Sunday, December 7, 2014


Our results became available last week. I ended up spending a large part of this weekend summarizing the results and re-organizing the graphs from AmGut into something I hope folks find a little bit more interesting and easier to digest (heh).

I hope to make the raw taxonomy data available later this week. Until then, please enjoy the slides. I'm going to hold off offering any of my own thoughts for a while. There are a lot of folks considerably more knowledgeable in this stuff than me anyway.

Finally, special thanks to Grace and Tim for offering suggestions on the slides, Mr. Heisenbug for offering suggestions on the experiment protocol, and last but by no means least, to Richard for bringing the considerable weight of his readership to bear on the fundraiser.

Obviously the slides on the large side, but you should be able to download them for more convenient side-by-side viewing. Enjoy!!

Update: Grace clarified to me that the genus Bifidobacterium is not necessarily part of the "Ancestral Core" as I show in the slides. One must look at the species. B. Longum is the Ancestral Core. AmGut only reports to the genus level of precision. However, it's possible to run one's own analysis to get species-level data. I plan to give it a try this week and report back.


  1. What does all of this mean? What is 4TB/day raw? What were you trying to change? Were the changes good or bad? Is reducing rare taxa a good thing? Was there a post prior to this explaining?

    1. Greetings,

      4TB/day raw means 4 tablespoons per day of raw, unmodified potato starch.

      We weren't trying to change anything. We were trying to measure the effect of supplementing various amounts of potato starch on an individuals gut biome.

      As for what it all means, it's open to considerable debate. The science is young here and about the only thing we can say definitively is that increasing one's intake of fermentable fiber is associated with far fewer chronic health conditions. Beyond that, I would recommend reading the various blogs I've linked to. Free the Animal, Mr. Heisenbug, Vegetable Pharm, and Animal Pharm all have a unique take on the topic.


  2. Why do you think your Akk was so high prior to the experiment? What where you doing different from your family?

  3. Great question! I had been meaning to write something on that, but then got busy with work and travel then it kind of fell off the radar.

    First, it definitely surprised me. When I first looked it up it surprised me even more as I do have what would be considered a thin build, and have had one my whole life. I've always been active, cross-country, track, wrestling, in high school, cycling to commute in college and work even to this day. But I'm also a stereotype for the hard-gainer. No amount of time in the weight room or extra servings in the cafeteria made a lick of difference. Sometime in college I gave up on eating more than I'd prefer as an effort to gain weight since it was obviously proving to be a futile endeavor. Over the last 20-22 years my weight has not appreciably changed, literally +/- 5lbs from my median. At present I'm on the lower half of my median, have been ever since going low-carb paleo in about 2009. Even after increasing my carb intake back to more typical for myself, circa 2012 or so, I've remained on the lower-half.

    From what I understand, that's classic high Akker. But what causes the high Akker? Chicken or Egg? This build seems to run in families so I gotta wonder if there's not a genetic component that makes some people better hosts for Akker. I have an uncle that eats like a goat. It's almost comical, and he's as rail thin he's ever been. I think he's about to turn 60 and to hear my Dad tell it, he's not gained 10 lbs in 40 years. Akker? It would be very interesting to get a sample on him.

    Now, all that said, there is one last little thing. I didn't know it at the time, this brouhaha wouldn't occur for a few months after my sample was at the lab, but how you gather the sample makes a big difference. Well, as I've subsequently learned, Akker primarily populates the intestinal wall lining. I have to assume this means it is going to be over-represented in the outer circumference of the stool. Well, without getting into too much detail, for reasons not entirely my own fault, I sampled directly from the stool's surface. Did that push my Akker all the way to 8x typical? I have no idea. Could it have pushed it from 2x or even 4x to 8x? Seems possible.

    HTH, and thanks for asking. I've been wanting to get that off my chest.

  4. Thank you for your answer! Assuming you took samples the same way for the rest of the family, won't that be the same confounding factor in all samples? The fact that your sample was so far off, but only in that specific category, I think would indicate you actually did have higher Akker.

    1. No, that sample was unique in its swabbing technique.

      (I guess I gotta say it…) AmGut suggests swabbing soiled T.P. For that sample, the T.P. was inadequately soiled; so the stool was swabbed directly. At the time, I was worried it would come back with strange results indicating bacteria associated with municipal water supplies. 17% Akker was totally off my radar. I'd never even heard of Akker until I got my results. HTH.

    2. It may be putting words in your mouth, but at Animal Pharm, the following blog post makes a point of saying you ate beans daily.
      I looked at your food logs, and while you did seem to eat more beans than the rest of the family on the days you kept a log, I didn't think it was significant. However, it was that post (on Animal Pharm) which led me to asking the question.