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How H. pylori causes vitamin B12 deficiency and pregnancy problems

H. pylori, vitamin B12 deficiency, fertility and pregnancy

This article is taken from my e-book, How H. pylori Causes Fertility and Pregnancy Problems, which you can download here for free.

Vitamin B12 is an important reproductive nutrient. It works in partnership with other nutrients such as folate (also known inaccurately as folic acid).

A chief role for B12 and its friends is to ensure optimal functioning of some key metabolic pathways called the folate and methylation cycles.

In fetal development, methylation is crucial for optimal development of the neural tube, which is a hollow structure from which the brain and spinal cord are formed.

Defects in neural tube development can result in congenital abnormalities such as spina bifida.

Inadequate folate (vitamin B9) and vitamin B12 levels during pregnancy have can lead to an increased risk of these neural tube defects by upsetting methylation and folate metabolism.

Folic acid food fortification

In the 1990s, governments and food companies started fortifying bread and cereals with folic acid––a synthetic form of folate––to reduce birth defects caused by neural tube issues.

This strategy was quite successful but in recent times it has transpired that synthetic folic acid may cause problems because, unlike naturally occurring folates in food, it cannot be metabolized properly.

Folate food fortification (a nice alliteration!) is evidence that governments and medical authorities acknowledge the importance of this nutrient in the context of fertility.

Can H. pylori cause folate and B12 deficiency?

It turns out that H. pylori can affect both vitamin B12 and folate levels.

With B12, the link is 100% certain. With folate, it’s slightly more controversial.

The 2014 World Journal of Gastroenterology article on H. pylori and fertility states:

“Several studies have reported that serum/plasma vitamin B12 and folate levels are lower in subjects with H. pylori infection compared to uninfected persons. Moreover, several investigations have also indicated that vitamin B12 and folate levels improve after H. pylori eradication.”

In the 2016 Maastricht Consensus Report, Dr. Malferheiner and colleagues point out that H. pylori may lead to increased blood homocysteine levels, which we’ll discuss later:

“Studies have shown a link between chronic H. pylori infection and malabsorption of vitamins, including deficiencies in the absorption of vitamin B12, which results in the accumulation of serum homocysteine.”

So we we know that H. pylori plays a role in B12 levels, but does it play a strong enough role to affect reproductive health?

The aforementioned World Journal of Gastroenterology article contains a section on vitamin B12 and neural tube defects, indicating that, perhaps, H. pylori increase the risk and incidence of this condition:

“Two case-control studies in a Mexican-American and in Iranian population reported that H. pylori could play a role in neural tube defect (NTD) causation by reducing folate and vitamin B12 concentrations. They showed that H. pylori seropositivity in pregnant women can increase the risk of occurrence of NTDs in newborns, since seropositivity was more frequent among mothers of newborns with NTDs than controls.”

I found a very interesting case study that’s not directly linked with fertility and reproduction, but which strongly emphasizes the severe issues that can result from H. pylori-induced vitamin B12 deficiency.

“A 23-year-old man presented with weakness in the lower limbs, numbness in hands and feet over past 6 months. Examination revealed a combination of absent ankle jerk, extensor plantar response and reduced sensations in a glove and stocking distribution. MRI of the spinal cord was distinctive of sub-acute combined degeneration (SACD) of the spinal cord. Serum vitamin B12 was low and anti-intrinsic factor antibodies were positive. A biopsy of the stomach revealed intense inflammatory infiltrates in lamina propria with grade III Helicobacter pylori infection. Other work-up for the cause of vitamin B12 deficiency was unremarkable. H pylori infection triggers autoantibodies by a mechanism of molecular mimicry. This case report highlights H pylori as a causative agent in vitamin B12 deficiency and culminating in SACD of the spinal cord. H pylori treatment reverses the underlying pathogenesis and corrects vitamin B12 deficient state in selected individuals.”

Gowdappa HB, et al. BMJ Case Rep 2013. doi:10.1136/bcr-2013-200380

Why would I include this case study?

It’s simple…

If H. pylori-induced B12 deficiency can cause spinal cord degradation in an adult, surely it can cause neural tube defects in a developing fetus!

The importance of H. pylori and genetics

H. pylori’s effect on any given individual depends on numerous factors, which include the H. pylori strain, a person’s nutrient status and diet, stress levels, and genetics.

It’s impossible to cover all of these here, but let’s briefly focus on genetics.

The folate and methylation cycles mentioned in this article depend on certain enzymes.

These enzymes are printed from genes with fancy names like DHFR, SHMT, MTHFD, MTHFR, MTR, MTRR and so forth.

We all have these genes, but we have different versions of them, known as SNPs, variants, or mutations.

The different variations can speed up or slow down enzyme function, which can adversely affect metabolic pathways.

These adverse effects can result in things like neural tube defects or other problems of fertility and reproduction.

Genes, enzymes and nutrient partners

Each enzyme needs nutrient partners, or “co-factors”, to function optimally.

For example:

  • MTHFR requires vitamin B2
  • SHMT requires B6
  • MTR requires B12
  • Folate (also known as vitamin B9) is required to “fuel” the entire cycle.

Nutrient deficiencies can have a dramatic impact on these enzyme functions and their metabolic pathways.

Gene variants: what’s the problem?

Genetic variants can speed up or slow down enzymes, increasing or decreasing the efficiency of metabolism.

A person with a mutated MTHFR gene will print an enzyme that is 30-75% slower than someone who doesn’t have the mutation.

This means that their capacity to run the folate and methylation cycles is lower than someone without the mutation.

As a result, people with MTHFR mutations are generally more sensitive to things that impact the methylation and folate cycles.

Folate and vitamin B12 are needed for these cycles, and we know H. pylori can reduce the amount of these nutrients in circulation.

Thus, H. pylori may well have a more dramatic impact on someone with MTHFR and other gene mutations.

This is a complex topic, and one that I address in more detail in the How H. pylori Causes Fertility and Pregnancy Problems ebook, which you can download here.

Key Points about H. pylori, B12, folate and fertility/pregnancy problems:

  • H. pylori infection can clearly impact vitamin B12 levels in the body, and possibly also folate.
  • This happens in some people but not all.
  • Low B12 and folate levels increase the likelihood of neural tube defects.
  • The folate and methylation cycles are central metabolic pathways in these issues.
  • The MTHFR gene and other associated genes are incredibly important.
  • Different people will be affected in different ways.
  • Individualised assessment is required

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