Central control of reflux; the Vagus nerve

The body has two safeguards against reflux, the diaphragmatic sphincter and the lower esophageal sphincter. Both are supposed to remain shut unless you swallow, burp, or vomit, but sometimes they malfunction and cause reflux. Typically, there are two kinds of malfunctions: (i) transient lower esophageal sphincter relaxations and (ii) weakness in one or both of the sphincters.

The first type of malfunction, transient lower esophageal sphincter relaxations, is basically a brief (i.e., a couple of seconds long) relaxation of the sphincters. Many things can cause these relaxations, including stomach distention, certain food items, and stress. Transient esophageal relaxations are likely the cause of most cases of GERD.

The second type of malfunction, sphincter weakness, is a more prolonged defect in one or both sphincters. Many things can cause such sphincter weakness, including stomach distention, abdominal pressure (such as from weight lifting or straining to go the bathroom), certain food items, certain medications, irritation of the esophagus, and stress. This type of malfunction seems to result in more serious GERD, especially when lying down at night.

Both types of malfunctions also seem to be under some form of central nervous system control via the Vagus nerve, with the result that reflux may be modulated, to some extent, by tweaking the neurotransmitters and receptors of the Vagus nerve. As I mentioned recently, cisapride seems to tighten esophageal sphincter pressure, likely by increasing the amount of acetlycholine in the Vagus nerve. Unfortunately for cisapride (and many other drugs in its class), it also increases the amount of acetlycholine elsewhere and can lead to some bad side effects (like cardiac arrhythmias).

Transient lower esophageal sphincter relaxations seem to be modulated by wide vareity of neurotranmitters, including GABA, glutamate, nitic oxide, and substance P, Cannabinoids. Melatonin, zinc, cholecystokinin, gastrin, atropine, and opioids may also play a role.

As you can see, there are many potential targets that could affect reflux. I will experiment with a number of substances that I know to affect one or more of these targets and that I consider safe. I am not interested in gambling (especially against the odds), so I am confining myself to only those foods & supplements that have been used well for long periods of time by large numbers of people. Results from these experiments will be the subject of numerous future blog posts.

Anatomical picture above is from here.

Oatmeal and Ayurveda

Recently I posted on colonic fermentation induced reflux. If you followed the links, you saw that the idea seems to be that the bacterial fermentation of carb by-products (what's left over after your digestive system absorbs what it can) produces something (maybe just gas, maybe something more complicated) that causes reflux.

One thing I discovered on my own is that if you go very low carb for a while (say 80% fat) and then have a bunch of carbs for lunch one day (oatmeal in my case), you might have a very burpy night. In my case, the experience went well beyond what I would normally expect from oats. So what happened?

I think that some of the good bacteria inside of me (probably the bifido ones) died of starvation during my 4 day long whipping cream binge. Then, when I ate Irish steel cut oats for lunch, the only thing left to ferment them were the more gas-producing bacteria. I guess the moral of the story might be to not eat whipping cream for 4 days straight. Or if you do, take a probiotic while you do it and introduce the carbs back gradually. I'll let you know if that works.

As a side note, after my oatmeal lunch, my reflux was so bad at night that I thought I should try to shut it down. I tried some strong decaf green tea, but that didn't help enough. So, I resorted to ashwaganda, an Indian herbal supplement known as an adaptogen (anti-stress medicine). In addition to promoting sleep, ashwaganda also inhibits acetylcholinesterase, an enzyme that degrades the neurotransmitter acetlycholine. Turns out, more acetycholine around (as a result of disabling that enzyme that degrades it) means less reflux because acetycholine helps to keep the LES closed.

It would be so perfect, but playing around with neurotransmitters makes me a little nervous because not enough is understood at this point. What's good in the short term may be very bad in the long term, especially in this area. Acetylcholinesterase inhibitors may have short term side-effects as well. In particular, acetylcholinesterase inhibitors can contribute to cardiac arrhythmias in some people. Likewise, Cisapride (a drug approved to treat GERD by increasing LES pressure) was pulled from the market over similar fears -- it's not an acetylcholinesterase inhibitor but does increase acetylcholine nonetheless via agony of 5HT4 (serotonin) receptors. So, can ashwaganda also contribute to cardiac arrhythmias? I have no idea, but I would guess it's unlikely as most of these things are dose dependent and I don't think ashwaganda is a particularly potent inhibitor of acetylcholinesterase. Also, people take ashwaganda and it's not known as the drop dead supplement. So, long story short, I took it and slept like a baby, without reflux.

EDIT: I tried Ashwaganda again and do not think it helped my reflux. In addition, it might have given me heart palpitations. Maybe psychological, maybe not. I have had palpitations before, but mostly after a hard night of boozing... The point of the update is to record that my ashwaganda experiment is officially over.