Category Archives: Constipation

Butyrate Series, Part 4

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 Review2.  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

Butyrate Series, Part 3

Bacteria

Bacteria (Photo credit: Wikipedia)

It all sounds like voodoo until you can find the sense (science) to understand it.

Recap Parts 1 and 2:

Part 1: Colons and colon bacteria make or break your health.  (Poop tubes and cooties.  Yes I know.  Voodoo.  True-doo.)  Although it is little known and little stressed, the intestines and the bacteria naturally found in colons are the foundations to a healthy human body, from the brain to the liver to the skin to food intolerances to fighting infections.  And you don’t have to have stomach pain, constipation, or diarrhea to have a broken gut.

Part 2:  Please pardon oversimplifications.

  • The colon is a world of bacteria; there are good bugs and bad bugs living there. Bad bugs take up space, overgrow, crowd out the good bacteria, eat up all the food, and make chemicals that don’t agree with the GI tract.  From a Discovery post on using how antibiotics harm the gut flora:  “…The facts and figures relating to the numbers and functions of the commensal bacteria, and those in the gut in particular, remain awe-inspiring.”  (1)  This stuff is simply amazing, folks.  Revolutionary.  And I didn’t learn a drop about it in medical school or residency.  What failures our academic institutions are in so many ways.
  • What we eat affects the bacterial world of the gut.  Processed foods lower levels of good bacteria. (2)
  • Bacteria in our colons make beneficial short chain fatty acids, including butyrate, from plant-based food sources.   Short chain fatty acids help in inflammation, fighting cancer, and protecting the GI tract. (3, 4)  They also promote the growth of good bacteria! (5)  And the demise of bad bacteria.  (6)

“Eat your fruits and vegetables, child.”  What colon cancer and ulcerative colitis may tell us about diets low in vegetables and fruits:

Colon cancer and inflammatory bowel disease tend to really hit the last part of the colon the hardest, particularly in developed countries.  So what?  Why would this be?  What can this suggest to us?  Colon cancer seems so far away, so removed from me (although with my chronic constipation issue, in reality it is looming over my shoulder:  Chronic Constipation Linked to Increased Risk of Colorectal Cancer— in case any readers have the audacity to question my open discussion of constipation).

Why should I ask you to think about colon cancer and inflammatory bowel disease?  Well, as we mentioned in the first two posts, body health depends on intestinal health, which in turn relies on bacterial health.  Colon cancer and inflammatory bowel disease are two significant problems arising in the colon.  Perhaps if we know what leads to these intrinsic intestinal problems, we have clues as to what leads to other problems in the human body.  So let’s look at what happens when a person doesn’t eat enough vegetables and fruits, based on bacteria and SCFAs and colons:

1.  Not enough plant matter is making it to the end of the colon for the bacteria to make the protective short chain fatty acids we discussed in our last post.  This can happen in somebody who eats mostly processed foods that are easily broken down and absorbed by the small intestine.  Or it can happen if someone is on a low carbohydrate diet.  (However, “low carbohydrate” is not the same as “no carbohydrate” because some low carbers work very hard to incorporate plants into their diet, such as onions, garlic, and diverse vegetables low in starch–although later in the series, low carbers may be intrigued by resistant starch.)  By increasing plant matter in the diet, more will reach the bacteria in the far ends of the colon to bathe the colon in sustaining and restoring SCFAs.

2.  Bacteria resort to less effective sources for fermentation since there’s not enough plant matter around (AND at a COST to us).  They start fermenting protein, mucous, and sloughed off dead cells.  Thankfully, SCFAs are still made for us, although not in as high of a quantity as from plants–but in exchange, toxins are made.  (Medical doctors just don’t use the word “toxin” loosely; we like to know specifics.  Specifically, ammonia, phenols, indoles, and nitrogen and sulfur-containing compounds are made from these inferior SCFA food sources, and they are detrimental to the colon and the body.) (6, 7)

Large intestine

***For those on or considering a low-carb diet, here are two studies of interest.  I know that some people feel and function better on a very low carb diet. But I think we need to be aware of potential pitfalls and personally explore if there’s a way to avoid these pitfalls without sacrificing quality of life and body function:

(Key point:  Colon cancer and ulcerative colitis hit the descending colon the hardest, possibly because the bacteria down here at this point don’t have enough carbohydrate to make abundant SCFAs AND they make compounds that are harmful to the gut when they ferment proteins. Since health begins in the colon, we can explore these two diseases as a possible illustration of why we need to eat more vegetables and fruits.)

Leaving microbiology and pathology and focusing on butyrate now:

All SCFAs are important, but butyrate seems particularly so.  Even if you don’t have bowel issues, if you just look over the effects of butyrate in the body, you will see it can affect many, many places!  Here is my original butyrate post:  Butyrate is important for YOU.  (By the way, the word butyrate is interchangeable with butyric acid and butanoic acid, if you ever see those anywhere.)  To briefly recap, butryate:

  • Reduces inflammation: both locally in the GI tract and likely in the rest of the body as, as well
  • Helps cancer cells get shut off and/or die
  • Helps stabilize blood sugars
  • Helps fight the hunger urge
  • Helps neurons damaged in the brain after strokes
  • Modulates oxidative stress in the colon (anti-oxidant actions)
  • Helps speed up GI transit
  • Helps regulate GI permeability

So you think this all sounds good.  Stop colon cancer and other cancers.  Help your blood sugars.  Suppress hunger.  Repair nerves.  Fine.  More specifics please.  How can a person get butyrate?

In my mind, I see four ways to increase butyrate.

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

Closing:  The next post will hone in on butyrate containing foods and maybe get started on butyrate producing foods.

~~Terri

Part 4

1.  The Impact of Antibiotics on the Gut Microbiota as Revealed by High Throughput DNA Sequencing.  Cotter, Paul et al.  Discovery Medicine.  March, 2012.  13(70):  193-199.

2.  Gut Reaction: Environmental Effects on the Human Microbiota.  Phillips, Melissa.  Environmental Health Perspectives.  May, 2009. 117(5): A198–A205.   http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2685866/

3. The Effects of Short-Chain Fatty Acids on Human Colon Cancer Cell Phenotype Are Associated with Histone Hyperacetylation. Hinnebusch, Shufen, et al.  J. Nutr. May 1, 2002 132(5): 1012-1017. http://jn.nutrition.org/content/132/5/1012.long

4. Anti-inflammatory properties of the short-chain fatty acids acetate and propionate: A study with relevance to inflammatory bowel disease.  Sofia Tedelind, Fredrik Westberg, Martin Kjerrulf, Alexander Vidal .  World J Gastroenterol  2007 May 28;13(20): 2826-2832.  http://www.wjgnet.com/1007-9327/13/2826.asp

5.  Short chain fatty acids and colonic health.  Hijova E and Chmelarova A.  Bratislava Medical Journal.  2007.  108 (8): 354-358. http://www.bmj.sk/2007/10808-06.pdf

6. Colorectal Carcinogenesis:  A Cellular Response to Sustained Risk Environment.  Fung, Cheng Ooi, Topping, et al.  SInt J Mol  Sci. 2013 July; 14(7): 13525–13541.  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3742201/

7.  Starches, Resistant Starches, the Gut Microflora and Human Health.  Bird, Brown, and Topping.  Current Issues Int Micro.  2000; 1:25-37. http://www.horizonpress.com/backlist/ciim/v/v1/03.pdf

8.  Review article:  the role of butyrate on colonic function.  Hamer, Jonkers, Venema, Vanhoutvin, Troost, and Brummer.  Alimentary Pharmacology and Therapeutics.  2008.  27, 104-119.  http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2036.2007.03562.x/abstract;jsessionid=92F8CCF91EDCE88AD7989649725CAEB3.f04t02

Butyrate Series, Part 2

It all sounds like voodoo until you can find the sense (science) to understand it.

Miscellaneous Info

A Working Goal of my blog:  Inspiring all people, but particularly parents with school-aged children, to understand that it is a true medical necessity to return our diets to a whole foods diet, free of processed foods, and lower in overall sugar (sugar, honey, maple syrup, agave, juice, corn syrup, date sugar, rice sugar, we-can-make-sugar-out-of-anything-sugar, and we-can-make-anything-taste-good-with-enough-sugar sugar).

What the upcoming series of posts will be about and why it is important to you:  The upcoming series of posts is going to be about butyrate.  It is a very important chemical that our body needs to function properly.  You probably haven’t heard about it, but it is important.  I guess if I had to try to compare it to something that you did know about, I’d liken its importance to vitamin C.  I am not saying it is vitamin C, but I am trying to relay the importance of the stuff.  The best source of butyrate comes, not from food, but from bacteria in the colon working on vegetable and plant matter.  It comes from bacteria that live naturally in your colon which ferment vegetable and plant matter and turn it into butyrate, which your body in turn uses to maximize health and function in many splendid ways.

Butyrate, then, is one specific retort to the statement and question:  “I don’t like vegetables.  Why do I have to eat my vegetables?”  You now have something concrete to say besides, “They’re healthy.”

Try this for a change:  “Aw, sweetie.  I know you don’t.  But the bacteria in your colon do!  And they will gobble them all up for you and turn them into butyrate.”

Or, “Tough.  I don’t care.  Eat them anyway.  Your bacteria do (like them).  You’ll be low on butyrate if you don’t.”

Short Chain Fatty Acids Overview

Recap from Part 1 (Part 1) Yesterday we talked about how we need the bacteria in our colon and how we want to help keep the “good” bacteria thriving.  Plant matter, like vegetables and fruits, feed the good bacteria and allow them to make important substances, like butyrate, which we absolutely depend on, see “Butyrate is Important for YOU.”  Sugars and processed carbohydrates can feed the growth of “bad” bacteria in our colons.  Bad bacteria are more likely to make chemicals that can be harmful to us, like ammonia, methane, hydrogen sulfide, and others.  Butyrate is a short chain fatty acid made by favorable strains of bacteria in the colon.  This series is honing in on butyrate because it seems to be a strong healer of the GI tract.  (1,2)

Butyrate is a short chain fatty acid:  There are several types of short chain fatty acids (SCFAs) besides butyrate, and each SCFA, in its own way, looks vitally important to the positive functioning of our bodies.  The most important way we get SCFAs is by eating food that comes from plants.  The “plant food” itself doesn’t give us SCFAs!  The bacteria ferment the plant-based food to make SCFA.  (Later we will learn that SCFAs are made best from certain types of plant foods, but for now we will just lump it all together.)  A brief explanation of digestion is needed to later understand which foods butyrate can be made from.  Allow us to deviate.

Line art drawing of an intestine

Line art drawing of an intestine (Photo credit: Wikipedia)

Brief explanation of digestion of carbohydrates up through the small intestine:  For butyrate’s purposes, we are concerned with carbohydrate digestion (even though butyrate is a fatty acid—forget that for now).  Let’s look at an apple.  Bite apple.  Chew apple.  Your saliva starts working on digesting the apple.  Swallow apple.  Apple goes to stomach.  Apple moves to small intestine where the bulk of digestion is done. The apple has some simple sugars (fructose, glucose, sucrose), a small amount of starch (starch is an energy form for the plant and is made up of glucose strings), and some fiber (and other stuff, but we’re focusing on the carbohydrate component for the purpose of this butyrate series).

  • The sugars of fructose and glucose get completely absorbed in the small intestine by most people.  The apple’s intrinsic sucrose sugar is broken down and then completely absorbed.  (Simple.  Simple sugars!)
  • The starch needs to get worked on by an enzyme called amylase, which is made by the salivary glands and pancreas.  The pancreas dumps its amylase into the small intestine (specifically the duodenum).  The amylase breaks down the apple starch into smaller units so it can be made into glucose by more small intestine enzymes. The glucose is then absorbed by the small intestine.  Nearly all of the starch in the apple will be broken down and converted to glucose to be absorbed.  More complex, eh?  Complex carbohydrates! (Even more complex is the fact that not all starches get completely digested and absorbed, although we used to learn that they did!  That will be explored later and is very important.)
  • Any kind of fiber in the apple (pectin and cellulose for example) doesn’t get broken down or absorbed.  We don’t have enzymes to do anything to the apple fiber.  It moves into the colon (large intestine) for the bacteria to feast on and make SCFAs.

The lovely colon (Aside:  I see it like a Star Wars world down there.): After the small intestine absorbs what it can, leftover foodstuff travels to the colon for further processing. The colon was not designed to function alone; it was designed to work in concert with billions of bacteria that naturally and ideally live there.  (You are not alone…)  The bacteria make many products that we humans absolutely rely on, such as B vitamins and vitamin K, but here today we will be looking at SCFAs.   The colon’s bacteria ferment what they can of the leftover foodstuff; that’s a fancy way of saying they eat the leftovers and turn it into energy for themselves.  They like to ferment starches, sugars, and fiber the best.  When they “eat” the fiber or starch, they make the necessary SCFAs for us to use and the colon absorbs them.  (The bacteria do care about us, by the way.  Don’t think they don’t.  Without us they’d die.  Is the feeling reciprocal?  I’m poking.  Grin.)

(Key point:  We have to have SCFAs, and we get them from the bacteria in our colons who make them best from plant-based foods.)                

Summarizing through highly sophisticated pictures: 

Small intestine as it relates to SCFA

Drawing of colon and SCFA

                                                                                                                      

“Sillily” simple structures:  SCFAs possess simple, simple structures that any high school chemistry student could draw, but their functions are so complex that even our most trained professionals are challenged to give us answers about them!

Scan

 

(Please note:  I STILL have not had time to upload the figure with the corrected structures for the SCFAs.  The structures you see are the alkanes.  Correct structures should show the final carbon on each as a carboxyl group, which is a COOH.)

No, you can’t just eat sugars and make these wonderful SCFAs:  Now I know at this point you’re thinking, “Whoo-ha!  Free ticket to eat sugar and starches.  She just said the bacteria like sugars and starches (oh, yeah—and fiber) the best!”

(Shout)  “NO!”  Because if you remember when we talked about the digestion of carbohydrates in the small intestine, I told you that most sugar and starch is broken down and completely absorbed by the small intestine.  So most of the processed foods, candy, soda pop, donut, what-have-you—those sugars and starches are for you.  They provide your calories (which many of you don’t want), not the helpful bacteria’s calories.  And, by chance, any simple sugars that do make their way down the intestines, they promote the overgrowth of “bad” bacteria and a decline of “good” bacteria.

Fate of the SCFAs after they are made by the bacteria:  Each SCFA has its own path once absorbed by the body.  Acetate mostly goes to the liver and to the blood to be circulated on to the peripheral tissues of the body.  Propionate gets sent to the liver.  Butyrate is immediately used as fuel and support for the lining of your colon (colonocytes; epithelial layer) and is also sent to the liver.  (I am focusing on butyrate because it is so vital to the maintenance and restoration of the GI tract.)  Valerate and caproate have not been quite sorted out yet.  We do know that valerate is poorly recovered in fecal matter, and so it may be highly used up like butyrate in the colon. (3)

(Key point:  SCFAs have different destinies in the body, and they are all important.  However, I’m focusing on butyrate because studies show that it hugely affects the function of the gut.  It may help so much more in the body, though!!  What starts in the gut–benefits or detriments elsewhere!  Acne, headaches, reflux, skin rashes, food intolerances, yada, yada, yada, can all be a sign of a disordered gut!!!)

Stop:  Okay.  We’re stopping here today.  The next post will discuss why a person would be low in SCFAs and butyrate and discuss some problems with this.  Then we’ll talk about how to get butyrate from food.  Which will lead us to resistant starch.  Thank you for reading.  Butyrate–it’s great.  🙂

Terri

Part 3

Sources:  All of these are available free on-line in full text.  Let me know if the links don’t work.

(1)  Targeting Enteric Neuroplasticity:  Diet and Bugs as New Key Factors.  deGiorgio and Blandizzi.  Gastroenterology.  May 2010.  138(5):  1663-1666.  http://www.gastrojournal.org/article/S0016-5085(10)00377-X/abstract

(2)  Review article:  the role of butyrate on colonic function.  Hamer, Jonkers, Venema, et al.  Alimentary Pharmacology and Therapeutics.  2008.  27:  104-119.  http://www.ncbi.nlm.nih.gov/pubmed/17973645

(3)  http://arno.unimaas.nl/show.cgi?fid=16226  Chapter 3 page 62

For GI Readers

My post and blog, they are not intended to treat or diagnose you.  It is meant to stimulate your desire to read and learn.  With your knowledge and research articles in hand, go visit your favorite healthcare practitioner.  Ask them what’s right for you.  The things I try may be detrimental to your health or have serious consequences that I may not even know about.

Dear Reader,

For about 20 months I have scoured the internet, looking to solve my lifelong, severe, medication-dependent constipation issue.  Constipation persisted for years as my only symptom, albeit worsening each decade of my life, until in my thirties other symptoms started creeping in like bloating, headaches, and fatigue.  In my stint as a practicing medical doctor, I saw at least two colectomies specifically for chronic constipation.  This scared me a lot because I do not want to have colon surgery.  However, nothing in my arsenal or in the arsenal of the doctors I chose could help me.

So about 20 months ago I started working with my diet (gluten-free, dairy-free).  About 17 months ago I started what sounded like a crazy, voodoo diet called GAPS, in an attempt to prove to myself that no diet “so extreme” could possibly be effective.  I wanted to check diet intervention off of my list as an alternative treatment choice.  “I am a trained medical doctor; I know that won’t work.  Diet won’t work.”  Actually, I had some minor success using GAPS, figuring out food intolerances, and piling on the magnesium to effect (which I had tried very unsuccessfully to do in the past).  I decided to stay on board with this strange, new way of eating (with a couple of boots by my husband when I cried around about it being too hard).

I have putzed along on GAPS, steady enough, but no real gains, trying this a bit and that a bit–all within the confines of GAPS.  I recently followed a lead regarding short chain fatty acids, particularly butyrate, helping restore the enteric nervous system.  In severe, lifelong constipation, researchers have found actual neurologic changes so I really thought this might be the tip I needed.

Resistant starch increases butyrate production in the colon.  But I am on GAPS, and many of the starches aren’t legal.  Plus, during my initial findings on butyrate, I was trying out very low carb to see if that would be my ticket.  So what to do?

How about just go get some butyrate?  I mulled it over.  It’s supposed to be absorbed before it reaches the colon and therefore not have its desired effect, at least in the common preparations.  But I went for it; I had nothing to lose except barrels of magnesium.  I bought some magnesium-calcium butyrate from Amazon, and I started taking two capsules three times daily.  It said to take it with food, but I thought I’d mix it up a bit.  I took it sometimes with meals and sometimes right before bed on an empty stomach.

For twenty days I have been on magnesium-calcium butyrate (250 mg total per day of magnesium versus the plus two grams of magnesium I’ve been taking).  For 19 days my GI tract peristalsis hasn’t missed a beat.  Best ever, even while on medicines.  I am trying to contain my excitement because perhaps it will stop working.  But I don’t know.  I mean, I’m completely off of my magnesium!  I am on nothing but a GAPS diet tailored for my hard-earned knowledge of my food intolerances, fish oil/vit D about three times a week, and VSL #3 probiotic at night.  None of that is new besides the butyrate.  I have not changed my diet, if anything I’ve pushed nuts too much trying to get butyrate to prove itself.  And it has.

I don’t like supplements.  My next goal is to see if I can add resistant starch to my diet and get the same effect.  I am very hopeful.  However, I think my pure GAPS saga may be winding to a close.  I believe my diet will now be GAPS but I will need to add in things like green bananas, cold potatoes, potato starch, and sweet potato.  I am not entirely sure yet.  I’m going to ride out a complete month on butyrate to complete a full monthly cycle.  However, when my problem was always at its worst before, it was smooth sailing!  I am very optimistic about this one.

I am currently composing a series encompassing all that I have learned going down this rabbit hole.  It will cover short chain fatty acids, butyrate, sources of butyrate, resistant starch, things known to increase and decrease butyrate/SCFAs.  My sisters are editing it for me now.

There is no perfect diet for anyone, but I think finding a good diet platform (such as Paleo, autoimmune Paleo, SCD, Whole30, Terry Wahls’, Perfect Health Diet, GAPS, etc) will allow you to slowly and surely figure your body out.  And then with some nips and tucks, you can achieve your endpoint.  I think.  But it takes the patience of Job.  Seriously.  The patience of Job.  And a good supporter; my husband has been super in helping me stay the course.  It has been hard because I am a “sweetaholic.”  I can’t tell you the diet and the supplements you need.  But I will be more than happy to be your cheerleader and encourager if you drop a comment or an e-mail.

In closing, a good diet, I think, must not only incorporate foods that are full of their own natural nutrients, but a good diet must also TAKE OUT COMPLETELY foods that are either commonly known to be inflammatory or known to cause symptoms–whatever they may be, acne, depressed-like mood, sore throat, eczema, bloating, etc–in a particular individual.  At this point, a broken body will need a little extra nutrition/supplementation in certain departments.  Perhaps a little magnesium, perhaps a little resistant starch, perhaps a little coconut oil, perhaps a little glutamine, perhaps a little fish oil, perhaps a few B vitamins, perhaps low-carb, and so on.

I wish you only success.

Sincerely,

cropped-hsd-line-drawing_edited-1.jpgTerri

 

Butyrate and Constipation

I have been excited about butyrate because rat studies showed that it increased the motility of the colon (please let’s not dwell much too long on the fact I’m reduced to rat status and writing about constipation).  I am going to summarize and explain an abstract to a study, from which the following quote is taken:

“Little is known about the environmental and nutritional regulation of the enteric nervous system (ENS), which controls gastrointestinal motility. Short-chain fatty acids (SCFAs) such as butyrate regulate colonic mucosa homeostasis and can modulate neuronal excitability. We investigated their effects on the ENS and colonic motility.” 

~  from Gastroenterology,  2010, “Short-chain fatty acids regulate the enteric neurons and control gastrointestinal motility in rats.”  Emphasis was mine.

Aside:  Please note that I am probably a fool and excited about nothing, but it is a path worth exploring for my slow transit constipation.  Also note, I do my best to simplify studies and concepts, some of which are difficult for my basic molecular biology background.  My husband, being an exceptionally logical and fact oriented doctor, hates it when I do this.  Big time scowls.  He is right, sometimes the explanations become kind of inaccurate.  So I will do the best I can.  If you have any questions or note any errors, I would like to know.  Gaps in my understanding will be bridged this way.  And one last note, don’t use my blog stuff to cause any harm to yourself.  Please.  See your doctor.

What did these researchers do? 

  1. Fed rats a resistant starch diet.  (I will write a resistant starch post soon.  Soon is always relative.)
  2. Inserted short chain fatty acids (i.e. butyrate) into rats’ cecums (a part of their colons).  (I only have an abstract so we are left to our imaginations for this lovely process.)
  3. Applied butyrate to some “free-standing” cultures of enteric nervous system cells in a “test tube.”
  4. In the “test tube” cells, they examined how the cell “looked”–its “phenotype.”  What kind of receptors did the nervous system cells have on their outer membranes?  What kind of proteins are expressed?  Knowing this kind of information helps us to know what the cell is capable of responding to and what substances the cell makes.  Special antibodies that will seek out these known proteins and receptors on the cells are used.   Researchers also used polymerase chain reaction (PCR), a way to amplify and increase certain material.  Specifically, these researchers looked for antibodies to Hu, choline acetyltransferase (ChAT), and nitric oxide synthase (NOS).  If you refer back to “Changes in Severe, Chronic Constipation,”  you will see a couple of these discussed:  Less neurons immunoreactive for ChAT and more neurons immunoreactive for NOS.  They also proceeded to analyze signaling pathways using various tests.
  5. Observed the motility of the colon both in the rat and outside the rat.

What were the results?

  1. Resistant starch diet (which increases butyrate) and butyrate (but NOT acetate and propionate, other short chain fatty acids made from resistant starch by the colon’s bacteria) both:
      A.  Increased the ChAT neurons, these are the ones partly responsible for increasing peristalsis.  Neurons with ChAT should make more acetylcholine, the neurotransmitter that encourages the bowel to move forward and empty.
      B.  Did not alter the NOS neurons’ proportion and number.  NOS would bring about nitric oxide, which slows down the bowel’s movements.  It makes the bowel relax rather than move.
  2. Bowel neurons have a transporter called monocarboxylate transporter 2 (MCT2), which helps bring butyrate into the colon cell after the bacteria graciously make it.  Well, the researchers were able to “stop” these transporters so butyrate wouldn’t move into the cell so much.  By stopping the MCT2 transporters, the increase in ChAT neurons–and therefore neurons that would increase colon motility–was halted.
  3.  Butyrate increased histone H3 acetylation in enteric neurons.  When DNA is acetylated, it allows the DNA to be transcribed.  So butyrate alters the actual genetic expression of cells.
  4. Resistant starch diet increased colonic transit.
  5. Ex vivo it was noted that butyrate increased the circular muscles contraction when exposed to acetylcholine.

Their Conclusion

“Butyrate or histone deacetylase inhibitors might be used, along with nutritional approaches, to treat various gastrointestinal motility disorders associated with inhibition of colonic transit.”  And that’s as far as I’ve seen it up to this post.  I’ll keep looking.

My Conclusion

I’m not trying to live forever.  I don’t have cancer yet.  I’m eons away from a stroke.  But my gut has a mind of its own.  In addition to more information on butyrate (and resistant starch), I need to explore the outcomes of slow transit constipation in 80 year-old women.  Do they have a study on that?  Right now, things are tolerable with all the changes I’ve made the last 18 months or so of my life, but what happens later?  Or when the magnesium stops working again?  Anyhow, here are my closing thoughts:

  1. Butyrate is made in the gut and absorbed by the gut.  The gut has been my constant, lifelong problem.
  2. Butyrate may affect the immune system and decrease inflammation.  We have studies supporting food intolerances causing severe, chronic constipation and these studies document subtle inflammatory changes in the mucosa.
  3. Butyrate may affect the nervous system through modulation of gene expression.  We know the enteric nervous system is messed up in slow transit constipation.
  4. Butyrate may stimulate the contractile activity of the colon and accelerate GI transit.  We know slow transit constipation has a reduction in high amplitude propagating contractions and a disruption of the coordinated peristaltic activity.
  5. Butyrate is increased by eating resistant starch, a type of “fiber.”  (This is a bit confusing, but I will clarify later.  Resistant starch would be high in diets rich in lentils, beans, tubers, etc.  Please see Butyrate Series, Part 6 for a better, more thorough explanation)  Fiber has long been recommended for constipation.  Perhaps it’s not the fiber.  It could be the fiber.  Or it could be a rich bacterial population capable of making more butyrate for an individual.
  6. Butyrate has been shown to possibly decrease colon cancer.  Colon cancer is higher in patients with chronic constipation (Chronic Constipation Linked To Increased Risk of Colorectal Cancer–summary article from Science Daily).

And finally, I’ll leave you with this quote:

If the promising results by Soret et al [the paper whose abstract I summarized and explained above] can be confirmed and expanded by controlled therapeutic trials, then butyrate-generating foods might become an effective and simple option to prevent or treat functional gut disorders via modulation of enteric neuroplasticity.” (2–a very good little commentary to read!)

Terri

Butyrate Series Page

Sources:

1.  Soret R, Chevalier J, De Coppet P, Poupeau G, Derkinderen P, Segain JP, Neunlist M.  Short-chain fatty acids regulate the enteric neurons and control gastrointestinal motility in rats.  Gastroenterology. 2010 May;138(5):1772-82.  Sadly, abstract only:  http://www.ncbi.nlm.nih.gov/pubmed/20152836

2.  de Giorio R, Blandizzi C.  Targeting Enteric Neuroplasticity:  Diet and Bugs as New Key Factors.  Gastroenterology.  2010 May; 138(5):1663-1666.

Also, if you will please see “Why Does My Gut Defy Gravity:  Changes in Severe, Chronic Constipation” and But What Causes All of Those Changes Found in Chronic, Severe Constipation?and “Cow’s Milk and Refractory Constipation”   then you can find further information plus sources for that information and information mentioned above.

Thanks,

Terri

I also have run a whole series on butyrate.  I need to come back and link eventually; the WordPress blogging platform used to have a feature to do that but not now.  If you look under GI Tracts Defies Gravity page, there are links there to the series pieces.

But What Causes All of Those Changes Found in Chronic, Severe Constipation?

Okay.  Great.  The slow movement of the colon in slow transit constipation occurs for a real reason.  There’s actually objective findings.  Super.

BUT WHAT CAUSED IT?  Here is where all of the great leads die.  All the fun and learning to get to this point–a hard, cold, concrete wall.  The etiology is unknown.  Don’t know.

Is there one of those changes discussed in the last post that could be a primary cause?  Or do these changes happen because of a discrete problem we haven’t connected and put together yet?  Or, more likely in my mind, are the changes a result of a multi-hit process in some of us?  I have had a problem with this since childhood, worsening, however, through the years.  Did it start as a dairy intolerance leading to inflammation?  The inflammation and food intolerance leading to constipation?  Constipation leading to chronic distention on the bowel wall?  Then worse constipation.  With the slowed transit did the bacterial flora get disturbed and changed?  Or did I have poor bacterial flora which in some way or other led to inflammation, constipation, distention, and worsening constipation?  I don’t know.  The hypotheses are endless for now.

  • Food sensitivities:  Would these be a source of chronic inflammation in the bowel which could bring about these insidious cellular changes?  Particularly if it was to something common like wheat, dairy or eggs?  I certainly don’t have an answer to this.  But studies do support food intolerances leading to severe, chronic constipation.  This next link is an excellent review article.  It starts out talking about cow’s milk and constipation, but near the end it starts talking about multiple food intolerances leading to constipation.  They go on to discuss inflammatory changes seen in chronic constipation patients, such as eosinophilia of the rectal mucosa.  (Full text, Review article: chronic constipation and food hypersensitivity –an intriguing relationship.)
  • Genetics:  Are you kidding me?  Of course!  Everything’s in your genes, slow transit constipation is no exception!  Researchers found an abnormal chromosome 1 in enteric neurons and glial cells.  (Abstract: Chromosomal study of enteric glial cells and neurons by fluorescence in situ hybridization in slow transit constipation.)  

These are the ones I found research supporting.  Fiber has been a mixed bag.  Bacterial flora is just starting to get sorted out.  So for now, this is it.  We are learning the structural, cellular, and hormonal changes that occur in slow transit constipation.  But we don’t know what initially causes all of it.

“Unfortunately, to date data are lacking on the possible factors causing neurenteric abnormalities in constipated patients. The current hypothesized mechanisms (often originating from experimental animal models) imply abnormalities in glial trophic factors leading to neural degeneration, and enteric localization of infective agents (bacteria, virus, prions) causing more or less selective degeneration of specific neurenteric cell populations (particularly EGC), whereas genetic factors or neurodegenerative changes due to aging seem to play a lesser role.”   (Full text,   Cellular and molecular basis of chronic constipation: Taking the functional/idiopathic label out.)

Citations are mostly links within the post.  Let me know if the links don’t work, please:

(1) http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2982.2008.01109.x/full

Next up when time allows, what I think about as I approach this problem personally and the Metametrix report on short chain fatty acids/butyrate stuff.

Terri

Why Does My GI Tract Defy Gravity: Changes in Severe, Chronic Constipation

What is the problem?  There definitely is a problem, even if knowing what we know of the problem won’t help you move your bowels any more frequently yet.  And of all these “problems,” we don’t know which is the primary problem, if any of them!  I guess what I’m saying is, it’s good to know, but I’m sorry it won’t help you.  Advances in science occur in spurts, and then it takes time to shape these advances into hypotheses and then theories.  Even then, we may arrive at an incomplete understanding–as we may have in leading you to believe “fat is bad for you.”

I will describe in a later post how I use this and other information to try to gain any edge I can on my bowel function.

Please let me know if any of these links don’t work, please.  It is fascinating information, and if it may help you with your disease process, I’d like to make sure you can read it!

  • Less Interstitial Cells of Cajal (ICC).  Normal movement of the GI tract requires interstitial cells of Cajal.  These cells act as pacemakers and signallers between autonomic nerves and smooth muscle, causing the colon’s neurons to fire and bring about peristalsis, and alterations in their number and function are thought to bring about drastic functional changes.  Decreased ICC numbers and abnormal integrity are considered a hallmark in the gut disorders of diabetic gastropathy and slow transit constipation. (1, 2, 4)
  • Increased number of mast cells.  Mast cells are immune cells which are often found in connective tissue, particularly in sites where there is close interaction with the “outside world”—the external environment—like in the GI tract.  They are often associated with allergic responses, including food allergies.  In the GI tract, mast cells are preferentially located next to nerve terminals in the region known as the lamina propria and play an important role in the regulation of gastrointestinal visceral sensitivity, vascular permeability, and motor function.  Interestingly, they have also have been found to be elevated in many cases of irritable bowel syndrome.  (1,3)
  • Abnormal neurotransmitters and response to these neurotransmitters , including but not limited to– serotonin, vasoactive intestinal peptide, and substance P.  (1, 3, 4, 9)
  • Too many progesterone receptors.  Progesterone slows the GI tract down.   It does this, in part, by decreasing the effect of acetylcholine (the neurotransmitter that, in the bowel, leads to increased peristalsis) and serotonin.  This may explain why constipation may worsen during pregnancy and at certain times in female cycles.  Check. (1, 5)
  • Reduced Substance P Fibers.  Substance P brings about an increased GI motility effect. (1)
  • Less neurons immunoreactive for ChAT.  Basically saying there are less neurons sensitive to acetylcholine, which is necessary for peristalsis.  (6)
  • More neurons immunoreactive for NOS.  Basically saying that there are more neurons sensitive to nitric oxide (NO), a substance that allows the distal gut to relax as peristalsis occurs.  Having more NO sensitive neurons will make the gut more likely to be “relaxed” rather than peristalsing.  (6)
  • Less neuron density  (50% less), decreased neuron numbers, reduced number of ganglia, reduced number of cells per ganglion, and reduced enteric glial cells.  (6, 9)
  • Reduction in high amplitude propagating contractions and a disruption of the coordinated peristaltic activity.  Basically saying that there are less of the sweeping contractions that bring about defecation and that the whole system just is not coordinated at all like in normal person.  (6)
  • Weaker contraction to acetylcholine in the colon. (7)
  • Relaxation to adrenalin stronger than a normal colon. (7)
  • Possible antibodies to GnRH with decreased GnRH and its receptor in enteric neurons.  GnRH is gonadotropin releasing hormone.  (8)
  • Excitatory nerve fibers present in the circular muscle are deficient in tachykinins and encephalin.  (9)
  • Expression of c-kit mRNA and c-kit protein was also found to be significantly decreased, which may lead to reduced interstitial cells of Cajal. (9)

In summary, your gut (and mine) doesn’t move, and we aren’t sure exactly why.  However, there are MANY identifiable differences in a gut with slow transit constipation and a normal gut.  The unique nervous system of the gut is disordered, in both the neurons, hormone production, hormone processing, and the supporting cells for the neurons.

More posts to follow along this topic:  What could cause this problem?  What I personally do about it.  The role of butyrate and short chain fatty acids (SCFA) on the gut/my Metametrix result for SCFA.

Take care,

Terri

Citations:

(1)  This requires a log-in.  So you may not be able to pull this little review article up:   http://www.medscape.org/viewarticle/770638_3

(2)  http://cdn.intechopen.com/pdfs/31218/InTech-The_role_of_interstitial_cells_of_cajal_icc_in_gastrointestinal_motility_disorders_what_the_gastroenterologist_has_to_know.pdf

(3)  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3033552/

(4) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3710411/#!po=11.363

(5) http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2982.2011.01705.x/full

(6)  http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2982.2008.01165.x/full

(7)  http://www.ncbi.nlm.nih.gov/pubmed/12397730

(8) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2885307/#!po=63.0435

(9) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3710411/#!po=11.3636  (I really liked this article for pulling things together and giving me leads to follow.)

Slow Transit Constipation: A True Enteric Neuropathy

Never apologize for a messy house.  (Reader, move on if this isn’t your deal.)

English: Pedestal squat toilet

English: Pedestal squat toilet (Photo credit: Wikipedia)

You’d think that being a not-so-old medical doctor, even now just eight years out of training, I would have known more about constipation than I did.  But I didn’t.  And the doctors I went to for help didn’t seem to know either.  I do remember one elderly OB/Gyn admitting that he didn’t know what to tell me to do, but to certainly do something; he had a friend who had severe constipation and had to have a colectomy (part of his colon cut out).  My OB/Gyn admitted, “I didn’t know constipation could get so bad.”  I appreciated his acknowledgement of the potential gravity of the situation.  However, nobody seemed to offer me anything helpful, and I just muddled through with various over the counter products with occasional, temporary success.  Luckily for most of my life, my slow transit was relatively asymptomatic (at least between bowel movements, which gave me quite a symptom-free interval—chuckle) and unaccompanied by too many other symptoms, until the last few years.

Since I got the awesome opportunity to homeschool my kids, I had just a couple of hours here or there to start reading for myself, so I could hopefully avoid that colectomy.  The first article that made me celebrate a couple of years ago was something about “fiber doesn’t help slow transit constipation (STC), in fact, it may make it worse.”  Validation of my own experience, counter to most suggestions from my own doctors and training!  However, mostly in my early searches, I came across depressing, belittling stuff like this (emphasis mine):

Now, I am beginning to read lines like this, helping me to see that, although research doesn’t know the answers, at least they’ve identified a REAL problem and there are researchers out there “fighting for me” (and my psychological profile):

Right.  So now I’ve got a nice review article to validate my personal knowledge that no matter what I try, nothing works great because I’ve got a real problem.  A problem that goes beyond trying  fiber, water, and yoga.  A problem beyond, “Well, you must have held your poop in too much when you were a kid so you wouldn’t have to poop in public places.”  Please.

So what is wrong down there?  A true problem with the nervous system and hormonal system of the gut, now in its early infancy of identification.  Science history in the making.

Thanks for reading.  I’m working up to my butyrate post.

Terri

Next up, Part Two:  Why Does My GI Tract Defy Physiology and Gravity?
(Alternate Titles To Amuse My Sense of Humor:  “Everybody Else Can Poop, Why Can’t I?”  or “Thank My ENS I Don’t Have To Touch The Toilet Bowl Brush!”)

Part 2: A Success Story In Using the GAPS Diet to Stop Absence Seizures!

If you subscribe to my posts or check-in regularly, you know I am following this unusual (poorly scientifically supported) diet called GAPS.  For me, it started out solely to fix my beyond slow, almost-to-stop, GI tract that NO medicine, activity, or dietary change was helping.  Over the year, on what I call my “dietary rehabilitation” program, I’ve seen lots of improvement in my GI situation, and I have observed (incredulously) the effect that foods, even “healthy” foods, has had on my family and me in many ways I never dreamed of.  These foods include dairy, wheat, eggs, chicken, and fruit:  “healthy foods.” Although I follow GAPS in a self-experiment, my blog is to encourage awareness that food treats the body like any drug, with good and bad effects varying in different people; most doctors don’t know or adhere to this.  I wouldn’t either, was I not living it.  Food culprits ought to be considered in many more illnesses.  I want to raise awareness that diet needs to be scrutinized and a dramatic change may help where no medicine or surgery does.  I am talking dramatic food changes, and some [most] people just aren’t willing to go there. Starting with a  traditional medical doctor is the correct place to start; I go to get new symptoms checked out, even for myself.  Bad problems exist, and I don’t want to miss them because I was blinded by nutrition or alternative health treatments.  My blog is not written to be a source of medical information, medical diagnosis or medical treatment, and I am no expert in nutrition or different types of diets, including GAPS.

Today, I am continuing to publish the Kinder Family’s story about how they feel nutritional intervention cured their son’s seizure disorder.  The story is unedited, despite the fact that I would have have perhaps explained things differently or sought help in different ways.  To me, the important thing is they recognized that food matters and they were willing to change.  Thank you, Dan and Tammy, for sharing:

Part 1 of “A Success Story in Using the GAPS Diet to Stop Absence Seizures!”

Part 2:  A Success Story in Using the GAPS Diet to Stop Absence Seizures!

by Dan and Tammy Kinder

…The ENT immediately recommended surgery and stated that he does dozens of sinus surgeries every month. Not wanting to go through surgery unless absolutely necessary, we started researching and reading alternative ways to resolve the chronic sinusitis. We came across lots of information that may potentially help. We read about changing our eating habit and avoiding certain type of food like dairy which causes the body to produce excessive mucus. We read about washing your sinus cavities out with salt water called a saline nasal flush. We read about many other things like supplements and other treatments, but these two made the most sense to us. So my husband stopped eating and drinking dairy products, he continued drinking carrot juice and started doing saline nasal rinse 3-4 times a day. He found out very quickly that the nasal rinsing worked was very effective. These rinses could turn a sinus infection that would normally last three or four week in to one that would last only three or four days. A sixty-nine cent can of salt was all it took to resolve the sinus infection each time symptoms appeared. Changing what we ate eventually gave his body the ability to prevent the infections from even appearing. As time went on the sinus infections disappeared altogether. This long drawn out experience with 13 different doctors contributed greatly to our decision to steer away from conventional doctors that would only give us their best guess and the best known drug at that time to try to resolve our son’s epilepsy, which leads me to my son’s story.

At about four and a half years of age, one of my sons started having what looked like staring or day dreaming episodes. When I first notice the episodes, my husband was convinced they were only day dreams and nothing serious. In fact, the episodes were so infrequent that he did not see one for himself until several months after they started. But as the months went by, the episodes came more and more frequently. They also became more pronounced in their characteristics and duration. The length of the episodes seemed to be mostly random, but would last anywhere from a fraction of a second up to as long as about eight seconds. The characteristics of our son’s body during the episodes also seemed to change as time passed. These characteristics included half-way drooping eye lids, the dropping of his arms to his side, looking towards the ground, staring at or through the person talking to him as though he was in his own world and ignoring his immediate environment. Along with these symptoms he also experienced reoccurring stomachaches. Early in this process we did not relate these stomachs to the episodes, but looking back over the years we now realize that his body was screaming for help yet we did not recognize or listen to what his body was trying to tell us. Another symptom was that certain foods would make him feel “weird.” Sometimes he would tell us that his head felt like it was spinning or vibrating. As he got older, it was certain foods he ate that made his head have these weird feeling or his body feel strange. Sometimes these odd feeling would cause him to want to do strange things. I recall one time that he told us that his body was telling him to scratch his fingernails on the concrete. That thought leads me to another symptom that was very strange. At times, he would tell us that his body was telling him to do things. On occasion he said he would hear voices telling him to do certain things. The older he got, the better he was able to elaborate on how he felt and and how he thought certain foods made him feel weird…

Part 3 to follow soon…

Dairy Causes Some Kids to Have Constipation

It's the picture of Italian ice-cream in a sho...

It’s the picture of Italian ice-cream in a shop of Rome, Italy (Photo credit: Wikipedia)

Tonight I found a site by Dr. John Briffa with a fairly recent post on cow’s milk and pediatric constipation:  Could dairy products be the cause of some children’s constipation?

I nearly wanted to explode “YES!” because I just can’t get this information out there loud enough!  Dairy causes constipation in (some) kids.  We saw this one year ago in my (then 6-year-old) daughter when we completely removed dairy several times and added it back in several times.  And what do you suppose happens to those constipated kids if dairy is never removed?  Well, maybe they turn into adults like me with severe, severe constipation.  I am not sure why (or if) dairy causes the initial constipation yet, but I do know that lifelong gut immotility has led me to have some issues with bloating, probably SIBO (small intestinal bowel overgrowth)–which makes sense because I was not getting the sweeping motion forward to keep the bacteria from creeping upwards.  I also have lots of food sensitivities (non-IgE) that I can’t help but wonder if they didn’t form through the years with the continued insult on the GI (gastrointestinal) tract.

It may be encouraging to know that my 7-year-old daughter was exceptionally sensitive to ALL dairy one year ago.   Even as a solely nursing infant, she would have longer than normal periods of no bowel movements, and I speculate it was due to my dairy intake.  She can now tolerate an occasional ice cream cone with no stalls in peristalsis.  We overhauled our diet in a big way, taking out “bads” and putting in “goods”, and maybe, just maybe, she can continue her dairy dalliances at times with exceptional nutrition otherwise.

The research article that Dr. Briffa was referring to was “The Role of Cow’s Milk Allergy in Pediatric Chronic Constipation: A Randomized Clinical Trial.”

For those who are following along regarding my GI progress, I am currently “taking my diet down” to I guess what would be considered Autoimmune Paleo, although I still adhere to GAPS.  I’ll let you know how it goes for my gut.  I’ve done it for four days now, and the last two days I’ve skipped my magnesium with success.  I believe any endeavor must have a goal.  By “taking my diet down,” I’m hoping to see improved bowel movements with either less magnesium or preferably none at all, less bloating, no irritable bowel symptoms, and no headaches.  I’m putting diet to the test.  We’ll see how much that honey, almond flour, egg, and fruit actually affect things here.

Other constipation related posts:

Slow and Steady Constipation Improvement (April 17, 2013)

Cow’s Milk and Refractory Constipation ((January 2, 2013)

A Doctor Visits the Doctor (December 5, 2012)

Whats’ Working (A Constipation Post) (November 3, 2012)

Is it Eggs (October 21, 2012)

Jordan and Steve (A Constipation Post) (October 17, 2012)

Bowels of Steel (October 8, 2012)