Some Early-Stage, But Promising, Science About the Microbiome and Cancer

Yesterday morning, I posted a story on my Biome Buzz’ Facebook page about 2 new studies that independently showed that there is a distinctive microbiome composition associated with colorectal cancer.[i]  One study “…identified a set of 29 species indicative of colorectal cancer across 7 countries,” while the other showed “…higher gut microbiome richness” than controls, which ordinarily sounds like it should be a good thing but in this case, that richness came from bacteria that are native to the mouth that had moved to the colon, where they are not meant to be.  This led to altered glucose metabolism in the large intestine, as well as the “putrification” of amino acids, etc.

I read that article with great interest as I was intending to start writing this post about a recent summary of what we currently know about using probiotics in treating and preventing cancer – and you all know I love coincidences![ii]

Upon reading this new article, the first thing that struck me was how long ago research into the connection of cancer to the gut bacteria began.  Back in 1980, two researchers (Goldin and Gorbach[iii]) first demonstrated an, “…association between a diet enriched with Lactobacillus and a reduced incidence of colon cancer (40% vs. 77% in controls)”!  That’s almost 30 years ago!  And so very little progress, really, has been made since then.  Of course though, thankfully, there has been at least some.

So a few highlights:

  1. The authors enumerate several potential mechanisms of action as to how probiotic bacteria prevent cancer.  Of course, “A specific mechanism associated with anti-tumor properties of probiotics remains unclear.”
    • Probiotics can help prevent excessive bile acids (which is carcinogenic) from adversely affecting the lining of the colon: “…probiotic bacteria such as L. acidophilus and B. bifidum have been demonstrated to be a promising tool in cancer prevention.”
    • Putrification (pathogenic) bacteria, like E. coli and Clostridium perfringens, both of which are naturally found in the human gut, create carcinogenic compounds using certain enzymes. In the late 1970s, the two researchers I mentioned above (Goldin and Gorbach), showed – in rats – that eating fermented milk products (ie. yogurt or kefir) had a beneficial effect on the amount of L. acidophilus in the rodents’ intestines which “…subsequently resulted in a reduction of putrefactive bacteria and decrease in the level of harmful enzymes.”  This has been confirmed in more recent research.
    • Lactobacillus and Bifidobacillus bind and degrade potential carcinogens. For example, these strains alleviate the effect of eating carcinogenic compounds found in unhealthy foods, like fried meats.
    • Many of the metabolites produced by the probiotic bacteria themselves play “…an essential role in maintaining homeostasis and suppressing carcinogens.” The authors specifically talk about short chain fatty acids (SCFAs), which you’ve heard me talk about many, many times on this blog. (For example, here and here.)  SCFAs beneficially affect the immune system, cell proliferation and cell death (which, in the case of tumor cells, you can imagine is pretty critical!), as well as help maintain “epithelial integrity” (ie. leaky gut).
      • At this point, the authors actually make a really interesting point: lactic acid producing bacteria are not directly involved in SCFA production, but they modulate the gut microbiota which, in turn affects the production of SCFAs.  That is, Lactobacilli and Bifidobacteria, are indirectly crucial in SCFA production.
      • “Colorectal cancer is strongly correlated with decreased levels of SCFA and SCFA-producing bacteria dysbiosis,” as I mentioned in the opening paragraph of this post. In mice, boosting levels of bacteria which produce the SCFA, butyrate, for example, inhibits the progression of tumor development.  So…eat your fiber (said Judy, for the millionth time…like here!)  Or, as these authors write, “…the prebiotic activity of fiber-enriched diet…is a promising strategy to prevent CRC [colorectal cancer].”
    • Probiotic bacteria also have the ability to increase and decrease inflammatory cytokines (chemical messengers) in the body, as well as modulating the production of prostaglandins, which are immune compounds which suppress cancer formation. They can also activate immune cells called phagocytes, which directly eliminate early-stage cancers.
    • Probiotic bacteria can suppress gastric cancers related to H.pylori infections, as well as clear the virus, HPV, which is associated with cervical cancer. A study on humans showed enhanced clearing of HPV with 6 months of consumption of probiotics.
  2. A 2012 meta-analysis of 19 different human cohort studies showed an “association between consumption of dairy products (except cheese) and a decreased colorectal cancer risk.” A second study confirmed these findings.  (However, high fat dairy does increase bile acid levels in the colon, which – as noted early – may be carcinogenic.) Also of note: a huge cohort study, on 45,241 subjects, “proved a significant association between single probiotic-rich product intake (yogurt) and decrease colon cancer risk.”
  3. The paper takes a brief look at the future, in terms of using probiotics to treat cancer. For example, scientists have used probiotic bacteria to modulate the immune response and have even been able to entirely inhibit tumor development.  Others are working on using probiotics as “vaccines,” manipulating the immune system to fight off various carcinogenic pathogens, like HPV (the virus that can cause cervical cancer).  And still others are using probiotics to more effectively deliver medicines to where they are most needed.


Unfortunately, as I said earlier, all this research – as promising as it is – is still pretty early stage, as most studies have been done in animals.  On the bright side, I hope with all my heart (considering how many people I already know who have had to fight (and all-too-often succumbed to) cancer:  “…evidence from the latest studies points towards the idea of possible implementation of probiotics in cutting-edge cancer therapy.”



[ii] Gorska, A, Przystupski, D, Niemczura, MJ, Kulbacka, J. Probiotic bacteria: a promising tool in cancer prevention and therapy. Current Microbiology.

[iii] Goldin BR, Gorbach SL (1980) Effect of Lactobacillus acidophilus dietary supplements on 1,2-dimethylhydrazine dihydrochloride-induced intestinal cancer in rats. J Natl Cancer Inst64:263–265.


Evolutionary Mismatch, the Human Biome…and a Bit More on Obesity

Recently there was a lot of discussion on the Biome Buzz’ Facebook page in regards to a post on obesity, wherein some people expressed their opinions that our current epidemic of obesity is due to nothing more than people eating too much junk food.  While there is zero doubt that diet is a (probably THE) major factor, I pointed out that it is not that simple.

Dr. William Parker,, of Duke University Medical School, wrote a paper back in 2013 which described the concept of “evolutionary mismatch.”[i]  This encompasses the idea that through evolutionary pressures (survival of the fittest), our bodies have developed in such a way as to account for the presence of our “old friends” (the trillions of organisms that co-exist in us) and modern living has deprived us of that which is now necessary for our bodies to function properly:  “Species depleted or even eliminated from the human biome include a wide range of pathogens, commensals and mutualists whose reproductive cycle is greatly diminished or even eliminated by modern sanitation, water treatment and medical practices…The absence of species from the human biome leaves the immune system in a hypersensitive state that, when combined with environmental triggers and genetic predisposition, leads to allergic and autoimmune disease. The wide range of evidence pointing incontrovertibly at this conclusion…”

My regular readers are very familiar with this idea as nearly every post I have written over the years describes the emerging science that connects biome depletion to our current epidemic (in the industrialized world) of chronic, immune-related illness.

I read a really interesting article yesterday that further explores this idea.[ii]  These authors, from the University of Louisville, examine the idea of evolutionary mismatch and natural selection, in light of biome depletion and the effect upon public health – and forward some ideas of how our society can (and must) deal with this threat.

So a few really interesting bits from the paper:

1. Many (if not most) microorganisms’ effects on human health are unknown.  They refer to these organisms as “indeterminate symbionts,” defining a symbiont as an organism that lives “intimately with other organisms.”  Commensal organisms are symbionts that have “neither a harmful nor beneficial overall effect.”  If you imagine a spectrum then, commensal is the dividing line between parasites and mutualists (those organisms that benefit the host while themselves, benefiting from the host).

2. Some organisms are “strong mutualists,” and are at the far end then of this spectrum on the beneficial side. They provide an example in the Bifido strain, infantis. In infants, “It releases antibacterial compounds that inhibit pathogenic bacteria, synthesizes vitamins, improves immunological responses, and protects premature infants against ulcerative colitis.” And guess what?  Human breast milk is uniquely suited to helping B. infantis grow, with its rich supply of human milk oligosaccharides (prebiotics), which are particularly suited for this organism.  “The diversity of HMOs produced in milk appears to have coevolved for B. infantis more than for any other bacterium.”  Thus, the increased use of formula – which contains neither the probiotic, B.infantis, nor the prebiotic, sets babies up for a myriad of health issues.

A paper appeared in 2018 from the American Academy of Pediatrics, that states “…breastfeeding has many established benefits for child health; in fact, previous meta-analysis of research found that breastfed infants have a 26 percent reduced risk of obesity later in life. In a study in the October 2018 Pediatrics (published online Sept. 24)… researchers found that breastfeeding was associated with lower body mass index (BMI) and a reduced risk of excessive weight gain in the first year of life.”

From an evolutionary standpoint, “The mismatch between formula feeding and breast feeding is a particular example pertaining to a dietary change because infant formula differs from breast milk.”[ii]  Thus, by not feeding the infant’s developing microbiome as nature intended, we have created an evolutionary mismatch that is associated with obesity (and other chronic diseases) later in life.  Another recent paper looked at the gut bacteria in 2 year old children (who had no weight issues), and correlated this to obesity by the age of 12: “One recent study in this regard showed infant gut microbiota could be used as a biomarker to identify the children who are at risk of becoming overweight and obese later in childhood. That study…concludes that gut microbiota composition at 2 years of age can be used as a predictor for obesity at age 12. Although the toddlers may not be overweight or obese at 2, the research identified a correlation between their gut microbiota composition at early stages and their body mass index (BMI) at 12.”

3. On this same subject (i.e. obesity): there have been many papers lately pointing out that gastric bypass surgery improves insulin sensitivity even before weight loss has occurred.  “The rapidly ameliorating effects of gastric bypass surgery are consistent with microbiome influences on diabetes, which could occur quickly as a result of the short generation times of bacteria.  Gut microbiota are strongly affected by gastric bypass surgery.”[ii]  Another coincidence (that you all know I love):  an article on this appeared this morning on Gut Microbiome for Health which states,   “…interactions between the gut microbiota and bile acids metabolism may partially mediate the success of bariatric surgery in the medium term…the authors showed specific core gut microbiome profiles, with patients from the success group showing the most diverse gut microbiome”  In fact, success of the surgery appears to be reliant upon the composition of the gut bacteria.

4.  The authors point out that different microbes have a greater and lesser affinity for glucose. Those that thrive on it are essentially competing with their host human for the molecule. For example, Staphylococcus aureus loves glucose.  Therefore, it releases a peptide (short string of amino acids) that binds to insulin and blocks it from uptake by human cells, thereby increasing the amount of available glucose to the microbe, and “favoring insulin resistance” in the human:  “In a study assessing the relationship between neonatal microbiota and obesity seven years later, S. aureus was found in the fecal samples that had been taken from obese 7-year olds when they were neonates, whereas bifidobacteria dominated the neonatal feces of children who did not become obese.  Accordingly, breast feeding is associated with a substantially reduced probability of being overweight or obese during childhood.”

5. And of course, our modern “western” diets are a complete evolutionary mismatch: “The evolutionary mismatch of a diet low in fiber and high in sugar and fat and the radical increase in formula feeding have led to near global disturbance of the human gut microbiome with shifts in species diversity and proportions.”

6. Other illnesses that are clearly associated with evolutionary mismatch, according to this article, include celiac disease, diabetes, obesity, as I just mentioned, autism and allergies.  (Dr. Parer’s paper has a far more extensive list.) A quick example:  in a mouse model, infantis ameliorates allergy:  “Has the nearly worldwide shift to vast numbers of children being formula fed…led to a reduction in the population level prevalence of important gut bacteria for the newborn?”

7. One new vocabulary word for all of us:   There are organisms, which I have actually written about several times before, that, depending on environmental circumstances, are either parasitic or mutualistic.  The paper provides an example:  the bacterium, Bacteroides thetaiotaomicron, which is a commensal organism that is ordinarily mutualistic (in that it breaks down non-digestible carbohydrates into sugars usable by us)…unless it is in the presence of E.coli, in which case, it exacerbates the damage caused by this parasitic bacteria.  From now on, I’ll be using that term – ambisymbiont – when talking about such organisms.  I like it!   It has a ring to it…

8. Back to my the paper I mentioned in the opening paragraph: Parker et. al. point out that our modern diet and the decrease in breast feeding are just two of the current evolutionary mismatches to which we humans (and our domesticated pets, by the way) are subjected.  Others include our general lack of exposure to sunlight, in regards to vitamin D production, potentially “unrequited psychological stress,” and the eradication of our native macrobiomes.  “The identification of biome depletion as the cause for pandemics of immune disease carries with it a solution:  biome reconstitution.  Although the extent to which biome reconstitution can reverse disease remains unknown at present, biome reconstitution is hypothetically a readily available means of preventing disease associated with biome depletion.”

Or…as today’s paper concludes:  “Public health efforts to counter negative effects of the Western diet, support breastfeeding, and assure access to high-fiber, low-sugar, and low-fat foods may have an outsized effect on seemingly unrelated widespread diseases such as diabetes, autism, and childhood obesity.”


[i] Parker, W and Ollerton, J.  Evolutionary biology and anthropology suggest biome reconstitution as a necessary approach toward dealing with immune disorders. Evolution, Medicine, and Public Health. 2013;89-103.  doi:10.1093/emph/eot008

[ii] Ewald, HAS, Ewald, PW. Natural selection, the microbiome, and public health.  Yale Journal of Biology and Medicine. 2018;91:445-455.

Can Helminths Help Alleviate the Obesity Epidemic? The Evidence (Slowly) Mounts

Remember last week when I told you all that I have a million great new pieces of research to write about?  Well, things have only gotten worse(or is it better?!) since then.  I found a bunch more stuff to keep us all very busy these next few weeks.

Which is good news, I guess!

Today I am turning back to the topic of helminths because I found a pretty incredible article on a topic that is of particular interest to me.  As a nutritionist, one of my biggest concerns is the growing epidemic of obesity plaguing the industrialized world, as my regular readers know. A quick look at the latest statistics:  according to the CDC, 39.8% of adults in the USA are obese (during 2015-2016)[i].  A 2017 article in Forbes points out that, “…nearly 4 in 10 U.S. adults have a body mass index classifying them as obese. Adult obesity rates have continued to increase steadily since the turn of the century, rising from 30.5 percent in 1999-2000 to 39.6 percent in 2015-2016, a record high. Young Americans have also been piling on the pounds and the obesity rate among the country’s youth (aged 2-19 years old) currently stands at 18.5 percent.”  But that’s only a part of an increasingly-grim picture as, “…just over 70 percent of all Americans are either overweight or obese, meaning people with normal weight levels are now a minority.”

70%!  Holy cow.

Over the years since starting this blog, I have looked at various pieces of research wherein scientists are trying to figure out the cause of this explosion of obesity.  There is no simple answer:  it’s most certainly not just “people are eating too much.”  Yes, diet is a major piece (probably THE major piece – remember my post of a few weeks ago about increased consumption of fructose? ), but there are many other factors to take into consideration.  For example, biome depletion also plays a major role.

In fact, back in April 2018, I wrote about research into bacterial microbiome alterations and obesity.  In that experiment, scientists from the University of Chicago “…started with germ-free mice and found that even when fed high fat foods, they did not gain weight as the fats were excreted with their stool.  However, mice who have a very high level of non-pathogenic gut bacteria, did gain weight.  Very rapidly, the microbes in their small intestines changed, with increasing amounts of Clostridiaceae and Peptostreptococcaceae, the former of which in particular appears to be responsible for fat absorption.  Levels of Bifidobacteriacaea and Bacteriodacaea, microbial families associated with leanness, rapidly decreased.”

So obviously diet is a key factor,  and also, research into microbiome alterations associated with obesity continues to grow.  But again, that is only one “ome” native to the human ecosystem. In March of 2018, I also wrote about research on the relationship of obesity to macrobiome depletion.  Those researchers found that colonizing mice with the helminth, Heligmosomoides polygyrus (Hp), resulted in “…significantly attenuated obesity.”  They noted that the colonized mice also had highly improved blood markers, like reduced glucose and triglyceride levels and higher levels of regulatory cytokines (which reduce inflammation), and they concluded, “The significant inhibitory effect of H. polygyrus infection on diet-induced obesity in our model supports the idea that helminth parasites, which infect millions of people worldwide, particularly in the developing world, may have beneficial metabolic effects. Our results also support the potential for helminths as a new class of biologics in treating inflammatory diseases and metabolic disorders….[R]esults from our study raise the intriguing possibility of using helminths as novel, safer and effective therapeutics in the treatment of obesity and other immune and metabolic disorders.”

So now, back to the pearl I discovered this past week.

Japanese researchers, expanding upon this helminth research, looked in detail at the mechanism by which helminths protect against obesity.[ii] As they point out, “Several lines of evidence indicate an inverse correlation between helminthic infections and obesity as well as inflammation-mediated disorders, suggesting that helminths may have suppressive effects on these diseases.”  They go on to say though that the “…protective mechanism involved in how helminths suppress obesity are largely unknown.”  So – they wanted to figure out how it all works.

There are several metabolic control systems in the body that are meant to protect us from obesity, including one that tells fat cells (adipocytes) to burn calories and convert them to heat, as opposed to storing them as more fat.  There is a protein expressed in the mitochondria (the powerhouse of every cell in your body) of adipocytes called uncoupling protein 1 (UCP1).  UCP1 tells the cell to convert fat and glucose (fuel) to heat as opposed to storing it as more fat.  UCP1 is activated by the hormone norepinephrine (NE), which is a major chemical messenger in your body.  NE is released from nerves, including those that are distributed through your body fat.  So to summarize this:  norepinephrine stimulates the production of UCP1, which, in turn, tells the fat cell to burn and not store fat.

Back then to our Japanese scientists…

They fed mice high fat diets which rapidly cause major weight gain.  Again though, as in the previous study, those mice who were given helminths first (also Hp) were protected from gaining weight.  In fact, the obese mice who were given helminths and who were still continually fed a high fat diet actually lost weight and had improved dyslipidemia (elevated bad cholesterol/low good cholesterol).  These findings completely replicated those of the 2018 study.

As these scientists knew that the presence of helminths beneficially improves the bacteria of the gut (increasing beneficial, anti-inflammatory species and decreasing pathogenic, pro-inflammatory ones), they hypothesized that this protective effect was due to this modulation of the bacterial microbiome. And guess what?  “We found that helminthic infection affected gut bacteria, resulting in increased NE production that upregulated UCP1 in adipose tissues.”  Wow, right?!

To double check that they had correctly pinpointed the mechanism of action, they first gave some mice an agent to essentially block norepinephrine in the adipocytes.  Sure enough, even mice with the helminths on board gained weight:  “Thus, the protective role of Hp infection against obesity is dependent on NE, presumably by inducing UCP1 for energy expenditure in adipocytes.”  They then wanted to make sure that the source of the increased norepinephrine was the gut bacteria and not the mice’ own nervous systems. They noted that giving a chemical to block NE production led to a “completely suppressed NE production in adipose tissue” BUT mice who had helminths “still contained substantial amounts of NE after treatment…suggesting the existence of other sources of NE besides sympathetic nerves.” They treated a group of mice with antibiotics to reduce the intestinal bacteria and found that doing so, “…decreased both the NE concentration and expression of UCP1 in Hp-infected obese mice, resulting in the attenuated suppression of weight gain.”  So yup, the source of the protective norepinephrine in the helminth-colonized mice was the gut bacteria.

Much to my delight, they did then zero in on which bacteria were producing the NE.  Mice that were given helminths had more Firmicutes and Proteobacteria compared to the mice without helminths and “…previous studies reported that two bacteria genera, Bacillus and Escherichia belonging to Firmicutes and Proteobacteria, respectively, produced NE in the intestines.”  Levels of both were greatly increased in the mice with helminths and “…NE concentration in Hp-infected obese mice was closely correlated with the amount of those bacteria.”  That is, the more Bacillus and Escherichia in the intestine, the higher the levels of norepinephrine.

Obviously, these findings have yet to be replicated in humans.  We can only hope, as always, that such studies happen soon as we, in the industrialized world, only continue to get fatter and rates of obesity-associated illnesses continue to climb.



[ii] Shimokawa, C, Obi, S, Shibata, M, Olia, A, Imai, T, Suzue, K, Hisaeda, H.  Suppression of obesity by an intestinal helminth through interactinos with intestinal microbiota.  American Society for Microbiology: Infection and Immunity. 2019. Apr 2019, IAI.00042-19; DOI: 10.1128/IAI.00042-19

Spondylitis and Microbiome Dysbiosis: Both Bacterial and Fungal

So  many interesting things to write about…so little time!

Last October, I wrote a post about spondyloarthropothies, which is a family of autoimmune diseases that affect the spine.  These include Ankylosing spondylitis, psoriatic arthritis, arthritis related to inflammatory bowel disease, reactive arthritis, and juvenile idiopathic arthritis.  There has been a suspicion for some years now that the gut biome was related to the onset and progression of these diseases.  As I emphasized in that post, while these diseases remain strangely unfamiliar to most people – as opposed to the well-recognized rheumatoid arthritis, multiple sclerosis, Parkinson’s disease, etc. –  at least 2.7 MILLION people suffer from these diseases in the USA alone, which is almost 3X the number of people that suffer from the way better known Parkinson’s disease alone,  for example!

I’ve thus kept an eye out for anything new, as you can imagine as I am quite sure I have readers who suffer from these illnesses, or know someone who does.  I was happy to see a newly published paper which took an in-depth look at the biome differences between those with Ankylosing spondylitis (AS), the best studied in this family of illnesses, and healthy controls.[i]  The results were fascinating.

The study included 22 patients with  AS and 16 healthy controls (HC).  They found major differences in the bacterial microbiomes between the two groups, including a “significant increase” in diversity in the AS group that included a nearly 3-fold increase in Proteobacteria and a decrease in Bacteroidetes species, including Prevotella.  The bacteria of the AS group, “…showed that the gut bacteria in AS patients expressed more abundant genes involved in human diseases….”  As I pointed out in that October post, “A 2007 study: patients with AS were given Moxifloxacin, an antibiotic that works against both Gram-positive and negative bacteria. The results ‘…have shown that AS patients treated with Moxifloxacin resulted in a significant and sustained improvement…Serum inflammatory markers were greatly reduced after 12 weeks.’” If these results hold up in further studies, i.e. the increased levels of disease-causing bacteria in the guts of those with AS, the improvements seen using an antibiotic actually make a whole lot of sense.

What really interested me even more though was this:  “…a more pronounced fungal dysbiosis than bacterial dysbiosis in AS patients was detected in this study.  We observed a significant decrease in the diversity of intestinal fungi in these patients….” The ratio of fungi to bacteria was also significantly decreased.  That is, there are proportionally way too many bacteria and too few fungi, in comparison to the healthy controls.  Seeing as these two kinds of organisms tend to keep each other balanced, it’s not surprising that this ratio is off, considering the high levels of bacteria found.  This study was the first time anyone has looked at this aspect of the human biome in sponylitis.

The results were so striking that the researchers flat out state that their findings “…suggest an alteration of the entire ecosystem in the guts of AS patients.”

Also of note:  the degree of mycobiome alterations coincided with disease severity:  “…the patients with level III and IV [i.e. more severe] damage in their spines had different fungal microbiota structure than patients with level II damage or healthy controls.”  They state, “These results suggested a possible role of the mycobiome in the development of AS.”

By the way, there was also a correlation between blood markers for inflammation (like C-reactive protein (CRP)) and fungal dysbiosis.  In fact, the scientists compared those undergoing treatment for AS (using the biologic medication, Enbrel, or using NSAIDS (non-steroidal anti-inflammatory medications)) to those newly diagnosed who had not as yet started treatment.  These anti-inflammatory treatments had “…profound effects on changing specific gut microbial and fungal groups, which may be associated with altered disease activities in AS patients…” That is, lowering inflammation levels via treatment seems to have a major effect on the composition of the gut biome.

Seems to me this is a pretty major step forward in spondyloarthritis research and almost more exciting to me, is to read a paper wherein more than just the bacterial content of the gut was taken into account.  I hope this becomes a trend as I am quite sure, similar dysbiotic issues are factors in other inflammatory diseases as well.


[i] Li, M, et. al. Altered bacterial-fungal interkingdom networks in the guts of Ankylosing Spondylitis patients. mSystems. 2019;4(2). DOI: 10.1128/mSystems.00176-18

Nutritional Treatments and Autism: Too Little Research but…Here’s Some of What We Currently Know

Well – I am feeling somewhat overwhelmed!  A brief internet search yesterday morning, in which I was looking for new and interesting research, led me to 10 papers that I want to read and write about for you.  Considering that it takes quite a while to make my way through scientific papers…I have my work cut out for me the next couple of weeks!  On the bright side, lots of interesting stuff for you to read about.

So for today, I’ve settled on a general review of nutritional approaches to treating autism (ASD).[i]  I’ve written many times before (here and here, for example) about biome alterations in the population and am, of course, always on the look out for “things you can do now” papers to treat this.  While far from comprehensive, there were enough items of interest in it to warrant a mention in my blog.

  1. A fact I did not know:  the central nervous systems of boys are “…innately more sensitive to environmental factors than those of females,” which may account for the greater number of boys affected with ASD than girls.  For example, two sex-dependent sensitivities include mycotoxins (toxins from fungi produced by Candida) and casomorphines (undigested peptides (short strings of amino acids) found in dairy products).
  2. Inflammation in the intestines of those with autism has been well documented, and can lead to many nutritional deficiencies. In fact, more than half of those with ASD have been found to have vitamin and mineral deficiencies, as well as abnormally low levels of amino acids (formed by the digestion of protein) and omega 3s.  “Multivitamin/mineral supplements have been reported to decrease cognitive, sleep, and GI problems.”
  3. There is some evidence that a ketogenic diet, which is high in fat but very low in carbohydrates, with adequate protein, can improve autistic behaviors. Same for the casein/gluten-free diets.  However, this latter is still controversial, as many studies have shown it does not help.  As always though, when I read papers like this, I wonder what other therapies are the parents doing, what they are really feeding their child, etc.  For example, the casein/gluten-free diet often leads to an excess consumption of carbohydrates.  After all, gluten-free cookies, chips, etc. are all fine on the diet and many of the children seem to crave carbs.  We know that those with ASD have carbohydrate-digestion issues (I’ve written about this before here) and also, carbohydrate-metabolism/mitochondrial issues.  So, I still keep an open mind.  (These authors do refer to the data collected by the Autism Research Institute on over 27,000 parents’ reports of how various therapies have affected their children.   At this point, the Specific Carbohydrate Diet is ranked highest in terms of percentage of parents who report it helping – 71%.  In my personal experience, that number is closer to 90%.  Again, though, it does depend on doing the diet right, making sure all nutritional needs are met, and so forth.)
  4. Curcumin: A 4 week long study done on mice in 2015, with 3 different doses of curcumin (50 mg, 100 mg, or 200 mg per kg of body weight) found that the spice could “…restore neurological, behavioral, biochemical and molecular changes related to the ASD phenotype…in a dose dependent manner.”  (The problem with curcumin is it is very poorly absorbed from the gut – huge doses are needed.  However, there is research going on now on ways to improve its bio-availability, including combining it with phospholipids (a kind of fat).)
  5. Probiotics: You all know by now that many studies have confirmed bacterial microbiome alterations in the ASD population.  You also know, if you regularly read my blog, that multiple studies have been done showing that probiotics (and fecal transplant) have both been used successfully to improve the quality of the gut bacteria and subsequently, improve the symptoms of autism.  While research remains “insufficient,” as this author says, there is enough to justify a trial of probiotics.  Of course though, as I have pointed out in this post, it is a good idea to first reduce inflammation in the body – via diet, targeted supplements, etc. – before starting probiotics as they can cause problems otherwise.  There are a couple of studies mentioned in this paper worth reporting to you.  Firstly, 22 children with autism were put on a sugar-free diet and Lactobacillus acidophilus twice a day for two months:  “…significant improvements were observed in the major behavioral domains, especially in the ability to concentrate and the ability to follow instructions.”    A second study mentioned in this paper was randomized, double-blind, controlled.  The children were put on Lactobacillus plantarum for 6 weeks, and “…improvements in destructive and antisocial behavior, as well as in anxiety and communication problems, was observed…”
  6. Food additives:  problematic in children with ASD.  (Well – problematic in everyone really, if you ask me!)
  7. Camel milk: has many beneficial properties.  One randomized study in 60 children with autism showed that 500 ml of camel milk over 2 weeks “…led to significant improvements in the behavior of children with ASD.”

The authors’ conclusion:  “It is reported than in individuals with ASD, while the gluten-free casein-free and KDs [ketogenic diets], camel milk, curcumin, probiotics, and fermentable foods can play a role in alleviating ASD symptoms, the consumption of sugar, additives, pesticides, genetically modified organisms, inorganic processed foods, and difficult-to-digest starches may aggravate symptoms.”

Helpful information to know but as I mentioned above, as far as I’m concerned it’s incomplete.  There are simply not enough studies done to really draw any conclusions, even about those treatments they mention, let alone therapies like the Specific Carbohydrate Diet, which anecdotally is unbelievably effective…but mostly untested in proper clinical trials.


[i] Cekici, H and Sanlier, N. Current nutritional approaches in managing autism spectrum disorder: a review. Nutritional Neuorscience. 2019;22(3):145-155.

Biome Bliss: An Interesting New Prebiotic Supplement

A week ago or so, I got an email from a company that makes a really interesting prebiotic product.  They offered to let me try it out on myself, and after looking through their website, I readily agreed.  (I took my first dose this morning.)  I also asked them for any literature they may have on the product and was sent 4 papers, including two small clinical studies.  There were certainly enough items of interest in these to share with you, even though I have not had time to test the product first.  After all, you know that I am always looking for “things we can do now” to improve our health!

The product is called Biome Bliss, and in the research papers, it is referred to it as a GIMM (gastrointestinal microbiome modulator).  It has 3 components:  the prebiotic fiber, inulin (isolated from agave); the prebiotic fiber, beta-glucan (isolated from oats); and polyphenols (anthocyanins, isolated from blueberries).  If you remember, I have written about polyphenols multiple times before, as they are not only powerful antioxidants but also have prebiotic properties.  In fact, I myself have been using grapeseed extract and Triphala  for many months now.  Polyphenols from blueberries also have profound effect on glucose/insulin metabolism.  These 3 ingredients were specifically chosen to work in harmony, encouraging the growth of specific gut bacteria that help modulate glucose levels (I have also written several times about this subject), improve short-chain fatty acid production (which you all know are highly anti-inflammatory), reduce feelings of hunger, improve bowel regularity and other health benefits, including improved GI health:  “B-glucans and inulin-type fructans are prebiotics that are not only preferentially fermented by specific types of bacteria, but also promote proliferation of the bacterial species such as Bifidobacteria.  These bacteria are associated with a beneficial impact on the host through their potential involvement in diabetes-related inflammation and the development of obesity.”[i]  B-glucan from oats also “…protects the intestine’s mucosal lining and supports the immune system.”[ii]  By the way, I should mention that the product is fine for those on low- or controlled-carbohydrate diets as the sugars have been mostly removed.

One of their studies was double-blind and placebo controlled, which involved 28  (randomized to 2 groups) overweight/obese individuals with high fasting blood glucose levels.  One group was put on the GIMM, the other a placebo, which they consumed twice daily for 4 weeks.  The experimental group did notice an increase in flatulence (which is not surprising as fiber should really be increased slowly to give the GI bacteria time to adjust), but reported no meaningful adverse effects.  The study found that, after eating, glucose levels rose less in the experimental group than in those taking the placebo and also, those taking the prebiotic showed a reduced desire to eat.  There was an increase in their blood levels of the hormone PYY (release of this hormone is stimulated by SCFAs), which makes you feel full, and a decrease in another hormone, ghrelin, which makes you feel hungry.  They did find an increase in the levels of fecal SCFAs, but this did not reach statistical significance.  However, they also saw a decrease in fecal pH, which indicates improved gut fermentation of the prebiotic fibers.

The 2nd study, which was done on overweight people with type 2 diabetes who were also taking the diabetes medication, metformin, found too that “…fasting glucose decreased more during the period when metofmin was combined with GIMM compared to metformin combined with placebo.”[iii]

The other two papers are general discussions of the importance of prebiotics to health, and there were several interesting items to share.[iv]

  1. On my blog, I have talked endlessly about the concept of biome depletion – the loss of diversity in our belly buddies.  Not only is the loss of diversity now well-established to be associated with so many chronic illnesses, but it’s also important to note that, “A greater biodiversity renders a greater resilience of the ecosystem to recover from or adjust to perturbations.” So the more diversity you have, the more resilient you are.
  2. Agricultural techniques – which are meant to increase our food supply, to satisfy our ever increasing human population – have led to terrible decreases in food diversity. And of course, “…the more diverse the diet, the more diverse the microbiome.” This paper points out that, “According to the Food and Agricultural Organization of the United Nations, 75 percent of the plant genetic diversity has been lost, as farmers worldwide have left their multiple local varieties for genetically uniform, high-yielding varieties.”  This decrease in diversity extends to food animals as well.  In fact, “75 percent of the world’s food is generated from only 12 plants and five animal species.”  Not to make a bad pun here but…holy cow.
  3. Of course the antibiotics used in animals has adversely affected human microbiome diversity, as has pesticides use on plants.  I’ve written about this subject before.  It’s a huge public health issue.
  4. Prolonged absence of certain foods in the diet – for example, low fiber – causes a non-reversible loss of microbiome richness.  (Remember that study I wrote about last November, which showed that microbiome diversity is lost through the generations, as people have emigrated to the USA and changed their diets?)

Over the years, I have worked with innumerable people, both adults and children, with a wide variety of inflammatory disorders as well as issues with weight, metabolic syndrome, and so forth.  There is a reason I write about prebiotics so often!  Research done in the last 15 years or so has shown that the addition of prebiotics to the diet is as important – if not MORE important – than the use of probiotics.  I am looking forward to giving this product a try and will report back to you all after a month or so of use.  I hope some of you will try it along with me so we can compare notes!  Email me and let me know!


[i] Rebello, CJ, Burton, J, Heiman, M, Greenway, F.  Gastrointestinal microbiome modulator improves glucose tolerance in overweight and obese subjects: a randomized controlled pilot study.  Journal of Diabetes and Its Complications. 2015;29(8):1272-6.  doi: 10.1016/j.jdiacomp.2015.08.023

[ii] Cervantes, ER and Pfost, D. Prebiotics & Metabolic Regulation Benefits Beyond the Gut.  Naturopathic Doctor News and Review. 2019.

[iii] Burton, JH, Johnson, M, Johnson, J, Hsia, DS, Greenway, FL, Heiman, ML. Addition of a gastrointestinal microbiome modulator to metformin improves metformin tolerance and fasting glucose levels.  Journal of Diabetes Science and Technology. 2015; 9(4):808-14.   doi: 10.1177/1932296815577425

[iv] Heiman, ML and Greenway, FL. A healthy gastrointestinal microbiome is dependent on dietary diversity.  Molecular Metabolism. 2016; 5(5):317-320. doi: 10.1016/j.molmet.2016.02.005

Introducing Archaea: Another Important Member of Your Inner Ecosystem

It’s not often that I get to write about the more esoteric members of our gut biomes.  Our bacteria get the most hype in the scientific literature, but as you all know, there are many other kinds of residents of our inner ecosystems.  I was excited, therefore, to spot an article late last week about Archaea.[i]

Let me start with a definition:  “Archaea [which is pronounced ar-key-a] are organisms whose cells lack a defined nucleus.  They are not bacteria (their cell walls are different) and they are not eukaryotes (which are complex, multi-celled organisms, including plants and animals, whose cells do have a defined nucleus).  Many are found in anaerobic (without air) environments, including hot springs, marshes and the guts of animals and humans.[ii]

A study just published in the Journal of Allergy and Clinical Immunology[iii] looked at the relationship of gut Archaea to the development of childhood asthma.  The researchers found that high levels of a species, Methanosphaera stadtmanae, were associated with a lower risk for asthma.  They analyzed 472 samples in total, and concluded that, “…the presence of M. stadtmanae was associated with a lower risk for asthma at 6 to 10 years of age.”  Higher levels of this organism are also somewhat associated with a lower risk for eczema, airborne allergies and food allergy, but not to the point of reaching statistical significance.  They have not, as yet, figured out the mechanism of action, but believe their results were meaningful enough to indicate that a beneficial link very likely exists.

I myself know very little about Archaea, so thought I’d do some snooping around to see what other kinds of information I could glean to share with you.  I did find some interesting papers.  For example, just this past February, a paper was published looking at Archaea’s involvement in the development of abscesses.  An interesting couple of sentences from the abstract:  “They have been implicated in dysbiosis of the oral microbiota…They have also been associated with dysbiosis of the digestive tract microbiota linked to metabolic disorders (anorexia, malnutrition and obesity) and with lesions of the digestive tract (colon cancer).”[iv]

Perhaps the most interesting thing I found was a paper from last year which took an in-depth look at what we currently know about Archaea’s involvement in human health and disease.[v]  They state that the role these organisms play has been vastly underrated: “It has been reported that the impact of methanogens [methane producing Archaea] of the gut microbiota on pathological conditions has been grossly underestimated. Methanobrevibacter smithii and Methanosphaera stadtmanae are specifically recognized by the human innate immune system, and it is considered that these species contribute to immune responses in the body, including inflammatory responses.”  These organisms are found in the gut, on the skin, in the vagina, and in the mouth, including in dental plaque (with one species, Methanobrevibacter oralis, being significantly associated with periodontal disease).  Whether or not though most are beneficial or pathogenic is currently unknown, but it seems likely that, like bacteria, helminths, etc, some species are good, some are bad, and perhaps, some can be both depending on circumstances.

An example of this (i.e. a species being beneficial or pathogenic, depending on circumstance):  higher levels of certain Archaea are found in obese people.  It is believed the organisms may improve the efficiency of energy (calorie) absorption from food.  However, in those with anorexia, higher levels of the species, M. smithii, have been found, which would “lead to increased energy efficiency in severely low caloric diets.”  The increased levels of the species may be the result of the body’s attempt to survive in the face of starvation.

There does seem to be a link between some Archaea and inflammatory bowel disease because they do seem to evoke an inflammatory response.  That said, a 2012 study showed lower levels of Archaea in those with IBD as opposed to healthy individuals but there is some belief this is because diarrhea would lead to a reduction in numbers.  No one is yet sure though.

There may also be associations between Archaea and irritable bowel syndrome, diverticulitis and periodontal disease.  Their conclusion, “Several studies in the last decade directly or indirectly suggested a link between methanogens and a number of metabolic diseases. In addition…methanogens should be considered as an important target for the studies relating to modulation of the gut microbiota in humans for improving health or reducing risk of disease. Consequently, there is merit in proposing dietary intervention studies targeting the manipulation of archaeal components of the gut microbiome…This concept could even be extended to consider their use as a probiotic whereby live preparations of archaea could be used as dietary supplements (archaeobiotic).”

I reckon we are a long way from being able to buy Archaea probiotics.  On the other hand, at least we know scientists are starting to take a meaningful look at these organisms which undoubtedly play a huge role in our biomes and thus, in our health.  I will of course keep a close eye on developments!




[iii] Barnett D, Mommers M, Penders J, Arts ICW, Thijs C. Intestinal archaea inversely associated with childhood asthma [published online February 20, 2019]. J Allergy Clin Immunol. doi:10.1016/j.jaci.2019.02.009

[iv] Sogodogo, E, Drancourt, M, Grine, G. Methanogens as emerging pathogens in anaerobic abscesses.  European Journal of Clinical Microbiology and Infectious Diseases. 2019. doi: 10.1007/s10096-019-03510-5

[v] Chaudhary, PP, Conway, PL, Schlundt, J. Methanogens in humans:  potentially beneficial or harmful for health.  Applied Microbiology and Biotechnology. 2018. DOI:



High Fructose Corn Syrup and the Growth of Colorectal Tumors

Today’s post is a little off topic but I can’t not share this research[i] with you, especially considering the post I wrote a few weeks back about “lysogenic” bacteria.  If you remember, it was about those types of bacteria that carry dormant viral DNA in them, which, when subjected to the right environmental circumstances, produce bacteriophages (viruses that kill bacteria) that kill their own bacterial hosts.  One of the factors that triggers this phage production is fructose.  The exact metabolic purpose of this is still unknown, but certainly there exists the possibility that the huge increase in our fructose consumption in the last 30+ years or so (from the addition of high fructose corn syrup (HFCS) in so many foods)  has adversely altered our bacterial microbiomes by excessively stimulating this production of bacteriophages.

In that post, I pointed out that, “…since the 1970s, and the ever-increasing inclusion of high-fructose corn syrup (HFCS) into our diets, our consumption of this sugar has increased fourfold.”  According to the Food Research and Action Center, “Obesity rates have more than doubled in adults and children since the 1970’s…The latest data indicate that 39.6 percent of U.S. adults are obese. (Another 31.6 percent are overweight…)”[ii]  A 2017 article[iii] on Medical News Today about research conducted by scientists from Imperial College London, in collaboration with the World Health Organization, points out that, “…obesity in children and teenagers is 10 times higher now than it was in 1975, and that 5 years from now, more will be obese than underweight.”  The study was massive:  1000 researchers looked at the records of 130 million people living in 200 countries around the world, and found: “… in 1975, there were 5 million girls who were obese, and in 2016, this number rose to 50 million. The report counted 6 million boys with obesity in 1975, but this number spiked to 74 million in 2016. Last year, an additional 213 million children and teenagers were found to be overweight.”

There isn’t actually much controversy over whether or not all the added fructose is a part of the reason for this increase in obesity – and subsequent type 2 diabetes rates.  How much it’s a factor though is of course still unknown.

Bearing all this in mind then:  I found a recent article out of the Baylor College of Medicine and Weill Cornell particularly interesting.  The study, which was published in the journal, Science, looked at the relationship between the consumption of even a “moderate” amount of HFCS (the equivalent of about 12 ounces of soda per day) and the growth of intestinal tumors.  Says one of the authors, “”An increasing number of observational studies have raised awareness of the association between consuming sugary drinks, obesity and the risk of colorectal cancer…The current thought is that sugar is harmful to our health mainly because consuming too much can lead to obesity. We know that obesity increases the risk of many types of cancer including colorectal cancer; however, we were uncertain whether a direct and causal link existed between sugar consumption and cancer.”[iv]

To find out more about this potential link between fructose and colon cancer, the researchers created a mouse model wherein they delete a gene responsible for creating a protein called APC.  Without APC, “…normal intestinal cells neither stop growing nor die, forming early stage tumors called polyps.  More than 90 percent of colorectal cancer patients have this type of APC mutation.”

When given sugar water (with HFCS) to drink at will, the APC mice rapidly became obese.  To prevent this, and to model humans drinking one can of soda, they limited the daily sugar water to a mouse equivalent.  After 2 months of this limited amount, the mice did not become obese but they did develop tumors that were “larger and of higher-grade” than the mice given regular water to drink.  The APC mice that were treated with the HFCS, “…showed a substantial increase in tumor size and tumor growth in the absence of obesity and metabolic syndrome.  HFCS increased the concentrations of fructose and glucose in the intestinal lumen and serum [blood], respectively, and the tumors transported both sugars.” [i]

Summarizing their findings, the lead researcher states, “These results suggest that when the animals have early stage of tumors in the intestines — which can occur in many young adult humans by chance and without notice — consuming even modest amounts of high-fructose corn syrup in liquid form can boost tumor growth and progression independently of obesity….[O]ur findings in animal models suggest that chronic consumption of sugary drinks can shorten the time it takes cancer to develop. In humans, it usually takes 20 to 30 years for colorectal cancer to grow from early stage benign tumors to aggressive cancers.”

Another scientist involved in the work states, “This observation in animal models might explain why increased consumption of sweet drinks and other foods with high sugar content over the past 30 years is correlating with an increase in colorectal cancers in 25 to 50-year-olds in the United States…”

Remember though too how rapidly the mice which were allowed as much sugar water as they chose to drink became obese.  And remember too that fat excretes huge amounts of pro-inflammatory chemicals.  So while the accelerated tumor growth was independent of weight gain, obesity is only going to worsen the issue.

To find out how the fructose led to this increased tumor growth, the scientists investigated further and found high levels of fructose and glucose (both of which are found in sugary sodas) left in the colon – and in the blood.  Cancerous tumors eat sugar.  Further experimentation showed that, “…colorectal cancers utilize high-fructose corn syrup, the major ingredient in most sugary sodas and many other processed foods, as fuel to increase rates of tumor growth….While many studies have correlated increased rates of colorectal cancer with diet, this study shows a direct molecular mechanism for the correlation between consumption of sugar and colorectal cancer.”

So to sum up, it appears that our increasing consumption of HFCS may be in part not only responsible for microbiome alterations, but also the ever increasing rates of obesity and type 2 diabetes found around the globe…as well as the increasing rates of colorectal cancers.   I obviously don’t know how all this is intertwined (after all, biome depletion also leads to increased inflammation, alterations in how food is digested, and so forth), but I’m sure it is somehow all connected.  How much of the guilt HFCS bears is still unknown, but certainly, I think we know enough to absolutely avoid the stuff in our diets.


[i] Marcus D. Goncalves, Changyuan Lu, Jordan Tutnauer, Travis E. Hartman, Seo-Kyoung Hwang, Charles J Murphy, Chantal Pauli, Roxanne Morris, Sam Taylor, Kaitlyn Bosch, Sukjin Yang, Yumei Wang, Justin Van Riper, H Carl Lekaye, Jatin Roper, Young Kim, Qiuying Chen, Steven S. Gross, Kyu Y. Rhee, Lewis C. Cantley, Jihye Yun. High-fructose corn syrup enhances intestinal tumor growth in mice. Science, 2019; 363 (6433): 1345-1349 DOI: 10.1126/science.aat8515




An Obvious Solution to Treating IBD?

A short article about helminths and inflammatory bowel disease [IBD] was just published, and is absolutely worth a read (and post).[i]  I’d almost call it an op-ed piece.  It reads like this researcher is berating a medical system that is ignoring an obvious solution to treating IBD.

The article starts by point out that “Inflammation plays a pivotal role in the pathogenesis of IBD that induces mucosal inflammation.  Hence, treatment of IBD mainly targets on inhibition of pro-inflammatory mediators.”  However, current treatments are pretty horrific. I wrote about the incredibly high side effect profile of the currently available medications almost 2 years ago, in April 2017.  If you remember, I described an FDA report that concluded, “Drugs used to treat Crohn’s disease and other autoimmune disorders are among those with the greatest number of reported side effects filed with the U.S. Food and Drug Administration…Drugs which suppress the immune system to fight inflammation can cause serious and sometimes lethal infections including tuberculosis, and have been linked with blood disorders, including lymphoma, a blood cancer.”

Back to this new little article: the author goes on to give a brief explanation of what we know about how helminths modulate the immune system, i.e. invoking a Th2 immune response that boosts levels of “…Treg cells to release immunoregulatory cytokines…”  He goes on to further state that bacterial microbiome alterations are known to lead to the inflammatory response in IBD, but that helminths, “…can maintain microbiota of the GI in order to induce anti-inflammatory responses.”  Thus, therapeutic helminths both raise levels of regulatory T-cells and cytokines (the off-switch to the pro-inflammatory system) while also improving and maintaining the quality of the bacterial microbiome, which also drastically reduces inflammation.

He then points out that benign helminths, like Trichuris suis ova (TSO) – which are whip worms native to pigs – have been shown in multiple human trials to have “no pathogenic potential for humans” and “has shown no side-effects.”

So his conclusion – which seems pretty obvious to everyone – except the world’s regulatory agencies:  “Inasmuch as the resolution of inflammation is a therapeutic target of IBD and helminths have great immunomodulatory properties, helminth-based therapy may be efficacious for patients with IBD.”

As I have said before, I continue to live in hope that someday, someone with actual power AND common sense will listen.


[i] Abdoli, A. Therapeutic potential of helminths and helminth-derived antigens for resolution of inflammation in inflammatory bowel disesase. Aarchives of Medical Research. 2019. doi: 10.1016/j.arcmed.2019.03.001

Early Life Biome Depletion and a Lifetime of Health Issues

Yesterday, I found a great complimentary article[i] to my Tuesday post regarding lack of exposure to commensal organisms and the development of asthma in children.  This is another “it’s biome depletion not the darn ‘hygiene hypothesis’” kind of story!

Background information:   babies are exposed to their first major onslaught of commensal organisms during the birth process. In an ideal world, the breast milk they are then fed for those first crucial few months leads to the development of a robust infant microbiome (consisting mainly of bifidobacteria and lacobacilli) with the oligosaccharides (prebiotics) in the milk being crucial for the developing biome.

Using a mouse model, researchers at the Institut Pasteur and Inserm looked at what happens in infants when solid food is first introduced and it’s pretty amazing.

Apparently, when solid food is introduced – typically between 3 and 6 months in humans (equivalent to two to four weeks for mice) – the number of bacteria increases 10- to 100-fold, and this rapid increase “…triggers an intense immune response,” which these scientists call a “weaning reaction.”[ii] This reaction occurs at a very critical time in immune development.

This rapid change in the microbiota (which of course also includes a major increase in bacterial metabolites) and the subsequent immune response (which consists of a huge increase in regulatory cytokines, which are the off-switch to the inflammatory system) is critical to normal immune development. When the scientists treated the infant mice with antibiotics during this crucial time window, disrupting this weaning reaction, they found that the mice were far more likely to develop inflammatory disorders, including allergies, colon cancer and inflammatory bowel disease.  Thus, they conclude that if the microbiome is decimated by antibiotics very early in life, the weaning reaction will fail to occur…and since the production of regulatory cells during the weaning reaction requires bacterial metabolites, like short chain fatty acids, the infant is set up for low levels of Treg cells and an abnormal immune response throughout life.

Says Dr. Gerard Eberl, the lead author of the study, “This is what is known as pathogenic imprinting…that is to say, events occurring in early childhood determine future susceptibility to inflammatory disorders.”

During the many years I’ve worked as a nutritionist, I have noted that the single most common thread in the children I’ve seen – many of whom had autism and/or ADHD as well as gastrointestinal issues – was early introduction of antibiotics.  (My own son, Alex, who is autistic and has a history of major immune issues and inflammatory bowel disease) was put on 5 days of IV antibiotics starting at 36 hours old, during which time he ceased to breast feed and I was forced by the hospital staff to start him on formula.) I’ve read many articles over the years exploring the connection of early antibiotics to later immune issues and finally, 25 years later, it looks like scientists have finally discovered the mechanism of action.  As sometimes antibiotics cannot be avoided, with all my heart, I hope this rapidly leads to a therapeutic solution.



[ii] Al Nabhani, Z, et. al. A weaning reaction to microbiota is required for resistance to immunopathologies in the adult.  Immunity. 2019.  DOI: