5 - Mercury, bilirubin, and the blood-brain
barrier
The focus of attention on the mercury preservative
in vaccines is astonishing. Implication of vaccine
injury is a lay movement that the professional
experts appear unable to credibly debunk. Mercury
affects the brain, and those on both sides of the
argument would do well to describe how and where
mercury does damage.
Mercury, like asphyxia, has been linked to damage
of the auditory system [1]. Lead and other toxic
chemical substances have also been linked to
damage of the auditory system, as have alcohol
intoxication and bilirubin [2-16]. Bilirubin, however,
appears to get into the brain only if the blood-brain
barrier has been compromised by a prior insult such
as sepsis or anoxia [13, 17-19].
The blood-brain-barrier is the natural defense that
must have evolved long ago as a protection against
high neonatal bilirubin levels. Bilirubin levels are
normally high in the circulatory system of newborn
infants until maturation of liver enzymes that can
remove it. If the blood-brain-barrier is intact, many
toxic substances (especially those of high molecular
weight, like bilirubin) should be prevented from
getting into neural tissue.
As can be seen in figure 4, Bilirubin staining is not
uniform in the brain, but affects the same subcortical
nuclei that are vulnerable to asphyxia at birth.
Asphyxia as inflicted in the experiments with
monkeys resulted in large part from diminished
circulation. The umbilical cord was clamped before
the infant monkey could take its first breath, leaving
a large volume of blood in the placenta. Respiratory
function is transferred from the placenta to the lungs
by transfer of blood from the placenta to the lungs
[20]. This blood fills the alveolar capillaries, making
the alveoli functional and capable of transferring
oxygen from the air to the bloodstream [21].
In their first publication on brain damage in the
monkey by asphyxia neonatorum, Ranck and Windle
made the comment, "The human neuropathologic
entity most closely resembling the effects of
asphyxia neonatorum in the monkey is kernicterus,"
[20, p153]. Kernicterus is a developmental disorder
thought to be caused by high bilirubin levels in the
neonatal period. However, in the experiments with
monkeys, Lucey et al. determined that bilirubin
staining in the brain only occurred in monkeys
subjected to asphyxia [19].
The finding that bilirubin is damaging only when
accompanied by asphyxia is an example of dual
mechanisms each compounding the effect of the
other. Unfortunately complications of this type
happen, and may partly explain why a brief period of
anoxia around the time of birth appears harmless to
most infants, but in combination with high levels of
bilirubin (or any toxic factor) can affect brain function
and lead to disability.
Likewise, most children are not injured by
vaccination. However, following any difficulty at
birth, routine vaccination in the neonatal nursery
might be dangerous. If the blood-brain barrier has
been compromised, the thimerosol preservative
could leak into neural tissue, and most likely in the
same pattern as caused by asphyxia. The mercury
theory should perhaps be reconsidered in this light.
The papers by Ranck and Windle (1959) and Lucey
et al. (1964) were, like that of Faro and Windle
(1969) published in the journal Experimental
Neurology. This journal has now made these papers
available as PDF files online. I have included them
here because I believe the data they report are of
such great importance.
barrier
The focus of attention on the mercury preservative
in vaccines is astonishing. Implication of vaccine
injury is a lay movement that the professional
experts appear unable to credibly debunk. Mercury
affects the brain, and those on both sides of the
argument would do well to describe how and where
mercury does damage.
Mercury, like asphyxia, has been linked to damage
of the auditory system [1]. Lead and other toxic
chemical substances have also been linked to
damage of the auditory system, as have alcohol
intoxication and bilirubin [2-16]. Bilirubin, however,
appears to get into the brain only if the blood-brain
barrier has been compromised by a prior insult such
as sepsis or anoxia [13, 17-19].
The blood-brain-barrier is the natural defense that
must have evolved long ago as a protection against
high neonatal bilirubin levels. Bilirubin levels are
normally high in the circulatory system of newborn
infants until maturation of liver enzymes that can
remove it. If the blood-brain-barrier is intact, many
toxic substances (especially those of high molecular
weight, like bilirubin) should be prevented from
getting into neural tissue.
As can be seen in figure 4, Bilirubin staining is not
uniform in the brain, but affects the same subcortical
nuclei that are vulnerable to asphyxia at birth.
Asphyxia as inflicted in the experiments with
monkeys resulted in large part from diminished
circulation. The umbilical cord was clamped before
the infant monkey could take its first breath, leaving
a large volume of blood in the placenta. Respiratory
function is transferred from the placenta to the lungs
by transfer of blood from the placenta to the lungs
[20]. This blood fills the alveolar capillaries, making
the alveoli functional and capable of transferring
oxygen from the air to the bloodstream [21].
In their first publication on brain damage in the
monkey by asphyxia neonatorum, Ranck and Windle
made the comment, "The human neuropathologic
entity most closely resembling the effects of
asphyxia neonatorum in the monkey is kernicterus,"
[20, p153]. Kernicterus is a developmental disorder
thought to be caused by high bilirubin levels in the
neonatal period. However, in the experiments with
monkeys, Lucey et al. determined that bilirubin
staining in the brain only occurred in monkeys
subjected to asphyxia [19].
The finding that bilirubin is damaging only when
accompanied by asphyxia is an example of dual
mechanisms each compounding the effect of the
other. Unfortunately complications of this type
happen, and may partly explain why a brief period of
anoxia around the time of birth appears harmless to
most infants, but in combination with high levels of
bilirubin (or any toxic factor) can affect brain function
and lead to disability.
Likewise, most children are not injured by
vaccination. However, following any difficulty at
birth, routine vaccination in the neonatal nursery
might be dangerous. If the blood-brain barrier has
been compromised, the thimerosol preservative
could leak into neural tissue, and most likely in the
same pattern as caused by asphyxia. The mercury
theory should perhaps be reconsidered in this light.
The papers by Ranck and Windle (1959) and Lucey
et al. (1964) were, like that of Faro and Windle
(1969) published in the journal Experimental
Neurology. This journal has now made these papers
available as PDF files online. I have included them
here because I believe the data they report are of
such great importance.
- Oyanagi et al. (1988) The
auditory system in methyl
mercurial intoxication: a
neuropathological
investigation on 14 autopsy
cases in Niigata, Japan - Bertoni & Sprenkle (1989)
Lead acutely reduces glucose
utilization in the rat brain
especially in higher auditory
centers. - Franken (1959) Étude
anatomique d'un cas
d'intoxication par le bromure
de méthyle. Goulon et al.
(1975) Intoxication par le
bromure de methyl: Trois
observations, dont une
mortelle. Etude neuro-
pathologique d'un cas de
stupeur avec myoclonies,
suivi pendent cinq ans. - Troncoso et al. (1981) Model
of Wernicke's encephalopathy. - Squier et al. (1992) Case
report: neuropathology of
methyl bromide intoxication. - Cavanagh (1992) Methyl
bromide intoxication and
acute energy deprivation
syndromes. - Cavanagh & Nolan (1993) The
neurotoxicity of alpha-
chlorohydrin in rats and mice:
II. Lesion topography and
factors in selective
vulnerability in acute energy
deprivation syndromes - Ross et al. (1996) Distribution
of bismuth in the brain after
intraperitoneal dosing of
bismuth subnitrate in mice:
implications for routes of entry
of xenobiotic metals into the
brain. - Irle & Markowitsch (1983)
Widespread neuroanatomical
damage and learning deficits
following chronic alcohol
consumption or vitamin B1
(thiamine) deficiency in rats. - Torvik (1987) Topographic
distribution and severity of
brain lesions in Wernicke's
encephalopathy. - Victor et al. (1989) The
Wernicke-Korsakoff syndrome
and related neurologic
disorders due to alcoholism
and malnutrition - Grünwald et al. (1993)
Changes in local cerebral
glucose utilization in the
awake rat during acute and
chronic administration of
ethanol. - Orth (1875) Ueber das
Vorkommen von
Bilirubinkrystallen bei
neugebornen Kindern. - Dublin (1951) Neurologic
lesions of erythroblastosis
fetalis in relation to nuclear
deafness. - Rozdilsky & Olszewski (1961).
Experimental study of the
toxicity of bilirubin in newborn
animals. - Worley et al. (1996) Delayed
development of sensorineural
hearing loss after neonatal
hyperbilirubinemia: a case
report with brain magnetic
resonance imaging. - Schmörl (1904) Zur Kenntnis
des Ikterus neonatorum,
insbesondere der dabie
auftretenden Gehirn
veränderungen. - Zimmerman & Yannet (1933).
Kernicterus: jaundice of the
nuclear masses of the brain. - Lucey et al. (1964) Kernicterus
in asphyxiated newborn
monkeys. - Redmond A, et al. (1965)
Relation of onset of
respiration to placental
transfusion. - Jäykkä, S (1958) Capillary
erection and the structural
appearance of fetal and
neonatal lungs. - Ranck & Windle (1959). Brain
damage in the monkey,
Macaca mulatta, by asphyxia
neonatorum.
- Oyanagi K, Ohama E, and Ikuta F (1989). The auditory system in methyl mercurial
intoxication: a neuropathological investigation on 14 autopsy cases in Niigata, Japan.
Acta Neuropathologica (Berlin). 77:561-568. - Bertoni JM and Sprenkle PM (1989) Lead acutely reduces glucose utilization in the rat
brain especially in higher auditory centers. Neurotoxicology 9:235-242. - .Franken L (1959) Étude anatomique d'un cas d'intoxication par le bromure de
méthyle. Acta Neurologica et Psychiatrica Belgica 59:375-383. - Troncoso JC, Johnston MV, Hess KM, Griffin JW, Price DL (1981) Model of Wernicke's
encephalopathy. Archives Of Neurology 38:350-354. - Squier MV, Thompson J, Rajgopalan B. (1992) Case report: neuropathology of methyl
bromide intoxication. Neuropathology and Applied Neurobiology 18: 579-584. - Cavanagh JB (1992) Methyl bromide intoxication and acute energy deprivation
syndromes. Neuropathology and Applied Neurobiology 18:575-578. - Cavanagh JB, Nolan CC (1993) The neurotoxicity of alpha-chlorohydrin in rats and
mice: II. Lesion topography and factors in selective vulnerability in acute energy
deprivation syndromes. Neuropathology and Applied Neurobiology 19:471-479. - Ross JF, Broadwell RD, Poston MR, Lawhorn GT. Distribution of bismuth in the brain
after intraperitoneal dosing of bismuth subnitrate in mice: implications for routes of
entry of xenobiotic metals into the brain. Brain Res. 1996 Jul 1;725(2):137-54. - Irle E, Markowitsch HJ (1983) Widespread neuroanatomical damage and learning
deficits following chronic alcohol consumption or vitamin B1 (thiamine) deficiency in
rats. Behavioral Brain Research 9:277-284. - Torvik A (1987) Topographic distribution and severity of brain lesions in Wernicke's
encephalopathy. Clinical Neuropathology 6:25-29. - Victor M, Adams RD, Collins GH (1989) The Wernicke-Korsakoff syndrome and
related neurologic disorders due to alcoholism and malnutrition, 2nd ed,
Contemporary Neurology Series v30. Philadelphia, PA : F.A. Davis Co. - Grünwald F, Schröck H, Biersack HJ, Kuschinsky W (1993) Changes in local cerebral
glucose utilization in the awake rat during acute and chronic administration of
ethanol. Journal of Nuclear Medicine 34:793-798. - Orth J (1875) Ueber das Vorkommen von Bilirubinkrystallen bei neugebornen
Kindern. Archiv für pathologische Anatomie und Physiologie und für klinische Medicin
63:447-462 - Dublin WB (1951) Neurologic lesions of erythroblastosis fetalis in relation to nuclear
deafness. Am J Clin Pathol. 1951 Oct;21(10):935-9. - Rozdilsky B and Olszewski J (1961). Experimental study of the toxicity of bilirubin in
newborn animals. Journal of Neuropathology and Experimental Neurology, 20, 193-
205. - Worley G, Erwin CW, Goldstein RF, Provenzale JM, Ware RE (1996) Delayed
development of sensorineural hearing loss after neonatal hyperbilirubinemia: a case
report with brain magnetic resonance imaging. Developmental Medicine and Child
Neurology 38:271-277. - Schmörl G (1904) Zur Kenntnis des Ikterus neonatorum, insbesondere der dabie
auftretenden Gehirn veränderungen. Verhandlung der deutschen pathologischen
Gesellschaft 6:109-115. - Zimmerman HM and Yannet H (1933). Kernicterus: jaundice of the nuclear masses of
the brain. American Journal of Diseases of Children, 45, 740-759. - Lucey JF, Hibbard E, Behrman RE, Esquival FO, Windle WF (1964) Kernicterus in
asphyxiated newborn monkeys. Experimental Neurology 9:43-58. - Redmond A, Isana S, Ingall D (1965) Relation of onset of respiration to placental
transfusion. Lancet 1 (6 Feb):283-285. - Jäykkä S (1958) Capillary erection and the structural appearance of fetal and neonatal
lungs. Acta Paediatr. 1958 Sep;47(5):484-500. - Ranck JB, Windle WF (1959). Brain damage in the monkey, Macaca mulatta, by
asphyxia neonatorum. Experimental Neurology 1:130-154.
PDF files:
Lucey JF et al.,1964 (Kernicterus, or
bilirubin staining of subcortical nuclei)
bilirubin staining of subcortical nuclei)
Ranck & Windle, 1959 (First report of
experimental asphyxiation of monkeys)
experimental asphyxiation of monkeys)
Figure 4: Non-uniform staining by bilirubin
(from Lucey et al. 1964)
Non-uniform staining by bilirubin
(From Lucey et al. 1964)