Autism- Rise in prevalence

Rise in autism prevalence

Data compiled from recent epidemiological studies- note that accuracy of study varies across countries. Figure 1-




Figure 1


In the 80s, official rates were round 5 children per 10,000 population (Figure 2).


Figure 2:





Incidence rates increased by 700% in children born in 1990 compared to those born in 2006. Hertz-Picciotto and Delwiche, The rise in autism and the role of age of diagnosis. Epidemiology 2009; 20: 84-90

Possible factors implicated:

1- Greater awareness and diagnosis criteria- Cannot explain the current rise. E.g. Figure 3

Figure 3: 8.2-fold increase over 1980-83 to 1995-97
Report: January 2005 - This study used current DSM-IV diagnosis criteria on historical records dating from the period 80-83. There is non the less a 8 .2 fold increase.

2- Genetic issues (Broad autism phenotype)- Asperger in the family, often undiagnosed.

Actual contribution to current rates is unknown but has been estimated at about 7%. The family history cen be seen as far as Asperger and HFA are concerned but rarely as far as regressive autism is concerned.

Many genetic studies in autism have been undertaken draining huge amount of funding. What has been found is:

• There is a higher rate of chromosomal abnormalities in a subset of autistic children compared to controls. (note this is consistent with environmental damage to genome see below).
• These include inversions, duplications and deletions visible by microscopic techniques.
• They have been found within all 23 chromosomes, but most commonly on chromosome 15 and 7.
• Based on location, a causal association might be inferred but has not been proven.
• This could account for up to 7% of cases.

Autism does not fit pattern for “classic” genetic diseases

3- What else? Genetic-environmental factors

Figure 4: The red bar represens the threshold level of an environmental insult. If the level is below toxicity, the population is spared of detrimental consequences. As the level increase, there is a progressivly greater number of susceptible indibiduals who are affected.

The response or ability to cope with toxins across the population can be modelled with a normal distribution curve (Figure 4). This is true of many types of exposure, e.g. alcohol, some individuals will tolerate it well, others will not. This particular sensitivity results from both environmental and genetic factors. This is true of most animal and vegetal species. Response to environment differ from individual to individual within the same species. Some species are more sensitive than others in a given environment. Canaries were used in the coal mines to detect rise in carbon monoxide (Figure 5). They were more sensitive than humans with regard to this factor. Their death was indicative of increased toxicity.

Figure 5

If the outcomes of rising toxic environmental factors in genetically susceptible individuals is autism, the number of affected cases would rise with the level and number of factors as shown in Figure 4.

What could these environmental factors be?

- Testosterone in the mother- Little evidence supporting the theory of testosterone being implicated in autism- see post on the subject here.

- Vaccinations: Epidemiological studies suggest no implication. We should remember that many epidemiological studies have disproved tobacco to cause cancer. Also thalidomide was not found to cause developmental abnormalities from epidemiological studies. What is needed is to investigate children and their progression in autism, not epidemiology investigations. A few cases were investigated suggesting strong correlation with vaccination, Poling, Bailey and more. More importantly, seeing parents of children with regressive autism, day after day, saying very similar stories of immediate deterioration after vaccination raised at the very least great concerns. In a group of 60 children, 18% were found to have loss and acute loss of function within 1 week of MMR (ATT report). The possible scenario of regression can take place more gradually and over a longer period of time and would not be picked up following parental account. We currently have no markers to prove or disprove of an association for cases of regressive autism with gradual and slow loss of function.

- Other factors: many factors are known to be toxic and found in increasing amounts in the environment. Heavy metals, bi-phenyls, phtalates, organo-phosphates, etc. Many are still unknown.

- Likely we have a combination of factors, again acting on genetically susceptible individuals.

- Autism is not the only condition that is found in much greater incidence; also rising are: ADHD, asthma, MS, chronic fatigue, Alzheimer disease, cancer and more.

How could these factors deteriorate development and behaviour:

A very common genetic feature in families of children with autism is a greater immune vulnerability. This is seen with increased rate of the following conditions: allergies, asthma, eczema, arthritis, MS, thyroid dysfunction (often associated with auto-immune abnormalities).

The sum of environmental factors would constitute a stress to genetically susceptible individuals, affecting either primarily their immune system, their gut or more directly their brain. It is also very likely that there will be epigenetic changes leading to alteration of gene expression (Figure 6), this could have the highest effect still on development and brain function. The common pathway of pathology amongst individuals would be the timing at which their neurological development is being affected. Studies are ongoing to unravelled each of these potential scenarios. Cascades of events leading to deterioration of brain function can be identified in animal models and consistent and testable paradigms (with each single step being documented and published in autism) have been identified supporting this theory.

Figure 6: Epigenetic in autism