Tag Archives: Butyrate

More Butyrate Series, Part 8: Clostridium butyricum for the Brain, for Colon and Bladder Cancer, and for Milk Allergy

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I hate disclaimers. I don’t feel like they should be necessary on an internet site, where people should be reluctant to believe anybody or anything. But, sometimes we’re gullible and vulnerable, especially when it comes to our health. So I just want to remind readers that I am not recommending Clostridium butyricum. I am not speaking against it either.  What you put in your mouth is as personal as who you let French kiss you. Have caution.  I do.

Do I think Clostridium butyricum sounds like a decent probiotic? On paper it does. But I’m aware that each person’s gut is unique beyond comprehension. Its function is as varied as each person’s diet, stress level, and sleep pattern. That’s pretty varied. Please never go out and buy or use a supplement because I mention it. I’d feel just horrible about that. Read the studies I reference. Read the internet anecdotes for the good AND THE BAD. Then, talk with your doctor about if he or she sees any harm for you based on what he or she knows about you.

Try hard to make your diet as real and whole as you realistically can. That’s a great start for health! And also try hard to savor each person you love in your life. Our life on Earth really is unpredictable, and each moment counts. For more on Clostridium butyricum on my site, read here, here, and here.  I’ve enjoyed searching for information about it and putting it in one “place.” I hope if you’re reading this far, you find what you’re searching for. If you can’t understand something, please ask.

Clostridium butyricum For Vascular Dementia

In a vascular model of disease, mice with carotid artery occlusion who were given Clostridium butyricum (strain WZMC1016 dosed at 5 x 10 ^6, 5 x 10^7, 5 X 10^8) had improved cognitive test scores.

In humans, this might translate into someone who has vascular dementia from atherosclerosis—“clogged arteries.” The probiotic-treated mice fared significantly better on motor skills testing and cognitive skills testing (numerically significant at the two higher doses). Their brains looked better in the hippocampal region, a region known to be exceptionally sensitive to low blood flow, than the non-treated vascular occlusion subjects. Please notice that dose did affect the outcome!

The specifics, if you’re interested, also indicated that the probiotic treated mice had:

  • Increased levels of BDNF (brain-derived neurotrophic factor)
  • Increased ratio of Bcl-2 to BAX (antiapoptotic to proapoptotic factors)  (10^7, 10^8 doses)
  • Increased ratio of p-Akt/Akt (Akt phosphorylation=p-Akt) (5×10^7, 5×10^8 doses)
  • Structural preservation of the hippocampus with reduced apoptosis of neurons in the hippocampus (dose of 5 x 10^8)
  • Increased butyrate in the feces
  • Increased butyrate in the brain (10^7, 10^8 doses)
  • Increased diversity of GI bacteria (“drastically changed” were the words) (10^7, 10^8 doses).

Source: Liu J, Sun J, Wang F, et al. Neuroprotective Effects of Clostridium butyricum against Vascular Dementia in Mice via Metabolic Butyrate. BioMed Research International. 2015;2015:412946. doi:10.1155/2015/412946.

Clostridium butyricum for Stroke

In a mouse study which simulated cerebral ischemia/reperfusion injuries, such as those which may be found in a stroke in humans, mice who were pretreated with Clostridium butyricum (strain WZMC1018 at 1 x 10^9 dose) had less neurological deficits than the other mice.

In addition, in the probiotic treated mice it was found that:

  • The expression of Caspase-3 and Bax were significantly decreased
  • The Bcl-2/Bax ratio was significantly increased
  • Butyrate content in the brain was significantly increased
  • Apoptosis in the hippocampus was ameliorated
  • Decreased contents of MDA; increased SOD in the brain tissue.

Source: Clostridium butyricum pretreatment attenuates cerebral ischemia/reperfusion injury in mice via anti-oxidation and anti-apoptosis.Sun J, Ling Z, Wang F, Chen W, Li H, Jin J, Zhang H, Pang M, Yu J, Liu J. Neurosci Lett. 2016 Feb 2;613:30-5. doi: 10.1016/j.neulet.2015.12.047. Epub 2015 Dec 28.

Clostridium butyricum in Traumatic Brain Injury

In a traumatic brain injury model, Clostridium butyricum administration in mice resulted in improved outcomes.

Specifically found were:

  • Improved neurological deficits
  • Decreased brain edema
  • Less impairment in the blood brain barrier
  • Increased GLP-1 production in colon and increased GLP-1 receptor protein expression in the brain  (GLP-1 is glucagon-like peptide-1 and is considered a mediator between the gut and the brain.)
  • An improved intestinal barrier, evidenced by decreased serum D-lactate levels.

Source: Neurogastroenterol Motil. 2017 Nov 27. doi: 10.1111/nmo.13260. [Epub ahead of print]Clostridium butyricum exerts a neuroprotective effect in a mouse model of traumatic brain injury via the gut-brain axis.Li H, Sun J, Du J, Wang F, Fang R, Yu C, Xiong J, Chen W, Lu Z, Liu J.

Clostridium butyricum for Prevention of Anxiety

Laryngeal cancer patients who required surgery (laryngectomy) had lower anxiety parameters when they received Clostridium butyricum before surgery.

Human laryngeal cancer patients received Clostridium butyricum (420 mg/capsule, two capsules twice a day) prior to surgery for about 14 days. When compared to placebo-receiving laryngeal cancer surgical patients, they had:

  • Lower corticotropin-releasing factor levels (CRF), a stress-related hormone, also commonly known as corticotropin-releasing hormone (CRH)
  • Lower morning and evening heart rates
  • Lower anxiety test scores.

Source: Yang, Hui & Zhao, Xiaoyun & Tang, Shan & Huang, Hua & Zhao, Xiulan & Ning, Zhuohui & Fu, Xiurong & Zhang, Caihong. (2014). Probiotics reduce psychological stress in patients before laryngeal cancer surgery. Asia-Pacific journal of clinical oncology. 12. 10.1111/ajco.12120.

Clostridium butyricum for Bladder Cancer and Colon Cancer

The association of Clostridia affecting cancer goes back to 1813, when it was noted that patients who acquired gas gangrene (Clostridium perfringens infection) had cancer regression! Because they are anaerobic organisms, they emerge from spore form to vegetative form in the anaerobic, necrotic centers of tumors, where the bacteria can promote tumor destruction. (1)

An in vitro and in vivo mouse study showed that Clostridium butyricum induced bladder cancer tumor cell death (apoptosis). 

Rather than oral administration, Clostridium butyricum (both in the in vitro and in vivo arms) was directly applied to the tumor cells. The study found the administration:

  • Increased TRAIL (tumor necrosis factor-related apoptosis-inducing ligand ) release from polymorphonuclear leukocytes (PMNs), perhaps more effectively and safely than the current therapy, BCG
  • Drastically suppressed growth of bladder cancer cells in vitro and in vivo.

Sources: (1) Mowday AM, Guise CP, Ackerley DF, et al. Advancing Clostridia to Clinical Trial: Past Lessons and Recent Progress. Dachs G, ed. Cancers. 2016;8(7):63. doi:10.3390/cancers8070063.

(2) Clostridium butyricum MIYAIRI 588 shows antitumor effects by enhancing the release of TRAIL from neutrophils through MMP-8. Masahide Shinnoh and Mano Horinaka et al. Journal of Oncology. March 2013. Volume 42 Issue 3. pp 903-911.

In a colon cancer model study, researchers found that Bacillus subtilis and Clostridium butyricum inhibited proliferation of colorectal cancer cells and promoted cancer cell apoptosis in vitro and in vivo.

Mice with induced colon cancer were used for the in vivo study, and human colon cancer cells used for the in vitro study. The researchers noted improved inflammatory markers and immune responses.

  • TLR4 mRNA was decreased with the probiotic administration.
  • NfKb was also decreased with the administration of the probiotics.
  • The probiotic treated cancer-model mice had downregulation of Th17 cells as compared to the non-treated cancer mice.

Source: Chen ZF, Ai LY, Wang JL, Ren LL, Yu YN, Xu J, Chen HY, Yu J, Li M, Qin WX, et al. Probiotics Clostridium butyricum and Bacillus subtilis ameliorate intestinal tumorigenesis. Future Microbiol. 2015;10:1433–1445. doi: 10.2217/fmb.15.66.

Clostridium butyricum to reduce food allergy (milk allergy)

Clostridium butyricum reduced intestinal anaphylaxis to beta-lactoglobulin in mice with induced allergy and the researchers felt the probiotic might have potential as a  supplemental therapy for food allergy.

Mice who had a milk allergy to beta-lactoglobulin were given Clostridium butyricum. When given the probiotic, the treated mice, as compared to the untreated mice, had:

  • Decreased diarrhea
  • Improved villus histological integrity with decreased amount of inflammatory cells [It really was pretty cool if you like histology.]
  • Increased CD4+ CD25+ Foxp3+ Treg cells in the MLN and high levels of TGF-β and IL-10 in the serum
  • High levels of TGF-β and IL-10 in the serum
  • Reversed imbalance of Th1/Th2 andTh17/Treg.

Source: Zhang J, Su H, Li Q, et al. Oral administration of Clostridium butyricum CGMCC0313-1 inhibits β-lactoglobulin-induced intestinal anaphylaxis in a mouse model of food allergy. Gut Pathogens. 2017;9:11. doi:10.1186/s13099-017-0160-6.

Closing and Personal Anecdote

I think that’s all the studies I’ll go through on Clostridium butyricum for a while. My eyes were kind of drooping near the end. Make sure and comment on typos or wrong information so I can address them!

I did try this probiotic several times off and on over the last couple of years at all kinds of doses. I had no major issues from it when I took it, but I did have some minor ones. (But my gut is not your gut.) Despite this probiotic reportedly being used for constipation in Asia, I found that my baseline constipation increased and I had to increase my magnesium laxative use while taking it. I also experienced bloating. I had a good sense of well-being on the probiotic, but I have a tendency to have that much of the time anyhow. I seemed to wake up earlier, but I think that could be anything. Due to the constipation and (painless but pretty significant) bloating, I could never extend my use of this probiotic more than two weeks. I didn’t know if it was the probiotic itself or the lactose in it.

That’s it for today.

Terri F

 

 

Butyrate Series, Part 8

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Hello! I have not stopped working on and constructing butyrate posts (or other posts, like recipes and homeschooling posts), but I haven’t been able to complete them in a very timely manner. Whew! Homeschooling is hard work! However, I’m ready to start posting the next installment of my Butyrate Series. Let’s look at another way to potentially increase butyrate production in the body. . .

Warning: Writing up what I’ve learned about certain topics is simply a hobby of mine. It’s my entertainment and way to unwind from motherhood, homeschooling, and housework. When you read my writing, I’d like you to enter into an agreement with me: you read it to see what I think I’ve learned, but you do not read it with the thought that I am some expert or that I can possibly help you. I can’t help you. Supplements and treatments discussed enthusiastically on the internet can be dangerous. You, however, armed with knowledge and curiosity, can take the initiative to safely and non-ignorantly make a difference for yourself. This site is not medical advice.

Probiotics to (directly) increase butyrate

The Japanese have used a strain of Clostridium butyricum, a direct butyrate-producing bacteria, as a probiotic since about the 1970s. Savvy health professionals know butyrate best for its gut benefits (healing leaky gut, improving the mucous barrier, and improving motility), but it also has positive effects on the kidneys, brain, and metabolism–not to mention colon cancer prevention. Despite its structural simplicity, the little short chain fatty acid called butyrate truly makes a powerful, all-encompassing health difference.

Personally, my favorite way to increase butyrate in the body is NOT to take supplements– but to eat green bananas, leftover boiled cassava root, and/or leftover potatoes. Aiming to eat whole, real food is always best, but it may not be enough for select problems.  I get that. So I’m curious about all the other ways to increase butyrate.

If you have read any of my butyrate posts, you may remember that I outlined and explored four potential ways to increase the body’s butyrate levels:

  1. Eat butyrate-rich foods, like butter from grass-fed cows.
  2. Eat foods that butyrate-producing bacteria like to metabolize, particularly green bananas, green plantains, refrigerated and then reheated potatoes, beans, lentils, cassava root, and/or rice.
  3. Take butyrate supplements directly.
  4. Take probiotics which contain bacteria known to make butyrate.

Since last writing, I’ve expanded my list of potential butyrate-producing methods that I’d maybe eventually like to write about:

5. Take probiotics which support butyrate-producing bacteria in the GI tract.
6.  Consume prebiotic fibers which enhance butyrate production by GI tract bacteria.
7. Maybe we could somehow upregulate our colonic butyrate importers, such as MCT1 and SMCT1. (1, 2)

My other butyrate posts have waded through points one through three. After quite a gap in my writing due to my work raising four wonderful people in the early stages of life, let’s talk about point number four: probiotics which contain bacteria known to directly make butyrate.

Commercially available butyrate-producing probiotics

The only direct butyrate-producing bacteria (that I found) that we have available as a probiotic for human consumption is Clostridium butyricum. Quite a bit of searching turned up only two different probiotic brands to buy with Clostridium butyricum. (Have you seen any others I’ve missed?) Although both probiotics contain spores of the same species, Clostridium butyricum, they are different strains of the species.

When ingested, the bacterial spores germinate and grow in the intestinal tract, making the short chain fatty acids butyrate and acetate (6). Both strains and brands have studies behind them for various health conditions which I’ll try to discuss in this thread of posts (but not in this post today). Both probiotics can be found on Amazon.

  1. MIYAIRI 588 (CBM 588) Miyarisan Tablets
  • A one-strain probiotic of Clostridium butyricum
  • Manufactured in Japan and distributed there as an over-the-counter medicine
  • Commonly available and used in Asia
  • Available in two strengths: standard and strong. If you look at my citation number 4, you’ll find the recommended dose and much, much more about this probiotic.
  • Other listed ingredients are lactose, corn starch, talc, microcrystalline cellulose, and magnesium stearate
  • History: First isolated from feces by Dr. Chikaji Miyairi in Japan in 1933. CBM 588 is the 588th MIYAIRI strain, isolated from a soil sample in Nagano, Japan in 1963.
  • As mentioned, the probiotic is composed of spores of C. butyricum (rather than “live,” active bacteria), which are then activated in the gastrointestinal tract, making the probiotic quite shelf stable with no refrigeration required. (3, 4)

2. Advanced Orthomolecular Research Probiotic-3

  • A three-strain probiotic which includes Clostridium butyricum TO-A, Enterococcus faecium (same as Streptococcus faecalis) T-110, and Bacillus subtilis TO-A (some places I see the label with Bacillus mesentericus)
  • Only the Clostridium butyricum is the direct butyrate-producing bacteria
  • Also contains lactose, potato starch, polyvinyl alcohol, providone, and sodium stearyl fumarate
  • If I understand correctly, it contains Bio-Three probiotic formula. I believe the “TO-A” implies that the strain was produced by the TOA Pharmaceutical company in Japan (inferred from Bio-Three website). The Bio-Three formulation is used in Japan, and has studies behind it.
  • No refrigeration necessary. As with the Miyairi probiotic, the Clostridium butyricum is in the shelf-stable spore form. (5)

About Clostridia and the bacterial species Clostridium butyricum in general

When we are about one month old, different commensal species of Clostridia start to colonize our gastrointestinal (GI) tracts. They are supposed to be there and provide specific and essential benefits to us without causing harm. Since we only typically hear of the toxic Clostridial diseases like botulism, tetanus, and “C. diff.,”  it may sound strange to some of you to know you healthfully have an abundance of clostridium residing in your GI tract! If you think of Clostridia as a “bad” class of bacteria, you might find it even more disturbing and confusing to know that a known pathogen like Clostridium difficile (the culprit in C. diff pseudomembranous colitis) can be part of a normal human gut biome or can actually prevent infection. (6-9)

[Opinionated aside: The fascinating idea that a strain of C. difficile, a bacteria we think of as toxic, can be normal flora supports why I would argue with people that we have to stop oversimplifying health, stop trying to peg things, and start convincing people to do complete overhauls to their modern lifestyles and mindsets to bring the body into rhythm with itself. Don’t just take butyrate supplements and butyrate-enhancing probioitics—investigate your life, eating, habits and make impact changes. Being honest with and scrutinizing oneself often hurts for several months, but if done properly, you move past the pain, and healing and change can begin. Perfection will never be reached in this realm, but progress feels so good to a mind and body.]

Clostridium butyricum is one species of Clostridia bacteria. It is Gram-positive, rod-shaped, and anaerobic. It lives in soil and in the GI tracts of birds and mammals and can be found on the skins of potatoes, Swedes, and even in cream and yoghurt. It ferments starches to produce butyrate. When C. butyricum is exposed to a stressful environment, it can form endospores, an alternative form which allows it to survive the stressful conditions, to later reactivate when exposed to desirable conditions. It is the spores which are used in the probiotic formulation, allowing them to be shelf-stable without refrigeration for several years. (3, 4)

Some of you may have read about the clusters of clostridia and wondered about that. The Clostridia microbiological class (to which C. butyricum belongs) is exceptionally diverse, and even the commonly accepted shared characteristics, such as being rod-shaped (bacillus), anaerobic, and spore forming, have variations and exceptions to the rules. In the attempt to break down, stratify, and classify the types of Clostridia, the species C. butyricum is categorized into what is called “Cluster I Clostridia.” Cluster I Clostridia aren’t common inhabitants of the human gut. Human guts seem to mostly contain butyrate-producing bacteria from Clostridium clusters IV and XIVa rather than cluster I, but some human GI tracts do contain Clostridium butyricum, so clearly it does naturally happen. Fecal studies have found Clostridium butyricum in about 10-20% of its surveys. (6-9)

For all practical purposes, C. butyricum is a non-toxic clostridium species, but there have been reports that it can acquire some of the toxic genes from other clostridia, leading to production of poisonous toxins which may contribute to infant botulism or infant necrotizing enterocolitis. Regarding adults, one case of sepsis from Clostridium butyricum has been reported in an intravenous drug user and one case of antibiotic associated diarrhea has been reported. The complexities of toxin acquisition/production depend on the strain, the host, and interactions with other strains. Some strains of Clostridium butyricum are probiotic and beneficial and other strains show virulence. The probiotic strains mentioned are tested for non-virulence.  (6, 7)

Closing

I’ll cut off this post for today and try to clean up my next writing segment regarding specific uses of the probiotic Clostridium butyricum. I do not have it “polished up” yet, but posting this half will force my hand to get the rest of it tidied up and posted for those interested. I’d like it if you’d point out typos or mis-information to me so I can make corrections. Thanks in advance.

Please keep in mind: I don’t really care about probiotics or bacteria or food. What I really care about is that you grasp your life, your whole life, and tenaciously latch on to the things that are good and real– and that you weed out the things that are bad for you and noxious. I love life. I’ve had my share of challenges, smaller than many, bigger than some. But no matter what, I try to choose to face life HEAD ON with as much transparency as I can. And each new day, each new week, each new stress, shows me how to become more true and real.

The best to you,

Terri F

Citations:

  1. Pedro Gancalves, Fa’tima Martel. Butyrate and Colorectal Cancer: The Role of Butyrate Transport. Current Drug Metabolism. Volume 14, Issue 9, 2013.
  2. Pedro Gonçalves, Fátima Martel. Regulation of colonic epithelial butyrate transport: Focus on colorectal cancer. Biomedical Journal. Volume 1, Issue 3, July–August 2016, Pages 83-91.
  3. Wikipedia site regarding Clostridium butyricum: https://en.wikipedia.org/wiki/Clostridium_butyricum
  4. Clostridium butyricum Miyairi 588 Novel Food Application, public version: C. butyricum MIYAIRI 588 as a novel food supplement.  Probiotic food supplement. Miyarisan pharmaceutical company, LTD. https://acnfp.food.gov.uk/sites/default/files/mnt/drupal_data/sources/files/multimedia/pdfs/clostridiumbutyricumdossier.pdf
  5. Bio-Three website: http://www.bio-three.com/
  6. N.Cassir, S.Benamar, B.La Scola. Clostridium butyricum: from beneficial to a new emerging pathogen. Clinical Microbiology and Infection. Volume 22, Issue 1, January 2016, Pages 37-45. Review. 
  7. Rousseau, Clotilde & Poilane, Isabelle & De Pontual, Loic & Maherault, Anne-Claire & Le Monnier, Alban & Collignon, Anne. Clostridium difficile Carriage in Healthy Infants in the Community: A Potential Reservoir for Pathogenic Strains. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America. 2012. 55. 1209-15.
  8. CS Cummins and JL Johnson. Taxonomy of the Clostridia : Wall Composition and DNA Homologies in Clostridium butyricum and Other Butyric Acid-producing Clostridia. Journal of General Microbiology.   (197 I), 67,33-46
  9. Lopetuso LR, Scaldaferri F, Petito V, Gasbarrini A. Commensal Clostridia: leading players in the maintenance of gut homeostasis. Gut Pathogens. 2013;5:23. doi:10.1186/1757-4749-5-23.

 

Eat Like A Vegetarian In The Garden of Eden

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This morning I’ve been reading on butyrate again, trying to put together the next post about probiotics and generating butyrate (which may still be a long way off, darn it).

Butyrate is generated by your gut bacteria for YOU to use in your own body.  It supports your gastrointestinal health and “a million” other things (diabetes and cancer, to mention a couple small problems).  It comes from your gut bacteria munching on the vegetables and fruits you eat.  (It can also be made from whole grains, such as oats.)  My go-to foods for butyrate production are leftover potatoes (baked potatoes, steamed potatoes, fried potatoes, you name it) and green bananas.

Foods rich in something called “FOSs” feed those butyrate machines too:  onions, garlic, and asparagus.  (And as much as I like garlic and onion powder, you need to go for the REAL onion and the real garlic to get butyrate).  We use no less than one onion a day in our home.  And I can’t even count how many cloves of garlic.

Well, this morning while butyrate-reading, I came across:

Butyrate, neuroepigenetics and the gut microbiome: Can a high fiber diet improve brain health?

Basically, it was explaining how butyrate may affect brain function.  It was fascinating.  I LOVE it when personal experience is validated with the science I read.  I never want to misinform and lead people down the wrong path, even if it applies to eating better.  (Because the battle a person has to fight now today to “eat right and real,” is a real battle.)

When I changed the way I ate a few or so years back, I noticed a dramatic improvement in moping days (as in they decreased in number).  Even now, when I eat too much sugar or grains or processed oils, my moping days like to come back.  Being a tiger for protecting my brain, I get back to eating as real as I can and how I know is best for me.

I was trying to think about how best to describe to people how I think we should eat.  From my varied reading, there is a huge allowable variation for human health.

But basically, I guess I’d sum it up as:

Eat like a vegetarian who is back in the Garden of Eden.  Round it out with the most connected- with-nature animal products you can find when you want them.  (If you don’t, no problem.  Just make sure you’re getting the nutrients you need in the place they’re lacking.)

What do you think of this thought?  Does this capture the idea?  Does this keep us focused on the food rather than the cholesterol, fat, and sugar content?  Does this take away the significance of labels and names?  Because that’s what it comes down to for MOST (not all, there will ALWAYS be exceptions—speak, Elijah) of us.  Eat it whole, baby.

Check out the article if you like science and you ever get moping funks.  Nah, I’ll bet none of you ever do that.  And remember, after you get it down to real food, you may need to make further tweaks to help with individual things like weight loss, headaches, irritable bowel, and so on.

The Homeschooling Doctor logoTerri

Slow Guts Need Tenacity

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256px-Pieter_Lastman_-_Jonah_and_the_Whale_-_Google_Art_ProjectTenacity.  Word for the day.  Word for a season.  Word for life.  I can hear mom’s voice even now, “Oh, Terrrr-rrrri.  You have a one-track mind.”  She said it like it was a bad thing!  Pshaw.  But, tenacity got her to buy me some black parachute pants; I think it’s restoring my gut too.  I’ve worked very hard to get this gut moving.  Very.  I’ll be laying out all that I can think of that I tried and how I think it affected my gut and me.  There is no ONE thing that worked for my colon regularity and stool consistency.  Geesh.  What would I have to write about if it was that easy?  I’ve turned down more cookies, cakes, and cheese platters than you can even imagine.  I’ve made myself go to bed early more than I’ve ever made my kids go to bed early.  I’ve attacked my gut on all fronts that I can.  Tenacity.

I’m starting out by writing about the supplements I’ve tried.  That does NOT mean that the supplements are the most important.  Just that I’m postponing talking about acupuncture and gargling and chakras.  I’ve already mentioned vitamin K2 in the last post.  These posts will just keep rolling.  So let’s continue.  Don’t use this as medical advice.  It’s my story.  If it gives you ideas to try, talk about them with your doctor.  Be SAFE.

Iodine

I’ve taken iodine for about two years now. I don’t have much in the way of a reliable iodine source in my diet, so I supplement. Iodine comes to a conventional diet via egg yolks, dairy, seafood, and iodized salt.   Iodine didn’t seem to have any particular impact on MY constipation, although other people have reported to me that when they started taking iodine it did seem to improve their constipation; I experienced other positive benefits from taking iodine. I was able to have my thyroid labs followed to make sure I was safely supplementing. Hypothyroidism (low thyroid) causes constipation. I was never categorized as hypothyroid. However, iodine supplementation did slowly drive my TSH down over time, which was medically interesting to watch.

Bottom line for me: Iodine did not seem to make my constipation better, but it helped other things for me. I think that a TSH needs periodically checked and symptoms need closely monitored if a person is going to take iodine.  In case you’re counting, this is the second supplement I take routinely.

Probiotics and Probiotic Foods

I’ve tried dozens of probiotics. Not A DOZEN—but DOZENS. There is no probiotic that makes my motility improve directly. I’ve tried soil based. I’ve tried VSL. I’ve now tried the Japanese kind. I’ve tried Klaire Labs. I’ve tried pickles, pickle juice, sauerkraut, sauerkraut juice and kimchi. I’ve made my own fermented pickles, sauerkraut, and beets. I’ve tried 24 hour homemade yogurt. I’ve tried homemade coconut yogurt. Tenacity.  There is one probiotic source I haven’t tried, but I’d like to try: Mutaflor. It has studies showing it helps constipation. However, it’s only available in certain countries, and the USA isn’t one of them.

Probiotics aren’t the “cure” for my STC.  I’ve tried many kinds, and I’ve tried driving up the doses.  Tenacity.  In fact, for a couple of months this summer, I even stopped probiotics completely!!!!  I suffered no ill GI effects and my gut still moved! Why did I stop them? I think that I have a mild case of small intestinal bowel overgrowth (SIBO).  (Why not test?  1) I already eat a tailored diet.  2) Things are improving.  3)  I’ve tried antibiotics before for it, and it came right back.  And now, I won’t take antibiotics because I’m nursing.  4)  My case isn’t that bad.)  I now waffle between probiotics and no probiotics.

What is SIBO?  This is where the bacteria from the colon track up into the small intestine in larger numbers and/or with different species than those that should be there. It leads to significant bloating, distention, bowel movement changes, fatigue, and other symptoms. There is a dispute in the SIBO arena about whether one should take probiotics with this disorder. Having no vested interest and an open mind, I could see both sides. So since I’d tried probiotics like crazy for years, I thought I’d try without. (Another aside: I have not always had SIBO symptoms. They started at about age 35. I think it was a result of chronic non-movement of my gut.  I think to effectively treat SIBO, a person HAS to address the underlying issues.)

Bottom-line for me: I tried coming off my probiotic. My gut still moved off the probiotic! However, my gut also moved normally for a couple of months before I got pregnant a couple of years ago and I was ON a probiotic. So for my body, I’m not yet sure whether it prefers a probiotic or not.  LOTS of people swear by probiotics for constipation.  I have been trying to utilize normal portions of Bubbie’s pickles, Bubbie’s sauerkraut, and eating my home-grown produce.

Butyrate

Butyrate has kick-started my gut twice in my life now. In 2013, I started taking it after a big dose of magnesium and immediately I had normal bowel movements daily. I then titrated up resistant starch using potato starch (which leads to natural butyrate production) and came off of the butyrate pills. I then titrated up food sources of resistant starch (green bananas, plantains, cooked and cooled potatoes and rice, raw potato and sweet potato sparingly) and stopped the powder forms of resistant starch.

BINGO. I thought I was a diet-controlled constipetic and the story was over! (I always told God I was going to stop blogging when my constipation was cured.  Never tell God what to do or what you think YOU’RE going to do.  Instead, when you hear “Jump.” from the Big Man, you say, “How high?”  Got it?) But I got pregnant in 2013 and I’ve been chasing GI rainbows ever since. Finally, late this summer of 2015, I decided to get back on butyrate. I took a good dose of magnesium to try to propel that butyrate deep into my intestines (just in case that would help, you know).  BAM.  My gut has been doing pretty well since then. Knock on wood. And I’m working on building back up my food sources of resistant starch again and working on other areas I’ll elaborate on through these posts (like stress management, core strength, etc). THIS IS NOT A SIMPLE QUICK-FIX JOURNEY. You want that? Go somewhere else.  Tenacity.

I KNOW butyrate does NOT work for all people. They’ve told me. More people have told me that butyrate did NOT help them than people have told me that butyrate DOES help them. I’d like to also point out that during pregnancy and post-partum, my gut kind of stopped working and I was on high dose magnesium. Butyrate did not work at this time—even though this summer I tried again and it did! This leads me to suspect that hormones play a huge role in constipation—which I already suspected and this simply pounded into my heat that I need to make sure and learn about this (and hopefully write it up too—although I must say the other day in my research, I saw a new review article that was downplaying hormones…).

Many people write to ask what butyrate I take. I simply tell this as part of my story. Listen. I do not support this brand, other than it has worked best for me out of all the ones I’ve tried. I don’t pretend to think this brand or even butyrate will help you. Heck, it may even set YOU back, while it sets me forward.  I use Body Bio Mag-Cal Butyrate 600 mg (two three times daily, usually, but not always with a meal). If you decide to try this, flash it to your doctor so he/she can make sure it’s going to be fine for you. A commenter, Vicki, has noted that Body Bio has received some reprimands. You may read about this by scrolling down to the comments and looking for an interchange between Vicki and me.  Sometimes, I have a strange feeling that some bottles work better than others.  I don’t know, though.  I have NO proof of that.

Bottom-line: Butyrate has some good evidence supporting its role in promoting gut motility.  I have many posts on that in my butyrate series.  Some people have tried it and found that it helped their food intolerances and gut motility. Others have tried it without success—and with a loss of hard earned cash.  If your’e counting, this is the third, and final, supplement that I currently take routinely.

Magnesium (Natural Calm)

What did I take during pregnancy and post-partum when hormones gripped my gut so tightly? I took three tablespoons of Natural Calm magnesium citrate in a tall glass of water nightly–every night. This is WAY too much magnesium. I am well aware that most of us are magnesium deficient, but this is a lot much! One electrolyte at a high dose is not good for the other electrolytes and their balances.  So even though this got things moving (diarrhea), this is not a good place to live for the rest of my life if I can help it.  Tenacity.

I tried some different forms of magnesium because the taste of this, although the unflavored is really okay, is becoming repulsive after four years or so of using it. The other forms, both topical and oral types of magnesium, just don’t work. And Epsom salts bath, although relaxing, don’t do anything at all for my GI.  This is the only brand of magnesium that has worked for me.  Again, I’ve no vested interest in this supplement, and I’m not saying it will work for you.

At my best right before pregnancy and also the last two months now, I was able to get off of the magnesium.  I still had/have to use it about once a week, and usually at a much lower dose– a heaping tablespoon.  But I only use it when I skip a day or things are too hard.

Bottom-line: Calm magnesium citrate now can keep my gut going (although with diarrhea) through thick and thin. Before I changed my eating and lifestyle four years ago, high dose magnesium did not work. So the fact that it works is great! But I still want off of it entirely! I am currently down to about once a week.  So I guess, if you are a nickel and dime counter, we would call this 3 and 1/2 regular supplements—since I only have to take it as needed and this only about once a week now.

Closing

I am going to stop now.  I have LOTS more to say.  You will be so bored by the time I finish.  You’ll think I talk and think about nothing but moving GI tracts. But, finish I will.  Tenacity.  Get those parachute pants.

Terri

Click here for Slow Guts Need Care, the first post in this series.

 

The Unglorious Call to Action

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IntestineThat is a personal problem.  Not a medical problem.

Here’s the poop.  No.  No.  I mean scoop.  My call to nutritional voodoo was, well, to say the least, not a glorious one.  Other nutritional blog hosts–oh such extraordinary, amazing recovery stories from horrible illnesses like multiple sclerosis and ulcerative colitis.  Motivating and inspiring us all to higher eating!  My issue–hmmm.  Right.  Not so inspiring.  Considered by the uninformed to be a personal problem, not a medical problem.  Ah, well.  Even if I arrived in Nutritional Nirvana via a clumsy fall on my derriere, I am here all the same.  My gut is working.  And the pursuit of that goal is pretty much what started this blog.

My History

I’m a 39 year-old female.  I have had chronic constipation all of my life.  Although not a common issue, I can remember twice in high school when I had horrible stomach cramps prompting me to head to the nurse’s office.  On the way, the visceral pain overcame me, and I passed out leaning against the lockers in the hall.  As a sixteen year-old girl I did not make the connection between constipation and these symptoms.  Neither did anyone else!  “You just need to eat more.”  Mmm-kay.  It never dawned on me that my gut was trying to move against a brick and it hurt!  I thought bricks were normal.  I mean, nobody talks about bowel movements at 16!  (I suppose I’m not supposed to talk about them ever.  But since I’m a medical doctor, no orifice or function makes me blush.)

Each decade, my GI function worsened, and I did finally realize in pharmacy school that my gut was abnormal.  The next ten years brought rounds of different fiber preparations (I can make darn tasty desserts with Metamucil wafers), docusate, milk of magnesia, magnesium supplements, suppositories, Miralax, yogurt, probiotics, prunes, shredded wheat (half a box a day), and finally, despite my attempts to only use them sparingly, daily stimulant laxative became required.  Mind you, even with those stimulant laxatives which were needed at doses which would kill a normal human being, my bowel movements still only occurred about every five to ten days and still were not easy to pass.  My gut was slowing down from slow to stop and becoming refractory to everything I knew to try.  I visited several doctors through the years and I always got the same answer:  more fiber and water.  Got a colonoscopy.  Pretty negative.  Got checked for low thyroid and celiac disease.  Negative.

I decided to think outside of the box and took to the wilderness of internet medicine.  Talk about crazy.  How do some of these people say these things without a license?  Guess I’m glad they can because it tipped me off in the right direction, and I embarked on the odd diet called GAPS (at least that founder has a medical license)–before I knew about Paleo which sounds way cooler than GAPS.  (Ha!  Ha!  I actually have landed on a diet which has no name but uses the templates of several diets.)  GAPS helped me identify food intolerances and taught me how to eat a nutrient dense diet.  It got my gut usually responding again to high dose magnesium (Natural Calm), but I don’t think high dose magnesium is good to take for the rest of my life.  So my endeavors persisted.  My goal is NO supplement for my constipation.  For myself, I try to use supplements as a bridge to achieve my health goals.  Once my health goal is achieved, I’d like to try to maintain it with food choices if I can.  However, I recognize there are conditions which will require lifelong dependence on medicines and/or supplements, not to mention declining content of certain nutrients in our food sources.

Achieving Success

This week I’ve lived large, taken a chance, and dropped the magnesium which sustained me through pregnancy.  My gut is working daily!  Back in November 2013, my gut was also working very well daily, and I was set to write this post back then.  I had started butyrate (butyric acid), and although it isn’t supposed to make it to the colon, it worked like a charm on my gut.  My GI tract moved daily and even my stupid food intolerances seemed diminished just in time for Thanksgiving.

But I hate supplements (please know that I do take some). I wanted to allow my body (I consider those bacteria in my gut to be part of my body.) to make its own butyrate, so  I tried to incorporate green bananas, green plantains, cold potatoes, occasional bites of raw potato and sweet potato, some legumes, and potato starch slurried up in water each night to get my own gut bacteria to make butyrate.  Things were going great.  Just great!  I was able to stop my butyrate and still have the same effects.  Wow.  Wow.  Wow.

Then, we were blessed with pregnancy.  Let me rephrase that.  We were blessed with a baby.  Pregnancy is no sleigh ride with jingle bells. (Increased constipation has always been in an issue in pregnancy.  This time was much better.  There was a time at about 14 weeks along where my gut completely stopped and nothing I did made it move.  I got worried, but after a couple of weeks, that lifted and magnesium helped again.)  However, I worked through all the food and supplement aversions and stomached magnesium, which I needed again every single day in excessive doses.  I bid “good-bye” to butyrate and resistant starch foods, which sounded disgusting during this time.  I delivered in July a beautiful, healthy girl.

About two weeks ago, I decided it was again time to get rid of that excessive magnesium and all that it was probably doing to my calcium balance.  Besides that, the magnesium didn’t always work daily.  I decided to take butyrate again and started incorporating resistant starch foods into my diet.  Would the experiment work for me again?  I was nervous since I had proclaimed success with butyrate in fall of 2013.  What if it failed?  I would have reported it, you know.  But I would have felt very stupid because I never want to lead anyone astray.  The experiment for me has successfully repeated itself.  Now all that needs to happen is to continue the resistant starch foods and see if I can taper myself off of the butyrate supplement.

Closing

So you see, mine is not the most glorious nutritional conversion story there is.  But it’s real.  It has convinced me that eating a nutrient dense diet, excluding inflammatory foods, and supporting the body’s bacterial flora is key to health and curing disease.  I am pretty much 100% convinced that this experiment would never have worked two and one-half years ago in the gut that I had then.  I’ve worked very hard and tried a lot of things to rehabilitate my broken colon.  In the next post, I am going to list what I feel has been most important for getting my gut peristalsis in working order.  I will report what worked for me.  Don’t assume that what works for me will work for you.  I want to make sure you seek the advice of your doctor; I don’t want you to overlook serious health conditions because you’ve given up on conventional medicine.  Don’t use my story as medical advice.  That it is not.  This is my story.

~~Terri
Photo credit:

Originally from en.wikipeida.  Author Dflock.  Now public domain.

Butyrate Series, Part 7

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Introduction:

We have made it to butyrate supplements.

Diet-wise, I follow the GAPS diet with modifications resembling a Paleo Diet/Autoimmune Paleo Diet –with some low carb stints thrown in to try to achieve my health goals.  I don’t have any lofty goals of looking like a runway model or movie star.  I’m still a little young to be much scared about cancer.  I don’t hang out with a fitness crowd to bring out my competitive inner edge.  My labs and ideal body weight have always checked out ideal.

I started the GAPS diet for exceptionally severe, idiopathic constipation and tweaked it here and there based on my research.  The symptoms I have changed include headaches, chronic allergy symptoms, fatigue, dry eyes, strange premature hot flashes, and I could go on.  My gut improved, but I still thought it could work better.  Several months ago, I started following some leads on nerve regeneration in the gut, and they lead me to butyrate.  I decided I would try an oral butyrate supplement, despite the researchers all saying a delayed release product was probably necessary.  If, by some chance, oral butyrate helped me, I would then focus on tweaking my diet some more to obtain butyrate naturally through food.  I was amazed when oral butyrate worked for me, particularly as I didn’t even choose a sustained release formulation.  If I stopped butyrate, my symptoms returned.  When I resumed it, my symptoms resolved.  So I’ve been working to try to increase forms of fiber and resistant starch that I tolerate–I’ve defined these in previous butyrate posts.

Ways I see to increase butyrate:

1. Eat foods with butyrate (butyrate-containing foods), like high fat dairy products such as butter. (Part 4)
2. Eat foods that your bacteria can make butyrate from (butyrate-producing foods), like fiber and
resistant starch.

3. Take butyrate supplements.
4. Take butyrate producing probiotics and prebiotics.

A bit about butyrate production.

Aside from the pharmaceutical industry, butyric acid is also used in the manufacture of plastics, varnishes, disinfectants, perfumes, and cosmetics. (Butyric acid and butyrate are interchangeable terms for our conversation.)  The American Food and Drug Administration has even approved it as an additive to food, beverages, and flavorings in the form of tributyrin. (1)  You’ll see more on tributyrin below.  (Humorous:  I also found it is used in fish bait: Carp Fishing Pellets.  Nice.)

The organic structure of butyrate is simple. It is just four connected carbons saturated with hydrogens with a carboxylic acid on the end of the chain. The manufacture of butyric acid is mainly from chemical synthesis using crude oil extracts. Crude oil extracts provide cheap, readily available ingredients. Butyrate can be extracted from butter, but the process is reportedly more difficult and expensive. Another way to obtain butyrate is through bacterial fermentation (the way we naturally get it from resistant starch and fiber in our colons). Bacteria are given the appropriate matter, and they ferment it to make butyrate. The fermentation method interests manufacturers because of the growing interest in “natural” sources for foodstuff. (1)  Butyric acid itself is a bit corrosive, and in supplements it will be found as a salt form.

My concerns with oral butyrate supplementation–and supplements in general.

My concerns with oral butyrate supplements are not unique to butyrate; they are the same concerns I have with supplements in general. Butyrate seems to have a pretty good track record. I mean, as I mentioned above, it’s even approved by the FDA for flavorings. But any time I take a supplement I ask myself a battery of questions. Could there be impurities, such as heavy metals? What is the proper dose? Does the supplement contain the amount of active ingredient it says it does? What if people take enormous amounts? Should there be a concern with unopposed supplementation? (What I am thinking of here pertains to “ratios.” For example the ideal ratio of calcium to magnesium supplementation. Or the ideal omega-3 to omega-6 ratio.) What are the side effects?

Butyrate seems pretty non-toxic as long as the manufacturer’s dosing guidelines are adhered to.  One study found that escalating doses in mice lead to kidney swelling– in humans the equivalent dose would be 7-8 grams in humans.  (2, 3)  To put it into perspective, the butyrate supplement I tried recommends a dose of up to 3.6 grams.  Another study specifically points out that in vitro, butyrate has positive effects until a certain point at which it has an opposite, detrimental effect:

“We conclude that the effect of butyrate on the intestinal barrier is paradoxical; i.e. whereas low concentrations of butyrate may be beneficial in promoting intestinal barrier function, excessive butyrate may induce severe intestinal epithelial cell apoptosis and disrupt intestinal barrier.” (4)

And finally, here is a nice toxicology report on butyric acid from the Environmental Protection Agency,  “Screening Information Data Sets” (SIDS). The report was accumulated for the SIDS Initial Assessment Meeting, referred to as the SIAM, in 2003.  It goes over just about anything you’d want to know about butyric acid, from its different uses to its stability in water to its effects on rats and their fetuses. For those interested in the toxicity profile as it at least relates to rats, scroll down a ways. It will talk about effects on male rats, female rats, pregnant rats, developing fetuses, chromosomes, etc. (5)

What are some commonly available butyrate supplements?

I Googled some supplements, and I will list those that I found. By listing them, I am not recommending any of them!  (Neither am I dis-recommending any of them.)  I’m simply listing in one spot just about all the supplements I could find and available consumer reviews.  If you think butyrate may be right for you, run it by your favorite healthcare provider. Maybe print off a couple of the studies I’ve linked to in my article and the EPA report above to help the provider understand toxicity, perhaps highlighting the sentences of interest to facilitate quick reading for them. I’m not in the situation to recommend anything, but I am happy to share my own personal experiences and research that I’ve come across.

Keep in mind the success of butyrate supplementation is going to vary from person to person. The pills will release their contents differently because of inter-individual differences in the pH of a person’s gut and transit time.  These supplements are salts, and the butyrate provided by these supplements will probably be absorbed very early in the GI tract, perhaps offering no benefit. There are other forms of butyrate used out there but not over the counter. I will mention them later.

P.S.:  Thank Amazon for the photos.  I didn’t realize the links came with photos.  Well, that saves you from my very bad drawings and “bubble-gum” photos.  (Sorry.  “Bubble-bum” is the word my dad used to describe the music I listened to as a kid.)   Rest assured this is still a hobby; I make no money from it.

• BodyBio/E-Lyte Butyrate 600 mg (Calcium/magnesium complex): This one has five reviews you can read on Amazon. The reviews revolve around fibromyalgia, collagenous colitis, excess ammonia, and multiple food sensitivities.

• BodyBio/E-Lyte 600 mg (Sodium Butyrate): This one also has five reviews on Amazon, around cancer, bipolar, substance addiction, and more nebulous issues. Quite interestingly enough, this also has medium chain triglycerides in it!

http://www.bodybio.com/main/products/sodiumbutyrate_qa.htm

http://www.amazon.com/BodyBio-E-Lyte-Sodium-Butyrate-caps/dp/B0058A9SF0/ref=pd_sbs_hpc_2

• BodyBio/E-Lyte 500 mg (Sodium-Potassium Butyrate): One review regarding autism.

http://www.amazon.com/BodyBio-E-Lyte-Sodium-Potassium-Butyrate-Capsules/dp/B0058A9SRI/ref=pd_sim_hpc_2

• Pharmax, Butyrate Complex: Three reviews. Constipation, yeast, and a nothing.

http://www.amazon.com/Pharmax-Butyrate-Complex-90-vcaps/dp/B0037V3WTA/ref=pd_sbs_hpc_3

• Nutricology/ Allergy Research Group ButyrAid: 5 reviews. IBS, dysbiosis.

http://www.amazon.com/Nutricology-Butyraid-Tablets-100-Count/dp/B0014TDVXE/ref=pd_sbs_hpc_4

• Cal-Mag Butyrate: 1 review. Leaky gut.

http://www.amazon.com/Ecological-Formulas-Cal-Mag-Butyrate-Capsules/dp/B003TV99EA/ref=pd_sbs_hpc_5

• T.E.Neesby – Butyrex Cal/Mag, 600 mg, Micro encapsulated design: Two reviews. GI related and insomnia.

http://www.amazon.com/T-E-Neesby-Butyrex-Cal-Mag-capsules/dp/B00014G70C/ref=pd_sbs_hpc_9

http://www.jigsawhealth.com/supplements/butyrex

• Butyren, Allergy Research (Nutricology): “ButyrEn, from Allergy Research Group, is an enteric-coated tablet of the calcium and magnesium salts of butyric acid, providing 815 mg of butyrate and 100 mg of both calcium and magnesium…the enteric coating is designed to provide delayed release in the intestinal tract.” Two reviews which don’t offer much.

http://www.amazon.com/Allergy-Research-Nutricology-Butyren-tablets/dp/B00014FOCY/ref=pd_sbs_hpc_11

• BioCare Butyric acid complex (magnesium and calcium): No reviews.

http://www.biocare.co.uk/default.aspx?GroupGuid=29&ProductGuid=11890

• Digestix: Two fair reviews.

http://www.pinnaclebio.com/products/digestix-%E2%80%93-calcium/magnesium-butyrate/

Forms of butyrate not available over the counter, per se:

Tributyrin:

In many butyrate research studies, tributyrin is used. Isn’t it fascinating that it is tributyrin which naturally occurs in butter? (6) Tributyrin serves as a delayed-release source of butyrate, and hence achieves more sustained plasma levels. It is made of a glycerol backbone with three butyrate molecules attached.  However, even still, it is absorbed before the colon:

“Oral tributyrin (glycerol tributyrate) is absorbed in the small intestine and at high doses increases free butyrate concentration in peripheral plasma for up to 4 h. However, the hepatic uptake of intestinal butyrate is known to be almost complete, suggesting that systemic delivery of butyrate to the colon would be limited.” (7)

Tributyrin has been used in many studies including, but in no way limited to, cancer studies, metabolic studies, and neurological disease studies.  Oncologists were hopeful that it could achieve the cancer-slowing benefits in vivo as is seen with butyrate in vitro; about 20% of cancer patients achieved long-term disease stabilization when receiving 200 mg/kg 3 times daily in a pilot trial. In diabetes and obesity, reports suggest tributyrin has the ability to suppress the induction of obesity and insulin resistance in mice fed a high-fat diet. Researchers speculate there may be an impact of tributyrin on the cognitive function of patients with early Alzheimer’s disease, although they express concerns:

“From the standpoint of practicality, however, it would be necessary to incorporate tributyrin into a functional food, as it would not be feasible to require the ingestion of many dozens of capsules daily.”  (3)

Phenylbutyrate:

Phenylbutyrate is an “orphan” drug used in rare conditions. What in the heck is an orphan drug?  An orphan drug is one that has been pushed through the typical drug approval process usually because the disease it treats is so rare. Phenylbutyrate has activity similar to butyrate (induction of apoptosis and histone acetylation) and is used for urea cycle disorders. I have listed it here as its actions seem similar to butyrate, and if one is exploring butyrate, they can also pursue study of phenylbutyrate. (8)

Butyrylated Starch:

Some studies have started using high amylase corn starch with butyrate attached.  You’ve seen high amylase corn starch mentioned in this series before when I discussed resistant starch. (7, 9)  Potentially, they’d like to consider adding butyrylated starches to food products to promote health.  (Darn it, folks.  Why do we keep letting ourselves be manipulated this way?  Instead of a cheap study looking at the safety or toxicity of raw potato to deliver resistant starch to the colon to bolster butyrate production and butyrate promoting bacteria, they’re coming up with more ways to modify your food source.  Why can’t we get it together?  When is enough enough?  Stop eating processed foods.  Even gluten-free ones.)

Enemas:

These may be helpful in ulcerative colitis. Research results are mixed.  The one formulation I found pre-prepared had been discontinued.  I read some forums, but I couldn’t really find any strong leads here.  It seems that to get these, you have to take your prescription to a pharmacy which compounds (makes) them specially for you. The smell and delivery mechanism are undesirable I read–not to mention the exposure time of the colon epithelium to butyrate will be brief.  If you have anything to leave in the comments regarding these, some Googlers may find it helpful in the future.

Conclusion:

Thanks for reading.  I’m sorry this has taken so long to prepare.  I hate that I pretty much came to a halt on a series.  I’m in my first trimester of pregnancy.  I’m not a very pleasant pregnant person.  Give me a baby.  Give me a kid.  Don’t give me pregnancy or a toddler.  (Joke.)

The next Butryate Series post will revolve around using probiotics to increase butyrate in the gut.  But I may have to write some “bubble-gum” posts in the meantime, if I can even type up anything at all.  I’m about shot.  Please point out typos and mis-information, please.  I appreciate it.  ~~Terri

Sources:  There are some interesting sources today.  Read and scrutinize carefully.

1.  Acetate adaptation of clostridia tyrobutyricum for improved fermentation production of butyrate.  Adam M Jaros, Ulrika Rova and Kris A Berglund.  2013.  SpringerPlus 2013, 2:47.  http://www.springerplus.com/content/2/1/47

2. Minamiyama M, Katsuno M, Adachi H et al. Sodium butyrate ameliorates phenotypic expression in a transgenic mouse model of spinal and bulbar muscular atrophy.  Hum Mol Genet 2004 June 1;13(11):1183-92.  http://hmg.oxfordjournals.org/content/13/11/1183.long

3.  Tributyrin May Have Practical Potential for Improving Cognition in Early Alzheimer’s Disease Via Inhibition of HDAC2.  Mark F. McCarty.  March 2013.  Catalytic Longevity.

http://catalyticlongevity.org/

http://catalyticlongevity.org/prepub_archive/Tributyrin-AD.pdf

4.  Effects of Butyrate on Intestinal Barrier Function in a Caco-2 Cell Monolayer Model of Intestinal Barrier.  Peng, He, Chen, Holzman, and Lin.  Pediatric Research (2007) 61, 37–41.  http://www.nature.com/pr/journal/v61/n1/full/pr20079a.html

5.  SIDS Initial Assessment Report.  For 16th SIAM.  May, 2003.  http://www.epa.gov/hpvis/hazchar/Category_ButylSeriesMetabolic_HC_SIAR_0108_Interim.pdf

6.  http://en.wikipedia.org/wiki/Butyrin

7.  Butyrate delivered by butyrylated starch increases distal colonic epithelial apoptosis in carcinogen-treated rats.  Clark et al.  Carcinogenesis. 2012 January; 33(1): 197–202.  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3276328/

8.  A Phase I Clinical and Pharmacological Evaluation of Sodium Phenylbutyrate on an 120-h Infusion Schedule.  Carducci, Gilbert, et al.  Clin Cancer Res.  October 2001.  7;3047.   http://clincancerres.aacrjournals.org/content/7/10/3047.full

9.  Butyrylated starch increases colonic butyrate concentration but has limited effects on immunity in healthy physically active individuals.  West et al.  2013.  EIR.  102-119.

Related articles

Butyrate Series, Part 6

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We’re working our way through butyrate and the foods that increase butyrate in the body.  We are on resistant starch today.  It’s a doozy.  [“Doozy” probably comes from the nickname (“Duesy”) for a kind of car called a Duesenberg.  It was a supreme, luxury car made in my home state of Indiana, in a tiny farming town called Auburn, north of Fort Wayne.  Each Labor Day weekend they host a huge car auction called the Auburn Cord Duesenberg Festival.]

Don’t be afraid to let your diet be unique.

Getting butyrate and short chain fatty acids in the gut seems pretty important, and there a few dietary Cute orange snackways to go about getting it.  No one way will work for every single person.  You must recognize absolutely how unique and special you are.  (Is this chick for real?)  Seriously, I do think you’re probably pretty special, but I am talking about nutrition here.  What makes one diet suitable for one person and detrimental to another?  (Why can’t I eat ice cream?  Whaaa-whaaa.)

  • Your genetics:  Yes.  Absolutely.  The genes we have will determine how well we can digest certain foods!  If your long ago ancestors are from an area who relied traditionally on more starches, you have more genes to make amylase (the starch break-down enzyme) and more amylase in your spit. (1)  Native Japanese people have genes to metabolize seaweed that people of European descent don’t.  (Ha!  For those who don’t like the flavor of seaweed, more power to ’em, eh?) (2)  But, ice cream.  Mmmm.  Does ice cream make you bloat?  Blame your genes’ inability to make lactase for you to break down the sugar in milk.  (3) And your mix of genes will be different than your sister’s or cousin’s.
  • Your gut bacteria.  With the trillions (edited post-writing) of bacteria in your body, you’re bound to be one-of-a-kind.  Some people will have more of one type of bacteria helping them eat than another kind.  I hope over the butyrate series you have come to see bacteria as an integral part of you, your diet, and your health.  Your bacteria will affect what you can comfortably eat or what happens when you eat it.  If the bugs you happen to have are strains that make lots of methane with cellulose, then cellulose may not be your friend.  Your bugs may do better with resistant starch. If you have significant overgrowths of putrefactive bacteria that make more toxic metabolites, maybe you’re at higher risk for disease from a high protein diet. (4) (5)  (Studies show, however, that diet can modify levels of bacteria.  So all is not lost!)
  • Your individual function:  We all have our own unique pathology.  FODMAPS, SIBO, slow transit, food intolerances, and glucose intolerance just to name a few.  If your small intestine is really bad at absorbing the sugars and sugar alcohols from foods (like in FODMAPS),  you’re going to have to watch and keep a food diary to figure out which vegetables and fruits you can tolerate.  If green bananas make you itch, you have to find another source for resistant starch.

Bottom line?  Short chain fatty acids and butyrate are pretty darn important for the gut and body.  Find a way to make your diet compatible with getting them.  You have several options.  For nearly any specialized diet, there is usually something you can tolerate to help boost needed nutrients.

Ok.  Rant over– resistant starch to boost short chain fatty acid and butyrate production.  This is going to be dry, dry, dry and long, long, long.  I thought about dividing it up, but I wanted all the resistant starch stuff on one page, not several.  And I figure those who actually read it are people really looking to learn about it– so they’ll like it on one page.  By the way, Merry Christmas-time.  I hope you are having a beautiful month.  May you be filled with joy and peace now and forever.

Is that a healthy diet?

What healthy diet removes beans, legumes, grains and potatoes?  When I began my food journey two years ago, I was SHOCKED to see grains and potatoes removed from many diets like Paleo, SCD, GAPS, Primal, and Whole30.  (Were you shocked when you started?) However, after much research, I decided there was no harm in removing them as I tried to treat my GI health problems.  I mean, my vegetable intake skyrocketed in compensation!  Now, though, my GI issues have plateaued, and I have been on the prowl again to see what else can be done.  I am tracking butyrate- producing foods.  In this series, I have covered dairy products, fermented foods, fiber, and now we are hitting resistant starch.

Resistant starch from foods makes it past the small intestine’s digestive process to enter the colon, where bacteria can ferment (“eat it”) it to make short chain fatty acids and butyrate as a result.  Great!  Resistant starch is a popular topic in health spheres now.  It has several possible health benefits.  Do you see anything which could help you?

  • Improved blood sugar control and insulin response to food.  Implications for diabetes, pre-diabetes, and metabolic syndrome.
  • Improved bowel health.  Implications for colon cancer, ulcerative colitis, Crohn’s Disease, diverticulitis, and constipation.
  • Improved cholesterol.  Implications for heart disease, high cholesterol, and metabolic syndrome.
  • Prebiotic to help stimulate the growth of “good” bacterial colonies in the colon.
  • Control of hunger and reduction of calories eaten.  Implications in obesity.
  • Increased micronutrient absorption.  Implications in overall mineral absorption for all and also in osteoporosis.
  • Thermogenesis.  Implications in diabetes and obesity.
  • Synergistic interactions with other dietary components, e.g. dietary fibres, proteins, lipids.  Implications for improvement of bowel health. (6)

Backtrack a second.  Working through the ways to Apples with almond butterpotentially increase butyrate:

The four ways to increase butyrate (as I see it) that I am working through:

  • Eat butyrate-containing foods.  (An aside:  I found something that said there was a form of butyric acid in butter AND honey!  The form is tributyrin, a form of butyric acid which is actually used in research studies to help the butyric acid not have such a short half-life.  No quantities listed in the abstract.  Isn’t that amazing?  Whole foods really can provide for us!) (7) 
  • Eat butyrate-producing foods like fiber and resistant starch.  (This is where we’re at in the series.)
  • Take butyrate supplements.
  • Take probiotics which contain bacteria known to make butyrate.

OK.  Back to resistant starch.  I know, some of you try not to eat starches.  So what is the difference between starch and resistant starch?  (Chemistry-wise, not much!  Actions in the body, HUGE!) 

What is starch?  Starch is plant carbohydrate.  A plant uses starch as a storage form for energy.  Starch is high in things like potatoes, corn, rice, other grains, and beans.  When we eat starch, it is usually completely broken down and absorbed in the small intestine by our amylase and other enzymes.  You know the rest– glucose, insulin, and calories.

Let’s talk a minute about the structure of starch because structure is going to help explain what makes starch resistant.  Starch is made up of two molecules, amylose and amylopectin.  Both molecules are simply made up of many glucose molecules hooked together—just hooked in different ways.  Amylose has many glucoses strung together in a tight, compact linear fashion.  Amylopectin has glucoses strung together in branching chains, forming a large structure.  Depending on the food/plant starch in question, these two players come together in different ratios and shapes.  They connect with each other through hydrogen bonding and form crystalline granules (an important point here in a bit) of varying sizes.  The crystalline granules are an effective way for the plant to store starch.  We have an enzyme called amylase, which works in the small intestine, and it is most often able to break apart the bonds of starch to make simple sugars which are easily absorbed.  (8, 9)

What is resistant starch?  Same stuff as starch!!!!  It’s just that for one reason or another (which we will talk about), it defies digestion by the small intestine and its amylase enzyme.  It moves into the colon and feeds bacteria, thus producing short chain fatty acids and butyrate.  Yeah!

How would the same stuff as plain, old starch do that?  We will look at that in minute.  First let’s mention the kinds of foods that have resistant starch.

What foods have resistant starch?

Obviously, starchy foods will have resistant starch, but how much resistant starch a food has– well, it willYellow pepper for Y keep your head moving like one of those darn, tiny bouncy balls your kids like to throw around.  Understanding resistant starch content is nearly insane.  So I’m going to list some examples of resistant starch values, but you have to keep reading to understand how truly variable and FICKLE resistant starch is.  For example, IT IS NOT ENOUGH TO SAY THAT A BANANA HAS LOTS OF RESISTANT STARCH—because sometimes it doesn’t!  I started to put together a nice table of resistant starch values.  I had research articles all over the schoolroom desk; I knew it was going to be a citation mess.  Every source had different values for resistant starch content and often even for the same food.  I decided making a chart was clearly was not a good time investment.  (Where do you want to invest your time?)  So here are some sources with lists of resistant starch contents for you to look over.  For your information, some sources suggest at least 20 grams of resistant starch daily; others suggest more.

Free the Animal.  Resistant Starch in Foods.  (Man.  What diligence.  Kudos.  This is what my table would have looked like.  He did a great job, and I’m grateful for his work!  This is a link to a PDF file which is featured on the blog.) (12)

An in vitro method, based on chewing, to predict resistant starch content in foods allows parallel determination of potentially available starch and dietary fiber  (10)

The Resistant Starch Report.  An Australian update on health benefits, measurement and dietary intakes.  (11)

Bananas (11)
8.5 grams/100 grams          Raw green, medium-size
2.4-5.4 grams/100 grams    Ripe, medium-size
Potatoes (10)
12.2 grams/100 grams        Boiled and stored at  5 degrees C –41 degrees F–fridge temperature
3.7 grams/100 grams          Boiled and not cooled
50 grams per pound           (Saw it on the internet gossip, but I need a legitimate source)  (About 97% of the starch in raw potato is resistant.)
1.3 grams/100 grams         Baked
Sweet potatoes (11)
1.1-2.1 grams                       Cooked
Raw  About 98% of the raw starch is resistant.  (Need source)
Plantains (12)
3.5 grams/100grams          Cooked
Raw much, much higher    (Need source)
Beans, white, boiled (10)
16.5 g/100 grams
Lentils, red, boiled (10)
13.83 g/100 grams
Chickpeas (11) 
6.6 g/100 grams
Nuts
Oats (12)
0.2 g/100grams                  Cooked
7.8 grams/100 grams        Raw
Pasta
1.4 grams/100 grams        Cooked whole wheat pasta (valemaisalimentos.com)
2.9 grams/100 grams        Boiled 9 minutes  (C)
Rice (11) (13)
3.1 grams/100grams         White, cooked
1.6 grams per 1/2 cup      Brown, cooked

The amount of resistant starch a food has will vary.  It will vary by the TYPE of resistant starch, the food source of the resistant starch, the food preparation, and many other factors I will try to point out.

There are four types of resistant starch RS:  Resistant starch type 1 (RS 1), resistant starch type 2 (RS 2), resistant starch type 3 (RS 3), and resistant starch type 4 (RS 4).

  • RS 1 is in seeds, legumes, and whole grains.  The starch is resistant because of the physical seed coat around the starch.  (Grinding and milling will decrease the amount of resistant starch.  Based on this, a wheat kernel has more resisant starch than ground flour.  Even chewing your food well decreases RS!)
  • RS 2 is in uncooked foods like potato, green banana, green plantains, sweet potato, cassava, yam, some legumes and high amylase corn.  The natural, raw shape of the starch granules in these particular plants does not allow our digestive enzymes to get in and break down the starch. (5)
  • RS 3 is in cooked and cooled starches, such as legumes, bread, cornflakes, potatoes, pasta salad or sushi rice. The starch when cooked becomes highly absorbable starch, but when it cools it forms a crystalline structure that won’t let enzymes in so it becomes resistant starch.  This is called retrogradation.  I will talk more about this below.
  • RS 4 is chemically modified starch and is not naturally found in nature.  It is often found in processed foods, but we don’t know if it acts the same as natural RS or not.  (So why are they putting it in our foods?  And why do people not care?  Ignorance is bliss.  But not really.) (6)

Both the plant species and the plant variety affects resistant starch content:  Bananas overall have more resistant starch than most rice.  Beans usually have more resistant starch than potatoes.  Within a species, long grain rice has more RS than short grain rice.  (14)  Jasmine rice has less RS than long grain rice varieties.  High amylose maize (corn) has been bred to have higher resistant starch than other corn.

Preparation method changes content of RS:  Long grain rice prepared in a pressure cooker has less RS than when prepared in a traditional rice cooker.  Baked potato has less resistant starch than potato salad.  Heated and cooled, heated and cooled, heated and cooled potato has more resistant starch than just potato that has been heated and cooled one time only.

Cooking at all changes RS:  Raw potato has immense amounts of RS.  Mashed potatoes have immensely less.

Foods can have more than one kind of resistant starch:  Potatoes have RS 2 when raw and RS 3 when cooked and cooled.

Ripeness decreases RS:  A green banana has great amounts of RS.  Ripe bananas have lots less.

Chewing decreases RS:  What are you going to do about this one?  LOL.  I think this is a great example of how you can find good in just about everything!  If you don’t chew well, you can get more resistant starch!

Remember how I mentioned amylose and amylopectin above?  In part, their association together will help determine how much RS there is:

  • Amylose and amylopectin come together in different ratios (maybe 20:80 or 40 :60 or 25:75) and will be different between species of plants and different varieties of the same plant, as I already mentioned.  The more amylose there is, the more resistant.  (5)  In fact, there’s this processed stuff called High Amylose Maize Starch that was bred to have high amylose.  It has great amounts of resistant starch.  1 tablespoon has 4.5 grams of resistant starch.  (13) Amylose takes higher heats to gelatinize so it is more resistant.  (When it gelatinizes, the body can digest it easier.)
  • Chain length of the amylose and amylopectin molecules will affect resistant starch content.
  • Size of the crystalline granules will affect resistant starch content. (15)

Non-starch components may affect the amount of resistant starch.  Amylase (our digestive enzyme) can bind with fats, and then change the breakdown of the starch.  If the amylase is all bound up, it’s not available to digest all of the starch.  Some plants come included with their own amylase inhibitors so we digest them less, allowing more RS to the colon.  Phosphorus can bind to the starch and make it more resistant.

Biological factors (such as transit time and menstrual cycles) can affect the digestion of starch. (6)

Yes.  Resistant starch values for any given food Water kefir with grape juicevaries dramatically. 

So when you look at different tables for resistant starch, you will see all kinds of different numbers.  The resistant starch values will be all over the place.  I know you don’t like it.  It’s just the way it is.  Nobody in life can give you an answer.  We just have to do the best we can.  God didn’t say, “Here.  Eat resistant starch.”  He gave you fresh vegetables, fruits, tubers, and yes, even grains.  And thankfully, He gave me a fridge to cool my tubers.

Why in the world does cooling change the amount of resistant starch?

When typical starch is heated, it becomes quite absorbable.  When it is cooled, it can form resistant starch and then not be absorbable.  This is termed retrograded starch or resistant starch type 3 or RS 3.  How does this happen?

Putting the starch in water and heating it allows the crystalline structure of the starch granules (made up of amylose and amylopectin) to swell.  Water can get into the starch granules, but it can’t break them apart because of hydrogen bonding between amylose and amylopectin.  The starch gelatinizes and swells.  With the swelling comes increased ease of getting amylase into the starch to break down the bonds holding it together.  So hot, cooked starch is easier to digest.

As the hot starch cools, its structure starts tightening back up and recrystallizing, becoming more like it was before water and heat was affected it.  Amylase can no longer get in to break the starch down into absorbable sugars.

The higher the amylose content, the more heat that is needed to gelatinize the starch.  Things with more amylose, such as high amylose corn starch, have more resistant starch.  In one study, high amylose corn starch showed an increase in butyrate formation, whereas low amylose corn starch did not. (15) (16) (5)

People often wonder why it matters if it’s cooled since when it is eaten it heats back up in our bodies.  I read that the answer to that is that it takes more heat than the temperature of your body to overcome the retrogradation.

Who might shy away from resistant starch?

SIBO people?  People with small intestinal bowel overgrowth (SIBO) may have problems with resistant starch.  (SIBO is a disorder which contributes to bloating, constipation, diarrhea, and stomach pain.  It occurs when bacteria inappropriately colonize the small intestine.)  I have seen the argument made that gastroesophageal reflux (GERD), SIBO, and some other GI disorders may be made worse by resistant starch.  Increasing the food supply for the bacteria that are inappropriately growing in the small intestine doesn’t seem like it would be helpful.  I can definitely understand this thought process.  However, on the other hand, production of SCFA has been found to increase the motility of the gut and make the environment more acidic.  These two mechanisms sound helpful!  Everything is an equilibrium.  Nobody right now knows the answer.  This is where you drag out a pen and a calendar, and you diligently journal what you eat and your symptoms and stop waiting to be told what to do.

FODMAP people?  One would think that FODMAP issues might actually do okay with resistant starch if there is no SIBO to go along and complicate the condition.  The gases usually made by the bacteria from FODMAP ingredients are not formed from resistant starch:  “However, RS [resistant starch] is believed to result in only a modest production of these gases [carbon dioxide, methane, hydrogen] compared with other non-digestible oligosaccharides, fructo-oligosaccharides and lactulose.” (6)  Potato, sweet potato, and rice are often well tolerated in those with FODMAP issues–although I read that sweet potato has mannitol which may cause some people problems.  (Sorry, no source.)

Diabetics:  They say that diabetics’ blood sugars will be fine on resistant starch and may even improve!  This seems like it would be quite variable and a diabetic should watch very closely.  (19)

Flatulence:  Excess gas.  Anecdotal evidence points out that there is excess gas as a person starts increasing their resistant starch.  The anecdotes say that it usually resolves in the first week at a stable dose.

Last tidbits with no good place to fit in above butFruit kabobs I want you to hear about:

Will resistant starch make me fat?  Resistant starch reportedly helps with the feeling of being full–so you’re not so hungry!  However, if it is metabolized by your bacteria, it does have calories (short chain fatty acids are made and absorbed).  Typical starch that is absorbed up in the small intestine supplies 4.2 calories per gram.  Apparently, resistant starch produces 2 calories per gram.  (6)  Want an anecdote?  I started potato starch as a resistant starch.  I stir one tablespoon in water twice a day.  I can honestly say that I’m not very hungry.  Of course, there could be a million and one other reasons for that.

Did you know we have a drug that makes starch resistant?  Acarbose is a diabetic drug.  It inhibits amylase and so increases the amount of resistant starch and also increases oligosaccharides.  It has been found to increase SCFA in the colon (but with side effects of bloating, diarrhea, stomach pain, etc).  (17)

Resistant starch versus non-starch polysaccharides (see last post for explanation) in butyrate production:  RS seems to do a better job than other carbohydrates at producing butyrate. Resistant starch acts as a prebiotic, raising the numbers of lactobacilli and bifidobacteria. (5)

Resistant starch diet helps increase the neurons that promote motility:  “After 14 days of RSD [resistant starch diet], the neurochemical phenotype of myenteric neurons of rats showed a significant increase of 35% in the proportion of ChAT-IR neurons complared with animals fed with the SD [standard diet]…As expected, RSD was associated with a significant increase in colonic concentration of butyrate compared with SD [standard diet].”   (18)  What is this saying?  On a resistant starch diet, the proportion of acetylcholine neurons increased!  Acetylcholine neurons play a large role in GI peristalsis and bowel movements.  Also, my friend butyrate, was found at increased concentrations.

Which form of resistant starch produces more butyrate?  This really seems to land you all over the place, trying to characterize all the different starch types and food types and how they each have a different effect.  Crazy.  Anyhow, RS 2 from raw potato starch is reported to increase the concentration of butyrate in humans and rats while RS 3 is reported to increase the concentration of acetate in pigs, but not in humans.  (5)

Great related reading:

I’m not saying I agree with all that is said.  I just like to see ALL that I can out there so I can think about how it applies to my body.  Does benefit outweigh risk in trying something?  Am I willing to accept that what somebody suggests could set me back significantly?  Does what they’re saying make sense in the context of what I know about physiology and biochemistry (which is NEVER enough!).

Free the Animal has about a million resistant starch posts, including posts on specific conditions (like SIBO, FODMAPS, high blood sugars, etc.)  This is really the place to go to read about resistant starch, although they have quite an enthusiastic stance.  I’m pretty excited, too, but I try to temper my excitement.  Nothing is a cure-all.  I haven’t had success coming off of butyrate with an increase in resistant starch using green bananas and Bob’s Red Mill Potato Starch (yet).

Animal Pharm:  HOW TO CURE SIBO, Small Intestinal Bowel Overgrowth:  Step #2 Eat Resistant-Starch-Rich Tubers, Grains, Legumes and Pulses (Guest Post: Tim/TATER)

Digestive Health Institute:  Resistant Starch–Friend or Foe

Done:

Please take good care.  Don’t be overwhelmed.  Track your symptoms.  Be patient with changes.  Don’t get frustrated.  Read.  Weigh benefits and risks.  Don’t flit from diet to diet to diet.  Pick a system, stick with it awhile, and then implement tweaks slowly and methodically.  Where you are at NOW does not reflect where you have to stay FOREVER!!!!!

As always, I need typos pointed out and faulty links.  I do the best I can, but this is a simply a hobby of putting together my findings for others to read.

Terri

Part 7

Sources:

  1. Diet and the evolution of human amylase gene copy number variation.  Perry, Dominy, Claw, et al.  Nature Genetics 39, 1256 – 1260 (2007) Published online: 9 September 2007.  (Link)

  2. Transfer of carbohydrate-active enzymes from marine bacteria to Japanese gut microbiota.  Hehemann, Correc, Barbeyron, et al.  Nature 464, 908-912 (8 April 2010). (Link)

  3. Archaeology:  The milk revolution.  Curry, Andrew.  Nature.  July 2013. (Link)

  4. Dominant and diet-responsive groups of bacteria within the human colonic microbiota.  Walker, Ince, Duncan, et al.  The ISME Journal (2011) 5, 220–230.  (Link)

  5. Starches, resistant starches, the gut microflora and human health.  Bird, Brown, and Topping.  Current Issues in Intestinal Microbiology.  2000.  1(1):  25-37.  (Link)

  6. Health properties of resistant starch.  Nugent, AP.  Nutrition Bulletin.  March 2005.  30 (1): 27-54.  (Link)

  7. (Abstract.)  Anticarcinogenic actions of tributyrin, a butyric acid prodrug.  Heidor, Ortega, de Conti, et al.  Curr Drug Targets.  December 2012.  13(14):1720-9. (Link to abstract.)
  8. http://www1.lsbu.ac.uk/water/hysta.html
  9. The synthesis of the starch molecule.  Smith, Denyer, et al.  Plant Carbohydrate Biochemistry.  1999.  Chapter 7.
  10. An in vitro method, based on chewing, to predict resistant starch content in foods allow parallel determination of potentially available starch and dietary fiber.  Akerberg, Liljeberg, et al.  The Journal of Nutrition.  1998.  128 (3): 651-660.  (Link)
  11. The Resistant Starch Report.  An Australian Update on health benefits, measurement, and daily intakes.  Landon, Colyer, and Salman.  Food Australia Supplement. 2012.    (Link)
  12. Link to a PDF file on Free the Animal blog listing resistant starch content:  http://freetheanimal.com/wp-content/uploads/2013/08/Resistant-Starch-in-Foods.pdf
  13. Natural Hi-Maize Starch website:  “Double Resistant Starch Intake.”  http://www.resistantstarch.com/NR/rdonlyres/DE2ADBB0-FF7D-40A7-B409-03493FEFFDFA/4601/Foodswithresistantstarch_LR.pdf

  14. Effect of variety and cooking method on resistant starch content of white rice and subsequent postprandial glucose response and appetite in humans.  Yu-Ting Chiu, Maria L Stewart. Asia Pac J Clin Nutr 2013;22 (3):372-379.  (Link)

  15. Understanding Starch Functionality.  Scott Hegenbart. Food Product Design.  January 1996. (Link)

  16. Butyrylated starch increases colonic butyrate concentration but has limited effects on immunity in healthy physically active individuals.  West, Shristophersen, et al. Exerc Immun Review.  2013.  19: 102-119.  (Link)

  17. Abstract for Effects of acarbose on fecal nutrients, colonic pH, and short-chain fatty acids and rectal proliferative indices.  Holt et al.  Metabolism.  1996.  Sep;45(9):1179-87.  (Link)

  18. Short-chain fatty acids regulate the enteric neurons adn control gastrointestinal motility in rats.  Gastroenterology.  May 2010.  138(5):1772-82. (Link)

  19. Consumption of both resistant starch and b-glucan improves postprandial plasma glucose and insulin in women.  Behall, Scholfield, et al.  Diabetes Care.  May 2006.  29(5): 976-981.  (Link)

Related articles

Butyrate Interruption, Kind of

22 Replies

My husband always passes along mainstream news clips on health that he sees relating to my studies.  I think he is super happy that we found this new way of eating and thinking, despite our doc-in-a-box trained brains.  (It has a made a huge difference in the health of every single family member.)

Anyhow here is today’s tidbit passed on to me by husband who noticed the word BUTYRATE.  The article relates to “potential new ways to prevent colon cancer” and discusses how there is growing evidence for a link between bacteria and colon cancer:

“Ahn and her colleagues also noticed lower levels of Clostridia – “good” bacteria – in the gut of cancer patients.  Clostridia – of which there are several forms – is important in the fermentation and digestion of fiber and carbohydrates.  Clostridia also creates a chemical butyrate, which is believed to moderate inflammation and cancerous mutations in the colon.”  (Emphasis mine)

So I continue to encourage you to eat for your bacteria!  Whole foods!  And I hope with the butyrate series that’s running, that you can say when you stumble across these news clips telling you it comes down to bacteria and the products they help make, “Yeah.  I knew that.  That’s old news.”

What you eat matters, from colon cancer to headaches to runny noses!  Don’t eat processed foods!  Here is the link to the article above:

Research points to potential new ways to prevent colon cancer

~~Terri

Butyrate Series, Part 5

59 Replies

It’s only voodoo until you understand the sense (science) behind it…so what’s the sense for fiber?

Introduction:

Part 4 of the Butyrate Series summarized naturally occurring sources of butyrate in food.  Today’s post explains another source of butyrate in the diet: fiber. (More correctly, fiber is a source for our colon’s bacteria to make butyrate for us.) Today we will cover:

  • What fiber is
  • Different kinds of fiber
  • Fermentability of different kinds of fiber
  • Which fibers bring about butyrate

(And if you think this sounds boring, you are probably quite right.)

There is a book out there called Fiber Menace by Konstantin Monastyrsky which demotes fiber.  I’ve not read it, but I’d have to say in my former Caterpillarseating life, I tried adding in high amounts of fiber: peas, hummus, beans, lentils, Shredded Wheat Cereal, Grape Nuts Cereal, Metamucil, and Fiber Con. I always swore in my head that this fiber did nothing but make my GI symptoms worse; however, this seemed like an insane fragment of my overactive imagination until 2011. In 2011, I read a little blurb in my American Family Physician journal about fiber not helping slow transit constipation and then found sources stating fiber may actually worsen slow transit constipation.  From a World Journal of Gastroenterology article:  “Muller-Lissner emphasized that a diet poor in fiber should not be assumed to be the cause of chronic constipation. In contrast, they found that many patients with severe constipation deteriorated when dietary fiber intake was increased.” (1)  Hmmm. Is that right?

In the past, I’ve tried high fiber and I’ve tried low fiber; I didn’t know what to think. Guess I still really don’t. Today, studies say that fiber helps this or that. Tomorrow they will say that it doesn’t. Depends on the wind. But considering how important short chain fatty acids (including butyrate) are, I’m thinking fiber may be pretty helpful, but not in the way I was trained to think.  It has nothing to do with the bulk or the drawing of water into the gut.  It has to do with good bacteria, what they like to eat, and what they make for me when they eat.  So for myself, in order to increase my butyrate naturally, I will keep vegetables and some fruit a priority.  I will watch my symptoms closely and adjust as indicated.

What I want you to know (because the rest of this post is like broccoli with no dip—pretty dry):

  • “Fiber” is an oversimplified, generic word for a hodge-podge of substances from plants. The words soluble and insoluble do not even come close to explaining the types of fiber.
  • Fiber is basically carbohydrates that humans cannot digest. There are many kinds of fiber which get “eaten” by the bacteria in different amounts and at different rates in our colon.  (More below.)
  • Some fiber, like cellulose (think of the stems of broccoli and the peel of an apple), gets fermented very little and very slowly.  Other fiber, like inulin (think onions) gets fermented very completely and very rapidly.
  • Each vegetable or fruit will contain several types of fiber, not just one type. Broccoli is not ONLY cellulose! Each vegetable or fruit has its own complex fiber identity! Find some that you tolerate.
  • I think to optimize butyrate production throughout the entire colon, it is good to eat a mix of vegetables and fruits. The quickly fermented fiber will bathe the first part of the colon in short chain fatty acids, and the slowly fermented fiber will make it to the end to bathe the final part of the colon.
  • Please don’t buy fiber in a box or plastic container. Please? Eat the real deal. Why? Because remember that vegetables and fruits contain multiple kind of fibers in one package, and they ferment at different rates. This provides valuable short chain fatty acids throughout the whole colon. In addition, different fibers have been found to influence the fermentation of other fibers, promoting more butyrate production than the given fibers alone. Not to mention all the vitamin C, vitamin A, magnesium, calcium, and other nutrients.  Again I say, find a mix of vegetables (and fruits) that you tolerate.  (2) (3) (6)  (And I still say, vegetable, fruits, and meats.  Wheat is a treat. Don’t get your fiber from wheat. My personal opinion.)
  • Good bacteria can be cultivated. Drugs that cultivate good bacteria are called PREbiotics, but foods can do the same thing. Vegetables and fruits carry fibers that are prebiotic. By eating vegetables and fruits, you are not just allowing the bacteria you have to make butyrate, you’re actually promoting their growth.  (4)

Caterpillar making attachmentReminder: All the information in this blog is information I have gathered and assimilated for my own purposes. I enjoy sharing it, but I certainly expect you to use it as fodder for learning and questioning, not as diagnosis and treatment.  Every individual is unique and may react differently (and badly) to what others find beneficial and helpful.  For your safety, present the information to your favorite trusted healthcare provider before making any changes. 

You know it’s bad when there’s a glossary:

Carbohydrates:  Carbohydrates are made up of polysaccharides, oligosaccharides, and sugars.

Sugars:  Sugars are monosaccharides or disaccharides.  Examples:  glucose, fructose, lactose, sucrose. They are usually completely absorbed in the small intestine. (But if they are not, they can continue to the colon to be fermented.)

Polysaccharides:  Polysaccharides are complex carbohydrates made by linking many, many, many sugars together. They can be starch polysaccharides or non-starch polysaccharides. Starches are commonly used as energy storage; amylose and amylopectin are two very common starches.  Non-starches are usually used for structure, like cellulose.

Oligosaccharides:  These are smaller chains of sugars linked together. They’re bigger than sugars and smaller than polysaccharides. They can be found in onions, jicama, and wheat. They are things like inulin and fructooligosaccharides (FOS—often a part of prebiotics).

Starches (amylose and amylopectin):  Starches are polysaccharides, which means many sugars strung together. Common starches in plant matter include amylose and amylopectin. Amylose has its glucoses linked linearly in a very compact structure, making it digest more slowly. Amylopectin has its glucoses linked in a large, branched structure, allowing more easy penetration of digestive enzymes. We used to think that all starch was digested and absorbed in the small intestine. We now know this is false.  Starches are in things like flour, potatoes, and sweet potatoes.  (Aside for SCD followers:  Breaking the Vicious Cycle’s explanation of amylose and amylopectin is incorrectly reversed.)

Non-starch polysaccharides:  A very hodge-podge group. It’s what you think of as classic fiber. Cellulose, pectins, gums, and more fit in this category. They often provide structure to plant cells. The small intestine can’t digest them.

Fiber:  Usually defined as plant matter that escapes digestion by the small intestine and continues undigested to the colon. But a true definition is evasive because calling something “fiber” is like saying a shoe is a shoe is a shoe. Well, stiletto boots are a far cry from my New Balances. Non-starch polysaccharides make up a huge chunk of “fiber.” Also included, depending on who is writing the definition, are resistant starch and oligosaccharides.

Resistant starch:  There are several kinds of resistant starches, but basically they are all starches that manage to escape digestion in the small intestine, and therefore they act like fiber. (5)

Eating for butyrate production by bacteria

Ok.  So the goal is to produce butyrate by eating food.  (The bacteria will do the work for me.)  Let’s take a moment to remember why anyone should care.  Studies indicate butyrate may—

  • Heal leaky gut, and therefore improve food intolerances
  • Stabilize blood sugar responses, even to carbohydrates
  • Lessen hunger and help weight loss
  • Stimulate bowel motility
  • Help damaged nerve cells to function again
  • Cure and fight cancer
  • Other unknown functions (7)

(I take a butyrate supplement. I have noticed a huge improvement in my peristalsis and in my ability to eat nuts and eggs baked in pies. Although my supplement seems okay, a person can never tell what impurities are in their supplements or how much of the nutrient the body needs!  Too much of a good thing can potentially turn on you. So I want off of my supplement, and this is where this butyrate series came from.)

What foods do bacteria use to make butyrate?  Fiber and resistant starch are the best ingredients for bacteria to make butyrate in your colon.  (Bacteria can make butyrate from proteins, mucous, and sloughed cells, but these ingredients lead to the formation of chemicals detrimental to your colon, like ammonia.)  We will talk about fiber today and resistant starch next time.

Fiber: 

You’ve heard of fiber. But what is fiber? Do you want functional fiber? Physiologic fiber? Soluble fiber? Insoluble fiber? Resistant starch “fiber?”  Caterpillar made cocoonViscous fiber? Fermentable fiber? Microfiber???? (No.)

Fiber is a hodge-podge (word of the day) of chemical substances.  Like my shoe analogy up there in the glossary: work boots, snow boots, running shoes, basketball shoes, platform shoes, and stiletto heels. They all go on the feet. They all have a similar function. They are all shoes. But you can break them down into boots and shoes. Or active wear and formal wear. Or open-toed and closed-toe. Or open-toed formal and closed-toe formal.

Fiber may be fiber, but it can be classified many ways.  My little ditty of a definition for fiber in the glossary– “plant matter that escapes digestion by the small intestine and continues undigested to the colon”—keeps it about as simple as it can get. (Shoe. Fiber.)

Maybe you have heard of soluble and insoluble fiber, this is NOT the only way to classify fiber.  (In fact, experts are trying to phase out the terms soluble and insoluble. They have come to realize that the function of the fiber does NOT depend on its solubility.) (8)

Bottom line: Fiber is a complex issue. The Paleo Mom has a great fiber series that she published recently:  The Fiber Manifesto.

Let’s look at the types of fiber—the ways to categorize fiber.  I’ll warn you, categories overlap.  Just remember that fiber is plant matter (usually) that makes it to the colon undigested:

Fiber can be classified based on solubility, fermentability, viscosity, whether or not it is a starch, or whether it’s a synthetic fiber with physiologic function.

Different ways to classify fiber:

Soluble fiber:
Pectin, mucilage, gums,   psyllium, wheat dextrin		 Insoluble fiber:
Cellulose, lignins, some   hemicelluloses, some pectins
Fermentable:
Oligosaccharides like FOS and inulin, gums (guar), pectins, wheat dextrins		 Non-fermentable:
Cellulose, hemicellulose,   lignin
Viscous (gel-forming) fiber:
Pectins, gums (guar gum), psyllium		 Non-viscous (non gel-forming) fiber:
Inulin
Resistant Starch:
Polysaccharides made of starch		 Non-starch   polysaccharides:
Celluloses, hemicelluloses,   pectins, and gums
Functional fiber (designed or extracted fiber):
Inulin, psyllium, FOS, some   resistant starch		 Dietary fiber (fiber found naturally in food)

(9) (10)

Now, you can take just about all of those and mix and match them!!!  For example, you can have:

  • Soluble, fermentable (example:  pectins)
  • Insoluble, fermentable  (example:  resistant starch)
  • Soluble, non-fermentable (examples:  alginates, carrageenans)
  • Insoluble, non-fermentable (examples: cellulose and lignin—cellulose is actually a bit fermentable, see below)
  • Resistant starch, fermentable  (example:  resistant starch)
  • Non-starch polysaccharides, fermentable  (examples:  FOS and inulin)
  • Non-starch polysaccharides, non-fermentable  (example:  cellulose)

You can keep going with this, but I’m stopping. Just remember, foods are composed of several types of fiber in one package—so a banana is NOT completely made up of soluble fiber! It also has (at least) resistant starch (an insoluble fiber!), pectin, and hemicellulose.  And it gets even more complicated than this because a ripe banana will have a different fiber composition than a green banana. Ahhhh!)

To make butyrate, we are mostly concerned with the fiber that is fermentable.  Solubility has nothing to do with it.

The table below summarizes the fermentability of the different fibers mentioned above. Percent of fermentability is important. Butyrate isn’t made unless the bacteria in the colon have something to ferment. Less butyrate will be made from cellulose (20-80% fermentable) than inulin (100% fermentable). HOWEVER, all the inulin will be probably be used up early in the colon, as soon as there are bacteria to feast on it. Since less cellulose will be fermented early on, more will be available throughout the whole colon, not just the beginning—like a “slow release” formulation.

Please note that our bacterial microflora are exceptionally unique and therefore our tolerability to different fibers will be unique. In a study on the fermentation of cellulose in the cell wall of spinach, one group of people fermented the spinach with one group of bacteria–while the another group of people fermented it with another kind of bacteria. (11)  Since we have different bacteria with different capabilities and metabolite production (such as gas), perhaps this is why some of us do well with fiber and not others?

Colonic fermentability of dietary fibres in humans

Dietary   fibre

Fermentability   (%)

Cellulose

20-80

Hemicelluloses

60-90

Pectins

100

Guar gum

100

Ispaghula

55

Wheat bran

50

Resistant starch

100

 Inulin, oligosaccharides

  100 (if they are not in excess)

(12)

So now you know that fermentable fibers make butyrate best. You can see above which fibers are fermentable (remember it’s probably good to mix and match high and low fermentable foods). But which fibers make a higher percentage of butyrate? Cellulose, inulin, raffinose (in beans), and resistant starch made higher percentages than guar gum, lactose, pectin, and sugar beets sources.  Oat beta-glucans were pretty high and so was wheat bran. (6) I’ve not tried to tease out grains, mostly because I don’t eat them. They are problematic for me and for many other people as well  Studies using them for fiber sources give so many mixed messages too.

Fiber acts as a prebiotic for good bacteria and also inhibits the growth of bad bacteria:

By eating vegetables and fruits with fiber and resistant starch, you are also promoting the growth of “good bacteria.”  Many of the good bacteria make butyrate for your body. You have commonly seen the term PREbiotic (not to be confused with the closely related term PRObiotic). All prebiotics are considered fiber. For a fiber to be a prebiotic, it must have the following characteristics:

  • “Resists gastric acidity, hydrolysis by mammalian enzymes, and absorption in the upper gastrointestinal tract;
  • Is fermented by the intestinal microflora;
  • Selectively stimulates the growth and/or activity of intestinal bacteria potentially associated with health and well-being.”

You can buy prebiotic supplements, and some probiotics come with prebiotics mixed in. However, prebiotics occur naturally in foods such as leeks, asparagus, chicory, Jerusalem artichokes, garlic, onions, wheat, oats, and soybeans. (Eat real food.)

(By the way, have you ever wondered what makes a bacteria a “good” bacteria? I have:  “Generally, bacteria having an almost exclusive saccharolytic metabolism (i.e., no proteolytic activity) can be considered potentially beneficial. Such a metabolic profile is typical for lactobacilli and bifidobacteria.”  Quote is just basically saying that good bacteria can’t break down protiens.) (9)

Prebiotics (including types of fiber) also inhibit the growth of bad bacteria! As the good bacteria ferment fiber, they produce short chain fatty acids and make the inside of the colon more acidic. A more acidic environment in the colon reduces breakdown of peptides (proteins), resulting in less formation of toxic compounds such as ammonia, amines, and phenolic compounds. Also, the more acidic environment decreases the activity of undesirable bacterial enzymes. So again, looks like eating real food that is fermentable will act as a prebiotic to encourage the growth of good bacteria and discourage the growth of bad.  (9)

What I wish I understood more:

1. The Inuits lived on a primarily fat and meat diet. Yet they had low rates of disease. Where did their butyrate come from? Did they forage enough when possible to get some? Did they ferment some of the plant matter when it was available for use later when it wasn’t available? Did the fermented meats they made provide them with butyrate? (Here we go again; I just can’t find good information on quantification of fermented food content. Anyone?) Does subsisting only on high quality animal protein and fat change the environment of the colon and body such that lower butyrate production is needed? Did their unique diet cultivate a unique micro flora that maximized butyrate production?

2. If grains and isolated fiber are removed as fiber sources from studies, how would this affect results?

Closing:

Man. Thanks for reading. If you have FODMAP problems and you just can’t tolerate any vegetables, come back next post. Next post we will move on to resistant starch, a huge producer of butyrate.  Only about two butyrate posts left to go. As always, comments, constructive criticism, and pointing out of typos is always welcome.

Terri

Part 6

Sources:

1.  http://www.wjgnet.com/1007-9327/13/4161.pdf

2.  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1374147/?page=6

3.  http://gut.bmj.com/content/34/3/386.full.pdf

4.  Starches, Resistant Starches, the Gut Microflora and Human Health.  Bird, Brown, and Topping.  Curr. Issues Intest. Microbiol.  2000.  1(1):  25-37.  http://www.horizonpress.com/backlist/ciim/v/v1/03.pdf

5.  Health properties of resistant starch.  Nugent.  Nutrition Bulletin.  2005.  30: 1(27-54)

6.  Short-chain fatty acid formation at fermentation of indigestible carbohydrates.  Henningsson, Bjorck, and Nyman.  Scandinavian Journal of Nutrition.  2001.  45:165-186.

7.  Review article:  the role of butyrate on colonic function.  Hamer, Jonkers, Venema, Vanhoutvin, Troost, and Brummer.  Alimentary Pharmacology and Therapeutics.  2008.  27: 104-119

8.  http://ajcn.nutrition.org/content/69/1/1.full

9.  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3705355/

10.  http://lpi.oregonstate.edu/infocenter/phytochemicals/fiber/

11.  http://www.ncbi.nlm.nih.gov/pubmed/20662929

12. http://www.fao.org/docrep/w8079E/w8079e0l.htm

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Butyrate Series, Part 4

34 Replies

Introduction:

We have had a most wonderful Thanksgiving week!  A warm thank you to my family for coming so far to visit and eat a gluten-free, dairy-free whole foods Thanksgiving dinner!  But let’s get this butyrate series rolling again.  Today’s post will start explaining dietary sources of butyrate after a few miscellaneous points.

1.  What does butyrate smell like?

Stravecchio Parmesan Cheese

A.  Chocolate
B.  Sauerkraut
C.  Stinky locker rooms
D.  Parmesan cheese
E.  A and C
F.  C and D
G.  All of the above
H.  None of the above

The smell of butyrate is quite characteristic.  I’ve heard it described as a vomit smell and a parmesan cheese smell.  Go figure.  My nose luckily errs on the side of parmesan cheese.  Today I opened a jar of ghee (ghee is clarified butter with the milk proteins removed and only the fat left behind) and a bottle of my butyric acid supplement capsules and had my sister smell them.  That distinct smell that greets you from a jar of ghee (or from butter if you have a good smeller) is butyric acid.  I wonder if I could sprinkle my supplement on my pizza meatballs… anyhow… butyric acid is what makes the locker room smell, stinky shoe smell, and certain cheesy smell.  So the correct answer is F (both C and D).

2.  How do you pronounce butyrate?

A.  Butt-eye-rate
B.  Byou-ter-ate
C.  Butt-er-rate
D.  Butt-yuh-rat

Butyrate:  byou-ter-ate
Butanoate:  byou-tan-oh-ate
Butyric acid:  byou-teer-ic acid
Butanoic acid:  byou-tuh-no-ic acid

The answer is B.

3.  Why do research articles use butyrate, butanoate, butyric acid, and butanoic acid interchangeably?

A.  Because they made mistakes in their writing and the editors missed it.
B.  All scientists, especially in nutrition, want to confuse everybody.  Like The Tower of Babel.  (Pssst.  Don’t let them do it.  Just eat real, whole foods.  Healthy food.)
C.  Because the terms apply to the same basic functional structure which the body can convert from one to the other with no difficulty at all.
D.  After lipase works on the short chain fatty acid butyrate, butyrate, butanoate, butyric acid, and butanoic acid are all made.  Although varying in structure, they do the same things in the body.

Butyrate, butanoate, butyric acid, and butanoic acid are interchangeable terms for our purposes.  In fact, butyrate and butanoate have exactly the same structure.  Butyric acid and butanoic acid have exactly the same structure.  And the only difference between butyrate/butanoate and butyric acid/butanoic acid is a hydrogen atom.  They all have the same structure plus or minus a hydrogen atom, and the body has no problems converting them back and forth.

The correct answer is C.

Back to Boring.  How Can You Get Butyrate?

There is no dietary guideline for butyrate, and you won’t see it mentioned on the nutrition label.   The best sources for butyrate come from eating certain foods that the bacteria living in your colon like to also eat (fiber and resistant starch).  However, this is not the only way.

I see 4 potential sources of butyrate for the body:

  • Eat butyrate containing foods
  • Eat butyrate producing foods
  • Take butyrate supplements
  • Take probiotics which contain bacteria known to make butyrate

Today we will look at “Eat butyrate containing foods.” 

What foods contain butyrate?

A.  Butter and cheddar cheese
B.  Bacon and ham
C.  Potato and sweet potato
D.  Beans and peas

There are not many food types with butyrate in them.  It pretty much comes down to food made from the milk fat of animals who eat grass, for example cows, sheep, and goats. These are called ruminant animals: animals who eat grass, have hooves, chew their cud, and have specialized stomachs.  The bacteria in their guts are very effective at making butyrate. (1, 2, 3)  So the correct answer was A.

Milk fat foods with butyrate:  Listed below are the butyrate contents for milk fat foods that I found on-line.

(Two asides:  1.  Here is a cool graphic “poster” glorifying the attributes of BUTTER:  Bulletproof–Grass-fed Butter in Bulletproof Coffee Review.  2.  If it is helpful at all as a useless reference, BodyBio makes a butyrate supplement.  BodyBio recommends a dose of 3600 mg daily of its butyrate supplement.  That may help you put the amounts I list below into some sort of perspective.)

  • 100 grams (one stick) of butter has 2700 mg
  • One pat of butter has about 216 mg (a pat of butter is 10 grams, 1/3 of an ounce, or 1/2 tablespoon) (3, 4, 5)
  • 100 grams (a little less than 1/2 cup) of cream has 1500 mg
  • 100  grams of whipping cream has 1200 mg  (I don’t know the difference between cream and whipping cream)
  • 100  grams (about 3.5 ounces) of cheddar cheese has about 1100 mg
  • 100 grams (about 3.5 ounces) of Camembert has about 780mg
  • 100 grams (about 3.5 ounces) of parmesan has about 730 mg
  • 100 grams of full fat ice cream has about 370 mg
  • 100 grams of “regular” milk has about 120 mg
  • 100 grams of whole milk yogurt has about 100 mg (5)

That’s it?

Well, that’s “pert near” about it.  Some fermented foods are claimed to have butyrate, but I couldn’t find Fermented foodsquantification of this, nor could I find any good list of sources from people who claimed this.  I spent hours searching, and I tried about a dozen or more different search terms.  I’ll list what I could find that showed/didn’t show butyrate in fermented foods.  If you have anything to offer in this area, please do!

Fermented Foods:

  • A study on commercial sauerkraut which showed no butyric acid in sauerkraut:  Chemical and Sensory Characterization of Commercial Sauerkraut. (6)
  • I found a rat study looking at the effect of fermented sugar beet fiber on cholesterol.  To make the rats’ food, they fermented sugar beet fiber with rat cecum bacterial contents in a fermentation jar.  The fermented “food” they made for the rats had higher levels of short chain fatty acids (including butyrate).  (Umm.  Is that how you make your sauerkraut?  Maybe we need to use their starter?  Makes you look at a Pickl-it-Jar in a whole new way…)  (7)
  • Kombucha.  I found a site called Happy Herbalist with a  post called “Analysis of the Kombucha Ferment.”  It lists butyrate (butanoic acid) as a potential substance in kombucha.  But I couldn’t determine the source of this information.  If you’re interested in kombucha, here’s a link to a research article about it.  Nothing about butyrate in it, though:  Changes in major componnets of tea fungus metabolites during prolonged fermentation.  In addition, I found something called “Teapedia.”  It also lists butyric acid as a potential component of kombucha:  Kombucha. 

So as far as fermented foods and butyrate go, I think there is probably a tad in some. Not much, if any, in the sauerkraut, kimchi, and pickles I eat. If there’s a strong smell like parmesan cheese or stinky locker room, there’s probably a good chance there’s butyrate there. Trust your nose.

Final Thought

Does the presence of butyrate in what you eat even make a difference?  If you surf around regarding oral butyrate (either via food or via supplements), you’ll see concern about how butyrate does not make it to the colon.  It seems to be important to have butyrate actually physically in the colon. (8,9,10)  Many human studies on oral butyrate use an enteric coated formulation so it can make it all the way to the colon (11).  Two things cross my small mind here:

  1. Although most butyrate seems to be absorbed by the small intestine, the absorption of butyrate is “saturable,” meaning at some point the transport of butyrate will become overwhelmed, and butyrate can scoot on by to make it to the colon without being absorbed.  (12,13)
  2. It appears that the butyrate that is absorbed makes it to the blood for beneficial effects, even on the colon, and this seems beneficial to the body too.  From a study looking at short chain fatty acids (SCFAs) and butyrate on mice with induced colitis: “It is now clear that the trophic [positive growth] effect of SCFA is due not only to the simple provision of energy to the host but also to the combination of local action and systemic metabolism of SCFA… We have demonstrated that this protection can be obtained by oral doses of SCFA.” (emphasis mine) (14)

Point one makes me think that if enough butyrate is taken through foods, there is a point at which absorption is overcome, and so some butyrate does actually make it to the colon.  Point two makes me think that even if it does get all absorbed, even that which is absorbed makes a difference both to the entire body and to the colon.

If you can’t eat dairy.  Don’t despair.  The next post will look at butyrate producing foods we can eat.

Take good care.

~Terri

Part 5

Sources:  (Most sources can be found in entirety or in significant portions on-line if you look for links to PDF files or look for little boxes that say “Full text.”)

  1. Milk Fats:  http://www.cyberlipid.org/glycer/glyc0073.htm
  2. Understanding the Ruminant Animal Digestive System from Mississippi State University Extension Service:  http://msucares.com/pubs/publications/p2503.pdf
  3. Foods High in Butyric Acid:  http://wholefoodcatalog.info/nutrient/butyric_acid/foods/high/
  4. The Ambiguity of a Pat of Butter:  http://www.ochef.com/1460.htm
  5. Butyric Acid Content of Food:  http://wholefoodcatalog.info/nutrient/butyric_acid/foods/
  6. Chemical and Sensory Characterization of Commercial Sauerkraut.  Trail, Young, Fleming, and McFeeters.  Journal of Food Quality.  1996.  19:  pp. 15-30.  http://www.ncsu.edu/foodscience/USDAARS/Acrobatpubs/P254-286/P258.pdf
  7. Fermentation Products of Sugar-Beet Fiber by Cecal Bacteria Lower Plasma Cholesterol Concentration in Rats.  Hara, Haga, Kasai, and Kiriyama.  The Journal of Nutrition.  April 1998.  128:4 (688-698).  http://jn.nutrition.org/content/128/4/688.full
  8. Butyrate and the Colonocyte.  Velazquez, Lederer, and Rombeau.  Digestive Diseases and Sciences.  April 1996.  41: 4(727-739).  http://link.springer.com/article/10.1007/BF02213129
  9. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3070119/  Potential effects of butyrate on intestinal and extraintestinal disease.
  10. Short-chain fatty acid formation at fermentation of indigestible carbohydrates. Henningsson, Bjorck, and Nyman.  Scandinavian Journal of Nutrition.  2001.  45: 165-168.
  11. Oral butyrate for mildly to moderately active Crohn’s disease.    Sabatino et al.  Aliment Pharmacol Ther. 2005 Nov 1;22(9):789-94 http://www.ncbi.nlm.nih.gov/pubmed/16225487
  12. Absorption of short chain fatty acids from the human ileum.  Schmitt, Konrad, et al. Digestive Diseases.  1977. 22:4 (340-347).  http://link.springer.com/article/10.1007/BF01072192#page-1      STEFF, MEMS
  13. Absorption of short chain fatty acids from the human jejunum. Schmitt, Soergel, and Wood.   Gastroenterology.  February 1976.  70: 2 (211-215).  http://www.gastrojournal.org/article/S0016-5085(76)70032-5/abstract
  14. Protection by Short-Chain Fatty Acids against 1-B-D-Arabinofuranosylcytosine-Induced      Intestinal Lesions in Germfree Mice.       Ramos, Bambirra, Nicoli, Cara, Vieira, and Alvarez-Leite.  Antimicrob Agents Chemother.  April 1999.  43:4(950-953).  http://aac.asm.org/content/43/4/950.full
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