Plants & Smoking: An Important Dot I Forgot To Connect

Sometimes an insight comes through the most random of things.

In a discussion about mucilage following this post, reader Roelm brought up something I hadn’t heard before. Mucilage is a soluble, gel-forming fermentable fiber in the class of non-starch polysaccharides. A good one to have in the mix. Okra is rich in mucilage (it’s my favorite source of it), but it can also be found in flaxseed, psyllium, cacti, and chia seeds. Roelm writes:

My neighbor who has blood sugar level problems told me a while back that he consumes okra mucilage and that helps him control his blood sugar. He cuts in two a couple of okra fruits, puts them in a water container and he then drinks from the container throughout the day. Apparently he is not the only one to do this as he got the idea from the wife of a medical doctor. I can surmise that the mechanism is at least in part increased butyrate production like that with scFOS and resistant starch.

I had never heard of okra as a diabetes or blood sugar remedy before. But a search for “okra” + “diabetes” or “okra” + “blood sugar” turns up a lot of results. But nothing about how or why, save for a bunch of unsubstantiated conjecture about sugar metabolization and cholesterol (we’ll get to that in a moment).

As I said, the mucilage in okra is a prebiotic, fermentable fiber. And that’s confirmed in the research. Mucilage has a prebiotic effect and a significant effect on SCFA production — specifically propionate and butyrate:

Increased levels of the short-chain fatty acids (SCFA) were attained in the cultures at rates of 35 and 16% in response to MO and PO treatments, respectively. Propionic acid (propionate) and butanoic acid (butyrate) production increased at least 50% throughout MO and PO treatments.

And okra has specifically been found to improve metabolic disorder in mice and have an anti-diabetic effect, as well as counteract hyperlipidemia, which is also a contributing factor to cardiovascular disease.

But if you read these studies, you’ll find that they can’t make any real conclusions about why or how it has these effects.

And then it came back to me: fiber in general has had a long-standing correlation with less heart disease. And it, too, has never been shown why or how.

If you’ve been following along, you’ll know that one of the more exciting and interesting discoveries we’ve made thus far is that the cessation of smoking — which is the number one predictor of heart disease — seems to cause the exact same microbial shift as consuming plant fiber. And what I found to be notable was that these are two acts that are completely different yet both considered to be healthful. But it was much better than that! They are completely different acts that are not only generally healthful, but are specifically correlated with less heart disease. And they result in the same microbial shift.

Like I said, as we find in the specific case of okra, there have never been very good explanations for why fiber has this effect. All you will find is a lot of conjecture about cholesterol-binding and displacement of dietary fat consumption. But if you read closely, you’ll find these claims are always preceded by “may” and “is said to.” That’s because there’s no research backing any of that up. (I’ve found that the medical establishment invokes the “evidence-based” requirement rather selectively.) This is likely due to preconceived biases, ie, “cholesterol and fat are obviously bad and cause heart disease so it must have something to do with that.” (How evidence-based of them.) And a meta-analysis has in fact shown that cholesterol-lowering is not the mechanism, which remains undefined.

So to put it all together:

Smoking is the number one predictor of heart disease, and happens to cause a microbial shift when you stop. That microbial shift is the exact same shift caused when consuming fermentable plant fiber. And plant fiber is correlated with less heart disease. (Oh, and we’ve also shown that same microbial shift to be responsible for the insulin sensitization caused in human subjects who underwent fecal microbiota transplantation.)

Identifying factors that are completely different (plants & smoking), yet have the same effect (less heart disease), is a very good way to isolate a mechanism of action.

And, for that reason, in my next post we’re going to drill down even more deeply into this line of inquiry by completely departing from the land of metabolic disorder and venturing into an entirely different, but no less significant, area of health. I’ll let you guess as to what I might be referring to.

Ok, hint: Some say it’s the reason that tiny gut of yours is so bad at converting all of that plant cellulose into anything useful, but why you’re capable of reading this right now.

Alright, I need a break. I’m hungry and I’m mentally drained. You might say I have a gut-brain problem.

— Heisenbug


17 thoughts on “Plants & Smoking: An Important Dot I Forgot To Connect

  1. Thanks for another gem, MrHeisenbug!

    I bet this explains why the Kitavans are apparently free of heart disease (as per Staffan Lindeberg), despite smoking like chimneys.

    Did you see how Emily Deans recently connected the rainforest in the gut to Obessesive Compulsive Disorder?

    Readers of my little Dutch blog are reporting many ‘psychological’ changes on RS. The gut-brain axis seems to be very real.

    • Hi Melchior,

      Yes that’s crossed my mind as well — given the long history of tobacco smoking, there must be protective factors.

      And yes I’m aware of your “little” blog. I’m going to have to take some time to give a closer look at what everyone is up to there. With the help of Google Translate!

  2. Little Dutch blog Melchior? 876,564 hits (Jan 12 2013) and the post ”Is Honig potato starch becoming the Paleo Hack of 2013” on Paleo Perspectief, has so far garnered 564 comments. And the tests that you got some of those participants running are just plain awesome.

  3. Mr Heisenbug, another test to add to my collection of things to test!! A couple of Okra’s cut in half and added to a jar filled with water, to drink throughout the day, is not too hard to do.

    • Not hard at all. And if you are also taking potato starch, it could have an interesting complementary effect. Mucilage and other NSPs have been shown to slow the rate of fermentation of RS and spread butyrate production more evenly throughout the large intestine, pushing it more distally.

      The theory is that if you were, say, trying to lessen your odds of colorectal cancer — which is known to occur more distally — then this would be an advisable thing to do.

      • I bought some Okra’s last Monday and started the experiment straight away. I noticed that the Okra floats on top of the water, so made sure the white fleshy part was facing down in the water. The next morning I fished the Okra out and drank the water. Just like drinking plain water. I noticed that the slime from the Okra stayed around the fruit.
        The third morning, I decided to give everything a brisk stir in the hope that more of the slime would get into the water. That worked as well.
        After a couple of days, I fealt it a shame that I was throwing the best part away, so I looked up on Google if I could eat the Okra raw, and it turns out that I can.
        So this morning I tipped everything into a blender and turned it into a greenish smoothie. I got the full effect of the slimy goop (tasted like jelly in my mouth) when I drank my Okra drink.
        So I will continue the experiment that way.
        I am doing the resistant starch experiment as well, but with Plantain flour instead as potato starch doesn’t sit well with me (I could be intolerant of night shades). I had immediate effect with lower blood sugars the next day.
        Having suffered constipation for over 40 years, it is pleasing to note that my bowels are moving, not spectacular, but I am definitely seeing an improvement.

  4. I must add that my neighbor also mentioned that he also cooks and eats the fruits afterwards since he likes okra and so I guess that muddies up the causation somewhat… At that time, I was completely at a loss as what could possibly be in the fruit/mucilage that was causing this anti-diabetic effect. It wasn’t until all these recent resistant start/gut biome discussions that a plausible mechanism arose. As with resistant starch, there may be a certain minimum amount required depending on the individual with regards to the blood-sugar effect.

    If it has an effect on mannose-binding pathogens, then that could also be a contributory factor…

    • I don’t think that muddies things up too much. If okra has been singled out for its antidiabetic effect, it must be something pretty unique to okra. And most of the explanations do in fact cite okra’s fiber as the cause, but again they focus on an ubsubstantiated cholesterol binding/lowering effect.

      Cooking/eating would only give you even more of the fiber. Smart neighbor!

  5. Very cool observation.

    This is probably stating the obvious, but it seems like a big problem here is with the endpoint: heart disease. Takes a long time to develop, lots of confounding variables. An interventional trial with enough statistical power would cost a lot!

    Compare that with an endpoint like blood sugar; responds quickly and is cheap to measure. Hypotheses (RS improves control) can be quickly evaluated and refined.
    Is there an intermediate, cheap-to-measure metric on the way to heart disease?

    • Yes, it’s a good point. That’s why most of the chatter WRT resistant starch revolves around diabetics/blood glucose. Easy, cheap home monitoring.

      A lipid panel or CRP is obviously nowhere near as easy or convenient. Perhaps blood pressure? Very easy to do with home blood pressure monitors.

  6. Yet, from my reading, CESSATION of smoking is related to a risk factor for developing chronic ulcerative colitis. Some colitis sufferers use a nicotine patch. Could you comment on this?

    • Smoking and IBD is a really interesting paradox. Smoking seems to aggravate Crohn’s Disease, and ameliorate UC.

      On the one hand, since these diseases seem to be so tightly intertwined with gut bacteria, the fact that smoking has such an effect on them lends a lot of credence to the smoking/microbial connection and its involvement in disease.

      As for why smoking seems to HELP UC, we’d really have to figure out what (if any) microbial impact it’s effecting with UC sufferers. Nothing is ever straightforward with this stuff.

      Also, most of the explanations out there for smoking’s impact on UC (which I wouldn’t put much stock in right now) seem to focus on nicotine, which would suggest that its effects are mediated by something other than microbiota. Lots we don’t know yet.

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