Problems with IBS? Personalized solutions based on your genes

We tend to take happy bowels for granted -- until something goes awry!  For many people, a daily battle seems to wage in their intestines. Pain, discomfort, bloating, diarrhea, and/or constipation...  a.k.a. IBS or irritable bowel syndrome.

There are multiple causes of IBS, and genetics can play a role in IBS symptoms. Pinpointing your cause can help you to figure out your solution.

Irritable Bowel Syndrome

IBS affects more than 10% of the population in Westernized countries[ref]

IBS is defined as a functional GI disorder defined as having:

  • abdominal pain, bloating, gas
  • diarrhea (IBS-D)
  • constipation (IBS-C)
  • OR - a mix of diarrhea and constipation (IBS-M)

To obtain an IBS diagnosis it often means eliminating other conditions -- such as celiac, Crohn's, or ulcerative colitis.

The causes of IBS are often a mystery -- both to the person who has it and to their doctor. The use of the word 'idiopathic' shows up frequently.

According to the National Institute of Health "Doctors aren’t sure what causes IBS."  Hmm...  not what someone with IBS wants to hear from their doctor![ref]

Often people will go through a series of dietary changes, trying to figure out which foods, if any, lead to their problems.

Researchers have come up with many theories about IBS.

I'm going to dig into a few of these theories and show how they link up to genetics. Then you can check your genetic data, and use that info to figure out the IBS solutions that may work best for you.

Digesting Carbs:

Carbs should be digested, broken down, and absorbed in the small intestines.  When that doesn't happen -- either due to lack of enzymes to break them down or increased gut motility -- the carbs end up in the colon. Extra carbs in the colon feed the bacteria there, and they party all night, giving off-gas.

While frank deficiencies of the enzymes that break down different carbohydrates are somewhat rare, researchers are now discovering that partial deficiencies could be causing IBS symptoms for some people.[ref]

Sucrase-isomaltase deficiency is a lack of the enzyme that breaks down the starches and sugars. SI deficiency leads to the accumulation of unabsorbed carbs in the intestines. This leads to a change in the gut microbiome, increased short-chain fatty acids, increased gas, and often diarrhea, abdominal pain, and bloating.[ref]

Lactose is a sugar found in milk and dairy products. Most people of European descent have inherited a genetic variant that still allows for the production of lactase as an adult. But for people who don't produce lactase as an adult (e.g. most Asians, 10% of Caucasians), drinking milk may aggravate IBS symptoms.

Serotonin makes things move:

Most of the serotonin (5-hydroxytryptamine, 5-HT) your body produces is in the intestines. It acts as both a neurotransmitter and an immune system regulator. It is the signaling molecule that regulates motility, secretion, and vasodilation. The stimulation of the intestinal tract produces more serotonin and more serotonin receptors.[ref]

The microbes in the gut are able to influence the amount of serotonin synthesized there.[ref] In essence, an overgrowth of certain bacteria could influence and increase serotonin synthesis.[ref]

There are several different serotonin receptors in the intestines. The overactivation of the 5-HT3R receptor has specific links to IBS with diarrhea. One study showed that people with IBS-D had double the number of 5-HT3R in the intestinal mucosa, compared with a control group.[ref]

Bile acid synthesis:

Your body produces bile acids for digesting fats as well as for getting rid of waste products, such as bilirubin. Adults produce between 400 and 800 ml of bile per day.

Typically, the gallbladder stores bile when you haven't recently eaten. When stimulated, the gallbladder releases the bile into the upper part of the small intestines. The bile acids then break up or emulsify fats so they can be easily digested by lipases.[ref]

About 95% of the bile acids are reabsorbed when they reach the end of the small intestines. From there, recycling occurs through the liver for reuse.

If too much of the bile acid ends up in the colon, diarrhea will ensue... This can be either from too much being produced or from not enough being reabsorbed at the end of the small intestines (at the ileum).

When excess bile acids reach the colon, they cause diarrhea by stimulating an increase in water in the stool.

Studies show that between 10 - 25% of patients with IBS-D had problems stemming from bile acids reaching the colon.[ref]

Enteric Nerve Irritation:

The enteric nerves in the intestines cause peristalsis or movement. Several studies point to increased expression of TRPV1 in the enteric nerves of people with IBS. TRPV1 is a pain receptor and that also may play a role in the response to mechanical stimulation (i.e. foodstuff pressing on the intestines).

TRPV1 stands for transient receptor potential vanilloid type-1. It is also the receptor that capsaicin binds to, causing you to sense spicy heat. A study that looked at the TRPV1 receptors in biopsies from IBS patients found that they had a 3.5-fold increase compared to normal people. Basically, it causes hypersensitivity to pain in the intestines (irritability!).[ref]

Another study points to histamine as a possible cause of sensitized TRPV1 channels in IBS.[ref] And to tie this back to bile acids, a study points to bile acids causing mast cell activation (releasing histamine) and increasing TRPV1 expression.[ref]

Variants in the TRPM8 gene have also been linked in large, genome-wide studies to an increased risk of IBS-C. This transient receptor potential channel is also thought to be associated with bile acid secretion.[ref]

Is IBS a genetic disorder?


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