A class I took this spring got me thinking about the multiple ways environmental health and nutrition interconnect and overlap.  In some cases, nutrition issues are environmental health issues.  In other cases, our nutrition may affect how we respond to contaminants in our environment.

Our food is a source of daily exposure to both protective and detrimental components, and we’re shifting more and more from protective to detrimental. We’ve moved meat production from grass-feeding to fattening in feedlots.  We’ve replaced natural fats like butter, beef tallow or lard with highly processed vegetable oils, changing the fatty acid profile of our diet.  We’ve shifted the source of our sweeteners, upped our corn and wheat intake, and invented new additives and preservatives. Through a shift to factory farming mixed with fast/packaged food, vegetable oil, high fructose corn syrup, and other delicacies of the modern age, our menus have changed significantly.

As the professor of that course frequently pointed out, “environmental health” itself is an extremely broad term, going far beyond contamination and pollution of land, air and water.  Food, particularly our exposure to more detrimental and fewer protective substances via food, is as much of an environmental health issue as, say the effects of methylmercury exposure via seafood and other sources.  And, curiously, these two kinds of environmental health -- poor nutrition and effects of contaminant exposure -- may be interrelated.

This brings me to a less intuitive, but extremely compelling way nutrition may have an impact on environmental health.  Research suggests that our diet may affect the way our bodies respond to contaminants like methylmercury.  Poor nutrition may make us more vulnerable to toxic exposure while adequate nutrition may actually mediate some of the effects.

While exposure to toxic heavy metals and other contaminants is a problem whether we’re eating well or not, it’s worth noticing if a poor diet is compounding the problem.  A double whammy of an increase in detrimental foods and a decrease in critical vitamin-rich foods may be increasing our vulnerability.  As usual, I’m concerned with the animal-form fat-soluble vitamins, particularly vitamin D3 and vitamin K2 MK-4 (aka vitamin K2 menaquinone-4). 

Some of this connection is still speculation, but intriguing speculation nonetheless.  Here’s an example: our class looked at two classically cited studies of childhood effects of prenatal methylmercury exposure via seafood, one in the Seychelle Islands, and one from the Faroe Islands, two regions with incidents of significant methylmercury contamination.  In the Faroe study, children exposed to methylmercury prenatally (measured through hair and umbilical cord levels) showed developmental effects such as cognitive and linguistic delays and social impairment.  Follow-up studies showed that effects persisted over time. 

In the Seychelle Islands, the results were different; effects from methylmercury exposure, which were lesser, seemed to decrease as children grew older.  While some sources have blamed the whale meat more popular in Faroe, allegedly absolving the fish eaten in the Seychelle Islands, I’m intrigued by the fact that the Faroe Islands are far north, near Iceland, whereas the Seychelles are close to the equator, off the coast of Kenya.  Vitamin D exposure might be a key difference, since people in northern latitudes can’t generate cutaneous vitamin D for a large part of the year.  (If you feel like geeking out, I wrote a paper on my recommendations for seafood consumption in light of methylmercury exposure; you can download it here.)

What if vitamin D and other fat-soluble vitamins counteract some of the effects of methylmercury and other toxins?   Evidence suggests they might. 

The case about childhood autism is particularly compelling.  Autism is often linked to methylmercury exposure -- the level of methylmercury correlates significantly with prevalence of autism.   Methylmercury seems to deplete an important peptide called glutathione.  Glutathione protects the developing brain from effects of methylmercury associated with autism.  Glutathione is found in diminished levels in children with autism (full text) (more information here).

So, what’s the connection to vitamins?  Vitamin D3 and vitamin K2 MK-4 counter the depletion of glutathione.  Vitamin D3 plays a protective role in glutathione metabolism, specifically by increasing and protecting glutathione and blocking neurotoxic agents. Vitamin K2 plays a protective role in the developing brain from the effects of loss of glutathione, specifically preventing oxidative cell death as a result of glutathione depletion.

So, having adequate levels of both vitamin D3 and vitamin K2 MK-4 is doubly protective: vitamin D3 is proactive, increasing the brain’s resistance to glutathione depletion and aids in creating more glutathione, while vitamin K2 MK-4 is responsive, mediating the effects glutathione depletion would otherwise have on the brain and on child development.

For the record, I don’t tend to think there’s generally only one root of any problem, nutritional or otherwise.  I’m not saying vitamin D3 and K2 MK-4 deficiencies are the sole cause of autism, just that there’s a compelling case that the vitamins might mediate the effects of methylmercury, and that deficiency in them might enhance the likelihood, and might do so significantly.

In the next few posts, we’ll explore this subject in much more detail, looking at how our changes in diet, including an increase in fast food and poor quality ingredients, may be relevant -- and not just because they’re lower in important vitamins.  We’ll look at statistics about autism incidence, biomarkers and effects of exposure to methylmercury and adequate/inadequate diets, the connection to nutrition, fast foods, and obesity, what’s going on in the field of public health, and what needs to be studied further.

Thanks to smithereen11 for the flickr CC photo.