Taken from: http://www.healthyfoodvision.com/wp-content/uploads/2016/05/gastritis.jpg

One thing that’s particularly frustrating about gut disorders is the individuality of it all.  If you look at 2 people with the same gut disorder you can see a completely different set of food and nutrient intolerances.  This is why an individual approach is heads and shoulders above the rest.

Another big issue is that symptoms can also vary from person to person.  One person may just have gastritis while another has gastritis and colitits.  That’s a whole lotta -itis.

Then you have the ass-backwards approach to treating something like gastritis.  The approach is to throw some proton pump inhibitors(PPIs) at it.

While proton pump inhibitors can be effective for short periods of time, they’re only temporary solutions.  Recurrence is common if a long-term approach isn’t also taken.

When used with antibiotics to treat one of the more common causes of gastritis, PPIs are effective.  But, there’s nothing to stop recolonization by the culprit once you’re off of the drugs.

Fortunately, a lot of people are turning away from this approach.  That’s a good thing because it doesn’t seem to work.  The typical road a person with gastritis takes with PPIs such as Prilosec is pretty well set.  A higher dose of the drug and eventual transition to a different proton pump inhibitor.

I’m not against using PPIs short-term, but long term not so much.  Long term PPI use can lead to nutrient deficiencies.  Particularly magnesium and vitamin B12 that need stomach acid for bioavailability.  That’s why it’s important to do other things to prevent relapse.

Helicobacter Pylori and the stomach

At the center of this gastritis problem is a little guy named Helicobacter pylori, or H. pylori for short.  The oft-maligned bacteria is found in over half the world population but only causes symptoms in 15% of people with it.

H. pylori is blamed for ulcers and gastritis, common problems today.  It’s important to note that these problems arise when H. pylori overgrows in the stomach.  This is why not everyone who has H. pylori in their stomach experiences symptoms.

H. pylori is even blamed for an increased risk of stomach cancer.  Preventing H. pylori colonization leads to a small, albeit measurable, reduction in risk of the disease.

While I believe the absolute risk of developing stomach cancer as a result of H. pylori overgrowth is small, it’s  drawn the attention of pharmaceutical companies.  A recent study has identified a mechanism that’s worth looking at.

Taken from: https://www.systemsbiology.org/wp-content/uploads/helicobacter.jpg

H. pylori overgrowth

For a bacteria to overgrow in the gut, many conditions must be present.  There’s never a single smoking gun in these situations.  Multiple environmental conditions often come together to cause the problem.

But sometimes there’s a singe mechanism we can manipulate to solve the problem.  Then it’s up to us to make sure the overgrowth never happens again.

Other times there are things we may be doing that can prevent resolution of a problem.  Proton pump inhibitors provide symptomatic relief but are bad in the long run.

Taking Prilosec can help you feel better because lowering stomach acid will prevent it from damaging your weakened stomach lining.  Over the long term, it can promote H. pylori colonization because one of the things preventing H. pylori overgrowth is stomach acid.

I’m ok with using PPIs for short-term symptom relief.  But this needs to be coupled with a proactive approach to fixing the problem.  Literally nobody does this.

New research shows that a vitamin that many people are taking for general health may also prolong the issue.  Another common supplement may be useful in preventing H. pylori colonization and recurrence.

Taken from: http://nattomk7.com/wp-content/uploads/2013/02/Vitamin-k_diagram.png

Vitamin K and H. pylori overgrowth

Vitamin K exists in 2 primary forms: phylloquinone(K1) and menaquinone(K2).  The vitamin Ks are important for all forms of life with K1 being the form for plants and K2 being the primary form for bacteria and animals.

Both animals and bacteria have endogenous means of producing K2.  In animals, vitamin K2 production comes from changing K1 in to K2.  In bacteria, many pathways are used and some don’t involve K1.

In bacteria, K2 serves a vital purpose in the generation of energy.  Bacteria use menaquinone to move electrons around in aerobic and anaerobic energy processes.  H. pylori is one of these bacteria.

Recent research in eradicating H. pylori overgrowth has focused on interfering with its K2 pathway.  This pathway is different than the ones humans and beneficial bacteria use to synthesize menaquinone(1, 2).  If you can block this pathway you should be able to keep H. pylori overgrowth at bay without affecting the host(you).

Blocking H. pylori overgrowth via the K2 pathway

A new study dug in to inhibitors of menaquinone synthesis in H. pylori.  In this study, the authors found that the Omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) inhibited the pathway that H. pylori uses to synthesize menaquinone(3).

Unfortunately, adding menaquinone in to the mix partially inhibited these effects.  This indicates that H. pylori needs vitamin K2 for colonization.  It may also mean that vitamin K2 supplementation isn’t a great idea in people suffering from gastritis caused by H. pylori overgrowth.

There are many different forms of vitamin K2 out there, and some may be more problematic than others.  Doing a little digging, I found that H. pylori uses 2 specific types of menaquinone: MK-6 and MK-4(4).  Unfortunately, MK-4 is one of the most popular forms of supplemental menaquinone.

There are, however, 2 other options.  The first is to use a vitamin K2 supplement that uses MK-7 instead of MK-4.  I use megaquinone from time to time and like it because it contains the cofactors that vitamin K needs to do its job.  This is probably the best route to improve a deficiency.

The other option would be to eat higher levels of vitamin K1 and rely on your own pathways to convert it.  Since the pathway that H. Pylori uses to make vitamin K2 doesn’t involve vitamin K1 and we convert K1 to K2 it in the intestine, it should provide no benefit to H. pylori in the stomach.

I think the K1 route is the way to go once you’ve improved a deficiency.  From an evolutionary perspective we come from a long line of heavy K1 consumers.  Vitamin K1 is in grass, leaves, basically anything that’s green.  Our prehuman ancestors likely ate a lot of it on a daily basis.  In my opinion, consuming higher levels of vitamin K1 is the best route.

The problem is determining a dosage.  The RDI for vitamin K is 120mcg and based on preventing defects in blood clotting.

Recent evidence points to many other roles for vitamin K, some specific to vitamin K2.  The science behind dosing of vitamin K2 also seems to be a little further ahead than dosing for vitamin K1.

Given the diet of our prehuman ancestors and the fact that 2 cups of spinach gives you around 300% of the RDI, I’m thinking the RDI is far too low.  Another issue is that vitamin K1 in foods is less bioavailable than K1 supplements.

Since most studies used supplements to determine the RDI, we don’t know what we need from food.  This means that someone looking to get adequate vitamin K1 from their diet needs to eat more than the RDI.

I’ll dig deeper in to vitamin K in the future as it deserves its own blog.

Taken from: http://www.newhope.com/sites/newhope360.com/files/styles/article_featured_standard/public…

Omega 3 fatty acids and H. pylori

In this new study, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) were able to inhibit growth of H. pylori by 96% and 78%, respectively.  These 2 fatty acids inhibited H. pylori by blocking vitamin K2 synthesis.

This is why adding vitamin K2 partially inhibited the effects, it gave H. pylori what it was unable to make.  Keep in mind that this study took place in a petri dish.  But there’s other evidence that DHA is effective at preventing colonization of H. pylori.

An earlier study looked at how DHA fares against H. pylori with and without standard treatment in mice.  DHA was effective without a PPI and antibiotics, but not as effective as it was with them.  Recurrence of H. pylori overgrowth was completely prevented in mice given both DHA and standard treatment.  Neither treatment on it’s own had the same effect(5).

DHA appears to be more of a prophylactic treatment for H. pylori overgrowth.  In other words, taking DHA is good for preventing H. pylori overgrowth and recurrence.  But it’s probably but not the best option as a standalone treatment. It doesn’t kill H. pylori, it just converts it in to a form that can’t colonize the stomach.

It’s also important to point out that eating fish isn’t going to be effective against H. pylori.  A supplement is necessary because the DHA in fish won’t be available in the stomach.

Conclusion

H. pylori overgrowth is a primary cause of gastritis.  The standard treatment of a PPI with antibiotics is effective at reducing colonization in the stomach but doesn’t stop recurrence.

Since the Mk-4 version of vitamin K2 is necessary for colonization in the stomach, avoid this form if you have an H. pylori overgrowth.  Two better options include increasing vitamin K1 intake or taking a supplement with Mk-7 instead of Mk-4.

Supplementation with the omega 3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) inhibits K2 synthesis by H. pylori.   This coupled with short-term treatment with a PPI and antibiotics can prevent H. pylori colonization long term.  Something the standard treatment has not accomplished.

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