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Comprehensive Guide to
Managing Autism
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Willis S. Langford
Slightly changed by Kees de
Vries, Drunen, Holland (june 2003)
Warning: Do not scan
and read this paper piecemeal. It must be studied to avoid mis-steps.
Introduction
There are several very
basic things discussed in this paper that can be done at home with little or no
expensive testing. Foremost is the home testing for thyroid function discussed
toward the end of this paper, and support of thyroid function. The “unloading
of the donkey” is vital to possibly 80% of these troubled children for they
are poisoned, drowning in their own toxic wastes. Elimination of bowel disorders
is very first on the list of vital action. It is often as simple as supplying a
digestive enzyme supplement, or removing milk. Some autistic children can be
helped dramatically by medical procedures such as an infusion of the intestinal
hormone secretin. The need and the beneficial response to secretin, I think, are
dependent upon the amount of damage to the duodenum and small intestine from
whatever cause, and on the stomach’s ability to produce adequate hydrochloric
acid (HCl) for proper digestion. Since proper functionality of these two things
largely determine proper digestion, it is vital that both be operative. Without
adequate HCl, secretin infusion can, at best, be only partially effective in
restoring digestion and proper physical and mental function. Secretin is reduced
in hypothyroid rats (Robberecht et al, 1981), so first support the thyroid. HCl
production is very dependent on adequate zinc levels, usually lacking in these
children. With support for the thyroid, adequate zinc, and possibly
supplemental betaine hydrochloride, secretin infusion may be totally
unnecessary.
The path of autism is
different for each child. Some are prone to seizures, some are not; some behave
aggressively while others are overly passive. However, children with autism and
with ADHD share several factors. There is a deep disturbance in their fatty acid
metabolism that impairs their utilization of amino acids, and often there is an
imbalance in their electrolytes. Electrolytes control what’s called membrane
traffic—what goes in and out of cells. This means that providing other
nutritional supplements is relatively ineffective until the electrolyte
(sodium-potassium-magnesium-calcium) imbalance is corrected. The delicate
balance of electrolytes also controls the electrical activity within the brain.
Practitioners suggest the extent of the nutritional problem in these
observations:
Nutritional
abnormalities:
a. Zinc deficiency
exists in 90% of autistic children
b. Copper excess exists
in 85%
c. Calcium and
magnesium deficiencies are common
d. Omega 3 fatty acid
deficiency exists in nearly 100%
e. Fiber deficiency
exists in nearly 100%
f. Antioxidant
deficiency exists in nearly 100%
Additionally, there is
heavy metals poisoning: A recent study found 85 percent exhibited severely
elevated Copper/Zinc (Cu/Zn) ratios in blood, suggesting a disorder of
metallothionein (MT), a short, linear protein responsible for homeostasis of
copper and zinc and many other metals. “The severity of the Cu/Zn imbalance
was far greater than that of any other population we have studied over the past
25 years,” said William J. Walsh, Ph.D., Physician, biochemist and chief
scientist of the Pfeiffer Treatment Center, Naperville, Illinois. His database
suggests that copper overload and zinc depletion are the most common
metal-metabolism abnormalities in behavioral conditions such as, ADHD, autism,
depression, bipolar disorders, and schizophrenia. In addition, these sufferers
are unusually sensitive to lead, cadmium, mercury, and other toxic metals that
they tend to accumulate rather than eliminate. Nevertheless, if a mouse cannot
make MT, then it should not get copper deficient when fed a high-zinc diet. We
fed some of these mice and some control mice (ones that can make MT) diets that
contained normal amounts of zinc and some that contained much more zinc. The
results showed that the mouse without MT got copper deficient when fed the same
high-zinc diet as the mouse that had MT. This study strongly suggests that the
old theory is not true and that stimulation of MT is not necessary for high-zinc
to bring about a copper deficiency. We suggest instead that the high zinc is
inhibiting a copper transport protein in the intestinal membrane, and copper
cannot be absorbed—Reeves PG, Copper Metabolism in Metallothionein-null Mice
Fed a High-zinc Diet. J Nutr Biochem 9:598-601, 1998.
Blood and urine
analyses yielded evidence of a metallothionein dysfunction in 499 of 503
patients (99%) diagnosed with autism spectrum disorders, according to Walsh,
suggesting that autism may be caused by either a genetic MT defect or a
biochemical abnormality, which disables MT protein. “An MT disorder may affect
the development of brain neurons and may cause impairments in the immune system
and gastrointestinal tract, along with hypersensitivity to toxic metals,” he
said. The excess copper in these kids is probably from two causes. Mercury
depresses zinc, and there is a high incidence of zinc malabsorption. To reduce
copper, you must use significant amounts of vitamin C and zinc.
Treatment for this
imbalance centers on stimulation of MT protein with divalent metals (such as
zinc and manganese) that are in depletion, and by providing N-acetylcysteine,
serine, selenium, and other constitituents of MT. Of secondary benefit are
vitamins B6, A, C, D, E, glutathione, genistein and biochanin A (both
from soy), and glucocorticoids (anti-inflammatory drugs). This treatment should
be gradual during the first 4 weeks of treatment to avoid rapid release of
copper from tissues, which could cause a sudden worsening of symptoms.
Mercury adversely
affects detoxification systems such as metallothionein, cytochrome P-450 (Phase
I), and bile. Mercury ties up this material so it cannot bind and clear other
metals such as lead, cadmium, and aluminum. Mercury inhibits sulfur ligands in
MT and, in the case of intestinal cell membranes, inactivates MT that normally
binds cuprous ions, thus allowing buildup of copper to toxic levels and
malfunction of the zinc and copper containing Super Oxide Dismutase (SOD).
Mercury induced reactive oxygen species and lipid peroxidation (forming free
radicals) has been found to be a major factor in mercury’s neurotoxicity,
along with its leading to decreased levels of the vital enzymes glutathione
peroxidase and superoxide dismustase (SOD).
Metallothioneins across
species are rich in cysteine (~30%) and have higher affinities for mercury (Hg)
and cadmium (Cd) than for zinc. Therefore, as Hg and Cd bind to metallothionein,
and are restricted from entering the mitochondria, zinc is released. The free,
ionized zinc, which would be toxic if permitted to accumulate, binds to a metal
regulatory element on the promoter region of the metallothionein gene and
“turns on” the synthesis of metallothionein. Increases of as much as 3-times
are reported. Such induction of metallothionein provides increased binding
capacity for both toxic metals (protective) and zinc (functional). The
displacement of zinc in the presence of toxic metal burden may explain in part
why increased levels of zinc are so commonly seen in the scalp hair of patients
exhibiting significant levels of toxic metals Hg, Cd, Pb (Quig, unpublished
observations).
Furthermore, their
minerals and amino acids are deficient and/or imbalanced. Their production of
red and white blood cells is irregular. They have a dysfunctional immune system
(often attacking “self”). Eighty percent suffer mitochondrial disorders
(lack of energy production) according to Dr. Colemen, George Washington
University Hospital. Ninety percent suffer some degree of hypothyroidism despite
“normal” TSH readings (Raphael Kellman, MD). Eighty-three percent suffer
dysfunctional Phase I and II, liver-enzyme activity (causing a build up of
toxins and heavy metals), and 85% of autistic meet criteria for malabsorption
leading to a multitude of nutrient deficiencies (Wm. Walsh). Both the autistic
and the ADHD children often suffer lymphoid modular hyperplasia (measles
infection in the gut—Wakefield). Thus, children with autism do not absorb food
properly, leading to nutrient deficiencies. The most common deficiencies of poor
diet and malabsorption are fatty acids, the minerals zinc, selenium, magnesium,
and calcium, and the vitamins A, B6, C, and D, and E. This
compromises immune function, and provides inadequate antioxidant protection to
offset the high oxidative stress these children suffer, thus causing significant
damage to cells throughout the body and brain. It is interesting to note that
uric acid plays a key antioxidant role in the plasma, and many of these children
have low urea/uric acid, possibly reflecting high oxidative stress. The nutrient
deficiencies can occasionally cause extreme behaviors; some children with autism
have been reported to have actually gouged out their eyes due to a calcium
deficit. If your child is pushing at his eyes, supplement calcium and vitamin D,
and get him in the sun.
Children with autism
have a lot of metabolic abnormalities as indicated, but that is a result of the
problems with their immune system. Heavy metals such as mercury induce a
dramatic activation of the immune system and autoantibody production in the
genetically susceptible. This autoimmune syndrome is dependent on T-Cells, which
are important for B-Cell activation and cytokine secretion. Studies have found
mercury impairs the body’s ability to kill Candida
albicans by impairment of the lytic activity of neutrophils. A population of
plant workers with average mercury excretion of 20 ug/g creatinine was found to
have long-lasting impairment of neutrophil function.
Another study found
such impairment of neutrophils decreases the body’s ability to combat viruses
such as those that cause heart damage, resulting in more inflammatory damage.
Samplings of immune data reveal that most of these autism-spectrum disorder (ASD)
children have atypical elevations of antibodies against otherwise common
pathogens such as Epstein-Barr virus, Cytomegalovirus, and/or Human Herpes Virus
6 (EBV, CMV, HHV-6), and in some 30%, elevated anti-measles antibodies
indicative of chronic infection from measles vaccine—Kawashima H, Mori T,
Kashiwagi Y, Takekuma K, Hoshika A, Wakefield A; Department of Paediatrics,
Tokyo Medical University, Japan. “Of the 160 autistic children we looked at,
only five did not have bowel disease”—Wakefield. (Attenuated vaccines
contain live viruses that don’t usually cause overt disease.) HHV-6 induces
synthesis of a broad range of host cell proteins, including interferon alpha,
CD4, interleukin-1 beta, and tumor necrosis factor alpha. Additionally,
HHV-6 kills Natural Killer Cells.
Human herpesvirus-6,
the etiologic (causative) agent of roseola, is ubiquitous, establishes latency
in the host, and can infect a variety of immunocompetent cells, with CD4+ T
lymphocytes being the targets in which it replicates most efficiently, and HHV-6
has an “Immunosuppressive effect... on T-cell functions” such as
“suppression of interleukin-2 synthesis and cell proliferation.”
HHV-6 is a commensal
inhabitant of brains. Various neurologic manifestations, including convulsions
and encephalitis, can occur during primary HHV-6 infection, or in
immunocompromised patients. HHV6 has been reported within oligodendrocytes and
microglia, and focal HHV6—encephalitis has been documented. It is considered
causative in CFS.
John O’Leary, Ph.D.,
a world-class researcher and molecular biologist from Ireland, using state of
the art sequencing technology, showed how he had found measles virus in the gut
of 96% of autistic children, compared to 6.6% of normal children. This virus did
not come from the natural disease; it came from the measles vaccine. In
addition, Dr. O’Leary found measles virus present in 75% of children with
Crohn’s Disease. Crohn’s has traditionally been an intestinal disease of
adults, following years of dietary abuse. Its appearance in children is a new
event, and Dr. O’Leary’s work points to measles virus from vaccines as the
likely cause. Additionally, Candida,
according to antibody studies done at the Atkins Center, is involved in more
than 80 percent of all cases of Crohn's and Colitis.
Their pathogenic
(disease producing) power is derived from the fact that they can set up
persistent infections within various lymph tissues (that of the gut, for
example, as shown by Wakefield) as well as within circulating cells of the
immune system. Wakefield found that controls had prevalence in the gut of HHV-6
DNA similar to that of those with ulcerative colitis—86%! Virus infected
monocytes (White Cells) travel freely throughout the body, and have been shown
to enter the brain, take up residence there, and secrete cytokines (chemical
messengers) toxic to brain tissue. They also serve as foci of infection. It is
not uncommon for infants to run fevers and show other signs of acute
inflammation after receiving multiple vaccinations. Interferon production is
stimulated by infection with a virus to protect the body from super infection by
some other microorganism. In this study, vaccination of one-year-old infants
with measles vaccine caused a precipitous drop in the level of alpha-interferon
produced by lymphocytes. This decline persisted for one year following
vaccination, at which time the experiment was terminated—Journal of Infectious
Diseases. Thus, this study showed that measles vaccine produced a significant
long-term immune suppression. Similarly, the report in the British medical
journal Lancet confirmed that a significantly higher percentage of these
children had received a DTP shot within 30 days of the onset of polio compared
to a control group of children without polio, 43 percent of polio victims
compared to 28 percent of controls. The DTP vaccine suppresses the body’s
ability to fight off the polio virus. Thus, we have evidence of long-term damage
to the immune system from vaccines. Starting at about 4 months, this leads to
the infections, antibiotics, more infections, and more vaccines that often
precede autism.
“Complete
Immunoglobulin E (IgE) deficiency was seen in 10% of the patients. Almost 20% of
the patients had low IgA, and 8% of them had a complete lack of it, which is
quite high compared to the general population (1 in 700-1,000). About 25% of the
subjects had IgG subclass deficiency. About 25% of the patients had a deficiency
of various subsets of lymphocytes (e.g., CD3, CD4, and CD8 Killer T-Cells). In
fact, almost 35% of these autistic children had a deficiency in Natural Killer
Cells. In general, the cytokines IL-2 and alpha-interferon are increased, while
IL-1 is normal”—Dr. Sudhir Gupta. IgG anti-brain autoantibodies were present
in 27% with ASD, and with 2% from healthy children. IgM autoantibodies were
present in 36% with ASD compared with 0% of controls. The presence of these
antibodies raises the possibility that autoimmunity plays a role in the
pathogenesis of language and social developmental abnormalities in a subset of
children with these disorders—Serum autoantibodies to brain in Landau-Kleffner
variant, autism, and other neurologic disorders. J Pediatr 1999
May;134(5):607-13.
“I firmly believe
that up to eighty percent (and possibly all) cases of autism are caused by an
abnormal immune reaction, commonly known as autoimmunity. The autoimmune process
in autism results from a complex interaction between the immune system and the
nervous system.
“Antibodies to
measles (rubeola) virus (MV) and human herpes virus-6 (HHV-6) are elevated,
which is a sign of a present infection, past infection, or a reaction to the
measles-mumps-rubella (MMR) vaccine. The HHV-6 and measles viruses are
etiologically linked to autism because they are related to brain autoantibodies
and demyelinating diseases.
“Recently, I
conducted a study of measles virus (MV) and HHV-6 in autism....This study showed
two things in particular: first, that the virus antibody levels in the blood of
autistic children were much higher when compared to normal children; and
secondly, the elevated virus antibody levels were associated with the brain
autoantibody titer. Interestingly, the viral antibody and brain autoantibody
association was particularly true of MV antibody and Myelin-Basic Protein (MBP)
autoantibody (i.e., 90 percent of autistic children showed this association).
This observation led me to hypothesize that a measles virus-induced autoimmune
response is a causal factor in autism, whereas HHV-6, via co-infection, may
contribute to the pathophysiology of the disorder. Although as yet unproven, I
think it is an excellent working hypothesis to explain autism, and it may also
help us understand why some children show autistic regression after the
measles-mumps-rubella (MMR) immunization.
“There is enormous
potential for restoring brain function in autistic children and adults through
immunology....The goal of therapy should be to normalize or reconstitute the
immune response instead of inducing immune suppression or stimulation. This will
maintain a balance within the normal immune response, avoiding major
fluctuations of overt immune activity which could be detrimental to the
patient”—Excerpts from Autism, Autoimmunity, and Immunotherapy: a Commentary
by Vijendra K. Singh, Ph.D. Department of Biology & Biotechnology Center,
Utah State University, Logan Scientific Board Member, Autism Autoimmunity
Project.
Reed Warren, et al,
mention how the IgA findings relate to infections and report a fascinating
double susceptibility in that 6 of 8 autistic kids with low IgA levels also had
null alleles of the complement C4b: “...IgA is also important in protection
against pathogenic infections and participates in the clearance of pathogens via
the alternative complement pathway. C4 proteins [e.g., from the C4a and C4b
genes] are involved in the other complement pathway, the classical complement
pathway. Therefore, it is interesting that of the eight autistic subjects with
decreased IgA levels, all but two also had a C4b null allele suggesting that, in
these patients, both pathways of complement activation [and response to
infections] are probably operating at less than optimal level.”
A test of thirty-six
children revealed grade I or II reflux esophagitis in 25 (69.4%), chronic
gastritis in 15 (42%), and chronic duodenitis in 24 (67%). Low intestinal
carbohydrate digestive enzyme activity was reported in 21 children (58.3%),
although there was no abnormality found in pancreatic function. Seventy-five
percent of the autistic children had an increased pancreatico-biliary fluid
output after intravenous secretin administration (indicating hypersensitivity of
the pancreas) —Gastrointestinal abnormalities in children with autistic
disorder. J Pediatr 1999 Nov;135(5):559-63.
Children with autism
produce higher levels of pro-inflammatory cytokines than children without
autism. Autistic children have been shown to exhibit many anomalies in
cell-mediated immunity, including abnormal T-cell activation (Warren et al,
1995), decreased relative numbers of helper-inducer lymphocytes, and a lower
helper-suppressor ratio. (Denney et al, 1996) These last 2 measures were
inversely correlated with severity of autistic symptoms. In children with
these abnormal antibody patterns, selenium supplementation at a dose of 10
mcg/kg body weight for six months significantly increased IgG-2 and IgG-4 levels
and reduced the number of infections. Low blood values of these two antibodies
are associated with intractable seizures. Selenium and vitamin E supplementation
has overcome intractable seizures that were resistant to drugs.
In workers exposed to
fluorine, those with subclinical hypothyrosis [reduced tri-iodothyronine (T3) in
51%] had immune alterations that were more evident. T-lymphocytes count rose,
but their functional activity declined, indicating impaired cooperation of
immunocytes as a result of imperfect control under low concentrations of T3 (Balabolkin,
1995). Their immune system is driving with no brakes!
Elevated serotonin
levels have been consistently found in 30% -50% of autistic patients, and may
represent a marker for familial autism. Hyperserotonemia in autism appears to be
due to enhanced 5-HT uptake, as free 5-HT levels are normal and the current
report of an excess of the long/long 5-HTTLPR genotype in autism could provide a
partial molecular explanation for high platelet serotonin content in autism—PMID:
11378854. Serotonin synthesis is decreased in the brains of autistic children
and increased in autistic adults, relative to age-matched controls (Chugani et
al, 1999), while whole blood serotonin in platelets is elevated regardless of
age (Leboyer; Cook, 1990).
Finally, these kids are
hypersensitive to everything: sound, light, touch, and colors. Typically, bright
yellow will drive them up the wall leading to all sorts of aberrant behavior.
This sensitivity is usually related to a deficiency of vitamin B6,
zinc, and magnesium.
These medical facts
show that every symptom of these dear children is treatable! These kids are
sick. They are not usually brain damaged. What seems to be occurring is an
immune mediated, abnormal “shut down” of blood flow in the temporal lobe
area of the brain, and therefore an interference with central nervous system
function.
This paper is not
meant as a medical prescription, nor do all the conditions and suggested
interventions apply to every child. You must study this paper until you see your
child’s face in it, and then use the parts that are applicable to him. In all
instances, it is good to consult with your medical professional when making any
major nutritional changes.
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