Wednesday, February 11, 2009





The risk that allegations of "shaken baby syndrome" may be based on faulty scientific assumptions is well articulated in an article written by Dr. Alan B. Clemetson.

Dr. Clemetson is Professor Emeritus in the Department of Obstetrics and Gynecology at the Tulane University School of Medicine.

Wikipedia tells us that: "Charles Alan Blake "Alan" Clemetson FRCOG, FRCSC, FACOG (October 31, 1923 – August 30, 2006) was a medical doctor, scientist and researcher who published over 48 medical papers and a three-volume monograph, Vitamin C.[1] During his hospital and teaching career he specialised in obstetrics and gynecology. After retirement in 1991 he devoted his time to researching and publishing papers on Barlow's disease (scurvy in infants), hypothesizing this to be a cause of Shaken baby syndrome...Dr. Clemetson had a long and distinguished academic career as a medical doctor, scientist and researcher. During his forty year professional career, he implemented numerous scientific studies and was instrumental in furthering scientific knowledge."

"Accusations are based on the findings of subdural hemorrhage, retinal hemorrhages, fractured ribs, etc., without any consideration of the possibility of Barlow’s disease (infantile scurvy)," the article begins, under the heading: "Was that baby really shaken?"

"Accusations are based on the findings of subdural hemorrhage, retinal hemorrhages, fractured ribs, etc., without any consideration of the possibility of Barlow’s disease (infantile scurvy)," the article continues;

"Routine blood coagulation studies are conducted to rule out hemorrhagic disease of the newborn; other diagnoses such as osteogenesis imperfecta and glutaric aciduria are also considered, but the possibility of infantile scurvy is usually dismissed because the typical white line between the epiphyses and the diaphyses of the long bones is not seen on the X-rays. It seems that there is now a new variant of Barlow’s disease, appearing earlier and developing faster, so that it does not show the usual radiological healing signs of calcification. As a result, plasma ascorbic acid and whole blood histamine levels are not carried out.

Such omissions are having very serious consequences in the United States and also in Britain, Canada, Australia, and New Zealand, where shaken-baby diagnoses are becoming all too common. Not only have so many infants died or been brain-damaged in these tragic events; but also many men and women have been accused, and some, convicted, of murdering their own children. This happens even though no one has observed any shaking, and each parent has testified to the innocence of the other.

The situation has become so bad in the United States that some parents are now afraid to take their children to an Emergency Room following a fall, for fear that someone will phone the child-abuse authorities: the parents may be beset by an army of nurses, social workers, child-protection workers, and the police -- who will cross-question them as though they were criminals. God forbid there should be an eye doctor who finds traces of retinal petechiae, for then one or other parent may be denied further contact with any of their children on suspicion of child abuse, without any court order.

Several physicians, including Donohoe (2003) and Geddes et al (2003) have questioned the histopathological evidence for such a diagnosis as shaken-baby-syndrome.

Barlow’s disease was well-recognized in bottle-fed infants in the first half of the twentieth century; it was characterized by broken ribs, subperiosteal hemorrhages, epiphysial separations, fractures of the long bones, skin bruises, and sores that would not heal. Physicians were slow to identify it at first, because the bleeding and spongy swollen gums typical of adult scurvy are never seen before the eruption of the teeth. Such findings were originally misdiagnosed as acute rickets (vitamin D deficiency), as the projecting costo-chondral junctions were mistaken as a “rickety rosary”, until Barlow in 1883 reported that it could be cured with orange juice. It occurred mostly in the poor, who did not know the need, or could not afford, to provide orange juice as a supplement to the bottled cow’s milk. Barlow’s disease also occurred in more affluent families who boiled the cow’s milk to be sure of killing all the tuberculosis bacteria, so destroying all its vitamin C content.

A new variant of Barlow’s disease -- occurring earlier in the first year of life -- is being wrongly diagnosed as “Shaken-Baby-Syndrome”, even though no one has ever witnessed the shaking. The diagnosis of shaken-baby-syndrome seems to have arisen from the work of Caffey in 1946, when he wrote on multiple long-bone fractures in infants suffering from chronic subdural hematoma. He noted that

“The large cortical thickenings associated with several of the fractures are similar to the cortical thickenings which develop in many cases of scurvy following sub-periosteal hemorrhage.”

However, most of the infants had supposedly been receiving orange juice daily, so he rejected that diagnosis and suggested physical injuries as the cause. No consideration seems to have been given to the possibility that subclinical scurvy with fragile bones, could be associated with the minor traumas of normal handling. The diagnosis does not have to be either trauma or scurvy; it can be a combination of the two. The ribs of some infants with scurvy crack when they are lifted by the chest. Likewise, there is the apopcryphal story of both femoral bones being broken when a nurse in hospital raised the heels of a scorbutic infant to change the diaper.

Kempe et al (1962), discussing the association between subdural hemorrhage and long-bone fractures in infants, reported that a combination of old and new fractures was indicative of child abuse; but, in fact, X-ray pictures showing fractures, at different stages of healing, are often seen in infantile scurvy.

Physicians accusing people of “shaken-baby-syndrome” today seem to have forgotten this differential diagnosis: they treat the patients and go to court without any proof of abuse and without analyses of plasma vitamin C or whole blood histamine levels. Such prosecutions should be thrown out of court for lack of evidence.

It seems that people do not want to believe that scurvy could possibly occur today in the modern world. Perhaps they are not aware that even ready-to-drink orange juice can lose most or all of its vitamin C content within a month, as shown by Johnston and Bowling in 2002. Moreover, few people are aware that hyperemesis gravidarum (excessive vomiting in pregnancy) can cause a rapid onset of scurvy in the mother and thus in the unborn child.

Lund and Kimble of Madison WI in 1943 wrote as follows:

"Hyperemesis Gravidarum may lead to dangerously low levels of vitamin C. Clinical scurvy may appear. The retinal hemorrhages of severe hyperemesis gravidarum are a manifestation of vitamin C deficiency and are similar to petechial hemorrhages seen elsewhere. The hemorrhages cease after adequate therapy with vitamin C; henceforth they are not necessarily an indication for the use of therapeutic abortion."

We used to consider retinal petechiae and jaundice as indications for therapeutic abortion, to prevent the mother from developing Wernicke’s hemorrhagic encephalopathy; that can now be prevented with proper treatment. Any woman complaining of excessive vomiting in pregnancy, who is found to have acetone and aceto-acetic acid in her urine, due to starvation, must be admitted to hospital without delay and treated with intravenous glucose, saline, and vitamins B1 and C.

Today, it is the fashion to give bottle-fed infants supplementary apple juice instead of orange juice, but apples are a poor substitute for oranges. One hundred grams of fresh orange juice (3¼ fluid ounces) contains about 49 mg of vitamin C, but the same amount of apple juice contains only 1 mg of this vitamin. So, unless the parent knows to buy apple juice with added vitamin C, there can still be a risk of vitamin C deficiency.

We now know that capillary fragility, which causes the bleeding of scurvy, is due to elevated blood histamine levels, which occur with even mild ascorbate depletion, as shown by Subramanian et al (1973) in guinea pigs and by Clemetson (1980) in human subjects. There is no change in the blood coagulation mechanism in the histamine intoxication of scurvy.

Similarly, Fung et al (2002) found no abnormality in the blood coagulation studies carried out on nine infants with retinal and subdural hemorrhages. They had been listed as NAI, or non-accidental injury, even though there was no suspicion of child abuse. These authors suggest that the prevailing pathognomonic association of unexplained subdural hematoma, retinal hemorrhages, and a diagnosis of child abuse is “a self-fulfilling prophecy.” It certainly seems to have become an self-propagating assumption.

We need to consider not only ascorbate depletion, but also other factors which can increase blood histamine levels and so precipitate new forms of Barlow’s disease. We may call them Barlow’s disease variants.

Chatterjee et al (1975) showed in guinea pigs that the injection of foreign proteins -- as in vaccinations, or inoculations -- causes an increase in the blood histamine concentration. These same authors also showed that L-ascorbic acid is needed to facilitate the removal of histamine by conversion to hydantoin-5-acetic acid and on to aspartic acid in vivo. As a result, it is clear that ascorbate-depleted individuals will not be able to cope with any further histamine excess.

Needless to say, infection can also raise the blood histamine level and thereby predispose towards a bleeding tendency, especially in ascorbate-depleted subjects. Work by Hume and Weyers in 1973 has shown that even the common cold causes a fifty percent reduction of the blood leukocyte ascorbic acid level within 24 hours. Moreover, Clemetson (1980) has shown that a mild reduction in the plasma ascorbic acid level below 0.7 mg/100 mL (39.8 µmol/L) in human subjects causes a highly significant increase in the blood histamine concentration (p<0.001).

One night of sleep-lack can more than double the blood histamine concentration of hospital interns and residents (p<0.001), without any change in the plasma ascorbic acid level, as reported by Clemetson in 1989. It would seem that any kind of stress could further increase the histaminemia of an ascorbate-depleted subject.

Gunn (1985) has reported subdural hemorrhages in utero, and Demir et al (1989) have reported atraumatic antepartum subdural hematoma causing fetal death -- so why should we consider the same occurrence after birth as being a criminal assault?

It seems that an increased blood histamine concentration can be the result of infections, vaccinations, vitamin C deficiency, and/or stress. They all contribute to the capillary fragility of scurvy. Even extremes of heat or cold increase blood histamine levels in guinea pigs, as reported by Chatterjee et al.

Now that it is a common practice to give infants as many as six inoculations at eight weeks of age, we must consider the combined effects of so many inoculants given all at once. An infant may have a head cold or other illness which has already depleted its vitamin C stores. In such a case, we can envisage the development of a major histamine toxicity.

Many of the deaths attributed to shaken-baby-syndrome nowadays occur within 21 days after vaccination. Clearly, research is needed to find out which inoculants cause the highest histamine levels, when they peak, and whether we should consider not giving so many inoculations all at once. In any event, we should give a vitamin C supplement, perhaps 500 mg of ascorbic acid powder (or crystals) in orange juice, at the time of all inoculations. Vitamin C is known to reduce the morbidity and mortality following inoculations both in animals, as reviewed by Clemetson in 1999, and in man, as shown by Kalokerinos in 1974.

Few hospital laboratories conduct plasma ascorbic acid levels routinely, so it may be appropriate here to provide a few suggestions to improve the accuracy of such determinations:

1) The laboratory must agree to a convenient time for receiving the blood specimen.

2) Blood must be taken directly to the laboratory and spun in a refrigerated centrifuge, as ascorbic acid losses occur at about 5% per hour at room temperature.

3) Care must be taken to avoid contamination by the buffy coat of leukocytes when removing plasma with a bulb aspirator.

4) A plasma sample showing any tinge of pink coloration must be discarded, as hemolysis causes rapid losses of ascorbic acid by oxidation and subsequent hydrolysis.

5) Ascorbic acid powder (crystals) is hygroscopic, so it must be dried in a dessicator over calcium chloride for about a week before being weighed to prepare standard solutions. Otherwise, plasma samples will give falsely high values."