Friday, July 28, 2017

CONSEQUENCES OF ACID BLOCKING DRUGS, AND NATURAL ALTERNATIVES

The topic of proton pump inhibiting drugs, or PPIs, otherwise known as acid blockers, has been a topic near and dear to my heart recently because my father, who is very medically indoctrinated, has been on a PPI for YEARS, and is now very sick with some of the side effects, such as extreme fatigue, stomach distension, and small intestine bacterial overgrowth, or SIBO.  He was also diagnosed with bladder cancer, and a 2011 study showed that PPIs are linked to cancer, although the form of cancer analyzed in that study was esophageal cancer. 

So in researching this topic for the benefit of my father, I discovered that PPI’s were never intended to be used long term anyway, even by the standards of the drug companies who make them.  Yet my Dad and countless other PPI users have been on them for years. 

If you know even basic physiology, it’s not really rocket science to know that suppressing the stomach acid at all, especially for stretches of years, is a really, really bad idea.  Stomach acid is the first line of defense against pathogenic bacteria, it stimulates peristalsis, it initiates bile secretion, and of course it helps to assimilate important nutrients like B-vitamins, minerals, and protein, just to name a few.

Let’s just consider SIBO for a moment.  If stomach acid is suppressed, it allows some pathogens to survive in the stomach that would otherwise be eliminated, leading to infections of the stomach like H. Pylori.  But then that pathogenic bacteria gets transported into the small intestine, and later the bowel, and can also go systemic, leading to all different kinds of potential maladies related to that circulating bacteria. 

Likewise, suppressing the stomach acid can lead to putrefaction of food in the stomach, leading to halitosis, distension, and more problems with indigestion.

And actually, this is where the whole maddening thing about using acid blockers in the first place needs to be addressed, because the whole idea about acid reflux being a manifestation of too much acid represents a lack of understanding, in some cases, of stomach physiology. 

Think about it.  Our stomachs have these cool little muscles at the top called the esophageal sphincter, which pinches off and blocks the acid from reaching the esophagus.  That muscle is activated by, guess what?  Stomach acid!  If a patient has hypchlorhydria, or low stomach acid, that muscle’s action can be inhibited, and it might not activate like normal, resulting in what little stomach is there reaching the esophagus.  Now, even a little acid in the esophagus is very irritating, and the medical interpretation is, “Oh! You have too much stomach acid.  Let’s block it.”  No, that patient probably has too LITTLE stomach acid, but the manifestation is burning in the chest and throat.

Here’s an example that I think will be helpful and applicable.  One Thanksgiving my older sister was at our house sharing the Thanksgiving meal with us, and afterward she sat down on my couch holding her stomach and moaning.  When I asked what was wrong, she said she had been struggling with indigestion and acid reflux for a long time, and she was having another episode.  So I gave her three tablets of a product containing betaine HCl and pepsin, or stomach acid.  In about 20 minutes she felt so much better that she had to ask me what it was that I gave her.   Sometimes if the problem is mild you can accomplish the same thing with apple cider vinegar.  I have had some success with that approach as well.

Now, having a patient go off a PPI can be tricky, because the parietal cells in the stomach have been suppressed for so long that sometimes it can trigger a strong rebound effect.  So to fight that, I would recommend having a combination powder containing DGL, aloe, and glutamine.  That combination is great in helping to soothe the discomfort associated with acid reflux while the patient is weaning off the drug. 

I also had a practitioner just this past week tell me that she gives magnesium to patients coming off long term PPIs because it helps get peristalsis going again, so I thought that was good insight. 


Feel free to reach out me if you need some product guidance.

Wednesday, July 12, 2017

Weight Control, Glucose Sensitivity, and the other Benefits of B. Lactis B420

As the research on probiotics continues to mushroom, some very compelling applications are being shown that would not have previously been attributed to the microbiome.  

Along those lines, then, there's some very interesting research surrounding a new probiotic strain called, Bifidobacterium Lactis B420.  

Now, before we examine the research on this strain, let's first note that medical science is beginning to make a connection between body weight and gut microbiota.  This was first discovered by accident with fecal implant patients.  Doctors began to notice that recipients of fecal implants would take on the characteristics of the donor in terms of body composition.  So a study was done on mice to try to reproduce this, and indeed they found the same thing in the laboratory.  A fecal sample was taken from an obese person and implanted into a mouse, and the mouse gained weight. 

So enter, then, the research on B. Lactis B420. 

Before we look at the research specific to body weight, let’s first look at the various other benefits of this impressive strain on other health paramters.

Experimental research has indicated that:

  • B420 increased tight junction integrity of epithelial cells, and therefore protected gut epithelial cells from the harmful effects of pathogenic microbes.
  • B420 protected against NSAID-induced GI side effects in a rat model by reducing an NSAID-induced inrease in stomach permeability
  • B420 reduced mucosal dysbiosis, bacterial translocation, expression of major pro-inflammatory cytokines in various tissues, and improved glucose metabolism in mice fed a high fat diet (HFD).
  • In HFD-fed mice, B420 modulated gut microbiota and improved glucose intolerance.  Further, the combination prevented the impairment of intestinal immunity due to metabolic abnormalities induded by the HFD.
  • In a mouse model of diabetes, B420 enhanced concentrations of ileum GLP-1, a protein involved in both insulin secretion and satiety signaling.
  • In an obese mouse model, increases in body weight and fat mass in mice fed with HFD for 12 weeks were significantly reduced if the mice were co-administered B420.  
  • In a diabetes mouse model, mice receiving both HFD and B420 had decreased fat mass compared with mice receiving only HFD.  B420 also improved glucose metabolism in this mouse model.


So this is already a very impressive list of benefits even without the benefits of weight control.  But now let’s turn our attention to that aspect, which is human data.

The goal here was to determine if the B420 could make a change in the incremental body weight that many people experience over time as they age.  The untreated group of overweight individuals gained 3.1% of bodyweight in six months.  The overweight group receiving 10 billion units per day of the B420 probiotic strain, however, did not gain any extra body weight in that same period of time, and they observed no dietary or lifestyle changes.  All they did was add the probiotic.  The probiotic group also showed a slight decrease in waist circumference of 2.4%, AND they ate less, showing improved satiety with the use of the probiotic strain. 

Another very positive benefit was the improvement in short chain fatty acids over that period of time, a huge benefit to gut health. 

Now, as we know, many people tend to gain weight as they age, some a little, and some a lot.  It’s too early to tell if the B420 can legitimately be called a weight LOSS probiotic, but it can certainly be called a weight CONTROL probiotic.  With that in mind, remember that those in the study didn’t change anything about their lifestyles.  So it could be, perhaps, that if this probiotic strain was added to a weight loss plan, it may amplify the effects of the other weight loss efforts….maybe.  Again, there’s not enough information to go on yet to verify that statement, but I think it’s a fairly good assumption that this could be the case. 

I’ll close by saying that weight gain with age is multi-factorial, and can be attributed to shifts in hormones and other factors.  However, we cannot and should not rule out the changes in the microbiome that occur with age as well.  And weight issues aside, there are enough other benefits with this remarkable strain that it should be considered for use with leaky gut and autoimmune patients, those with gut dysbiosis, and even glucose and insulin intolerance. 

References available upon request



Thursday, April 27, 2017

The Emerging Understanding of Probiotics and Colonization

Recently I was asked a good question by a doctor about oral probiotic supplements and whether they survive transit in the GI, particularly very acidic stomachs, and whether or not there are studies confirming colonization of various probiotics strains.  Since this question represents the more widespread thought process of probiotics -- a thought process that is becoming antiquated -- I thought I would pass the answer on.


To answer this question, let's consider the strain studied in weight control.  The genus, species, and strain are: B. Lactis B420.  B420 is not a human-strain. It was first identified in dairy. However, as fermented dairy foods are common in human diets, B420 can be grown from a stool sample from non-supplemented humans (proof of survival in GI transit). Also, in the current study, B420 was cultured from stool samples of the treatment arms as proof of survival in GI transit. So is this same culturing required for all human-strain probiotics? Not really. If they are human-strains, how did they get there in the first place? Orally, through foods, through the gut. Non-protected, no 'encapsulation' was needed naturally. And one would assume that this is the case even with very low pH (high acidity), since probiotics from fermented foods appear to still colonize the guts of people in all pH ranges.  (i.e. People with very high acid stomachs with a pH of, say, 1 or 2, do not have sterile GI tracts.  They are still colonized with all kinds of bugs.)

Regarding survivability of stomach acid, then, what is well understood is that the stomach is acidic pretty much all the time (while food may actually act as an acid buffer), and that human-strain probiotics should 'naturally' be able to survive GI transit (i.e. how did they get their in the first place?).


Now, here's the biggie: 
Colonization. 


It used to be thought that the rationale for use of oral probiotics was to repopulate the gut. That is out of date. The current understanding of probiotics is strain-specific activity. In other words, residency in the gut microbiota seemed to be the marker of a strain's hardiness/survivability in times past.  But not anymore. The modern understanding is that oral probiotics are not about colonization.  Oral probiotics are about their transient effects, helping to make the neighborhood a better place. A healthy gut is a diverse one, made up of hundreds, even thousands of species. How can one create diversity through oral probiotics of one, two, or even eight strains? It likely cannot be accomplished with so few strains.  The oral probiotic stays for a little while, does its job, and then leaves.  Job done.  


Part of the definition of oral probiotics​ is proven efficacy in humans proven by reams of research, which, by the way, is why you want the genus, species, AND strain -- all three -- identified so that you can correlate the strain with the research.  Said another way, according to sources like the International Scientific Association of Prebiotics and Probiotics, a TRUE probiotic must have two things in particular in order to be legitimately called a probiotic: 1) genus, species, and strain identified, and 2) they must have proven oral benefit - including survival through the GI tract. If a product simply says on the label, for example, lactobacillus acidophilus, but no strain, then you cannot connect it to specific research, and thus, you don't know if it survives digestion or not, and you don't know what, if any, benefit it has in humans.  A product without the strain identified can probably rightly be called a bacteria, but NOT a probiotic.  If the strain is not identified on the label it is absolutely impossible to make any claim of being orally effective

Typically, part of the evaluation of a probiotic is observation of its traits (phenotype). The probiotic strain is tested for acid and bile tolerance. If tolerant, this is recorded. Once understood it is no longer necessary to test each generation of this proven strain trait. What is necessary is to test the DNA to ensure that each generation is the same as previous (genotype). 

The third factor to GI survival is the use of human microflora. As stated above, these species/strains ‘natively’ survive passage through the GI tract,​ as this is their normal abode. Once againhow do the hundreds of species of good flora get to the gut in the first place? Nearly a​ll orally. Ninety-percent of the bacteria that enters the body does so through the mouth. ​The genus/species of bacteria that live in our gut survive and thrive,​ as they are inherently adapted to do. 

As an example, consider the genus and species of one common probiotic family, Lactobacillus acidophilus.The latter term, acidophilus, is​ from the Latin, and refers to ​"acid-​loving."​
  
So, in short, yes, most probiotics survive digestion (some strains much better than others), even in very acidic stomachs.  And yes, part of the research in identifying a true probiotic is its effectiveness in humans. But again, colonization is not the true marker of a probiotic's effectiveness: strain-specific activity is.  And that is another reason why the genus, species, and strain listed on the bottle is so important.


In closing, I should add that some companies choose to list the strain in their promotional literature, but not on the bottles.  This, too, is a quality issue because by not listing it on the label of each bottle, companies don't have to prove that the strains are in THAT bottle or lot.  Companies who do random batch assays and then list the strains in their promotional literature are not proving anything in regards to all the different batches and bottles.  If a company lists the strains on the bottle, however, they have bound themselves to being able to provide documentation of the presence of those strains in that bottle and batch.