Part 2 in the series based on a paper I wrote this past spring.
Previously:
Autism, Vitamin D and Vitamin K2 MK-4 Part I:
Does nutrition play a role in environmental health?
Autism is a broad term used to classify “autism spectrum disorders,” a category referring to a spectrum of neurodegenerative/neurodevelopmental disorders beginning in early childhood and
marked by physiological and behavioral effects on brain function, social behavior, and communication.
While children and adults with autism have a wide range of functionality and unique ways to contribute to society, the disorders pose challenges for those experiencing autism. Some challenges are internal, such as impaired function, and some are external, such as social biases against those with developmental or behavioral differences. Both such challenges can be difficult for children and their families and caregivers. Diagnosis raises questions about who is getting autism, why it is occurring, and whether it may be treated at present and prevented in the future.
As discussed in
part 1, I’m interested specifically in the potential relationship between certain fat-soluble vitamins and prevalence of autism spectrum disorders.
In recent decades, the scope of autism diagnosis has
risen astronomically, with recorded cases among ages 6-22 increasing nine-fold in eleven years (1992 - 2003;
www.fightingautism.org ) and the majority of the increase beginning
in the 1980s and 1990s (Figure 1).
While autism appears across all populations,
prevalence is higher in boys than in girls, in people with darker skin than those with lighter skin, and, some data suggests, in some recent immigrant populations to northern regions.
As discussed in the last post, autism is often
linked to methylmercury exposure. However, other factors may contribute to autism’s rapidly-increasing prevalence, perhaps exacerbating effects of methylmercury exposure. It seems, as with many areas of children’s environmental health, autism may not be caused by only one factor, but by a combination of elements. A simultaneous increase in detrimental variables and reduction in protective ones may cause a significant rise in incidence while confounding the process of isolating exposure factors and how they interact.
The timing of the recent autism increase (Figure 1) has aligned interestingly with the recent increase in childhood obesity, which started to rise significantly in the mid 1980s and has continued to climb dramatically (NHANES) (Figure 2)
raising risks of chronic disease, metabolic syndrome, and earlier morbidity.
While, of course, correlation does not imply causation, it is worth examining whether some of the same factors that are correlated with the recent obesity epidemic may also be contributing to a rise in autism and related illnesses linked to variables of environmental health.
This brings us back to the decrease in certain protective fat-soluble vitamins, due to changes in sunlight exposure, metabolism, and in diet, and an increase in detrimental foods, such as fructose and omega-6 fatty acids. As I mentioned in the
last post,
vitamins D3 and
K2 MK-4 (menaquinone-4) protect against effects of the depletion of glutathione, an important tripeptide in the brain. Glutathione protects the brain from effects of methylmercury associated with autism, and glutathione is
found in diminished levels in children with autism. Fructose, omega-6 fatty acids and other ingredients which
promote obesity interfere
with glutathione development and
affect levels of leptin in a way that limits metabolism of fat-soluble vitamins.
Other explanations for the increase in autism prevalence have been suggested. One hypothesis is that the rate of reporting has increased as awareness of the disease has risen. This may account for some of the change in incidence, but not all, due to the extent of change; overviews of data
have established the increase exists independently of awareness and diagnostic biases. Another argument, as
this paper pointed out and thoughtfully debunked, is that autism is strictly genetic. While environmental factors may change how genes are expressed, genes themselves have not spontaneously generated in the population in the last several decades and so this factor cannot serve as an explanation strictly on its own.
This is a relatively new topic, one which merits rigorous investigation due to the importance of addressing childhood autism and the critical role fat-soluble vitamins play in health. The possible relationship between vitamin D deficiency and autism has been addressed in a number of places, although it is still considered controversial. The only mention of a relationship to vitamin K I could find, other than what I’ve written, is
here and not yet in any formal research.
The question of fat soluble vitamin deficiency is not yet part of public health and public policy intervention and prevention systems for autism. Recommended intakes of vitamin D and K do not take into account factors like autism prevention or potential interaction with detrimental environmental factors, although vitamin D deficiency, and a push for a higher recommended daily dose, is starting to
appear in media and on the public’s radar, in connection to health concerns like cardiovascular disease. I hope public exploration of a connection to environmental health and neurodegenerative diseases will also increase.
The next post will be an exposure assessment, aka a discussion of what we’re being exposed to -- or not exposed to-- that may be contributing to the rise of autism prevalence.
Thanks to
Norma Desmond for the flickr CC photo
Previously: Autism, Vitamin D and Vitamin K2 MK-4 Part I:
Does nutrition play a role in environmental health?
Autism is a broad term used to classify “autism spectrum disorders,” a category referring to a spectrum of neurodegenerative/neurodevelopmental disorders beginning in early childhood and marked by physiological and behavioral effects on brain function, social behavior, and communication.
While children and adults with autism have a wide range of functionality and unique ways to contribute to society, the disorders pose challenges for those experiencing autism. Some challenges are internal, such as impaired function, and some are external, such as social biases against those with developmental or behavioral differences. Both such challenges can be difficult for children and their families and caregivers. Diagnosis raises questions about who is getting autism, why it is occurring, and whether it may be treated at present and prevented in the future.
As discussed in part 1, I’m interested specifically in the potential relationship between certain fat-soluble vitamins and prevalence of autism spectrum disorders.
In recent decades, the scope of autism diagnosis has risen astronomically, with recorded cases among ages 6-22 increasing nine-fold in eleven years (1992 - 2003; www.fightingautism.org ) and the majority of the increase beginning in the 1980s and 1990s (Figure 1).
While autism appears across all populations, prevalence is higher in boys than in girls, in people with darker skin than those with lighter skin, and, some data suggests, in some recent immigrant populations to northern regions.
As discussed in the last post, autism is often linked to methylmercury exposure. However, other factors may contribute to autism’s rapidly-increasing prevalence, perhaps exacerbating effects of methylmercury exposure. It seems, as with many areas of children’s environmental health, autism may not be caused by only one factor, but by a combination of elements. A simultaneous increase in detrimental variables and reduction in protective ones may cause a significant rise in incidence while confounding the process of isolating exposure factors and how they interact.
The timing of the recent autism increase (Figure 1) has aligned interestingly with the recent increase in childhood obesity, which started to rise significantly in the mid 1980s and has continued to climb dramatically (NHANES) (Figure 2) raising risks of chronic disease, metabolic syndrome, and earlier morbidity.
While, of course, correlation does not imply causation, it is worth examining whether some of the same factors that are correlated with the recent obesity epidemic may also be contributing to a rise in autism and related illnesses linked to variables of environmental health.
This brings us back to the decrease in certain protective fat-soluble vitamins, due to changes in sunlight exposure, metabolism, and in diet, and an increase in detrimental foods, such as fructose and omega-6 fatty acids. As I mentioned in the last post, vitamins D3 and K2 MK-4 (menaquinone-4) protect against effects of the depletion of glutathione, an important tripeptide in the brain. Glutathione protects the brain from effects of methylmercury associated with autism, and glutathione is found in diminished levels in children with autism. Fructose, omega-6 fatty acids and other ingredients which promote obesity interfere with glutathione development and affect levels of leptin in a way that limits metabolism of fat-soluble vitamins.
Other explanations for the increase in autism prevalence have been suggested. One hypothesis is that the rate of reporting has increased as awareness of the disease has risen. This may account for some of the change in incidence, but not all, due to the extent of change; overviews of data have established the increase exists independently of awareness and diagnostic biases. Another argument, as this paper pointed out and thoughtfully debunked, is that autism is strictly genetic. While environmental factors may change how genes are expressed, genes themselves have not spontaneously generated in the population in the last several decades and so this factor cannot serve as an explanation strictly on its own.
This is a relatively new topic, one which merits rigorous investigation due to the importance of addressing childhood autism and the critical role fat-soluble vitamins play in health. The possible relationship between vitamin D deficiency and autism has been addressed in a number of places, although it is still considered controversial. The only mention of a relationship to vitamin K I could find, other than what I’ve written, is here and not yet in any formal research.
The question of fat soluble vitamin deficiency is not yet part of public health and public policy intervention and prevention systems for autism. Recommended intakes of vitamin D and K do not take into account factors like autism prevention or potential interaction with detrimental environmental factors, although vitamin D deficiency, and a push for a higher recommended daily dose, is starting to appear in media and on the public’s radar, in connection to health concerns like cardiovascular disease. I hope public exploration of a connection to environmental health and neurodegenerative diseases will also increase.
The next post will be an exposure assessment, aka a discussion of what we’re being exposed to -- or not exposed to-- that may be contributing to the rise of autism prevalence.
Thanks to Norma Desmond for the flickr CC photo