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Month: February 2023

Post biotics, are you kidding me?

Post biotics, are you kidding me?

This newsletter attempts to update its readers on the hot areas in medical research.  If you have read even a few of these newsletters you will know the frequency of articles on the human microbiome and immune health. 

Much research is being done on the complex physiology of the microbiome.  In keeping with that theme is research on promoting a healthy microbiome.  To date most of this research has been on probiotics either natural as in yogurt or kefir or as supplement containing active strains of healthy bacteria and yeast.  

Then research segued to prebiotics.  Prebiotics can be provided through healthy foods, primarily fruits and vegetables, or also though a supplement. In both cases support is provided to “nourish and flourish” the healthy gut microbes. 

Now enter post biotics.  These are available only as a supplement.  They contain dead bacteria and useful products excreted by live microbes.  One might ask “what good is a dead albeit good bacteria much less the things they excrete”?  As it turns out they are quite useful.  First of all, they don’t run the very slight risk that probiotics have in immune compromised individuals of “running amuck”.  Secondly, some of the key benefits of the bacteria come from their protein structure, and the enzymes, vitamins, polysaccharides and short chain fatty acids they secrete.  All of these moities play a favorable role in digesting food properly, reducing inflammation, and in proper signaling via nerve transmitters and nerve fibers.  One example is the short chain fatty acid butyrate.    It is a multi-tasker: reduces chance of food allergy development and strengthens the gut wall thereby reducing the inflammation that can contribute to obesity and to inflammatory bowel disease such as Crohn’s disease.  In fact, butyrate enemas have been used with success in patients with difficult to control ulcerative colitis. 

A second example is the bacteria metabolite urolithin A (UA) which maintains mitochondrial function.  Mitochondria are the “batteries” that power all of our cells, to the degree that if they

underperform or decline in number, we have less energy and we age more quickly. 

Melatonin: Medicine, Myth or Mischief

Melatonin: Medicine, Myth or Mischief

The sale of melatonin is a two billion dollar a year business which must mean that a lot of people have trouble sleeping. 

Sleep is an intricately choreographed neurologic process.  Critical to good sleep is the circadian variation of the reticular activating system.  Melatonin produced in our brains has a mild modulating effect on our sleep cycle.  However, people who have had their pineal gland (a major source of melatonin) removed are able to sleep just fine. 

Because melatonin sales are not regulated by the FDA, scientists decided to do controlled studies to determine its potential benefit.  Multiple studies comparing melatonin to placebo found the same results.  Sleep latency (the time required to fall asleep) was decreased by 7 minutes and total sleep duration was increased by 8 minutes.  So, there is a measurable benefit, albeit very modest. 

The flip side of the coin is safety.  Accidental or purposeful overdoses with melatonin occur in one out of 20 ER visits for overdose.  Some children have died or

required ventilator support to recover. The other issue is content of the product.  Chemical assays of melatonin products have shown that the actual content can vary from 83% lower to 478% higher than what was claimed on the label.  One chewable tablet for children contained 9 mg rather than the 1.5 mg noted on the label.  Moreover, a quarter of the products sampled contained serotonin (not on the label) in addition to melatonin. 

Twenty-five years ago, the science journal “Cell” cautioned about melatonin madness.  They advised ignoring the hyperbole and histrionics of advertising and instead to focus on sound science.    

 Dear Dr. K; Is it just me or is there a

 Dear Dr. K; Is it just me or is there a

he- –  of a lot of cold and flu this winter?

It’s not just you.  Covid-19 is adding to its historical legacy by this resurgence of other respiratory infections.  According to epidemiologists (scientists who study the incidence and distribution of diseases) this is unprecedented.   For instance, hospitalization rates for both adults and children for influenza are the highest in over twenty-five years. 

The simple explanation is that the cumulative load of infections that would have occurred over the past three years, but didn’t due to mask wearing and social isolation, are now making up for lost time. 

Another factor that markedly attenuated influenza was the decrease in global travel.  The influenza virus has always relied on our “small global community created by travel” to infect the maximum number of humans.  Now with global travel returning to pre-Covid frequency the flu virus has hitched a ride. 

RSV (respiratory syncytial virus) has used a different strategy.  Normally RSV infects a small portion of young children each season.  The small numbers have kept it from being epidemic or pandemic.  Also, once infected the child develops resistance.  But for three years many children have “missed the illness” leading to a very large population of susceptible hosts.  With more children all getting sick at once, the trickle-down effect has been a spread to older adults whose immunity has waned over the years.  So once again hospitalization rates for children but now also older adults are unprecedented.   Then add on all the other “cold viruses” such as Rhinovirus and Coronavirus into the “catch-up” mix and you have a lot of sick people out there. 

Respiratory bacteria also follow the Darwinian mantra of survive and propagate.  Some of the leaders in the bacterial pack are Pneumococcus, Streptococcus, Hemophilus, Moraxella and Mycoplasma.  The relaxing of social isolation and mask use have allowed them to play “catch up”.

A few practical strategies to lessen your chance of illness include the usual hand washing advice.  But, nasal saline rinses at the end of the school day or work day can provide an additional mechanism of protection.  Finally, getting a flu vaccine has value.  Many Americans are fed up with all of the Covid vaccines and have consequently avoided their usual annual flu shot.

EBV and MS

EBV and MS

The cause of MS (multiple sclerosis) has long been sought.  Although many factors are felt to predispose to it, genetics and environment top the lists.  For instance, the illness is much more common in Europe and North America than in the rest of the world. 

Viral infections have long been suspects.  Now there is mounting evidence that the Epstein Barr Virus (EBV) may be the culprit.  Two recently published research studies lend credence to this possibility. 

The first study was done on service members on active duty who came down with MS.  Over the study period 801 patients developed MS and all but one of them had evidence of active EBV infection.  Now, don’t over interpret this finding.  Evidence for prior EBV infection (the main cause for Mono, although CMV can also cause Mono) can be found in 90 plus percent of young adults and MS is a comparatively rare disease. 

But the other recent study done by immunologists at Stanford University found that 25% of the MS patients they studied had a blood antibody that reacted to both EBNA1 protein and GlialCAM (glial cell adhesion molecule) protein.   These two proteins are very similar in their chemical structure even though one is a viral protein and the other is a protein found in myelin sheaths.  This is a phenomenon called molecular mimicry.  Long story short what seems to be happening is the immune systems attempt to irradicate the virus via the anti-EBNA1 antibody ends up attacking the GlialCAM protein in the myelin sheath of nerves.  The myelin sheath can be thought of as the plastic or rubber insulation on an electric wire.  Damage to the sheath leads to altered nerve conduction and hence the numbness and muscle weakness found in MS. 

The Stanford scientists extended their research in a mouse model.  In one group of mice they injected EBNA-1 protein into their brains and in the control group a non-viral protein of similar size.  A handful of the EBNA-1 injected mice developed neurologic disorders whereas none of the control group did.