases of scurvy.

Hess, page 212-213, states:
To this end the 'capillary resistance test' was devised. A blood-pressure band, or torniquet, is placed about the arm, and the pressure increased until the forearm becomes cyanosed and the radial pulse is almost obliterated. The pressure is then maintained at this level for 3 minutes. The principle of this test consists in subjecting the capillaries and venules to increased pressure to observe whether this strain results in the escape of blood. In infants the pressure was raised to 90 mm; in some cases it had to be raised higher in order to entirely obstruct the return flow of blood.

The test is considered to be 'positive' when the forearm shows many petechial spots. In normal infants petechiae were almost always absent, or there were few to be seen. This is not a specific test for scurvy, but demonstrates a weakness of the vessel walls, whatever may be the cause. It is found to be positive in the majority of cases of scurvy.


Your Support is Greatly Appreciated. . .

Click Here to Donate

(Why reversing this conviction will help many people)

Alan Yurko


Problem with or question about this website: