Tag Archives: Short-chain fatty acid

Butyrate Series, Part 6

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)

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.

A Kid’s Conversation on Butyrate (Fiber–To Way Oversimplify)

A trashcan at a food court in Salt Lake City, Utah

A trashcan at a food court in Salt Lake City, Utah (Photo credit: Wikipedia)

“Whatcha’ doin’?”
“I’m reading about butyrate.”
“What’s butyrate?”
“Oh my goodness.  It’s amazing.  Do you remember those little bacteria I told you about that live in your colon?”
“Uh-huh.”
“Well, lots of fruits and vegetables and certain foods have this stuff called fiber.  And a there’s a special kind of fiber your body can’t use.  [Resistant starch for those of you who want a more intellectual conversation.]  But those bacteria take this special fiber, and they use it for food!  Then, they make this stuff called butyrate, which they can’t even use!  And guess what!  Our body likes butyrate!  Our colons eat up that butyrate and use it for food and energy, and it helps the cells fight infections and cancer.”
“So, they eat the trash we can’t.  Then, we eat their trash, and it helps us?”
“Yes.  That’s right.  Even the body recycles.  So that’s why we have to eat fruits and vegetables [and for those who know, also beans, lentils, and I have to keep working on my butyrate post…].”

♦♦♦♦♦

I am reading and working on a butyrate post, a short chain fatty acid that the bacteria in your colon make–much to your benefit–the bacteria making butyrate that is–not my article.  I have told myself I can’t post anything else until I finish it.  But it’s Monday.  And that’s the day you all read blog articles, based on statistical analysis.  So I hate to let an opportunity slide.

My kids just woke up.  I try to read and blog in the morning before they wake up, which luckily for me as homeschooled kids, is quite a bit later than most other kids.  They file into our schoolroom where I read and write, one by one, in the morning to see what I’m doing.  Today, I was very happy that I was reading about butyrate.

I try to almost never use the word “healthy” when I talk to my kids about food choices.  If I have to use the word healthy, it means I don’t understand why it is “healthy.”  I HAVE to be able to tell them what it is that makes a particular substance beneficial or NOT beneficial.  And I have to be able to see the food from all angles:  psychological angles, physical angles, physiologic angles,  net-gain versus net-loss angles.  If I have to say “healthy for you” or “that’s not healthy for you”–I don’t understand the food well enough.  They’ll never stick with it all their life, which is what I’m trying to do here for them.  If you haven’t explained to your kids that you are SO lucky to have bacteria in your colon, you have missed a HUGE chunk of their nutritional education.  That’s a great thing to tell them, and then you can use conversations like this, which happened this morning in our home.

It’s time to take back our kids’ nutrition.  Take it back from the boxes and packages.  Take it back from the commercials.  Take it back from the schools.  Take it back from the well-meaning dance teachers, coaches, and Sunday school teachers.  (Ouch.  That sounded really harsh.)  Take it back from convenience.  Kids’ bodies and brains function way better on whole foods without dyes and preservatives.  You can do it.

Terri