A review of P3-OM

A reader asked me to review this heavily marketed on some channels.

In terms of marketing, their home page is thick like thieves with hype.

Just one single probiotic species in it. I must admit, I chuckled when I saw the distributor “Rush Order

So it is a proprietary “super strain”: Lactobacillus Plantarum OM. Checking the patent application, we see it is “L. plantarum, OM ATCC 55981”  and a patent was originally file in June, 1997, almost 20 years ago and the patent is expired. So, immediate RED FLAG, “patented proteolytic probiotic, P3-OM™. ” – it is no longer patented, a false claim.

Checking PubMed, there are ZERO hits for plantarum 55981; so no peer-reviewed studies.

Origin: Remember human source is your only hope of it taking up residence. The patent application states “L. plantarum, OM may be isolated from a fermented meat. “

Price Analysis

One bottle is $79.95 and contains 120 capsules with 2.5 billion CFU. or a total of 300 BCFU in a bottle or $0.27 per BCFU. Going to Custom Probiotics which also offers a one strain only version of Lactobacillus Plantarum we can get 100g at 400BCFU/gram for $190. That computes to $0.00475 per BCFU … or FIFTY-SEVEN (57x) better price. The custom probiotics strain is Lp-115 or SD-5209. And I found four pubmed citations for this!

Bottom Line

The firm “Rush Order” seems to be trying to get you to rush your money to them for an undocumented, out of patent strain originated from fermented meat at an unrealistic price. I would give it a wide pass.

To be clear, there is nothing known wrong with this product. If you are interested, I have this excellent product that I am selling for just $500 for 8 oz. It’s the very rare and extremely well documented for healthy living,
hydroxylic acid . Just send me a certified check and an address!

Feel free to ping me to do other reviews.

Ozone Therapy – A Review

A reader forwarded me a link to: “Ozone therapy is an effective therapy in chronic fatigue syndrome:result of an Italian study in 65 patient” My initial take was that I was not surprised — why? Ozone kills some bacteria… but we need to dig deeper. Note: both Ozone and Hydrogen peroxide have one abnormal Oxygen atom that easily reacts. Hydrogen peroxide does wonders for killing bacteria on wounds.

First this study

What was done: “therapeutic shock of ozone autohemotherapy”

What was the result: “> 50% improvement in symptoms”

  • No one went into remission.
  • “symptoms” is way too subjective
  • “The practice of autohemotherapy carries significant risks without any health benefit. Patients have died. Plus, autohemotherapy has been an illegal practice in Germany since 1984, but you will find naturopaths advertising ozone therapy as “commonly used in Europe.” [www.naturopathicdiaries.com] – a very good read on legality in the US.

On PubMed

There are some 70 articles on ozone autohemotherapy many of them are from China.

Bottom Line

I would recommend a pass on this approach for three reasons:

  • No studies suggesting remission, just symptom improvement (whatever that means — especially given the placebo risk)
  • Real significant risks of adverse effects
  • Those offering it are likely violating laws or naive in understanding the full picture.

” Ozone as a medical therapy has been used in many medical conditions; unfortunately, however, like every other therapy, ozone therapy has side effects. The literature concerning ozone therapy supports possible strong vasoconstrictor and prothrombotic effects of ozone therapy, further supporting our suggestion that ozone can lead to acute coronary syndromes in human beings. In conclusion, to our knowledge, our case report reveals a possible complication of ozone therapy that has never been reported before. We think that this article will raise the awareness of the possibility of thrombotic complications after ozonated autohemotherapy. ” [2015]

Blood Type: Microbiome and Diet

One of my favorite sources for information on the microbiome is run by Dr. Peter J. D’Adamo. For many years he has advocated eating for your blood type. In this week’s issue of New Scientist. an article “Your gut bacteria may match your blood group – but we don’t know why

The difference between many blood types are sugars. [PDF]

These sugars are called antigens and help tell your immune system that your blood cells belong to you and shouldn’t be attacked. If an A person were to accidentally receive a transfusion of B blood, antibodies made by their immune system would react with the B sugar and flag these cells for destruction. ..
The team found that blood type wasn’t linked to any differences in the kinds of bacteria a person had. However, they noticed that bacteria seemed to be recognised by antibodies from different blood types, in a similar way to when antibodies detect incompatible blood cells.
This suggests that gut bacteria make sugars that match their host’s blood type. “We were very surprised to see this,” says Yin.

While some bacteria are already known to carry molecules that are similar to B antigens, this is the first indirect evidence that bacteria can have sugars that behave like A antigens too.

Gut microbiota have blood types as human
A blood antigen (GMA) and B blood antigen (GMB)

You can help build Blood Type Profiles of Microbiomes

Microbiome site is updated with the ability to record blood type with your microbiome. http://microbiomeprescription.azurewebsites.net

  • Login to see your uploaded sample.
  • Click on Analysis for your microbiome sample.
  • Click the item highlighted below

You will now see the ability to associate your blood type to your sample.

Remember to do this for each of your samples.

Bottom Line

Consider reading Peter’s eating for your blood type. Food impacts bacteria. I will be looking at the effort of filtering some suggestions by blood type in the next few weeks.

KEGGs and Inflammatory Bowel Disease

I often have attended the yearly talks of futurist/predictionist
Mark Anderson. This year there was talk about Mark’s new company, Pattern Computer.On that site I saw this interesting item

Insights in Inflammatory Bowel Disease

Using the Pattern Discovery Engine™ coupled with a hypothesis-free approach, we analyzed a large dataset of 50 human microbiome samples, each with the relative abundance of the ~10,000 KEGG protein families. We identified 39 KEGGs that were significant in differentiating the disease states from each other and from healthy, with 9 of the KEGGs (out of 10K total) being most associated with a dynamic path from disease to health in the human-gut microbiome. Using our approach we were able to reduce the size of the dataset to be analyzed by three orders of magnitude.

What is a KEGG?

KEGG (Kyoto Encyclopedia of Genes and Genomes) is a knowledge base for systematic analysis of gene functions, linking genomic information with higher order functional information. The genomic information is stored in the GENES database, which is a collection of gene catalogs for all the completely sequenced genomes and some partial genomes with up-to-date annotation of gene functions. The higher order functional information is stored in the PATHWAY database, which contains graphical representations of cellular processes, such as metabolism, membrane transport, signal transduction and cell cycle.

KEGG: Kyoto Encyclopedia of Genes and Genomes [2000]

Or in plain english, it is show what produces, consumes or influence processing of chemicals in nature (including the human body and the microbome in your gut).

We are getting into complex areas which makes a Gordian knot look like a straight piece of rope.

Their Draft Paper

Read the paper here. A chart from it is very interesting:

Further research into these nine KEGG protein families revealed that six of the nine KEGG protein families identified are related to oxidative phosphorylation. IBD, like other inflammatory diseases, may be associated with abnormal oxidative phosphorylation or oxidative stress [10]. Oxidative phosphorylation produces reactive oxygen species (ROS) in both prokaryotes and in the mitochondria of eukaryotes. Microbial ROS production affects the innate immune response, influencing the integrity of the intestinal epithelial barrier (2) which is compromised in IBD.

Path ways: K00330, K00348, K00351, K00434, K00604, K00607, K00609, K00633, K03671.

Bottom Line

While the sample sizes were small (and likely not widely distributed geographically), the results are definitely interesting. It does point to reducing oxidative phosphorylation and inhibiting reactive oxygen species as desired paths forward (and likely topics for future posts).

For people interested in watching the talk:

Mark Anderson’s 2019 Predictions

Lecithin: Friend, Foe or Neutral

I received several questions about Lecithin on Facebook and this blog after my last post on Emulsifiers. I cited one study that I found for illustration purposes:

Dietary carnitine (present predominately in red meat) and lecithin (phosphatidyl choline) are shown to be metabolized by gut microbes to trimethylamine (TMA), which in turn is metabolized by liver flavin monoxygenases (especially FMO3 and FMO1) to form trimethylamine-N-oxide (TMAO). High levels of TMAO in the blood strongly correlate with cardiovascular disease and associated acute clinical events.

Dietary modification of the microbiome affects risk for cardiovascular disease.[2013]

Many of the questions came from the belief that lecithin helps heal the gut. My goal is to see what has been found in studies listed on PubMed – my gold standard for separating urban-(medical)-legend from reasonable facts. I first look at conditions: There was nothing for Chronic Fatigue Syndrome.

Irritable Bowel Syndrome

There are no studies except with boswellia where it was used as a delivery mechanism.

Crohn’s Disease

“The most promising approach in UC seems to be the use of probiotics or the natural compound lecithin as a stabilizer of mucus structure to enhance the barrier…. ongoing phase III study … “

Improvement of a ‘Leaky’ Intestinal Barrier. [2017]

Note: that we have an “or” and “seems to be” — so no concrete results yet.

“Children with CD frequently consume food additives, and the impact on disease course needs further study. ( Mean exposures per day for xanthan gum was 0.96 ± 0.72, carrageenan 0.58 ± 0.63, maltodextrin 0.95 ± 0.77, and soy lecithin 0.90 ± 0.74.  )”

Children with Crohn‘s Disease Frequently Consume Select Food Additives. [2018]

Note: The authors are stating concerns about all of these food additives for Crohn’s Disease children

Ulcerative Colitis

In randomized controlled studies, delayed-release lecithin [phosphatidylcholine (PC)]  was proven to be clinically and endoscopically effective, which now awaits a phase III authority approval trial.

Lecithin as a therapeutic agent in ulcerative colitis. [2013]

Note: There were no results published for the phrase III study. If there are old studies indicating positive results and plans for more studies, but nothing is published, THEN most researchers would conclude that no positive results were obtained and thus the study was not published because it failed to produce intended results.

Issues Associated with Lecithin

 lecithin, choline, and carnitine) are converted by closely related gut bacterial TMA lyases to TMA, which is absorbed and converted predominantly by flavin mono-oxygenase 3 to the toxic trimethylamine N-oxide (TMAO). TMAO causes atherosclerosis in animals and is elevated in patients with coronary heart disease

New Insight into the Dietary Cause of Atherosclerosis: Implications for Pharmacology. [2016]

 No scientifically valid clinical studies exist on the safety and efficacy of high-dose lecithin supplementation in nursing mothers or infants. 

Lecithin. Drugs and Lactation Database (LactMed) [Internet]. Bethesda (MD): National Library of Medicine (US)

Bottom Line

It appears that some early studies saw improvement when a delayed- release dosage of lecithin was used (no information on the dosage). As these studies were on what appear to be a potential commercial product, the missing phrase III studies suggest that positive results were not found. What is more interesting to infer is the decision to use delayed release — it implies there were issues seen with direct lecithin (which likely were not published but known to the researchers).

There are reports of lecithin overdose and drug interference. There are no safety studies to determine what dosage is beneficial (and what level is harmful).

I conclude that current published evidence does not support the use of lecithin supplements.

Emulsifiers – making autoimmune flare again!

My eye caught a news story today Common food additive may impact gut bacteria, increase anxiety.

Earlier studies have shown that emulsifiers can alter the microbiome of mice, causing low-grade inflammation and increasing the risk of obesity and metabolic disorders.

study in humans concluded that gut bacteria “can be directly impacted by these commonly used food additives, in a manner that subsequently drives intestinal inflammation.”

The scientists showed that the emulsifiers did impact gut bacteria, but in different ways for male and female mice. They also showed that the changes in behavior were different between the sexes.

Specifically, they saw an increase in anxious behavior, particularly in male mice. In female mice, there was a reduction in social behavior.

A common one is polysorbate 80, which I have a page on the bacteria that it is known to change, here. It is often found in ice cream and cottage cheese. It is also in some vaccines.

Another one, cited above is carboxymethylcellulose (CMC)

Other emulsifers used in the US include [2017]:

  • lecithin [phosphatidylcholine (PC)]  ,
  • mono- and diglycerides (MDGs),
  • stearoyl lactylates,
  • sucrose esters, and
  • polyglycerol polyricinoleate.

For lecithin, we read:

Dietary carnitine (present predominately in red meat) and lecithin (phosphatidyl choline) are shown to be metabolized by gut microbes to trimethylamine (TMA), which in turn is metabolized by liver flavin monoxygenases (especially FMO3 and FMO1) to form trimethylamine-N-oxide (TMAO). High levels of TMAO in the blood strongly correlate with cardiovascular disease and associated acute clinical events

Dietary modification of the microbiome affects risk for cardiovascular disease.[2013]

Bottom Line

Checking products for any emulsifiers before buying (and asking your waiter when eating out, which menu items contains no emulsifiers) is strongly recommended — especially if you have any gut or anxiety issues.

Foods commonly containing emulsifiers are:

  • almost every processed food, from ice cream, to low fat cookies and salad dressing contains a wide range of emulsifiers that keep ingredients from separating, improve the texture and taste especially of low-fat foods, and increase shelf life. ” [src]
  • salad oils
  • some cottage cheese, some cheese (especially processed) and many yogurts [src]
  • ice cream
  • bread
  • chocolate
  • margarine
  • processed meat

Some of this list from an article entitled “The perfect mixture: emulsifiers make our food enjoyable” . IMHO, it needs a subtitle, “and do a number on your microbiome!’

A list of various names that may be on products [src]:

  •  Soya Lecithin Granules G
  • Soya Lecithin Powder P
  • (Ultralec® P & G)
  • Soya Lesithin-Powder,Granulate,Liquid
  • Distilled Glycerin Monostearate(D…
  • Potassium Stearate
  • Calcium Stearoyl Lactylate(CSL)
  • DATEM
  • Glyceryl Monostearate
  • Mono Propylene Glycol
  • SPAN 80
  • Sodium stearoyl lactylate(SSL)
  • Tween
  • Sodium Stearate
  • Glycerol Triacetate
  • Sugar Esters
  • Polyglycerol Esters of Fatty Acid…
  • Non dairy creamer
  • Calcium Stearate
  • Polyglycerol Polyricinoleate (PGPR)
  • E No: E476
  • Soya Lecithin Liquid (Yelkin® TS)

Bottom line: Use the raw ingredients to prepare meals. Beware of all processed foods.

Intrinsic Factor and low Vitamin B-12 levels Cognitive Impact

What is Intrinsic Factor?

Intrinsic factor (IF), also known as gastric intrinsic factor (GIF), is a glycoprotein produced by the parietal cells of the stomach. It is necessary for the absorption of vitamin B12 later on in the ileum of the small intestine.[5] In humans, the gastric intrinsic factor protein is encoded by the GIFgene.[6]:989

Wikipedia

With CFS/ME, Lyme and other conditions being low in Vitamin B12, suggests that an issue with GIF could have developed. This may be due to an epigenetic event. The incidence of defects in the GIF Gene is very low.

However, wikipedia is incomplete, because it is not only parietal cells.

These findings demonstrate a potential for cellular expression of human intrinsic factor in nonparietal cells. Because such expression occurs normally at the margins of anatomical gastric regions, it suggests that local factors may influence expression of intrinsic factor.

Human gastric intrinsic factor expression is not restricted to parietal cells. [1996]

These data in humans with and without gastritis are consistent with the hypothesis that local factors influence ectopic gastric IF expression, arising from either the anatomical location, the focal inflammation, or both.

Production of ectopic gastric intrinsic factor in gastric mucosa of humans with chronic gastritis [2011]

The earliest recorded history of autoimmune gastritis can be traced to 1849 in London, when Thomas Addison described “a very remarkable form of anemia” later called pernicious (fatal) anemia (PA). This was followed by the recognition of a gastric mucosal defect suspected to have a nutritional basis, the discovery of the megaloblast that characterized the anemia, the insufficiency of a dietary extrinsic factor characterized as vitamin B12 (cobalamin), and a gastric-secreted intrinsic factor. Treatment with vitamin B12 proved curative. The link between PA and gastritis and atrophy was first confirmed histologically after immediate fixation of the stomach postmortem and later, in the 1940s, by peroral tube biopsy. The causes of gastritis remained enigmatic until the era of autoimmunity, when autoantibodies were detected first to gastric intrinsic factor and then to gastric parietal cells. Hints of a dichotomy in pathogenesis of gastritis were crystallized by the description in 1973 of Type A (Autoimmune) and Type B (later, Bacterial) gastritis.

Autoimmune gastritis: historical antecedents, outstanding discoveries, and unresolved problems. [2005]

Proton pump inhibitors also reduce the absorption of vitamin B(12) probably by inhibiting intragastric proteolysis 

Effect of proton pump inhibitors on vitamins and iron [2009]

 The results suggest that IF insufficiency may occur during cimetidine treatment in patients 

Effect of cimetidine on intrinsic factor secretion stimulated by different doses of pentagastrin in patients with impaired renal function. [1983]

Issues reported in the literature with low B12, includes:

  • “The most common psychiatric symptoms were depression, mania, psychotic symptoms, cognitive impairment and obsessive compulsive disorder. Neurological involvement includes mainly combined spinal sclerosis, peripheral neuropathy and dementia. ” [2015]
  • “These symptoms seem to fall into several clinically separate categories: slow cerebration; confusion; memory changes; delirium, with or without hallucinations and/or delusions; depression; acute psychotic states; and (more rarely) reversible manic and schizophreniform states. ” [1988]

Bottom Line

From the literature, it is well established that one bacteria influences GIF, Helicobacter pylori. In terms of drugs that reduces GIF, we see these drugs impact a lot of bacteria families (linked to from drug below):

It appears that GIF production is influenced by the local environment/factors. An important factor for this is the microbiome – bacteria involved.

Treatment

First choice is always to stop drugs that reduces GIF. Second choice, is to eliminate any known bacteria that reduces GIF, explicitly, testing for
Helicobacter pylori (you may lack symptoms and still have it). Third choice is supplementing with Vitamin B12.

Fourth choice (which may also impact the 2nd choice), probiotics that produces or processes B12.