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Saturday, September 4, 2010

The Case for Evolution - Octopuses, Grandmothers, Iceland, and Poor Dr. T. Colin Campbell

It has been a while since I reviewed my basic premise, that homo sapiens walk around in bodies and brains exceptionally well suited for hunting and gathering in small family groups in the wilderness, and that we are not evolved for agriculture as a whole, and industrial agriculture in particular. I subscribe to the concept of Evolutionary Medicine, that diseases of civilization (I'm focused on mental health in my blog) are caused by differences between our current lives and our evolutionary suitability, and that replicating a hunter-gatherer life in many ways (as makes scientific and practical sense) can lead to better health, both physical and mental.

Here's what T. Colin Campbell, PhD and full professor (of nutritional biochemistry) at Cornell has to say about that (1): "Those who follow evolutionary history and who support the inclusion of substantial amounts of animal protein as a recommended dietary practice, make this error. Our dietary evolutionary history, while interesting, absolutely does not yield critical clues for optimal nutritional practices. Human evolution required that our ancestors make dietary choices that maximized gene proliferation."

To which I say - maximized gene proliferation means living past 30 and well into old age. Humans have grandmothers. Women are designed to live 20-30 years past menopause in order to favor a higher overall birthrate as grandmothers helped gather for their offspring's offspring and taught valuable cultural information (Textbook of Evolutionary Psychiatry: The origins of psychopathology). How could tens of thousands of generations not have selected for relative longevity and freedom from disease (both mental and physical) based on our evolutionary diets? For me it honestly makes no sense to view health data from another perspective. Bizarrely, Campbell goes on to write of how chimpanzees eat a plant-based diet (we split off from chimpanzees 5 million years ago) so the preponderance of evolution data must lean towards a plant-based (low protein) diet. So evolution (of an entirely different species) is important when it explains his theories, but not so when it doesn't.

If you watched the television series "Life," you might have seen the segment about the octopus that reproduces once then dies, leaving a zillion offspring who feast on mom's dead body, and hopefully a few make it to go on. I am not an octopus! Humans are rather on the extreme "k" side of the r versus k selection species. We have few, quality offspring and spend a lot of energy nursing them to reproductive age and beyond. Our genes want us to live for a very long time, to teach our toddling young and their toddling young how to make it in this big, bad world. What plants to eat, how to chase down a large land mammal, how to set fishing traps, where the best water holes are, how to select the "Children and Family ages 2-4 movies" on netflix and how to get the kangaroo through the alphabet maze on starfall.com (seriously, I never get to use my own computer anymore) - all of this is knowledge we are not born with, and is most efficiently learned from our elders. Though my youngest figured out how to post on facebook all on her own at 12 months. Darned intuitive apple iPhone technology!

(An aside - I definitely recommend Evolution's Captain: The Story of the Kidnapping That Led to Charles Darwin's Voyage Aboard the Beagle if you are a student of evolution. Darwin was selected to go on the voyage as a gentleman companion to the young Captain Fitzroy, who had a family and personal history of depressive mental illness, in order to offer him company and hopefully to forestall any depression on the long voyage returning some kidnapped Tierra del Fuegans back to the southernmost part of South America (no, I am not making this up). Sadly, Fitzroy, who ended up being the second governor of New Zealand and was also a devout Christian, eventually killed himself a few years after watching a debate on evolution between the Archbishop of Canterbury, Thomas Huxley, and Samuel Wilberforce.)

But what about those genetic diseases that occur after reproducing? Diseases such as Huntington's Chorea? Clearly those genes survived and are genetic, not dietary, so that evolutionary (dietary) paradigm doesn't support links to those aspects of ultimate human health. Cardiovascular disease and those other diseases of civilization (let's leave out acne and many autoimmune diseases which strike young) get us when we are old and no longer contributing to the gene pool (tell that to my 9th grade band director who died in his late 40s of an MI). Okay, decent argument, but that brings me to Iceland.

Way back in the infancy of my blog, a commenter from Iceland left me two links to some very interesting information. Turns out there is an autosomal dominant genetic disease in Iceland called Hereditary Cystatin C Amyloid Angiopathy. It is caused by a mutant protein that is deposited in the walls of small arteries, leading to brain hemorrhage and death in young adults (average age of 30). Since this is Iceland, and everyone knows everybody, the family trees of everyone with the disease were deciphered and studied. Turns out the deadly hereditary cystatin C mutation occurred in Iceland sometime around 1550, and carriers of the gene lived normal lifespans until 1830, when over the next 70 years the lifespan of those afflicted decreased from 65 to 30. "This change in life-span is an indication of a strong environmental effect on the penetrance of the mutation. The effect must have been very common as it happened in [almost] all families simultaneously in all parts of the country." In the time from 1830 to 1900, Iceland changed from a traditional cow and milk based diets to a more "Western" diet similar to Europeans. In one remote region of Iceland, the lifespan shortening occurred 20 years later than in the other related family groups - that was one of the later regions to adopt the Western diet. So here we have an example of how an autosomal dominant genetic disease seems to be affected by diet.

Which brings me back to Huntington's Chorea. In my last post, I mentioned a study that showed that carriers of the mutant huntingtin gene (an autosomal dominant gene with complete penetrance, meaning everyone with the gene gets a progressive, deadly neurological illness with no cure but steady and inevitable degeneration leading to death over 20 years that begins between the ages of 20 and 44, thereabouts) had a much higher rate of positive test for anti-gliadin (wheat protein) antibodies than the general population. The huntingtin gene probably codes for a type of microtubule or vesicle protein, basically structural proteins that anchor the mitochondria in nerve cells. The mutant, deadly gene has extra trinucleotide repeats of CAG, coding for an unstable version of the huntingtin protein. A normal gene will have less than 20 CAGs in a row. A mutant gene 36 or more. The more trinucleotide repeats, the earlier the disease seems to strike. What does this have to do with wheat?

Here's the really weird part. That CAG DNA code repeat I was talking about? CAG is the genetic code for the amino acid glutamine. The mutant extra repeats is called a "polyglutamine repeat", and there are a number of genetic diseases that are also caused by this polyglutamine repeat. Turns out that polyglutamine tracts are also present in gliadin - the wheat protein. A possible explanation is that the body recognized the abnormal polyglutamine tracts made in the cells with the abnormal gene, and the wheat proteins looked a lot like the abnormal protein so that the people with Huntington's mounted an immune response to the wheat proteins. But wheat protein exposure has also been associated with non-Huntington's ataxias. Could wheat gliadin polyglutamine exposure itself and an abnormal autoimmune response lead to the protein aggregation in Huntington's disease? In other words, does our ubiquitous exposure to dietary wheat protein modify the natural history of Huntington's disease? Somewhat like Western dietary exposure seems to modify the natural history of Hereditary Cystatin C Amyloid Angiopathy?

No one knows.

But an evolutionary perspective would lead one to pursue those questions.

For decades, the U.S. government has been freewheeling with sugar and heart disease, repeating the fact that there was no data to suggest sugar had anything to do with it. Well, here's an abstract from a study in JAMA in April of 2010, showing a strong correlation between dietary sweetener consumption and a bad cholesterol profile (low HDL and high triglycerides). The money quote from the abstract? "No known studies have examined the association between the consumption of added sugars and lipid measures."

That's right. No one bothered to publish a study on sugar and blood lipid profiles until 2010.
The jury on wheat is still out. In the mean time, I'll fall back to the safe evolutionary medicine position, and avoid it.

17 comments:

  1. When I read "I am not an octopus" my brain set it to Marina & The Diamond's I Am Not A Robot. Awesome blog BTW. I was just in Robb Wolf's nutrition cert and he spoke on the connection between wheat and Huntingtons.

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  2. Btw chimps do eat meat. It was first observed by Jane Goodall see http://www-bcf.usc.edu/~stanford/chimphunt.html

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  3. Good post. I learned some things. Btw, the plural of octopus is octopuses, not octopi. I used to make the same mistake, but now that I know an octopus researcher, I've been corrected. It turns out octopus derives from Greek, not Latin, and so the plural of Greek words ending in -us is -uses. I'll get off my pedantic soap box now.

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  4. Melissa - I'm waiting fir my copy of Robb's book to arrive. I would love to attend one of his nutrition certifications. He seems like a mad genius.

    Raven - my roommate in med school was an anthropology major and told me gorillas eat meat too, on occasion.

    Aaron - I stand corrected. Now what word does end in us where the plural is i? Hmmm. It's very early in the morning here and I can't think of one now.

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  5. Cactus and cacti (although cactuses is also acceptable in most quarters).

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  6. e e cummings reckoned the plural of rectum was ...

    "Auden & spender political poyds
    even whose recti are covered by Lloyds"

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  7. I asked Cordain about Huntington's Chorea. Here is his response:
    http://thepaleodiet.blogspot.com/2009/12/paleo-diet-q-8-december-2009.html
    He says "Plain and simple, it's wheat". He seems a bit too confident.

    I later also asked Robb Wolf about the disease. On his podcast show he said that there is some research being done right now in Portugal on Huntington's Chorea and gluten. I have tried finding more information about that research, but I couldn't find anything. You are more familiar with research, maybe you know where to look?

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  8. Hi Tim - I would say no way it is a slam dunk caused by wheat. Here's what I could find - Portugal happens to be a hotspot of another polyglutamine hereditary diseass (http://www.dizziness-and-balance.com/disorders/central/cerebellar/sca.htm) and it looks like they are doing research there. Here's an abstract from pubmed about gluten sensitivity in hereditary and spinal ataxias: http://www.ncbi.nlm.nih.gov/pubmed/11310636

    Here's an article suggesting that gluten is the cause of 74% of sporadic (non hereditary) ataxias: http://brain.oxfordjournals.org/cgi/content/full/126/3/685?view=long&pmid=12566288

    On the con side, there are many models where scientists have been able to create protein aggregates just using the abnormal huntingtin gene protein, no extra gluten required.

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  9. And I was able to find this here (http://members.cox.net/hal.kraus/glossary.htm#_Poly-Glutamine)

    "Poly-Glutamine

    Poly-glutamine (poly-Q) is a chain where the molecule glutamine (Q) is repeated many times within a protein. This is actually quite rare. Long poly-glutamine chains are really only found in three places:

    1) Normal transcriptional regulation proteins, which are found especially in the central nervous system and which are normally short lived and regulated by Ubiquitin.

    2) Specific protein "mutations" associated with degeneration of the central nervous system.

    3) Gliadin in wheat (Alpha and beta). (Shorter glutamine chains are found in other grain storage proteins.)

    Excessive long chain poly-glutamine is associated with neuron toxicity. Toxicity of poly-glutamine is implicated in poly-glutamine diseases, which include Huntington’s Disease and some types of ataxia. This mechanism provides (hypothetical at this time) means by which gluten triggers, aggravates, or seems to cause degenerative CNS disorders and provides means by which gluten mimics genetic CNS disorders when the genetic disposition is not present."

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  10. Very interesting and informative post! What you wrote about wheat gliadin reminds me of what I have read about grain leptines in general (that their amino code resembled the ones of proteins that occur naturally in the human body and therefore could elicit cell reactions that wouldn't occur naturally, and thus fostered a various range of autoimmune diseases). I haven't digged into that deeply enough to make a scientifically proved statement, but for now I feel much better without grains on my plate.

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  11. I´m the one who told you about the icelandic research. It´s the reason I´m reading blog like yours because I knew something was off with the dietary guidelines.

    I´m glad you found some use of it, at least it shocked me when I heard about. I had known for a long time about this disease but I always assumed they had died young from the beginning.

    I´m just surprised it hasn´t been discussed more but I guess it´s the same struggle as anywhere else. I at least have lost my appetite for grains, I just don´t want to take the chance.

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  12. Thanks again for the info, Anna. Anyone who comments - I do look at the links, and the information always percolates. Thanks very much, because the collaboration is so important to refine ideas, theories, and to gather knowledge.

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  13. Hey. I just wrote a post that fits a lot with what your saying from an ecological viewpoint. HOpe you don't mind but here is the link -

    http://www.darwinstable.com/2010/09/16/big-brained-humans-a-dangerous-idea/

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  14. Hey Emily,

    Whenever I hear that line about men being evolved to 'spread their seed' far and wide, I always think of the 'r vs k' thing and wonder, 'what are we, E. coli?'

    I think the grandmother case has a lot of merit, but I still wonder how many grandmothers a population really needs for a selective advantage. It seems those roles could be filled with a moderate survival rate for grandmothers. I'd rather keep all the grandmothers though. Mine is awesome. :)

    Chris

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  15. Hi Chris - you know the pelvic inlet size was bigger back then (vitamin K2?), but I'm still betting a lot of women died in childbirth. Would make it all the more important for any surviving children to have grandmothers around. I think the only other animal with long-lived grandmothers (meaning a decade or more past menopause) is a species of whale that also lives in family groups as we do.

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