For many people, going poop isn’t as regular as it should be.  But whether or not you poop isn’t the only sign that your gut motility isn’t what it should be.

The consistency of your stool can also be telling.  A looser stool is indicative of motility that’s too rushed while a hard dense stool that’s difficult to pass is indicative of lagging motility.

There are many factors that can play in to altered motility.  But this post isn’t meant to be a comprehensive analysis on gut motility.  It’s simply a, “This is what I do because I feel it’s important and it works” type of blog.

I consider going #2 regularly to be a pretty important indicator of health.  During my chubbier and unhealthy days I never had a problem with going #2 and doing it often.  That all changed when I “cleaned up” my diet and dropped 40lbs.

Granted, I don’t believe weight loss is specifically the problem.  The problem is that as you decrease the amount of food you eat daily to lose or maintain weight, the likelihood that you aren’t meeting your nutrient requirements increases.

For many people, this includes nutrients that are involved in gut motility.  In this blog I’ll go over what I feel is important and has worked for me to maintain good motility.  What better way to start than to take a look at what makes your gut move.

The enteric nervous system and cholinergic nerves

Your gut has its own nervous system that can function on its own called the enteric nervous system.  One of the primary functions of the enteric nervous system is to regulate peristalsis, the muscular contractions that propel your food through your gut.

Nerves are often classified by the type of neurotransmitter they use to communicate with other nerves.  Acetylcholine is one of the most abundant neurotransmitters in the gut and the neurotransmitter that causes all muscles to contract.  Nerves that use acetylcholine as their neurotransmitter are called cholinergic nerves.

Note: This gets a little science-y and may not be something you’re interested in.  The reason I put it here is to show how important it is for a nerve to make acetylcholine.  It also explains why coffee works as a motility aid which I’ll describe at the end of the blog.  If you aren’t interested, you can simply skip to the next section.

Nerves are separated by a gap known as the synapse.  The synapse is the area where a neurotransmitter is released in to.  When referring to nerves, the pre-synaptic nerve is the nerve releasing the neurotransmitter in to the synapse and the one receiving the neurotransmitter is called the post-synaptic nerve.

When a nerve fires, it causes the release of its neurotransmitter in to the synapse.  The neurotransmitter binds to a receptor on the post-synaptic nerve and causes it to fire.  This in turn causes the post-synaptic nerve to release its neurotransmitter in the next synapse, and so on.

Taken from: http://faculty.pasadena.edu/dkwon/chap%208_files/images/image61.png

Simply put, for a nerve to fire and cause another nerve to fire, it must synthesize its neurotransmitter.  Since we’re dealing with cholinergic nerves and they cause muscles to contract, we want to make sure we have what we need to make acetylcholine.

For proper peristalsis, you need muscles to contract and relax.  For a muscle to relax, acetylcholine gets kicked out of its receptor on the postsynaptic nerve and the enzyme acetylcholinesterase breaks acetylcholine in to acetate and choline.  They are then reabsorbed back in to the pre-synaptic cell that released it.

This stops the nerve impulse and will cause the muscle that the nerve communicates with to relax.  Without acetylcholinesterase, acetylcholine will just float around the synapse until it repeatedly simulates the nerve or muscle.  More on this a little later.

Now that we got through the technical science stuff that you don’t really care about, let’s look at ways we can optimize acetylcholine synthesis.

Optimizing acetylcholine synthesis

Taken from: http://biology-forums.com/gallery/medium_321806_30_03_15_4_25_00_211361912.jpeg

For nerves to fire they have to be told to fire by another nerve.  This isn’t really under our control save for managing stress and all of the things that help you do that.  What is at least partially under our control is making sure our nerves have enough of the raw materials to create acetylcholine.

Acetylcholine is a fairly simple neurotransmitter that gets formed when the enzyme choline acetyltransferase(ChAT) combines acetyl CoA with choline.  This process is also easy to manipulate.  You just need to provide ample acetyl CoA and choline while stimulating ChAT.

Increasing acetyl CoA

Taken from: http://www.pnas.org/content/101/13/4584/F1.large.jpg

Producing acetyl CoA can be done multiple ways, but in the nerve cell it’s primarily accomplished by converting glucose in to acetyl CoA.  Glucose primarily comes from carbohydrate intake, so an important step is to make sure you’re getting enough carbohydrates in your diet.

This wasn’t a big problem for me, I was still eating enough carbohydrates.  My problem was that I cut out processed carbs like bread and cereal which are typically fortified with an important B vitamin known as thiamine.

Thiamine is also known as vitamin B1 and added to many processed foods with higher carbohydrate content.  This reason for this is thiamine needs are dictated by your carbohydrate content and an imbalance leads to neurological problems(1).  In fact, this was discovered when the Japanese began processing rice which eliminated thiamine from their diet.

Processed white rice induced a neurological disorder known as beriberi in the Japanese Navy.  Beriberi is now know to be the result of an imbalance between thiamine intake and carbohydrate intake(2). The more carbohydrates you consume the more thiamine you need to process them.

Thiamine and acetylcholine

Thiamine is a co-factor for converting glucose in to acetyl CoA, and a really important cofactor.  Thiamine is needed for activity of pyruvate dehydrogenase(PDH) which converts pyruvate in to acetyl CoA.  Without adequate thiamine, pyruvate is converted in to lactate instead of acetyl CoA and leaves the cell.

For this reason, most processed foods high in carbohydrate are fortified with thiamine to prevent this from happening.  Lactate isn’t bad, we have ways to process it.  A lack of acetyl CoA is bad because we form acetylcholine from it and also use it for energy.

When removing processed food from your diet, you have to be aware of this.  This is a major problem for people with digestive disorders because processed foods are one of the first things to go for SCD, GAPS, and low FODMAP diets.  The result could be poor acetyl CoA synthesis from glucose which will impact acetylcholine synthesis.

Increasing choline

Taken from: http://www.foodnavigator-usa.com/var/plain_site/storage/images/media/images/foods-rich-in-choline/9383205-1-eng…

Increasing choline is pretty straightforward, just eat more of it(3).  When choline isn’t provided in the diet, you use up methyl groups creating it from scratch.  For people with polymorphisms in the folate and choline cycles, this means you probably aren’t going to meet your choline needs.

There are pretty simple ways to improve this.  As I said, either eat more choline or supplement with it.  For a supplement I prefer sunflower lecithin, but there are other types of lecithin as well as choline and phosphatidylcholine supplements.

Another way is to supplement with creatine.  Creatine synthesis uses up about 40% of the methyl groups you make.  Eating more of it will allow more methyl groups to be used for choline synthesis.

Another benefit to creatine use is that it provides energy in cells.  Since nerve cells primarily use glucose for energy and much of that energy comes from using acetyl CoA, creatine intake can spare acetyl CoA for acetylcholine synthesis instead of using it for energy.

Increasing ChAT

Now that we’ve hit on providing the raw materials for acetylcholine synthesis, we need to light a fire under ChAT to get it to put acetyl CoA and choline together.  There are 2 great ways to do this.

First, studies show that vitamin A stimulates ChAT activity(4, 5).  Vitamin A also increases acetylcholine storage(5).  The combined effect leads to higher acetylcholine levels in cells with sufficient vitamin A.

Next, butyrate also increases ChAT levels(4).  Butyrate is produced via the fermentation of fiber by bacteria in your gut.  This may be one of the primary mechanisms by which fiber increases motility.

Does coffee make you poop?

Taken from: http://www.retroplanet.com/mm5/graphics/00000006/54713_plain.jpg

This may sound like a loaded question, literally.  But aside from its role as a stimulant, caffeine is also an acetylcholinesterase inhibitor(6).  This means that caffeine prevents the breaking of acetylcholine in to acetyl CoA and choline.  Therefore, acetylcholine floats around in the synapse and repeatedly stimulates the nerve or muscle.

The reason I mention this is that it can indicate that one of your problems may be poor acetylcholine synthesis.  Making more acetylcholine is one way of increasing stimulation of cholinergic nerves.  The other way is preventing its breakdown, which caffeine does. An interesting note: Acetylcholine is partially responsible for gastric acid secretion and coffee is known to increase acid production.  This may be due, in part, to the acetylcholinesterase inhibiting effect of caffeine.

This doesn’t mean that coffee is the answer, but it can indicate that you will benefit from increasing acetylcholine synthesis.  No matter how difficult of an issue I had going #2 during the dry times, coffee always made me go.  In fact, it’s what brought me to look in to acetylcholine for sluggish motility.

Optimizing motility with taurine

I’ve been beating the hell out of the taurine for gut health drum as of late.  Although, I haven’t really touched on its effect on motility which I’ll do now.

There aren’t a ton of studies on taurine and gut motility, but an interesting one in rats found that taurine has a way of balancing motility in the gut.  In states where there is too much motility it slows it down and when motility is too slow, taurine speeds it up(7).

Part of this effect is due to modulating acetylcholine signaling.  Specifically, when acetylcholine receptors were blocked, the stimulatory effect of taurine on gut motility stopped(7).

This, coupled with multiple studies showing taurine to improve ChAT activity imply that taurine may be a great way to increase gut motility through increasing acetylcholine levels(8, 9).  Of course, there is also the added benefit of taurine correcting for increased motility, which may be through another mechanism.

Conclusion

There are many factors that regulate gut motility, acetylcholine is just one of them.  Luckily for me, it was the first thing I looked in to and it worked.

My issue was partly due to a lifestyle change that also happened to induce a few nutrient deficiencies that impact acetylcholine production.  This coupled with some genetic polymorphisms that open me up to choline and methylation cycle problems likely contributed to my ills.

My solution was pretty simple and worked.  It’s a motility shake that gets things moving.  I’ll share my recipe with members of the private facebook in a private blog on next week.  I’ll also share some personalization techniques you can use to make it suit your needs.  If you want access join here.

Interested in improving your digestion, protecting your digestion while taking pharmaceutical drugs, or deciphering your digestion woes ?  Shoot me an email by clicking the “contact” page on the menu at the top and we can see if I can help.