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Mercury Poisoning vs Autism ... "81 Clinical Symptoms Are Almost All Identical !!!
Mercury Poisoning |
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Autism |
Psychiatric Disturbances |
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Social deficits, shyness, social withdrawal |
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Social deficits, social withdrawal, shyness |
Depression, mood swings; mask face |
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Depressive traits, mood swings; flat affect |
Anxiety |
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Anxiety |
Schizoid tendencies, OCD traits |
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Schizophrenic & OCD traits; repetitiveness |
Lacks eye contact, hesitant to engage others |
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Lack of eye contact, avoids conversation |
Irrational fears |
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Irrational fears |
Irritability, aggression, temper tantrums |
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Irritability, aggression, temper tantrums |
Impaired face recognition |
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Impaired face recognition |
Speech, Language & Hearing Deficits |
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Loss of speech, failure to develop speech |
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Delayed language, failure to develop speech |
Dysarthria; articulation problems |
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Dysarthria; articulation problems |
Speech comprehension deficits |
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Speech comprehension deficits |
Verbalizing & word retrieval problems |
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Echolalia; word use & pragmatic errors |
Sound sensitivity |
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Sound sensitivity |
Hearing loss; deafness in very high doses |
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Mild to profound hearing loss |
Poor performance on language IQ tests |
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Poor performance on verbal IQ tests |
Sensory Abnormalities |
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Abnormal sensation in mouth & extremities |
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Abnormal sensation in mouth & extremities |
Sound sensitivity |
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Sound sensitivity |
Abnormal touch sensations; touch aversion |
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Abnormal touch sensations; touch aversion |
Vestibular abnormalities |
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Vestibular abnormalities |
Motor Disorders |
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Involuntary jerking movements - arm flapping, ankle jerks, myoclonal jerks, choreiform movements, circling, rocking |
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Stereotyped movements - arm flapping, jumping, circling, spinning, rocking; myoclonal jerks; choreiform movements |
Deficits in eye-hand coordination; limb apraxia; intention tremors |
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Poor eye-hand coordination; limb apraxia; problems with intentional movements |
Gait impairment; ataxia - from incoordination & clumsiness to inability to walk, stand, or sit; loss of motor control |
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Abnormal gait and posture, clumsiness and incoordination; difficulties sitting, lying, crawling, and walking |
Difficulty in chewing or swallowing |
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Difficulty chewing or swallowing |
Unusual postures; toe walking |
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Unusual postures; toe walking |
Cognitive Impairments |
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Borderline intelligence, mental retardation - some cases reversible |
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Borderline intelligence, mental retardation - sometimes "recovered" |
Poor concentration, attention, response inhibition |
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Poor concentration, attention, shifting attention |
Uneven performance on IQ subtests |
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Uneven performance on IQ subtests |
Verbal IQ higher than performance IQ |
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Verbal IQ higher than performance IQ |
Poor short term, verbal, & auditory memory |
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Poor short term, auditory & verbal memory |
Poor visual and perceptual motor skills, impairment in simple reaction time |
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Poor visual and perceptual motor skills, lower performance on timed tests |
Difficulty carrying out complex commands |
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Difficulty carrying out multiple commands |
Word-comprehension difficulties |
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Word-comprehension difficulties |
Deficits in understanding abstract ideas & symbolism; degeneration of higher mental powers |
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Deficits in abstract thinking & symbolism, understanding other’s mental states, sequencing, planning & organizing |
Unusual Behaviors |
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Stereotyped sniffing (rats) |
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Stereotyped, repetitive behaviors |
ADHD traits |
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ADHD traits |
Agitation, unprovoked crying, grimacing, staring spells |
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Agitation, unprovoked crying, grimacing, staring spells |
Sleep difficulties |
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Sleep difficulties |
Eating disorders, feeding problems |
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Eating disorders, feeding problems |
Self injurious behavior, e.g. head banging |
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Self injurious behavior, e.g. head banging |
Visual Impairments |
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Poor eye contact, impaired visual fixation |
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Poor eye contact, problems in joint attention |
“Visual impairments,” blindness, near-sightedness, decreased visual acuity |
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“Visual impairments”; inaccurate/slow saccades; decreased rod functioning |
Light sensitivity, photophobia |
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Over-sensitivity to light |
Blurred or hazy vision |
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Blurred vision |
Constricted visual fields |
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Not described |
Physical Disturbances |
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Increase in cerebral palsy; hyper- or hypo-tonia; abnormal reflexes; decreased muscle strength, especially upper body; incontinence; problems chewing, swallowing, salivating |
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Increase in cerebral palsy; hyper- or hypotonia; decreased muscle strength, especially upper body; incontinence; problems chewing and swallowing |
Rashes, dermatitis/dry skin, itching; burning |
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Rashes, dermatitis, eczema, itching |
Autonomic disturbance: excessive sweating, poor circulation, elevated heart rate |
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Autonomic disturbance: unusual sweating, poor circulation, elevated heart rate |
Gastro-intestinal Disturbances |
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Gastroenteritis, diarrhea; abdominal pain, constipation, “colitis” |
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Diarrhea, constipation, gaseousness, abdominal discomfort, colitis |
Anorexia, weight loss, nausea, poor appetite |
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Anorexia; feeding problems/vomiting |
Lesions of ileum & colon; increased gut permeability |
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Leaky gut syndrome |
Inhibits dipeptidyl peptidase IV, which cleaves casomorphin |
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Inadequate endopeptidase enzymes needed for breakdown of casein & gluten |
Abnormal Biochemistry |
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Binds -SH groups; blocks sulfate transporter in intestines, kidneys |
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Low sulfate levels |
Has special affinity for purines & pyrimidines |
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Purine & pyrimidine metabolism errors lead to autistic features |
Reduces availability of glutathione, needed in neurons, cells & liver to detoxify heavy metals |
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Low levels of glutathione; decreased ability of liver to detoxify heavy metals |
Causes significant reduction in glutathione peroxidase and glutathione reductase |
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Abnormal glutathione peroxidase activities in erythrocytes |
Disrupts mitochondrial activities, especially in brain |
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Mitochondrial dysfunction, especially in brain |
Immune Dysfunction |
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Sensitivity due to allergic or autoimmune reactions; sensitive individuals more likely to have allergies, asthma, autoimmune-like symptoms, especially rheumatoid-like ones |
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More likely to have allergies and asthma; familial presence of autoimmune diseases, especially rheumatoid arthritis; IgA deficiencies |
Can produce an immune response in CNS |
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On-going immune response in CNS |
Causes brain/MBP autoantibodies |
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Brain/MBP autoantibodies present |
Causes overproduction of Th2 subset; kills/inhibits lymphocytes, T-cells, and monocytes; decreases NK T-cell activity; induces or suppresses IFNg & IL-2 |
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Skewed immune-cell subset in the Th2 direction; decreased responses to T-cell mitogens; reduced NK T-cell function; increased IFNg & IL-12 |
CNS Structural Pathology |
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Selectively targets brain areas unable to detoxify or reduce Hg-induced oxidative stress |
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Specific areas of brain pathology; many functions spared |
Damage to Purkinje and granular cells |
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Damage to Purkinje and granular cells |
Accummulates in amygdala and hippocampus |
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Pathology in amygdala and hippocampus |
Causes abnormal neuronal cytoarchitecture; disrupts neuronal migration & cell division; reduces NCAMs |
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Neuronal disorganization; increased neuronal cell replication, increased glial cells; depressed expression of NCAMs |
Progressive microcephaly |
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Progressive microcephaly and macrocephaly |
Brain stem defects in some cases |
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Brain stem defects in some cases |
Abnormalities in Neuro-chemistry |
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Prevents presynaptic serotonin release & inhibits serotonin transport; causes calcium disruptions |
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Decreased serotonin synthesis in children; abnormal calcium metabolism |
Alters dopamine systems; peroxidine deficiency in rats resembles mercurialism in humans |
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Possibly high or low dopamine levels; positive response to peroxidine (lowers dopamine levels) |
Elevates epinephrine & norepinephrine levels by blocking enzyme that degrades epinephrine |
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Elevated norepinephrine and epinephrine |
Elevates glutamate |
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Elevated glutamate and aspartate |
Leads to cortical acetylcholine deficiency; increases muscarinic receptor density in hippocampus & cerebellum |
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Cortical acetylcholine deficiency; reduced muscarinic receptor binding in hippocampus |
Causes demyelinating neuropathy |
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Demyelination in brain |
EEG Abnormalities / Epilepsy |
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Causes abnormal EEGs, epileptiform activity |
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Abnormal EEGs, epileptiform activity |
Causes seizures, convulsions |
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Seizures; epilepsy |
Causes subtle, low amplitude seizure activity |
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Subtle, low amplitude seizure activities |
Population Characteristics |
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Effects more males than females |
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Male:female ratio estimated at 4:1 |
At low doses, only affects those geneticially susceptible |
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High heritability - concordance for MZ twins is 90% |
First added to childhood vaccines in 1930s |
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First "discovered" among children born in 1930s |
Exposure levels steadily increased since 1930s with rate of vaccination, number of vaccines |
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Prevalence of autism has steadily increased from 1 in 2000 (pre1970) to 1 in 500 (early 1990s), higher in 2000. |
Exposure occurs at 0 - 15 months; clinical silent stage means symptom emergence delayed; symptoms emerge gradually, starting with movement & sensation |
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Symptoms emerge from 4 months to 2 years old; symptoms emerge gradually, starting with movement & sensation |
http://www.vaccinationnews.com/DailyNews/July2001/AutismUniqueMercPoison.htm
http://www.vaccinationnews.com/scandals/feb_15_02/comparison_symptoms.htm
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Autism - A to Z
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Autism - Coral Calcium - Can Natural Nutritional Supplement Assist in Behaviour Modification of Autistic Children & Parents |
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The results indicate that there was a significant difference in favor of the nutrition group. This study strongly indicates that Coral Calcium or other nutritional supplements like them can greatly benefit both autistic children and their parents. Also, parents reported better rest and satisfaction in the nutritional group.
For instance, Coral Calcium contains calcium which has been show to aid in sleep. Also, this supplement contains lithium which has greatly helped bipolar individuals. People who suffer from bipolar disorder have strong mood swings similar to autistic children tantrums. Perhaps this mineral helps balance the brain of this population as well.
Studies have shown that calcium plus vitamin D helps the population in a variety of ways and even prevent cancer (Tang, 2011). More studies are needed on the benefits of such supplements and effects on physiology and neurology of special needs children and general population. |
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Autism - Information / Articles - Vitamin D Deficiency - Mercury Controversy - Hyperbaric Oxygen Therapy (HBOT) |
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Seemingly overlooked is the fact that the MMR vaccine contains 3 different live viruses, although attenuated, they are all of a type that in heir natural state can infect the brain and potentially cause brain damage. In light of a number of equivocal and contradictory research studies attempting to incriminate the mercury preservative in this vaccine, the live virus explanation needs more study.
Fetal exposure to environmental insecticide residues may also provide clues.
The widespread addition of of MSG to many, many foods (added to most processed foods in cans and boxes), and disguised by terms such as as "hydrolyzed protein," "yeast extract," "natural flavorings," etc., also needs to be looked at. |
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Autism - A Patient Friendly Summary |
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The autism spectrum disorder (ASD) is a group of developmental disabilities. Autism is just one disorder on the spectrum. It affects both the brain and body of young children. These children have atypical development in socialization, communication, and behavior.
In 2006, approximately 1% of all children or one child in every 110 was classified as having an ASD.
Risk factors
Risk factors for autism include:
- Environmental toxins (exposure to chemicals and heavy metals)
- Environmental conditions leading to vitamin D deficiency
- Genetics
Environmental risk factors may lead to DNA mutations and increased risk for autism. Vitamin D protects against DNA damage. Vitamin D also repairs the damage once it occurs.
Sunlight exposure and autism risk
Dr. John Cannell of the Vitamin D Council has studied the link between autism and lower levels of sunlight. There is increased prevalence of autism in regions of greater cloud cover and rainfall.
According to many studies, more children with autism are born during the spring. March is the time of lowest vitamin D levels in northern mid-latitudes. These areas are further from the sun and get less light. This corresponds to brain damage around the sixth month of pregnancy.
Vitamin D and Autism
Vitamin D levels
Several findings suggest that low vitamin D levels (in mothers during pregnancy and in infants) may affect the risk of autism:
- Dark skin is a risk factor for development of autism. Those with dark skin produce less vitamin D from sunlight.
- Low maternal vitamin D level is a risk factor for premature delivery. The risk of autism increases with each week a baby is born early.
- Maternal seafood consumption during pregnancy may lower the baby’s risk of autism. Cold water ocean fish are a good source of vitamin D and omega-3 fatty acids. Both are important for brain health.
These and other findings do not prove that vitamin D reduces the risk of autism. However, the theory is strong enough that Dr. Cannell states, “[The possibility] deserves immediate attempts to disprove it.”
How vitamin D works
Every cell in the brain has vitamin D receptors. The receptors control gene expression or how genetic material is used. Therefore, vitamin D may have many beneficial effects for the brain.
Dr. Cannell pointed out that infection during pregnancy could increase the risk of autism. Some adverse birth outcomes, such as schizophrenia, are associated with maternal influenza during pregnancy. Influenza during pregnancy raises the maternal body temperature. This can have adverse effects on the developing fetus. High levels of vitamin D may lower the risk for influenza.
One of the hallmarks of autism is oxidative stress. This leads to early cell death. There are many papers in the literature reporting that vitamin D reduces oxidative stress.
Prevention
The risk of autism could be lowered significantly by women using vitamin D supplements before conception, during pregnancy, and after birth. Research suggests that pregnant and nursing women require 6000 IU (150 mcg)/day of vitamin D3 (cholecalciferol) during pregnancy and lactation for best pregnancy outcomes and in order to give the infant sufficient vitamin D3 during nursing.
Treatment
There are no peer-reviewed papers reporting the use of vitamin D to treat children with autism. However, some of Dr. Cannell’s newsletters report improvement in autism after increasing vitamin D blood levels.
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There is mounting evidence that low serum 25-hydroxyvitamin D[25(OH)D] levels during pregnancy and early life are associated with increased risk of developing autism.
The ultraviolet-B (UVB)-vitamin D-autism hypothesis was originally proposed by John Cannell1 2. Evidence in support of this hypothesis includes increased prevalence of autism with increasing latitude, excess birth rate for autism in spring, low serum 25(OH)D levels for those with autism, increased risk of autism for those with darker skin, increased risk for autism born to mothers likely to have low serum 25(OH)D levels due to darker skin, increased risk of autism associated with preeclampsia, and diametrically opposed social behaviors of those with Williams syndrome.
The mechanisms whereby high serum 25(OH)D level increase the risk of autism may include protection against DNA damage of spermatocytes and ova prior to conception, impacts on fetal brain development, and reduction of oxidative stress.
To reduce the risk of autism, pregnant and nursing women should consider keeping serum 25(OH)D levels above 40-50 ng/mL, which would keep serum vitamin D levels high enough for the fetus/infant, and making sure their infants and children maintain adequate serum 25(OH)D levels.
Autism is a disease that affects both the brain and the body.
“Autism spectrum disorders (ASDs) are a group of developmental disabilities characterized by atypical development in socialization, communication, and behavior. ASDs typically are apparent before age 3 years, with associated impairments affecting multiple areas of a person's life. Because no biologic marker exists for ASDs, identification is made by professionals who evaluate a child's developmental progress to identify the presence of developmental disorders…..In 2006, on average, approximately 1% or one child in every 110 in the 11 ADDM sites was classified as having an ASD” 3
“Recent clinical studies have revealed a high prevalence of gastrointestinal symptoms, inflammation, and dysfunction in children with autism. Mild to moderate degrees of inflammation were found in both the upper and lower intestinal tract. In addition, decreased sulfation capacity of the liver, pathologic intestinal permeability, increased secretory response to intravenous secretin injection, and decreased digestive enzyme activities were reported in many children with autism. Treatment of digestive problems appears to have positive effects on autistic behavior4.”
John Cannell's original hypothesis1 2 was based on a thorough review of many lines of evidence regarding the characteristics of autism and the roles of UVB and vitamin D on neurological function. Given the importance of this hypothesis and since the reasoning involved is an excellent example of how such hypotheses can be formed from available evidence, the entire abstract is presented here:
Any theory of autism's etiology must take into account its strong genetic basis while explaining its striking epidemiology. The apparent increase in the prevalence of autism over the last 20 years corresponds with increasing medical advice to avoid the sun, advice that has probably lowered vitamin D levels and would theoretically greatly lower activated vitamin D (calcitriol) levels in developing brains. Animal data has repeatedly shown that severe vitamin D deficiency during gestation dysregulates dozens of proteins involved in brain development and leads to rat pups with increased brain size and enlarged ventricles, abnormalities similar to those found in autistic children.
Children with the Williams Syndrome, who can have greatly elevated calcitriol levels in early infancy, usually have phenotypes that are the opposite of autism. Children with vitamin D deficient rickets have several autistic markers that apparently disappear with high-dose vitamin D treatment. Estrogen and testosterone have very different effects on calcitriol's metabolism, differences that may explain the striking male/female sex ratios in autism. Calcitriol down-regulates production of inflammatory cytokines in the brain, cytokines that have been associated with autism. Consumption of vitamin D containing fish during pregnancy reduces autistic symptoms in offspring.
Autism is more common in areas of impaired UVB penetration such as poleward latitudes, urban areas, areas with high air pollution, and areas of high precipitation. Autism is more common in dark-skinned persons and severe maternal vitamin D deficiency is exceptionally common the dark-skinned. Conclusion: simple Gaussian distributions of the enzyme that activates neural calcitriol combined with widespread gestational and/or early childhood vitamin D deficiency may explain both the genetics and epidemiology of autism. If so, much of the disease is iatrogenic, brought on by medical advice to avoid the sun. Several types of studies could easily test the theory2.
Page last edited: 17 May 2011
References
- Cannell, J. J. Autism and vitamin D. The Vitamin D Newsletter. 2007 May;
- Cannell, J. J. Autism and vitamin D. Med Hypotheses. 2008; 70 (4): 750-9.
- Prevalence of autism spectrum disorders - Autism and Developmental Disabilities Monitoring Network, United States, 2006. MMWR Surveill Summ. 2009 Dec 18; 58 (10): 1-20.
- Horvath, K. Perman, J. A. Autism and gastrointestinal symptoms. Curr Gastroenterol Rep. 2002 Jun; 4 (3): 251-8.
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Autism - Vitamin D and other Vitamin Deficiencies in Autism - A Case Study |
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John is a seven-year old boy living in the northeastern U.S. with a long-standing diagnosis of autism. Symptoms include temper tantrums, repetitive self-stimulatory behavior, impaired language, mood swings, fear of being alone, toileting problems, dysbacteriosis, and impaired muscle strength. John spends a lot of time outdoors starting in the spring and his mother noticed a distinct seasonal variation in his symptoms in that he improved in the summer and regressed in the winter.
A 25-hydroxy-vitamin D in April of 2008 was 25 ng/ml and obtained after John had begun to play outside. Due to the seasonality of John's symptoms the mother consulted me and I advised the mother to stop all products containing vitamin A including cod liver oil and begin John on 5,000 IU of vitamin D3 per day for two weeks followed by 2,000 IU per day in the form of powdered vitamin D dissolved in juice. Within a week of starting the vitamin D language began to return and he was no longer as fearful of being alone.
At the end of two weeks his language showed further improvement, he began to toilet himself, counted to 10 and knew the spelling of his name. After three weeks language continued to improve and some improvements were noted in his dysbiosis. After four weeks of vitamin D treatment, the mother noted improvements in muscle strength as well as continued improvements in language. A repeat 25-hydroxy-vitamin D is pending while John continues taking 2,000 IU of vitamin D per day. |
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Autism - What if Vitamin D Deficiency is a Cause of Autism |
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A few researchers are turning their attention to the sunshine vitamin as a culprit, prompted by the experience of immigrants that have moved from their equatorial country to two northern latitude locations
As evidence of widespread vitamin D deficiency grows, some scientists are wondering whether the sunshine vitamin—once only considered important in bone health—may actually play a role in one of neurology's most vexing conditions: autism.
The idea, although not yet tested or widely held, comes out of preliminary studies in Sweden and Minnesota. Last summer, Swedish researchers published a study inDevelopmental Medicine and Child Neurology that found the prevalence of autism and related disorders was three to four times higher among Somali immigrants than non-Somalis in Stockholm. The study reviewed the records of 2,437 children, born between 1988 and 1998 in Stockholm, in response to parents and teachers who had raised concerns about whether children with a Somali background were overrepresented in the total group of children with autism.
In Sweden, the 15,000-strong Somali community calls autism "the Swedish disease," says Elisabeth Fernell, a researcher at the Karolinska Institute in Stockholm and a co-author of the study.
In Minnesota, where there are an estimated 60,000 Somali immigrants, the situation was quite similar: There, health officials noted reports of autism among Somali refugees, who began arriving in 1993, comparable to those found in Sweden. Within several years of arrival, dozens of the Somali families whose children were born in the U.S. found themselves grappling with autism, says Huda Farah, a Somali-born molecular biologist who works on refugee resettlement issues with Minnesota health officials. The number of Somali children in the city's autism programs jumped from zero in 1999 to 43 in 2007, says Ann Fox, director of special education programs for Minneapolis schools. The number of Somali-speaking children in the Minneapolis school district increased from 1,773 to 2,029 during the same period.
Few, if any, Somalis had ever seen anything like it. "It has shocked the community," Farah says. "We never saw such a disease in Somalia. We do not even have a word for it."
What seemed to link the two regions was the fact that Somalis were getting less sun than in their native country—and therefore less vitamin D. The vitamin is made by the skin during sun exposure, or ingested in a small number of foods. At northern latitudes in the summertime, light-skinned people produce about 1,000 international units (IUs) of vitamin D per minute, but those with darker skin synthesize it more slowly, says Adit Ginde, an assistant professor at the University of Colorado Denver School of Medicine. Ginde recommends between 1,000 to 2,000 IUs per day, calling current recommendations of 200 IUs per day outmoded.
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Autism - Autism and Vitamin D: The Sun is Not the Enemy |
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In recent years we have been told to avoid the sun. Anyone reading women's magazines, in fact, will have been advised to put on sunscreen on face and hands "just in case" as those few moments walking from the car to the workplace or grocery store might be enough to cause aging and cancer cells to go nuts in our vulnerable skin.
We slather on sunscreen and sunblock, which for the most part completely blocks the UVB sun rays that increase our cancerprotective vitamin D and allows in some cancer causing UVA - to me that sounds like a silly thing to do!
Why not get enough sun to get a little color, obtain a healthy amount of the essential vitamin D and then cover up to avoid sunburn and further problems? It is certainly what our ancestors, absent suncreen, must have done for hundreds of thousands of years.
Vitamin D is minimal in the diet (fortified dairy products and cod liver oil provide a small amount), and we have historically obtained 90% or so of our vitamin D through our skin. In fact, someone with fair skin in the midday hours of the summertime can make up to 12,000 IU vitamin D within 20 minutes or so with arms and legs exposed. A more typical amount in someone with an adequate blood level of vitamin D would be 4,000 IU - a cup of milk has 300 IU. So you can see you have to drink an awful lot of milk to make up for sun avoidance.
In recent decades, near-complete sun-avoidance is what we've been told to do (particularly in the midday, which is when we make the most vitamin D.) Health-conscious folks blocked those dangerous rays from our vulnerable hides and definitely protected the soft skin of our most precious children. But could that increased vigilance have a terrible cost? Could a lack of sunshine and suboptimal amounts of vitamin D be a possible cause of autism spectrum disease in our children?
Vitamin D researcher Dr. John Cannell has spent a great deal of time covering this topic, so I don't need to reinvent the wheel here. I'll note the highlights and link his articles for the full discussion. He began with an article in 2007, followed by a comprehensive update in 2010. (My thanks to fellow blogger Jamie Scott for pointing me to these articles originally.)
Cannell's 2007 article
Update, August 2010
Dr. Cannell's major points (he has several more, but I'll note the more compelling ones):
1) Autism is increasing, as is vitamin D deficiency, and the autism epidemic came upon us at the same time the major health authorities advised us to eschew the sun.
2) Vitamin D is likely central to brain development as a key helper in neural development and neuroprotection. In addition, autism is likely mediated by inflammation, and vitamin D is a key player in anti-inflammatory processes. Also, vitamin D enables glutathione, the "masterantioxidant," clear our system of free radicals, and glutathione also acts as a chelating agent to bind toxic heavy metals such as mercury, which kids with autism have a tough time clearing from their systems.
3) Williams syndrome, a chromosomal disease which (among other things) results in abnormally high levels of circulating active vitamin D in early childhood, results in kids who are especially social and overfriendly - rather the opposite of autism symptoms.
4) During pregnancy, boys' brains are bathed in testosterone, and girls' brains in estrogen. Estrogen is known to have many vitamin D enhancing properties. This could account for the 4:1 ratio of boys to girls suffering from autism.
5) Studies show autism births occur most often in March, at the end of winter, when vitamin D levels would be lowest.
6) African Americans seem to suffer from a higher rate of autism, and they also have a higher rate of vitamin D deficiency than people with lighter skin. In Europe, the children of darker-skinned immigrants have higher rates of autism also.
7) Rickets, due to vitamin D deficiency, is characterized by hypotonia (poor muscle tone) and developmental delay, as is autism.
8) Autism seems to be higher among the kids of highly educated women, and they are more likely to follow guidelines for sun restriction for themselves and their children.
All told, it makes for a compelling theory, and Dr. Cannell has a point in that "this theory deserves immediate attempts to disprove it." My only major issues with it are that rickets is not autism, and that there may not be a new autism epidemic after all, but we are only now recognizing how prevalent the disorder actually has been all this time. But I could certainly be wrong about that second bit. And, by all means, let's please give pregnant women guidelines for sufficient vitamin D and get the kids to play outside! And let's study vitamin D and autism directly.
Dr. Cannell touches on this next part in his 2010 article - we have a lot to learn from history. If vitamin D deficiency is the cause of autism, then all of this has happened before . Rickets, characterized mostly by bone growth abnormalities in children, became endemic during the industrial revolution , when people in cities, especially, seemed to spend very little time outdoors, diets were poor, and many children died, as there was no cure. Eventually, cod liver oil and sunbathing were shown to prevent and improve the disease.
Here is Dr. Cannell's quote: "If adequate amounts of vitamin D prevent autism, one would expect children with rickets to have an increased risk of autism. To my knowledge, the neuropsychiatric symptoms of rickets have not been studied in the modern era. However, at least two old papers have addressed it, both published before Kanner described autism in 1943. Both papers describe ‘weak mindedness,'‘feeble minds,'‘mental dullness,' unresponsiveness and developmental delays. Even more intriguing, both papers report that the mental condition in rickets improved with vitamin D."
In Nutrition and Physical Degeneration , first published in 1939, a writer named Laird had the following to say about the state of mental health at the time - keeping in mind this was published without a thought for political correctness, and certainly researchers or bloggers would phrase some things quite differently these days! (1 ):
The country's average level of general ability sinks lower with each generation. Should the ballot be restricted to citizens able to take care of themselves? One out of four cannot. . . . The tail is now wagging Washington, and Wall St. and LaSalle Street. . . . Each generation has seen some lowering of the American average level of general ability.
Although we might cite any one of nearly two dozen states, we will first mention Vermont by name because that is the place studied by the late Dr. Pearce Bailey. "It would be," he wrote, "safe to assume that there are at least 30 defectives per 1000 in Vermont of the eight-year-old mentality type, and 300 per 1000 of backward or retarded persons, persons of distinctly inferior intelligence. In other words, nearly one-third of the whole population of that state is of a type to require some supervision.
Dr. Weston Price summarized the thinking about medicine and disease at the time thusly:
The problem of lowered mentality and its place in our modern conception of bodily diseases has not been placed on a physical basis as have the better understood degenerative processes, with their direct relationship to a diseased organ, but has generally been assigned to a realm entirely outside the domain of disease or injury of a special organ or tissue. Edward Lee Thorndike, of Columbia University, says that "thinking is as biological as digestion." This implies that a disturbance in the capacity to think is directly related to a defect in the brain.
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Of course back then they did not have the diagnostic categories or laboratory tests to differentiate between the varieties of autism, mental retardation (most commonly due to hypothyroidism), and cerebral palsy. But even Dr. Price complained that medicine was becoming too specialized, without an holistic view. And it is nice to see him recognize that mental illness is biologic, way back in the early part of the century. Pretty good considering that psychiatry is something of the red-headed stepchild of modern medicine even today.
It does make you wonder. This "mental degeneration" of that time period, in part, led to the rise of eugenics, and even Nazis. In the late 1800s, admissions to mental asylums skyrocketed. The mental health of the western world seemed to improve after World War II, when bread began to be fortified with B vitamins, and people recognized the importance of at least a small amount of vitamin D. But anxiety, depression, and "bodily degeneration" is on the rise again with our change to industrial processed food, and perhaps this change in nutrition and increase in sun avoidance has contributed to an increase in autism spectrum disorders as well.
In historical novels, a curative practice for what ails you is always to take some time visiting on the seashore. One would expect to get more sun then, and eat more nutrient-rich seafood, and be bathed in the magnesium-rich waters of the ocean. Sounds like an excellent curative course to me!
Don't get burned, but don't hate the sun - those midday rays (in moderation) are the best source of a healthy amount of vitamin D. Skin cancer is usually easy to catch early and have removed, whereas higher levels of vitamin D have been shown to be protective against may different kinds of much more common cancers that are generally moredifficult to catch early - including colon, breast, and prostate cancer . Melanoma is the deadly exception to the relatively easily managed and removed rule of skin cancer - but melanoma often occurs in areas not exposed to the sun, and its incidence seems to be increasing the more we use sunblock . And, of course, melanoma is much rarer than colon or breast or prostate cancer.
The full impact of lack of sunshine on mental health in general is unknown, but I do suspect there is a connection. In the future I will publish articles about links between depression and schizophrenia and vitamin D levels. One final plug for sunshine, not just vitamin D supplementation - according to Dr. Michael Holick in The Vitamin D Solution, we make 5-10 additional photoproducts in our skin. It seems prudent to think that if our skin is spending time and energy making something, it will likely be a molecule we need. While these issues are not fully understood, I like to fall back to evolution as a sensible guide. Our species has exposed a lot of skin to the sun. We need to fully comprehend the risks and benefits (for total health, not just skin cancer) of hiding from it before we make general recommendations to never let skin go exposed. |
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Autism - The Link Between Autism and Low Levels of Vitamin D |
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An epidemic of autism appears to be underway in the United States. According to several respected leaders in child and adult nutrition from across the United States, the current meteoric rise in autism and autism spectrum disorders (ASD) may well be a direct consequence of significant vitamin D deficiencies in pregnant women and their infants.1-6And evidence points to vitamin D deficiency as the cause of other debilitating brain conditions as well.5,7-10 This insidious deficiency is readily remedied—yet tragically often missed.
For years, Life Extension has been exploring the potentially devastating consequences of vitamin D deficiency, ranging from cardiovascular disease to cancer. Now in this report, Life Extension magazine examines the link between low levels of plasma vitamin D and autism. At the forefront of this research is Dr. John J. Cannell, executive director of the Vitamin D Council and a forensic psychiatrist at Atascadero State Hospital in California. The stunning findings suggest that rampant vitamin D deficiency is causally related to brain dysfunction, and may be readily preventable by adequate supplementation.2-4,11
Autism—What’s Known, What’s Guessed, and What’s Still to be Learned
Autism, or the Autistic Spectrum Disorders (ASD), involves poor social and verbal functioning accompanied by repetitive or “stereotyped” behaviors.12 Symptoms begin sometime in early childhood. Just what the deficits are, when they first become evident, and what causes them are still unknown, though both genetic and environmental factors seem to play major roles.12-14 Similarly, it seems apparent that there are many different developmental conditions that meet at least some of the definitions of autism or ASD.12
In fact, scientists agree that we actually know very little about this puzzling, multi-faceted, and tragic condition, which ranges in severity from very subtle alterations in social behavior to full-blown developmental delays that may result in placement in long-term care facilities.15-17
What is undeniable is that there has been a marked increase in the number of children being diagnosed with autism over the past two decades, not just in the US but in most industrialized nations.18-21 Some experts argue that this rise is due to increased detection by parents and physicians, as well as changing criteria and diagnostic categories.22-25 By now, however, most agree that the increase is real, and probably represents an interaction of basic genetic tendencies with something new and different in our current turn-of-the-century world.3,19-21 One report showed the incidence of autism rose 30-fold in just seven years.25 This 2006 British study estimated that one in every 86 children met criteria for autism or ASD20—a shocking figure that alone justifies use of the term “epidemic.”3
What is causing this apparent dramatic rise in autism cases? The answer or answers have been elusive, generating heated controversy among (and between) physician groups, other scientists, and many parent groups. Considerable attention has been given to mercury and other environmental toxins that cause oxidative stress,26,27 and scientists are conducting further studies to determine if mercury in the environment and mercury preservatives in vaccines are casually linked to autism. Genetic factors are also important, as demonstrated by high rates of occurrence in other family members, particularly in twin studies.28,29 Today’s consensus identifies both genetic and environmental factors as being relevant to the causes of autism.14,30
The “Vitamin D Deficiency Theory” of Autism
What possible factors involving both genetics and environment could account for the dramatic change in autism rates in just 20 years? Our genes surely aren’t changing that fast, and while our environment is clearly being altered, no serious scientist suggests that anything radical enough to cause an epidemic of brain dysfunction has taken place in the past two decades. That’s correct, argues Dr. John Cannell, but in fact our behavior with regard to our environment has indeed undergone significant changes—changes that, because of their effects on the vitamin D neurosteroid system, can and do account for many of the observed facts about the autism epidemic.
Dr. Cannell, a widely-published expert on vitamin D’s many-faceted effects,4,31-33 believes that these facts line up in a compelling fashion to implicate vitamin D deficiency and support the “vitamin D deficiency theory” of autism.3 Let’s follow Dr. Cannell’s line of thinking as he lines up the extraordinary evidence that we may be able to stop the autism epidemic in its tracks with simple vitamin D supplementation.
Cannell starts with the incredible increase in our understanding of vitamin D’s fundamental contri-butions to human health. Though most people (sadly including many physicians) still associate it only with bone mineralization, we now understand that the active form of vitamin D, called calcitriol, plays an equally important role as a neurosteroid hormone, directly responsible for many elements in brain development and behavior34 (other examples of neurosteroids include the sex hormones estrogen and testosterone, which have effects on the full spectrum of human behaviors). Vitamin D obtained from supplements or sunshine must undergo two biochemical processes before it becomes active. First, it is metabolized by the liver to 25-hydroxyvitamin D, the main circulating form of vitamin D and the only vitamin D metabolite that should be measured to assess vitamin D status.
Circulating 25-hydroxyvitamin D then undergoes a final biochemical step to form calcitriol, a potent neurosteroid that controls brain cell growth, and acts on receptor molecules found in brain cells from the first days of embryo formation.35 Because of these potent effects, researchers in 2001 labeled vitamin D the “neglected neurosteroid” and concluded that vitamin D deficiency “should be examined in more detail as a candidate risk factor” for neurodevelopmental disorders such as autism.36 More recently, researchers have suggested that vitamin D, acting as a neurosteroid, offers “neuroprotection, antiepileptic effects, immunomodulation, [impact on] several brain neurotransmitter systems and hormones, as well as regulation of behaviors,”37 stressing the importance of prenatal, neonatal, and postnatal vitamin D supplementation for normal brain functioning.38
But what has happened in the past 20 years that could affect the neurosteroid function of vitamin D and relate it to the explosion of autism cases? Plenty, argues Cannell: put very simply, we have become excessively “sun-phobic” in our efforts to reduce the very real risk of skin cancers.3,39 Couple this with our decreasing natural exposure to sunlight as we’ve moved from agricultural to manufacturing to service-based activities, and you have the “perfect storm” for vitamin D deficiency.1,11Vitamin D levels in industrialized countries are known to be much lower than those of fully sun-exposed individuals.40 Thus, our behavior has had the paradoxical and unintended consequence of limiting our blood levels of the only known precursor of a vital neurohormone that, in turn, can influence the very organ of behavior itself, the brain.3
What is the evidence to support the vitamin D deficiency theory of autism? A recent review by Dr. Cannell provides a substantial and cogent evidence base,3 starting with the characteristics of the vitamin D neurosteroid system itself. Calcitriol acts as a “molecular switch” in brain tissue, turning on powerful genes that influence brain development. There are about 1,000 genes already known to be targets of calcitriol activity, and that number is growing fast.37,41
But unlike any other vitamin system, the bulk of human vitamin D stores come not from oral intake but from skin production under the influence of sunlight.42,43 As Dr. Cannell notes in his review, “Large populations of pregnant women putting small amounts [of vitamin D] in their mouths—in the form of prenatal vitamins—instead of generating large amounts in their skins, is novel to human brain development;”44 since we no longer get ample sun exposure, we need to pay closer attention to how much vitamin D we do get through our mouths.
The case for significant oral supplementation is made even clearer when one considers that skin production of vitamin D is vastly more efficient than oral intake.2 In fact, just 10-40 minutes of summer sunbathing by a fair-skinned adult, notes Cannell, produces about 20,000 units of vitamin D which is presented to the systemic circulation over the next 24 hours45—to get the same amount orally a pregnant woman would have to drink 200 glasses of milk (at 100 IU per glass) or take 50 standard prenatal multivitamins (400 IU per tablet) to realize the same gains!3
But, as Cannell goes on to point out, we’ve been assiduously avoiding sun exposure for the past 20 years, dutifully following AMA guidelines.39 It is precisely during that same 20-year period that we’ve seen the rapid rise in autism rates,14 though as Dr. Cannell acknowledges, “Thousands of other environmental changes occurred during this same time and such associations, on their own, mean little.”3
But there are plenty of additional persuasive arguments supporting the theory. The calcitriol neurohormone system is different from all the body’s other steroid hormone systems. While other steroids are produced directly from the body’s natural store of cholesterol “precursor” compounds, the amount of calcitriol produced is completely dependent on having enough precursor 25-hydroxyvitamin D present in the first place. And brain levels of activated vitamin D, as Cannell observes, “directly depend on the amount of vitamin D the mother makes in her skin or puts in her mouth.”3
Cannell’s dramatic conclusion is that “Human behavior, be it the step into the sun, the step to the supplements, the step into the shade, or the step to the sunscreen, determine brain calcitriol levels.”3 In the case of the human fetus, as we’re about to see, brain calcitriol levels are directly linked to very early cognitive development, with tremendous implications for the developing baby’s brain.
WHAT YOU NEED TO KNOW: AUTISM AND VITAMIN D |
- An epidemic of autism is sweeping the US and other industrialized nations.
- Causes and cures for autism have long eluded researchers, with often conflicting data making progress difficult.
- At the same time a less well-publicized but undeniable epidemic of vitamin D deficiency has been underway as a result of diminished sun exposure.
- The inspired leadership of several forward-thinking experts has finally tied the two epidemics together and may allow for the first real progress in preventing and treating autism since the epidemic began.
- Since most Americans don’t get nearly enough sunlight to meet their daily vitamin D needs, and since too much sun exposure can be dangerous, experts now recommend oral supplementation of vitamin D far in excess of standard government recommendations.
- Pregnant and nursing mothers as well as young infants need special attention to vitamin D status, since vitamin D works as a neurohormone to stimulate proper brain development and potentially reduce risk for autism.
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Calcitriol—Nutrient and Neurohormone of Brain Development
A wealth of animal data has emerged demonstrating just how essential calcitriol is in early fetal brain development. Offspring of vitamin D-deficient rats, for example, have abnormal cell growth, structure, and functions in their brains,46-48 excessive and undirected movements,49-52 and subtle alterations in learning and memory.8 Even when the deficiencies occur only late in gestation, they are capable of causing disruptions in adult brain functioning,48demonstrating the exquisite dependence of brain development on this vital neurohormone.
A group of French researchers has in fact found 36 crucial brain proteins that are disrupted when vitamin D is deficient during fetal development,7,53 and others have shown increased brain size and enlargement of the fluid-filled ventricles of the brain9—both abnormalities that are common in autism.54,55
Toxins and Oxidants—Another Important Role for Calcitriol in Autism?
What about the apparent importance of toxins and inflammation in autism? Does the vitamin D deficiency theory of autism offer an explanation? Resoundingly yes—for example, it is already known that autistic people have abnormalities in immune functions similar to those that are affected by vitamin D—including increased inflammatory cytokine levels.12,56,57 And we know that much of the ongoing inflammation in autistic brains is the result of oxidative stress12—just where vitamin D’s powerful anti-inflammatory properties are most useful (and most critical if missing).
Calcitriol has nootropic properties—that is, it protects brain tissue by reducing inflammatory cytokine levels which, when elevated, are strongly associated with cognitive impairment.3,58 Calcitriol also protects brain tissue by stimulating production of neuro-trophins, chemicals that combat toxicity from a number of sources including toxic levels of intracellular brain calcium.59 Calcitriol also increases brain levels of glutathione,60,61 a powerful natural antioxidant that is the body’s most important tool for detoxifying and excreting heavy metals and that is rapidly consumed during oxidant stress from toxins and other sources.
Cannell argues convincingly that it is especially this calcitriol-induced increase in glutathione levels that can explain the link between autism and heavy metal toxicity.3,62 Heavy metals deplete intracellular glutathione,63 however, animals supplemented with calcitriol show a reduction in iron- and zinc-induced brain injury.64,65
A study by Dr. Jill James sheds further light on the connection between heavy metals, glutathione, and autism. Children with a variant of autism called regressive autism demonstrated a severe imbalance in the ratio of active to inactive glutathione, compared with healthy children. Regressive autism occurs when previously healthy children lose acquired language or behavioral skills and go on to develop autism. Children with regressive autism displayed chronically elevated levels of oxidative stress, which would make them more vulnerable to damaging neurotoxic agents such as heavy metals.66
Vitamin D Interactions—An Answer to the Gender Issue in Autism?
The fact that vitamin D metabolism differs markedly under the effects of the sex hormones may go a long way towards explaining yet another puzzling fact about autism, namely its strong predilection for boys over girls.3 For example, researchers in Sweden and in Utah have now shown that estrogen has effects on developing brain tissue that serve to make it more responsive to the neurohormonal growth-stimulating effects of calcitriol—results which suggest that estrogen can enhance any beneficial effects of vitamin D on the brain.67,68 It has been found that estrogen increases the activity of an important vitamin-D-related calcium binding protein in neurons69,70 that plays several important roles during central nervous system development.
Though complex, these studies do support the notion that the developing brain of a female fetus, with its predominance of estrogen relative to testosterone, could make more efficient use of available vitamin D than would the brain of a male fetus. In a situation where there was plenty of vitamin D present, such differences would go unnoticed—but introduce the all-too-prevalent maternal vitamin D deficiency state, and the stage is set for possible impairment in boys more commonly than in girls, which is of course precisely the situation we see with autism’s gender discrimination.3
Vitamin D Intake and Cognitive Performance
If even some of the damage done by vitamin D deficiency during fetal development is reversible, we’d expect to find that vitamin D supplementation would help reduce autistic symptoms at least to some extent. There aren’t yet many good studies on this subject, but what we know is encouraging. A multivitamin supplementation study of 20 autistic children in 2004 showed improvements in sleep and gastrointestinal problems that are common in autism (that study only provided 150 units of vitamin D per day, which as we’ll see is probably well below the minimum requirement).71 Similar multivitamin studies have shown improvements in cognitive function even in apparently normal schoolchildren, according to one review of 14 separate studies.72
What’s remarkable (and heartbreaking) is that while these studies show very little effect on most of the children evaluated, about 20% of the children had substantial gains in performance.72 This 20% might represent a vitamin D-deficient subgroup of children—a tremendous number if these figures hold nationwide.3
We would also expect that consumption of vitamin D-rich foods by pregnant women would improve cognitive performance in their infants, and indeed Cannell provides evidence that high maternal consumption of fish, rich in vitamin D, is associated with better cognitive outcomes in infants.73,74 Another recent study demonstrated that infants born to mothers with very low seafood intake had higher risks for having low verbal IQs, less well-socialized behaviors, and poorer fine motor and communication skills.75 As Cannell persuasively argues, these deficiencies are “eerily similar to [those found in] autism.”3
A WORD ABOUT DOSING |
To reach the 25-hydroxyvitamin D blood levels that Life Extension recommends for optimal health of 50-60 ng/mL, most typical Americans will need to use dietary supplements, given the real risks ofprolonged exposure to sunlight or UV tanning lights.
But neither officially-recommended daily intakes of vitamin D (400 IU/day) nor consumption of vitaminD-fortified foods can effectively prevent vitamin D deficiency.4,85,86 As leading researcher Dr. John Cannell points out, “Adequate oral supplementation will require doses that might make a practitioner initially uncomfortable, as physiological doses of vitamin D, in the absence of sun exposure, probably range between 400 IU/day for premature infants to 10,000 IU/day for the morbidly obese.”4
Cannell goes on to cite another expert, Dr. Robert P. Heaney of Nebraska’s Creighton University, who estimates that 3,000 IU/day is required to assure that 97% of Americans obtain levels greater than 35 ng/mL.87 The Canadian Pediatric Society recommends that pregnant women should take 2,000 IU vitamin D daily to reduce the risk of autism and other adverse health conditions in their children.88 In a recent comprehensive review, Dr. Cannell recommends that “parents supplement breast-fed infants with at least 800 IU of vitamin D daily, while formula-fed infants need 400 IU per day.
Toddlers and young children who do not get regular sun exposure should take 1,000-2,000 IU daily year round, depending on body weight, keeping in mind that current Food and Nutrition Board recommendations state doses up to 2,000 IU per day are safe for children over the age of one.”4 Dr. Cannell and other experts believe that autistic children may require even higher blood levels of vitamin D than other individuals, and should take enough vitamin D to maintain serum 25-hydroxyvitamin D levels of approximately 70 ng/mL. |
Exposure to UV Light—Another Clue?
We know that certain brain diseases such as multiple sclerosis are much more common in high latitudes where sunlight is scarce, and many scientists suspect that those conditions are directly related to chronic or seasonal vitamin D deficiencies.1,2,76 A strong positive association between latitude and the prevalence of autism has been reported for groups of children before 1985, which is what we’d expect if autism were related to vitamin D deficiency.3,4 Additional support comes from recent data from the Centers for Disease Control and Prevention (CDC), which found the highest prevalence of autism in New Jersey (the second most northern state in the survey), and the lowest in Alabama.18
One might expect that babies born in late winter would have higher rates of autism if vitamin D deficiency were involved, since their mothers would have spent most of their pregnancies in fairly low-sunlight settings. While one report suggests that late winter birth dates are associated with higher rates of autism,77 the literature isn’t consistent on this topic. Cannell argues that in fact this would be expected if the critical time for the deficiency to cause damage was not only during gestation, but also in early childhood, and indeed animal studies suggest just that.46,50 Lower rates of autism have been found in rural compared with urban areas, further supporting the idea that low sunlight exposure may be a contributor.78 And a fascinating study recently demonstrated that autism rates are substantially higher in geographic areas where precipitation is highest79 (the implication is that people in such areas spend less time outdoors, thereby reducing their vitamin D-producing sun exposure).
Finally, air pollution is now known to reduce UV light exposure sufficiently to lower vitamin D levels to the point at which experts are recommending supplementation,80 and one recent study demonstrated an association between air pollution and autism27 (of course this particular association could as easily be due to toxins in the air—demonstrating how much we still have to learn about this mysterious condition).
UV-Blocking Skin Pigment—Further Support for the Vitamin D Deficiency Theory
If fetal vitamin D deficiency is at the root of autism, we should expect to find higher rates of autism among children born to dark-skinned mothers, because melanin, the major skin pigment, is an extremely efficient blocker of UV light.42As Dr. Cannell points out in his review, studies of this nature are difficult to perform and interpret, though there is limited evidence of higher incidence of autism in American black children.81 Two European studies published in 1995 also showed higher rates of autism among children of dark-skinned immigrants (up to 200-fold higher in one study).82,83 Since some studies suggest that darker-skinned individuals are more likely to be deficient in vitamin D than those with lighter skin tones,84 this provides another compelling reason for those with darker skin tones to diligently monitor their vitamin D status.
Table 01: http://www.lef.org/magazine/mag2009/images/apr2009_vitamind_09b.jpg
Summary
There seems to be little doubt that a significant proportion of the epidemic of autism is real, and not just a fluke of over-reporting and over-diagnosis by anxious parents and physicians. As many Life Extension reports have documented, there’s equal certainty that we also face an epidemic of vitamin D deficiency as we steadily move away from old ways that exposed us to more vitamin-D producing sunlight. The theory that the two epidemics are inextricably linked is supported on myriad independent grounds, and as Dr. Cannell himself points out, is readily susceptible to rigorous testing.3
While we are awaiting those results, however, it seems prudent to maximize vitamin D status in pregnant women, infants, and young children and infants, aiming for levels found in humans living in a sun-rich environment, between 50-60 ng/mL (blood testing for 25-hydroxyvitamin is recommended as the only way to make the diagnosis and to assure treatment is adequate and safe).4 One recent study noted, “Supplemental doses of vitamin D and sensible sun exposure could prevent deficiency in most of the general population.”2 Under the leadership of brilliant scientists like Dr. John Cannell, we may be privileged to witness at least the beginning of the end of the scourge of autism among our children.
If you have any questions on the scientific content of this article, please call a Life Extension Health Advisor at 1-800-226-2370.
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