Tuesday, August 25, 2015

Starchy stable isotopes? I don't think so!

Have a read at this statement from Hardy et al 2015:

“…stable isotope analyses indicate a mainly carnivorous diet for Neanderthals; a wider range of isotopic values have been observed in contemporary Middle Pleistocene H. sapiens (Richards and Trinkaus 2009), indicating that considerable differences in the levels of starch consumption existed between these two species.”

Now, if you read this I think you might be led to believe that stable isotope analysis indicates that Neanderthals were carnivores and H sapiens ate a different amount of starch to a carnivore. I feel the implication of this sentence is that H sapiens ate "more-than-zero starch" during the Middle Pleistocene.

You would believe wrongly. Did you check the reference? No? Naughty. Richards and Trinkaus (2009) actually say this:

“As the method only measures protein intake, many low-protein foods that may have been important to the diet (i.e., high caloric foods like honey, underground storage organs, and essential mineral and vitamin rich plant foods) are simply invisible to this method.”

The data do not deny starchivory. But the data equally do not in any way support its occurrence. Starch, fruit and honey are invisible on stable isotope analysis. This is a gross mis-citation of Richards and Trinkaus by Hardy et al. Never believe stuff like this without checking the refs. Easy when it is a freebie in PLOS. What do Richards and Trinkaus actually say about diets of carnivorous Neanderthals vs H sapiens? Try this:

“There are now enough isotopic data to see patterns in the data, and they show that the Neanderthals and early modern humans had similar dietary adaptations, obtaining most of their dietary protein from animals, although some of the early modern humans obtained significant amounts of their protein from aquatic, and not just terrestrial, sources.”

You can tell H sapiens ate fish because aquatic food chains are long. The longer the food chain the greater the effect visible in stable nitrogen isotopes. They make fish eating carnivores look like hyper-carnivores. That's how they show up in the paper. Had humans eaten any significant amount of protein rich plants (hazel nuts get cited as a possibility) it would show a lower stable nitrogen ratio. There is no evidence for this.

Did early humans consume starch to grow their brain size? Stop laughing! No one knows, certainly to the point where a starchivorous paper has to mis-cite a completely non-supportive paper as being actually supportive of their rubbish hypothesis.

I love it.

Did you hear the one about Jennie Brand-Miller? Passthecream linked to this gem in the comments of the last post. Some things are just too funny not to share. Have a giggle. J B-M is second author on the starch-is-needed-to-grow-brains paper...

Peter

36 comments:

Tucker Goodrich said...

Hardy also doesn't discuss at all the one clear marker we have for starch consumption in early humans: dental caries.

They don't appear until just before the emergence of agriculture with its high starch consumption.

I covered some of the evidence a year ago in this post:

"Yes Virginia, The Paleo Diet Was Low-Carb"

http://yelling-stop.blogspot.com/2014/09/yes-virginia-paleo-diet-was-low-carb.html

Peter said...

Excellent post Tucker. We both know we carry our biases around with us. What I hope is an accurate view of the world is one which does not force us to lie due to our biases!

Peter

raphi said...

I read your post Tucker - nice!

Denisovans/Neandertals have 1 copy of AMY1 and modern humans 4.31 to 14.25 copies. This increase in AMY1 copy number happened post-Neandertal/Denisovan divergence around ~550-590kya. Estimates of controlled fire use (aka cooking) ranged from 300-400kya (Roebroeks et al. 2010) or as soon as 250kya (Wrangham et al. 2010).

So AMY1 have evolved in response to eating more starches via cooking - that is, if like me you still believe in cause preceding effect.

1ofMany Sugaraholics said...

"Starchivory": love the new word you've added to the nutritional lexicon.

Miki said...

For a more detailed rebuttle of this (very wrong) hypothesis see my post http://www.paleostyle.com/?p=2152

Miki said...

and my AHS 13 presentation http://www.slideshare.net/mikibendor/carnivourus-paleolithic-diet-miki-bendor-ahs13-24907026?qid=2ba97b3a-0dc9-4c7a-9de4-c73b7f9e030a&v=default&b=&from_search=1

Tucker Goodrich said...

Thanks, Peter. That means a lot coming from you.

@Raphi: AMY1 copy number increase also evolved in dogs in the same period. Both wolves and chimps have two copies, both dogs and people vary in number. So there's pretty clearly severed pressure to adapt to a high-carb diet. The question, of course, is why?

It turns out that the bacteria that turn starch into tooth-decaying acids use salivary amylase to do the conversion: they can't do it themselves.

There's exactly one (that I could find) study that looks into the effect of multiple AMY1 copies on dental health. They found that people with multiple copies have lower rates of caries.

If this is correct it means that the evolutionary pressure is a defensive one: to protect the teeth from rotting out.

Sort of speaks against the health benfits of starch... ;)

The other interesting thing I've learned is that, while we evolved from frugivores who had a high sucrose diet, we do not have salivary sucrase enzyme to break it down. Salivary sucrase is a sign of bacterial activity. So it's not a great argument to make to say salivary amylase is needed for digesting starch.

It's an interesting question why we have salivary amylase then in the first place, let alone why wolves have it.

Peter studies protons in mitochondria for a hobby, I study teeth. ;)

Peter said...

Miki, I've enjoyed reading your blog and listening to the AHS presentation immensely (I never listen to podcasts!). There are so many problems when anyone falls in love with an idea. The cooked starchers clearly have problems with reality and the omega 3 and DHA-ers have some ridiculous ideas on board, some quite funny. I like your self questioning and methodical approach through energetics. Thanks for putting your ideas out there.

Tucker, the teeth speak well!

Peter

raphi said...

@Tucker,

Would you mind linking to that paper looking at AMY1's effects on dental health? raphi.inter@gmail.com. Thanks.

"Both wolves and chimps have two copies, both dogs and people vary in number" ==> You make a good point that the adaptation, so far, appears to have been more of a defensive move rather than an 'embracing' one.

"It's an interesting question why we have salivary amylase then in the first place, let alone why wolves have it." ==> I don't know what the what the timeline says about dog domestication & their AMY2B (pancreatic amylase) CNV increase but...could they have adapted alongside us to make the best of our scraps? But then why no AMY1?

What we DO know about AMY1 is that it doesn't help our metabolism deal with carbohydrate better since you're as likely to be obese whether you have 4 or 14 copies. Seems like this riddle is going to be a slow process of eliminating hypothesized functions...

Spittin'chips said...

Seems to be a lot of money up for grabs at the moment - Rory Robertson and Anthony Colpo have thousands of our (currently pathetic) $AUD on offer, albeit for different things. Coincidentally, they also both have thoughts on offer re the Australian Paradox.

I wonder if Rory would have gotten any better response from Sydney Uni if he'd gone "Full-Colpo" on them.

Stipetic said...

Hi Tucker. I read your blogpost. Excellent stuff.

Above you say:

It turns out that the bacteria that turn starch into tooth-decaying acids use salivary amylase to do the conversion: they can't do it themselves.

If this is correct it means that the evolutionary pressure is a defensive one: to protect the teeth from rotting out.


I didn't get the jump to the conclusion here. If bacteria need salivary amylases to convert starch to acid, then wouldn't more amylase produce more acid? If so, how is that protective? Seems it would be more damaging.

Passthecream said...

@Raphi


Instant hypothesis, just add water and research : grains contain amylase inhibiting enzymes, greater amounts of amylase would counter the effect of greater (relative) inputs of seed based food. This is a zero sum game for calorie intake but gives an advantage in terms of novel food choices.


C.

raphi said...

@Passthecream,

interesting. i can see that.

Passthecream said...

And perhaps you might find other neolithic detoxifying adaptations eg in areas where legume consumption is higher there might be a greater capacity for dealing with phytohaemagluttenins.



C.

Tucker Goodrich said...

Stipetic: "I didn't get the jump to the conclusion here. If bacteria need salivary amylases to convert starch to acid, then wouldn't more amylase produce more acid? If so, how is that protective? Seems it would be more damaging."

Unless more salivary amylase prevents the bacteria from getting the starch.

If it's digested into glucose before the bacteria can do it, it would prevent them from producing the acids that actually rot the teeth. Not a 100% solution, but an improvement.

Tucker Goodrich said...

@Tucker,

Would you mind linking to that paper looking at AMY1's effects on dental health? raphi.inter@gmail.com. Thanks.

Will do, when I can find it again: it wasn't a great study: it was from Iran, but it was the only one I could find. I don't seem to have saved the link or the study...

"...could they have adapted alongside us to make the best of our scraps?...

Yes, I think that's exactly what happened.

"What we DO know about AMY1 is that it doesn't help our metabolism deal with carbohydrate better since you're as likely to be obese whether you have 4 or 14 copies...."

I can give you this link:

"The chance of being obese for people with less than four copies of the AMY1 gene was approximately eight times higher than in those with more than nine copies of this gene. The researchers estimated that with every additional copy of the salivary amylase gene there was approximately a 20 per cent decrease in the odds of becoming obese."

http://www.sciencedaily.com/releases/2014/03/140330151318.htm

That's a huge signal for an epidemiological signal, btw. On the order of the signal that smoking tobacco causes lung cancer—indicative of a likely strong causal relationship.

The cause appears to be that people with more AMY1 copies detect the glucose earlier, secrete insulin earlier, and therefore can secrete less insulin to deal with the bolus—that's another paper that I don't have time for find the link for right now...

We'll leave the insulin/obesity discussion on the side for now. ;)

Tucker Goodrich said...

@raphi:

""It's an interesting question why we have salivary amylase then in the first place, let alone why wolves have it." ==> I don't know what the what the timeline says about dog domestication & their AMY2B (pancreatic amylase) CNV increase but...could they have adapted alongside us to make the best of our scraps? But then why no AMY1?"

Yes, thanks for correcting me. It's AMY2B, not AMY1. That's why I hate doing this stuff from my lousy memory!

But the point and implication are the same.

"Amylase activity is associated with AMY2B copy numbers in dog: implications for dog domestication, diet and diabetes"
http://onlinelibrary.wiley.com/doi/10.1111/age.12179/full

Tucker Goodrich said...

This one is fun too:

"...the strongest association of α-amylase activity measures were found to be a negative correlation with blood pressure."

"Salivary Alpha-Amylase Activity, a New Biomarker in Heart Failure?"

http://www.omicsonline.org/salivary-alpha-amylase-activity-a-new-biomarker-in-heart-failure-2155-9880.S2-005.php?aid=6829

They did find it's not a great marker for heart failure, but the inverse relationship with blood pressure is pretty fascinating... :)

Tucker Goodrich said...

"...These observations are interpreted to suggest that [high-amylase] individuals may be better adapted to ingest starches, whereas [low-amylase] individuals may be at greater risk for insulin resistance and diabetes if chronically ingesting starch-rich diets."

"High Endogenous Salivary Amylase Activity Is Associated with Improved Glycemic Homeostasis following Starch Ingestion in Adults"

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3327743/

raphi said...

@Tucker,

http://www.nature.com/doifinder/10.1038/ng.3340 Usher et al. 2015 'Structural forms of the human amylase locus and their relationships to SNPs, haplotypes and obesity' ==> 3 cohorts for a total of 51,535 Estonians.

1) "Obese and lean individuals show indistinguishable distributions of AMY1 copy number (P > 0.05)...We had >99% power to detect (at nominal significance) effects as strong as those reported. However, we did not observe even a nominal association between obesity and the copy number of any amylase gene (P = 0.70 for AMY1)"
2) The previous strong association you cite were due to "low-resolution, poorly clustering molecular data conceal technical effects that can create the false impression of strong association"
3) Authors believe that the "the difference from the reported observation likely comes from our use of higher-resolution approaches for both molecular and computational analysis"

Point 3 has to do with read-depths relating to sequence coverage. The latter is the number of times a nucleotide is read during the sequencing process [Formula: N x (L x G)] N = # of reads, L = average length of reads, G = length of original genome.
>x7 = deep ... >x100 = ultra deep.

The association (AMY1-obesity) has been pretty much definitively put to rest in my mind.

Tucker Goodrich said...

@raphi:

Thanks for posting. I will take a look.

169-page (!) PDF available for free here:

http://dash.harvard.edu/bitstream/handle/1/17467224/USHER-DISSERTATION-2015.pdf?sequence=1

http://www.sciencedaily.com/releases/2015/06/150622122840.htm

"...This is a younger field having its birth pangs."

Guess so...

raphi said...

@Tucker,

Nice find for background on the study! I enjoyed it actually & although I didn't get much of the stats I can appreciate the genetics rationale that went into them.

You mean the field of genetics as it relates to obesity? If so, agreed. The genetics angle on obesity has generated 0 practical interventions as far as I know. Not to say it won't one day but...

Tucker Goodrich said...

As discussed above:

"Conclusion: Generally it can be concluded that low levels of alpha-amylase may promote early childhood caries. On the other hand, dental caries may subsequently reduce the level of salivary alpha-amylase. This vicious cycle may promote and then accelerate caries formation among susceptible people with low level of salivary alpha-amylase."

"Effect of alpha amylase on early childhood caries"
PDF: http://ojs.fosjc.unesp.br/index.php/cob/article/viewFile/873/795

Ash Simmonds said...

Don Matesz - King Of Evidential Ignorance - for some reason doesn't agree:

- http://donmatesz.blogspot.co.nz/2015/08/paleo-diet-big-brains-needed-carbs.html

Stipetic said...
This comment has been removed by the author.
Stipetic said...

Thanks for responding, Tucker. I'm still trying to understand. You said,

If it's digested into glucose before the bacteria can do it, it would prevent them from producing the acids that actually rot the teeth. Not a 100% solution, but an improvement.

I thought bacteria use glucose to make acid (your original post seems to imply bacteria can't utilize starch directly, that it needs amylase to convert it to a usuable form; glucose). If so, more amylase should produce more sugar, which bacteria would use to produce more acid, which would then lead to more caries (and this process would likely grow more bacteria too and lead to a vicious cycle). Inversely, less amylase would lead to more starch going unprocessed directly to the stomach, leaving less glucose for the bacteria to turn into acid--fewer amylase copies = beneficial (less caries). But that's not what you are saying and not what's been shown empirically (Iranian paper).

However, if bacteria utilise starch directly, then the availability of usable substrate to bacteria is inverse and the argument works.

The evolutionary pressure argument doesn't seem to work if bacteria use glucose directly. Sweets cause caries, right? In essense, I'm not seeing how the number of copies appears to be defensive in order to protect teeth from rotting. Unless it does so by some other mechanism. Did I missunderstand or misinterpreted? Cheers.

Tucker Goodrich said...

@Stipetic:

I expected that AMY1 multiple copies would produce more caries, as you describe. We have one not-great study showing the opposite. I was trying to come up with an explanation as to why that might be the case. Pure speculation on my part, in other words.

S. mutans uses glucose, or, given salivary amylase, it uses that to digest starch, releasing lactic acid. My thought was that a higher amylase enzyme level may reduce the time the starch is in the mouth, thereby reducing the amount available to S. mutans for acid production.

The other major characteristic of starch that causes caries is stickiness: likeliness that starch is stuck to the teeth, where S. mutans lives. Less sticky starch like rice is less cariogenic.

So reducing that sticky starch to glucose and getting it off the teeth as fast as poassible would reduce the amount that S. mutans could convert to acid.

But again, it's pure speculation, as I was hoping to explain an effect contrary to what I was expecting to see.

john said...

Ash,

What an odd story Matesz is. I wonder if he feels bad about charging people for dietary consultations when he was "paleo." Did they all get refunds? Give him some more time, and he'll be praising Ray Peat.

Since you mentioned Matesz, I thought I'd also check out Guyenet, who of course is also proud of the recent low fat win. He seems to support statin use now, and has an anti-meat tone, though, to be fair, it isn't so aggressive (yet?).

Tucker Goodrich said...

"...I wonder if he feels bad about charging people for dietary consultations when he was "paleo." Did they all get refunds?..."

I donated $50 to his blog before he lost his mind. I did not get a refund.

But I got good value from his old posts, so I'm not complaining.

Passthecream said...

@Tucker Seems as though he has fallen prey.


What do other seed eating, non-ruminant animals do about starch, birds for instance?


Where I live we have a big problem with sparrows as an invasive species. These are thought to be another of the 'diseases' of civilisation, following the neolithic crops across from the middle east until they have almost come back full circle around the planet.



C.


Stan (Heretic) said...

Re: Mrs JBM,

www.theaustralian.com.au/news/health-science/a-spoonful-of-sugar-is-not-so-bad/story-e6frg8y6-1226090126776

8-:D

Regards,
Stan (Heretic)


Passthecream said...

Lovely display of supposedly healthy foods there ( puke).

She's probably not so cocky any more, but this latest starch paper does have an aspect of zombie to it.


C.

Peter said...

Zombie w/o bwains... Non-living proof of the shrinking human brain size! Stan, these people always make me think go JK's ideas about the slave temperament and a carb based nutrition. Intelligence is not required, contribution to the hive is what matters. What intelligence remains is used to claw up the carb society pyramid.

Peter

Tucker Goodrich said...

@Passthecream:

"What do other seed eating, non-ruminant animals do about starch, birds for instance?"

I don't know, but birds are pretty far down a different evolutionary path from us, so it's not really relevant what they do.

Pigs are more interesting to look at, as they're extremely close to us and they are clearly well-evolved to eat tubers.

What's really interesting is that they're not prone to the tooth-eating bacteria that feed on our starch using our amylase.

http://jdr.sagepub.com/content/73/10/1627.short

Passthecream said...

Rats and mice are seed based creatures but maybe they don't live long enough to get tooth decay? I don't know how they deal with agglutenins etc. but I guess they must have specific enzymes and digestive processes to handle them. I had a thought this afternoon that the high (10%) Western European prevalence of haemochromatosis might be a useful mutation wrt a diet heavy in grains and legumes.



C.

Passthecream said...

Probably I'm wrong about rat diets there; one thing I remember about uncovering rats 'nests' in the garden when I was young was that were huge piles of almond and other stone fruit seeds from which the kernels had been eaten and just as many empty shells of garden snails. That looks like a high fat/high protein diet.



C.