Part of the problem is the rise in bisphenol A (BPA) and other endocrine disrupters, linoleic acid, and other substances that interfere with GAP-43 expression (including inflammation).

From an excellent study done on post-mortem human autistic (and control) brains, Changes in prefrontal axons may disrupt the network in autism (emphasis mine):

Neuronal migration appears to be intact in autism, since neither neuronal density nor cortical depth was affected, at least in the parts of the three areas studied (Supplemental data: Cytoarchitecture of ACC, OFC, and LPFC). Our data suggest that the insult occurs later, when axons connect with other areas in the presence of high GAP-43 expression, and possibly other growth factors, which may remain elevated in adulthood in response to inflammation (Vargas et al., 2005). The associated signaling pathways need to be investigated for therapeutic interventions in autism.

GAP-43 is up-regulated by a variety of external factors as well, including estrogenic agents that disrupt endocrine function, such as bisphenol A, used for lining plastic food and drink containers, linoleic acids found in some oils, and by immunosuppressive and psychiatric drugs used for a variety of common disorders, including psoriasis, asthma, rheumatoid arthritis, depression and anxiety (Wong et al., 1989; Jyonouchi et al., 2001; Granda et al., 2003; Croen et al., 2005; Ostensen et al., 2006; Sairanen et al., 2007; Nguyen et al., 2009; Brown, Jr., 2009). Several of these substances came into heavy use in the early 80s at a time when the prevalence of autism began to rise (Blaxill, 2004). Epidemiologic studies are necessary to investigate if these events are merely coincident or if the cumulative effects of dietary factors and drugs change the uterine and postnatal environment and perturb the expression of factors implicated in axon growth and guidance in autism.

The key here is that the rise in ADH ASD highly correlates with the increased use of BPA, especially in things like baby bottles. When the bottles are heated in hot water on the stove, or in the microwave, the BPA can leach out into the formula. This doubtfully accounts for all of the increase, but I bet it accounts for a lot of it. Here we have a clear mechanism for neural changes that are found in autistic brains. I think the question above is a great one, and I think this study shows that there are things we can do to reduce the incidence of ASD, one being, get rid of BPA in plastic bottles (and in can liners), and cut out linoleic acid from infant formula (and other foods).

Part of the problem is the rise in bisphenol A (BPA) and other endocrine disrupters, linoleic acid, and other substances that interfere with GAP-43 expression (including inflammation).

From an excellent study done on post-mortem human autistic (and control) brains, Changes in prefrontal axons may disrupt the network in autism (emphasis mine):

Neuronal migration appears to be intact in autism, since neither neuronal density nor cortical depth was affected, at least in the parts of the three areas studied (Supplemental data: Cytoarchitecture of ACC, OFC, and LPFC). Our data suggest that the insult occurs later, when axons connect with other areas in the presence of high GAP-43 expression, and possibly other growth factors, which may remain elevated in adulthood in response to inflammation (Vargas et al., 2005). The associated signaling pathways need to be investigated for therapeutic interventions in autism.

GAP-43 is up-regulated by a variety of external factors as well, including estrogenic agents that disrupt endocrine function, such as bisphenol A, used for lining plastic food and drink containers, linoleic acids found in some oils, and by immunosuppressive and psychiatric drugs used for a variety of common disorders, including psoriasis, asthma, rheumatoid arthritis, depression and anxiety (Wong et al., 1989; Jyonouchi et al., 2001; Granda et al., 2003; Croen et al., 2005; Ostensen et al., 2006; Sairanen et al., 2007; Nguyen et al., 2009; Brown, Jr., 2009). Several of these substances came into heavy use in the early 80s at a time when the prevalence of autism began to rise (Blaxill, 2004). Epidemiologic studies are necessary to investigate if these events are merely coincident or if the cumulative effects of dietary factors and drugs change the uterine and postnatal environment and perturb the expression of factors implicated in axon growth and guidance in autism.

The key here is that the rise in ADH highly correlates with the increased use of BPA, especially in things like baby bottles. When the bottles are heated in hot water on the stove, or in the microwave, the BPA can leach out into the formula. This doubtfully accounts for all of the increase, but I bet it accounts for a lot of it. Here we have a clear mechanism for neural changes that are found in autistic brains. I think the question above is a great one, and I think this study shows that there are things we can do to reduce the incidence of ASD, one being, get rid of BPA in plastic bottles (and in can liners), and cut out linoleic acid from infant formula (and other foods).

Part of the problem is the rise in bisphenol A (BPA) and other endocrine disrupters, linoleic acid, and other substances that interfere with GAP-43 expression (including inflammation).

From an excellent study done on post-mortem human autistic (and control) brains, Changes in prefrontal axons may disrupt the network in autism (emphasis mine):

Neuronal migration appears to be intact in autism, since neither neuronal density nor cortical depth was affected, at least in the parts of the three areas studied (Supplemental data: Cytoarchitecture of ACC, OFC, and LPFC). Our data suggest that the insult occurs later, when axons connect with other areas in the presence of high GAP-43 expression, and possibly other growth factors, which may remain elevated in adulthood in response to inflammation (Vargas et al., 2005). The associated signaling pathways need to be investigated for therapeutic interventions in autism.

GAP-43 is up-regulated by a variety of external factors as well, including estrogenic agents that disrupt endocrine function, such as bisphenol A, used for lining plastic food and drink containers, linoleic acids found in some oils, and by immunosuppressive and psychiatric drugs used for a variety of common disorders, including psoriasis, asthma, rheumatoid arthritis, depression and anxiety (Wong et al., 1989; Jyonouchi et al., 2001; Granda et al., 2003; Croen et al., 2005; Ostensen et al., 2006; Sairanen et al., 2007; Nguyen et al., 2009; Brown, Jr., 2009). Several of these substances came into heavy use in the early 80s at a time when the prevalence of autism began to rise (Blaxill, 2004). Epidemiologic studies are necessary to investigate if these events are merely coincident or if the cumulative effects of dietary factors and drugs change the uterine and postnatal environment and perturb the expression of factors implicated in axon growth and guidance in autism.