Note: None of this information constitutes medical advice. We are all individuals, and what works for one person may not be all that great for another. In this blog I cover some of the basics of what I did to improve my microbiome and digestion. However, there’s quite a bit of nuance in doing this. Some of the things I did should be implemented slowly as I believe they have a pretty big effect on digestion. I believe everything I did to be perfectly safe for most people, but what’s good for the goose may not be good for the gander. Please consult your healthcare provider for guidance.
If you’ve been following my “Hacking your gut…” series you know that I’ve been trying to improve my general digestion and microbiome for a bit of time now. My initial plan was to see what antibiotics would do to my microbiome using Ubiome testing. My goal was to see if taking prebiotics and probiotics along with a healthy diet prevents antibiotic induced dysbiosis.
I guess I got started off on the wrong foot because my diversity was in the 3rd percentile to begin with and only improved to the 4th percentile during the 3 tests I did spanning 2 months.
However, a little later on in 2016 I decided to see what would happen if I switched my focus. Rather than going for the bargain basement approach of fiber and probiotics, I decided to dig in to my 23andme data and see if a more personalized approach would work.
As you can see, that approach worked much better…
The top test results are the same ones that my older results were compared to in both of my “Hacking your gut…” blogs. During this test, I was 2 weeks in to my new approach and in the bottom one I was 10 weeks in.
So what did I do and what did I take? Well, our journey begins at livewello.com.
Note: If you haven’t followed this series, click the links below:
23andme, livewello, and my gut
A few years back I had my genome sequenced via 23andme to help identify ways I could improve my health. At the time, 23andme didn’t have a useful dashboard so I used prometheus to look at my raw data.
Unfortunately, prometheus is as bare bones as you get so I went to a site called livewello.com. Unlike 23andme and prometheus, livewell has interesting information as well as a user-friendly interface. I simply uploaded my 23andme data to livewello and used some of the free reports available to me.
Using livewello, I looked through the health reports available to me. I found out I have reduced MTHFR enzyme activity which I already knew and that I don’t convert plant-based vitamin A in to the active, retinol form.
Vitamin A is a pretty important nutrient for gut health. Probably the best way to describe what it does is to say that it makes basically every other function work better. This includes detoxification, inhibiting inflammation, and sealing up a leaky gut.
Prior to my new direction, my vitamin A came mostly from sweet potatoes. I occasionally ate liver and I like it, but I wasn’t on top of eating it every week. Since my DNA shows that I need to eat animal-based forms of vitamin A, I made it a weekly staple in my diet. You can clearly see this in my ubiome data under retinol metabolism.
Adding liver in once per week increased the retinol metabolism in my microbiome by more than 150%. I definitely feel this is a major contributor to my improvement in diversity. I’m not sure exactly what my gut bacteria are doing with it, obviously. But the fact that those bacterial pathways are being upregulated indicates that my new intake is probably better.
You may have noticed how I brushed right by my inefficient MTHFR enzyme. From my perspective, I really don’t care that I have impaired folate cycle efficiency. In my opinion most people put way too much emphasis on MTHFR and the folate cycle.
It’s not that methylation isn’t important for digestion, it is. It’s just that when I look at the pathways I put a lot more weight in the choline cycle. One spin through the choline cycle creates the same number of methyl groups as folate and makes 3 precursors to methylfolate that MTHFR can act on. More importantly, having to synthesize choline because you aren’t eating enough of it uses up 3 methyl groups in one of the major pathways.
Another reason I put more weight behind the choline cycle is because of what phosphatidylcholine does. Phosphatidylcholine is a primary component of bile that protects against bile acid induced injury to the intestinal wall(1).
Phosphatidylcholine is also the primary phospholipid in cell membranes. This basically means that phosphatidylcholine makes up a big chunk of the intestinal wall and helps form the water impermeable barrier in the gut.
Because of all this, I began supplementing with lecithin which is a combination of phosphatidylcholine, phosphatidylethanolamine, and phosphatidylinositol. Liver also happens to be a good source of phospathidylcholine as well as folate so that covers 2 bases as well.
Taking a look at my ubiome lipid metabolism data kind of tells the story…
My sphingolipid metabolism doubled. Sphingolipids, specifically sphingomyelin, are synthesized from phosphocholine which is made from choline. They work with phosphatidylcholine to shore up the outer leaflet of the cell membrane and are also components of the myelin sheath that covers nerves.
Another important consideration here is that acetylcholine is one of the important neurotransmitters in the gut. When you aren’t consuming enough choline to make acetylcholine, cell membranes are broken down to get sphingomyelin and phosphatidylcholine(2). Obviously not an ideal situation.
Working around MTHFR and improving energy with creatine
While livewello has nice little user-friendly tidbits like the one I showed you on Vitamin A, it’s actually quite a bit more useful than that. You can take a look at health and variance reports that were developed by other people such as Dr. Yasko’s methylation report.
There are also subscription based reports that look to be useful but I’ve never tried them. You can also make your own reports if you know which genes you want to look at. I’ve done this, and my folate and choline cycles have multiple polymorphisms that indicate poor enzymatic activity. This is why I take lecithin.
Another important factor that creeps up in my 23andme results involves the substance creatine. Creatine basically functions as an energy donor in cells by recycling ATP. Much like my choline cycle pathways, I have polymorphisms in the enzymes that synthesize creatine.
The problem with the genes involved in creatine synthesis is that they aren’t as well studied as the ones in the folate and choline cycles. We just don’t know for sure if having a single copy of a defective gene leads to lower creatine levels, but it is expected(3).
Creatine deficiency syndromes are caused by a defect in one of the genes necessary for creatine synthesis. People born with 2 copies of a bad gene in each enzyme suffer from mental retardation, autism-like behaviors, and early onset epilepsy(4).
The genes with relevance to creatine synthesis are arginine:glycine amidinotransferase(AGAT or GATM) and Guanidinoacetate methyltransferase(GAMT). People with 2 copies of AGAT respond very well to oral creatine supplementation and require nothing else(4).
People with polymorphisms in GAMT do well with oral creatine but must also supplement with the amino acid ornithine and reduce arginine and protein intake. In both scenarios, supplementation can prevent manifestation of the disease altogether if caught early enough(4).
This seemed pretty powerful to me. Being born with a mutation in a gene that blocks a single enzyme can cause someone to become mentally retarded, autistic-like, and/or epileptic. If you catch this person early enough in development and give them a simple supplement you can find anywhere that costs $20 a year they live a perfectly normal life.
Digging through my data revealed to me that I have a couple of polymorphisms that could be problematic in creatine synthesis. But this in and of itself didn’t raise a red flag to me because the data isn’t solid. My history with creatine tells me that it’s a probable issue, though.
What piqued my interest with creatine is that people fall in to one of 2 groups with creatine: responders and non-responders. Creatine non-responders see no effect from taking creatine. Creatine responders tend to see immediate results in strength and energy with creatine use.
I’ve used creatine many times in my life and I can tell you unequivocally that I’m a responder. My energy levels are much greater and my strength goes up within a week or 2. The best way to describe what creatine does is that it continually replenishes ATP to be used for energy. For more on creatine check out this blog.
Perhaps in responders there is lower creatine synthesis through the defective pathways because they have a single bad copy of a gene. Taking creatine as a supplement increases the amount of creatine in cells and makes up for lower production by your liver.
Since I’ve used creatine safely for long periods of time, I saw no harm in it. It’s also damn cheap so it made no sense not to try.
My thought process is that it will not only increase my energy levels, it will lower my methylation demand while allowing more of the acetyl CoA produced in cells of my gut to go to acetylcholine synthesis rather than energy.
Acetylcholine is an important neurotransmitter in the gut that plays a big role in regulating motility and reducing inflammation(5). I want fertile ground for my bacteria to grow, not a burning wasteland.
The final piece of the puzzle doesn’t require any fancy 23andme testing or livewello reports. It’s simply a free amino acid that plays a big role in bile production and regulating inflammation in the gut. I’m talking about taurine.
I could talk at length about why I think taurine is important, but I’ve covered it in blogs on this site. I’m simply going to give you the crib notes version and a link to one of the blogs I discussed these things in.
When you produce bile acids in the liver, they’re fat soluble and toxic. Before they can be sent to the gallbladder, they get conjugated with glycine or taurine to make them water soluble and less toxic.
Most carnivores conjugate bile acids exclusively with taurine while herbivores conjugate with glycine. The only exception being ruminants who are herbivores that conjugate exclusively with taurine.
Omnivores can conjugate with both, but the extent to which they conjugate with taurine is dictated by the amount of taurine in their diet. Since taurine is found exclusively in foods of animal origin, the more meat you eat the more taurine you get.
Now, an important distinction here is that eating more taurine changes the ratios of the conjugated bile acids by increasing total bile acid output. What I mean is that you don’t make fewer glycine-conjugated bile acids when you eat meat, you just make more taurine-conjugated bile acids. Given that bile acids aid in the digestion of fat, it makes sense that you would make more bile acids when you eat meat because you’ll also eat more fat.
In my opinion, more bile is great for your microbiome provided you have the machinery to deal with it. Most bile acids are recycled back to the liver when they reach the ileum and a few stragglers make it to the colon. If you’ve had your ileum resected due to Crohn’s disease, more bile acids would probably give you a massive case of diarrhea.
The few bile acid stragglers that make the colon are acted on by bacteria that remove their conjugate and further process the bile acid. In the specific case of taurine, free taurine activates something called the inflammasome.
Activating the inflammasome in the colon blocks inflammation and increases mucus production. These are 2 very important factors for gut health and regulating the microbiome. In fact, there are multiple inflammasomes throughout the body and this specific inflammasome directly regulates the microbiome. That’s why I threw some taurine in there.
Truth be told, if there was one thing that moved the needle the most, it was taurine. Many of the changes in my most recent Ubiome test are indicative of higher bile output because a few bile tolerant individuals showed up.
Update 6/2017: I dropped taurine for a while and saw a huge drop in diversity(From 42nd percentile to 12th) and Firmicutes now outnumber Bacteroidetes, although they are about 50/50 now. I have a distinct feeling taurine has a large impact on the microbiome and this is probably due to a combination of increased bile output and inflammasome signaling. It’s important to point out that I probably changed a few things, but I’m fairly certain taurine was the big one.
For more on why this is, check out this blog.
I think the results speak for themselves. I saw absolutely no improvement in microbial diversity messing around with fiber and probiotics but a pretty substantial change focusing on improving my gut via the above nutrients.
Above are my taxonomy results from my last 2 Ubiome tests showing the species of bacteria in my gut. The one on the left is from diversity data putting me in the 7th percentile and the one on the right is the data putting me in the 42nd percentile. Both are in the same font so the difference in size is due to the larger number of species. I’d like to point out that even as bad as the one on the left is, it’s still more than double what it was when I started.
Before I can really call this a major success I have to wait until my last results from 11/11/2016 are tabulated. My digestion is definitely better so the question is, “Do I really care?”
I have one more test to take but I’m not sure when I’ll take it. I’ve recently done some more tweaking and will figure that out before the end of the year. Once my results from 11/11 are back I’ll be sure to update you on my progress.