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C. Difficile Gut Infection Or Even IBD May Be Due To Low Vitamin D Or PPI Drugs

haidut

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As the study says, the direct cause is high intestinal levels of calcium but as the study also says these are usually due to poor calcium absorption. And unless a person has IBD (which is rare) the low vitamin D status or PPI drug (GERD) use stand out as the most likely causes, even more so considering how prevalent both vitamin D deficiency and PPI use is. The study seems to vindicate glycine, which up until now was apparently considered crucial for establishment of C. difficile infection.
The same mechanism seems to be at play in other severe gut bacteria infections including the one now officially claimed to be the cause of Chron's disease - Mycobacterium paratuberculosis (Mycobacterium avium subspecies paratuberculosis - Wikipedia). Ray has spoken many times about the role of low vitamin D in chronic inflammatory conditions including IBD and this study seems to confirm his position. Yet another reason to ensure optimal levels, which seems to be in the 50 - 60 range. And whoever is using PPI may want to consider switching to the safer H2 antagonists like famotidine. The link between PPI and gut infection/inflammation is really scary as these drugs are commonly prescribed to pretty much everybody who endures a hospital stay and most people acquire C. difficile infection at a hospital.
Hey, @aguilaroja you may want to take a look at this as it is another black mark for the PPI drugs.

Intestinal calcium and bile salts facilitate germination of Clostridium difficile spores
‘Superbug’ may depend on calcium to multiply

"...Clostridium difficile (known as “C. diff”) bacterial infections are commonplace in hospitals and nursing homes. C. diff is responsible for large numbers of deaths every year and is the leading cause of hospital-acquired diarrhea."

"...The researchers suggested that individuals with high gut levels of calcium could be at higher risk for C. diff infection. High intestinal calcium may be the result of supplementation, poor absorption resulting from low vitamin D status, medication use (including Proton Pump Inhibitors (PPIs)), or gut diseases such as Crohn’s or colitis. The researchers noted that all the individual elements above are established risk factors for C. diff infection and critically, that “deficient intestinal calcium absorption (i.e., increased calcium levels) is associated with these risk factors.” However, Hanna advocates caution to patients considering ceasing medications or doctor–recommended supplements (or starting new ones). Nevertheless, avoiding excess calcium and ensuring adequate vitamin D status appear prudent in the light of the findings. The discovery that calcium germinates C. diff spores is also significant; as the amino acid, glycine was previously thought necessary to the process. This study demonstrated that spore germination could occur without glycine. Travis Kochan, a graduate student in the research team, observed that the liquid used for growing C. diff for their studies contained calcium. When he chemically removed calcium from the growth medium, spore germination ceased. FDA researchers subsequently conducted further research in mice using C. diff spores modified to prevent glycine acting upon them. As spore germination still occurred without glycine, this demonstrated that calcium was the critical trigger."
 

Drareg

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I know of a man in his seventies prescribed ppi's for almost 2 years who has developed cancer in the rectal area,he collapsed one day and was taken to hospital,they found low sodium,he was also taken x-a-n-a-x and statins,his ppa was high so they looked at prostate and found cancer there also. It took 2 and half months to diagnose this.
He was in hospital he still had acid reflux so an intern prescribed a different ppi that has a side effect of possible stomach cancer,they still give him this as well as the castration therapy for prostate. Radiotherapy is next,no t3,Rt3 will be measured,still gets X-a-n-a-x statins and now the occasional sleeping pill which can be given by a nurse.
He was told 50 out of 100 men live for 2 years,no more,isn't this hilarious word play! I mean it's the height of psychotic,it's an apology for the coming radiotherapy which will be the final straw.
 

aguilaroja

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As the study says, the direct cause is high intestinal levels of calcium but as the study also says these are usually due to poor calcium absorption. And unless a person has IBD (which is rare) the low vitamin D status or PPI drug (GERD) use stand out as the most likely causes, even more so considering how prevalent both vitamin D deficiency and PPI use is....
And whoever is using PPI may want to consider switching to the safer H2 antagonists like famotidine. The link between PPI and gut infection/inflammation is really scary as these drugs are commonly prescribed to pretty much everybody who endures a hospital stay and most people acquire C. difficile infection at a hospital....

“As if” other evidence is needed, this review indicates a 38% higher risk for Clostridium Difficile gut infections for people treated with PPI’s compared with famotidine/other H2 blockers.

Comparison of the Hospital-Acquired Clostridium difficile Infection Risk of Using Proton Pump Inhibitors versus Histamine-2 Receptor Antagonists fo... - PubMed - NCBI
“PPIs increased the risk of CDI by 38.6% (pooled odds ratio, 1.386; 95% confidence interval.… Subgroup analyses of the purpose of study medication use, study site, and study design confirmed the consistency of a greater CDI risk with PPIs than with H2RAs.”
 

haidut

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Amazoniac

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So, one possible explanation of the widespread low vitamin D levels would be its increased utilization to oppose inflammation/TLR4 due to the endotoxin overload most people suffer from nowadays, right?
This is what a few liver injury reviews have hytope- hytopo- have suggested as well. I believe that even John Cannell wrote about it on his blog.
 

Amazoniac

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https://link.springer.com/article/10.1007/s00198-008-0764-2

"Vitamin K and D deficiency and decreased bone mineral density (BMD) were highly prevalent in patients with inflammatory bowel disease (IBD), especially Crohn's disease (CD). Dietary intakes of these vitamins, however, were above the Japanese adequate intakes in IBD patients, suggesting that malabsorption is the basis for hypovitaminosis K and D and decreased BMD."

"Food intake could be evaluated in 25 patients (15 with CD and 10 with UC). Fat intake was significantly lower and protein intake was significantly higher in patients with CD than those with UC. The results were similar when expressed as the percentage of total energy intake. The adequate intakes (AI) for calcium in Japan are 600–650 mg for men and 550–600 mg for women. AI for vitamin K is 75 μg for men and 65 μg for women, respectively, and that for vitamin D is 5 μg [30]. As a whole, although the average calcium intake was below AI, vitamin K and D intakes apparently exceeded AI (Table 4)." :ss

"Patients with IBD have been reported to be at high risk of malabsorption of these vitamins due to intestinal inflammation or intestinal resection in some patients [6, 18, 21–24]."

"Vitamin K absorbed from the gastrointestinal tract is transported to the liver via the portal vein where it is used for the γ-carboxylation of clotting factors [42, 43]. Only the vitamin K unutilized in the liver will be available to the bone. Therefore, the bone is likely to be much more susceptible to vitamin K deficiency than the liver."

"Tangpricha et al. [44] reported that vitamin D dissolved in fat-free orange juice was effectively absorbed from the intestine and indicated that fat content of the diet little influenced vitamin D absorption."

"In summary, BMD was decreased and plasma concentrations of PK, MK-7 [japanese study], and 25OH-D were quite low in patients with IBD, especially CD, despite apparently sufficient intake of these vitamins. Impaired intestinal absorption of these fat-soluble vitamins is likely to be associated with vitamin K and D deficiency and bone loss in IBD."​

These were posted by my incubator here.
 

haidut

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Only the vitamin K unutilized in the liver will be available to the bone

Thanks. I think this needs to be a sticky because I get so many emails and messages about why would one want to use topical vs. oral vitamin K. I think the same thing applies to the other vitamins - i.e. the organs get whatever remains unutilized in the liver. So, with topical, you give more to the other organs and the liver still gets some but just not as much as with oral.
 

Wagner83

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Growth of M. avium subspecies paratuberculosis in culture is enhanced by nicotinic acid, nicotinamide, and α and β nicotinamide adenine dinucleotide. - PubMed - NCBI
might have been bad taking niacinamide (nicotinamide) if it actually feeds m. avium tuberculosis that wagner83 maybe suggested is a problem ?!
The fascinating thing about that study was also the fact that they've proven that salicylic acid also enhances growth of these M. Avium subspecies. On the contrast something called "Para-amino salicylic acid" is bactericidal. But I believe it's completely different compound.

This would explain all the intestinal bleeding and kidney issues people have after taking aspirin.

METHODS​

As experimental controls, we use two well-established antibiotics to inhibit mycobacterial growth. Isoniazid (INH; isonicotinylhydrazine (used to treat tuberculosis [39] and leprosy [40]) and para-amino salicylic acid (PAS) used to treat tuberculosis [41]. In 1940, Bernheim first reported the enhancement of growth of mycobacteria by salicylate [42]. Accordingly, our experimental control for enhancement of growth was salicylic acid.

Results​

The initial experimental control to document that growth enhancement can be achieved is salicylic acid. To contrast with the enhancing effect of salicylic acid, our inhibitory control is PAS (Table 1; Fig. 1) [41]. PAS is probably bactericidal on M. avium and BCG.
Our antibiotic inhibitory control for the structural analogs of nicotine is isonicotinylhydrazine [INH] [45]. INH is bactericidal on M. tb (99%–DcGI at 1 (one) lg/ml) (Fig. 3) and has dose dependent inhibition on BCG and M. avium: 101(C98%– DcGI at 64 lg/ml).
 

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