Well, there’s good news and there’s bad news.
First, a quick summary: the good news is that the first human trial was just conducted using fecal microbiome transplant (FMT) to treat obesity. The bad news is that the treatment did not result in either weight loss or changes in the hormone, GLP1, which is involved in feelings of satiety (feeling full).[i]
There is more mixed news though so some more details for you:
22 obese, but otherwise healthy, adults took part. For 12 weeks, half of them took a daily capsule of microbes from thin people, while the other half took a placebo. On the good news front, the treatment proved safe.
Also more good news: “The overall microbial makeup of the treatment group did become more similar to that of the lean donors, and a specific decrease in a type of bile acid was particularly noted.” Remember – there is unlikely to be one cause of this epidemic, as I’ve been writing about. The lead author of the study states, in fact, “The bile acid data is certainly intriguing and suggests that maybe there are one or more different pathways at play…Obesity is a very complex disorder, and a multifactorial process is probably at the heart of its development.”
The actual paper has not yet been published, as it’s preliminary results are just being presented at a conference. I cannot, therefore, as yet comment on their methodology and so forth. For example, what were the people eating during the study? In fairness (and to be silly for a moment while making a valid point): if the adults in the experiment group continued to eat 10,000 calories a day while sitting on the couch watching TV, I don’t care what kind of capsules they were taking. I find it impossible to believe anyone could lose weight under those circumstances.
Still…this is a step forward. I am always happy to be able to report to you actual human trials. I do believe that someday in the future, FMT (purified microbiota from healthy donors, given via oral capsules) will become a treatment norm. In fact, I recently posted the news (on my Biome Buzz Facebook page) that the autism trials have been so successful that the FDA is fast-tracking the treatment for that population.
I will, of course, continue to keep an eye on all this research!
A great article appeared last week on Gut Microbiota for Health,[i] on the overlooked mycobiome in digestive diseases. I’ve written about this topic several times before and am always very happy to see new research focused on the topic.
The authors of the paper[ii] point out that while the gut bacteria greatly outnumber fungi, this in no way diminishes fungi’s effects on the host. Cell size too, for example, must be taken into account – and many fungi cells are 100X bigger in volume than many bacteria. They produce, therefore, much larger amounts of byproducts which, even in low concentrates, may have profound impact. And, like bacteria, fungi “talk” to the immune system both locally (in the gut) and remotely (in the body as a whole).
Factors that influence the make-up of the mycobiome include diet, because foods like cheese, vegetables, etc. have fungi in and on them. The host interacts with all the microbiota it houses: for example, things like bile acids and so forth, can alter the mycobiome make-up. Finally, the other organisms of the gut influence the composition of the mycobiome. In fact, the bacteria are not alone in their influence: archeae, viruses (bacteriophages), and so forth likely play a role in determining mycobiome composition, although very little research has been done on this to date.
Some research points to fungi having a role in metabolic syndrome as well as cancer but…we are nowhere near having enough information on this to determine true relevance yet, let alone, mechanisms of action. Evidence is mounting for connections between fungi and other diseases ranging from autism to spondylitis to schizophrenia. And it looks very likely that the mycobiome is involved in the development of inflammatory bowel diseases, as I’ve written about before: “…a role of the mycobiota in disease, notably in IBD, is indicated by both descriptive data in humans and mechanistic data in mice.” There are distinct differences between those with IBD and healthy controls, confirmed by two independent studies.
In a mouse model, fungi have been shown to aggravate the severity of inflammation in IBD. This research supports the idea that the fungi work with the bacteria in such a way as to worsen IBD symptoms. In fact, another study in humans (which I described back in 2017) showed that the fungi, C. tropicalis, and the bacteria E. coli and S. marcescens, work together to form a biofilm (kind of a slimy mass that protects the organisms inside – think about the plaque on your teeth) that evokes an inflammatory immune response.[iii]
A 2018 study was conducted in Saudi Arabia on 15 children with Crohn’s disease.[iv] Their mycobiomes were compared to 20 healthy controls to see if they could accurately predict which children were sick or healthy. They found that Saccharomyces cerevisiae and S. bayanus were at significantly higher levels in the children with IBD, while overall diversity of the mycobiome was lower…and indeed, they absolutely could use these levels to correctly predict if the sample came from a child with IBD or a healthy child.
I sincerely hope I have more frequent opportunities to write about research into our commensal organisms other than our bacteria. Each element of our internal ecosystems probably plays an equally important role in determining our health status. The bacteria though are best known and most numerous, so they get all the press (and money). I have high hopes though that this is all going to change in the very near future.
[ii] Richard, ML and Sokol, H. The gut mycobiota: insights into analysis, environmental interactions and role in gastrointestinal diseases. Nature Reviews. 2019.
[iv] El Mouzan, M, et. al. Fungal dysbiosis predicts the diagnosis of pediatric Crohn’s disease. World Journal of Gastroenterology. 2018:24(39):4510-4516. doi: 10.3748/wjg.v24.i39.4510.
Just a couple of weeks ago, I wrote about ways in which modern food processing may be related to our growing epidemic of obesity (or globesity, as those authors called it). In that post, I mentioned that many food additives are potentially thought to be contributing to the problem, in that they may adversely affect the microbiome, and thus, the way we digest food.
Well, just yesterday, I spotted an article out of the University of Sydney, in Australia, wherein researchers looked at the effects of the additive titanium dioxide on human health.[i] It is apparently used as a whitening agent in high quantities in more than 900 food products (like chewing gum and mayonnaise), and in many medicines as well. While it is an approved additive, relatively little safety testing has actually been done.
These researchers found, in a mouse study, that titanium dioxide adversely affects the activity of the bacterial microbiome (i.e. it altered the production of their normal metabolites) and also stimulates gut inflammation, potentially triggering inflammatory bowel diseases and colorectal cancer. It seems to promote the formation of biofilms – those slimy masses of bacteria that protect the organisms inside: ““This study investigated effects of titanium dioxide on gut health in mice and found that titanium dioxide did not change the composition of gut microbiota, but instead it affected bacteria activity and promoted their growth in a form of undesired biofilm. Biofilms are bacteria that stick together and the formation of biofilm has been reported in diseases such as colorectal cancer…”
The article states: “The interaction between gut microbiota and host plays a central role in health. Dysbiosis, detrimental changes in gut microbiota, and inflammation have been reported in non-communicable diseases. While diet has a profound impact on gut microbiota composition and function, the role of food additives such as titanium dioxide (TiO2), prevalent in processed food, is less established….[Our] findings collectively show that TiO2 is not inert, but rather impairs gut homeostasis which may in turn prime the host for disease development.”[ii]
Says the co-lead author, Dr. Laurence Macia: ““Our research showed that titanium dioxide interacts with bacteria in the gut and impairs some of their functions which may result in the development of diseases. We are saying that its consumption should be better regulated by food authorities.”
So…I did a quick search of my kitchen. I buy organic and found no titanium dioxide (so far) in my foods. But, I then did an internet search of my medicines and supplements, and low and behold, there it was.
Titanium dioxide is in so many things, in fact, that I don’t know if there’s any way to avoid all of it. It’s everywhere!
[ii] Pinget, GV, et. al. Impact of the food additive titanium dioxide (E171) on gut microbiota-host interaction. Frontiers in Nutrition. 2019. doi: 10.3389/fnut.2019.00057
I continue to make my way through the stacks of articles I’ve collected these last few months and decided today to treat myself to a description of a paper from 2015 that used survey data to analyze the effects of the Specific Carbohydrate Diet (SCD) on those suffering from inflammatory bowel disease. Of course there are issues with using such data, and this is far from the gold-standard double-blind, placebo controlled cross-over studies that eventually prove scientific certainty (or…at least as much certainty as science ever gets). Still, it’s a valuable paper, especially as there is dearth of studies on using diet to treat disease (there’s simply no money, and thus no motive, to do them). In spite of that fact that the few studies that have been done have been 100% successful, SCD continues to get generally ignored by the medical community.
My regular readers know I have a very personal SCD story: the diet saved my son, Alex, from inflammatory bowel disease hell. It was my experience with SCD, in fact, that led me to change careers from teaching special education to becoming a nutritionist. I witnessed a miracle that changed me forever. You can read more about that here.
Thus, I am always thrilled to be able share any kind of published study on SCD.
50 patients filled out a survey and also included their medical records, a 3 day diet diary and validation from an American physician confirming their diagnosis of IBD (via endoscopy, radiology, and pathology reports by a board certified gastroenterologist). The survey included a wide variety of accepted measurements of disease severity, quality of life measurements and so forth. 36 of the patients had Crohn’s disease, 9 had ulcerative colitis, and 5 had other forms of IBD. A few interesting notes on the breakdown of the patients:
a. “The mean time the SCD was followed was 35.4 months.” I found that fascinating as I have always told my nutrition clients that the diet must be strictly followed for 3 years (minimum) to achieve full effect and not risk relapse.
b. “The patients followed SCD strictly with a mean adherence rating of 95.2%.” Good for them! Compliance is crucial to success!
c. “Mean time to see some improvement when following SCD was 29.2 days. Thirty-three subjects (66%) noted complete symptom resolution, which did not occur until a mean of 9.9 months after starting the SCD.” I am truly astounded by the nearly exact match, in terms of time frame, with what I have seen in using the diet for the last 16 years with clients. I personally found that most patients begin to see improvement in symptom closer to 35-48 days but still…my anecdotal experience is not far off this paper’s findings. And almost everyone I have ever worked with, my own son included, got complete resolution of symptoms between 9 and 10 months on the diet. The consistency is truly incredible.
From the paper’s conclusion: “This is the first clinical description of a large series of patients with IBD following the SCD. Our survey results suggest that SCD can potentially be an effective tool in the management of some patients with IBD…”
Not to sound like the world’s biggest cynic, but if you are wondering then why SCD is not recommended as the medical norm as a part of a treatment plan for those suffering with IBD, you probably need look no further than this sentence: “Our results also suggest that in some patients with moderate to severe disease who follow this diet, discontinuation of immuno-suppressive agents has been feasible.”
The authors point out the strengths and weaknesses in their study, many of which are apparent. But they conclude:
“…we now show that at least a subgroup of patients with IBD may notably improve as a result of following the SCD and/or dietary interventions in general. Our findings enhance those of prior limited case reports of dietary therapy with SCD…Further evidence suggesting diet can be an effective treatment for some patients with IBD stems from the fact that diet has the potential to change the intestinal luminal environment, specifically the intestinal microbiome. Our prior preliminary findings hint at a change in the microbiome of patients with IBD who follow the SCD. If following the SCD changes the microbiome significantly and/or reverses some of the dysbiosis reported in patients with IBD, this may be a low-cost intervention to induce and maintain remission with little or no known adverse reactions. As such, further interventional studies of SCD and diet therapies in general for IBD are urgently needed.”
I’m not holding my breath.
Kakodkar, S, Farooqui, AJ, Mikolaitis, SL, Mutlu, EA. The Specific Carbohydrate Diet for inflammatory bowel disease: A cases series. Journal of the academy of nutrition and dietetics. 2015. 115(8):1226-1232. doi: 10.1016/j.jand.2015.04.016.
I just finished reading an article from 2018 on mental health and the microbiome that describes some of where we are now, knowledge-wise, and where we need to be before psychobiotics become a treatment norm.[i] There were multiple pieces of information in it which were either new to me, or worth repeating.
The history lover in me very much enjoyed the first section which points out that while we are currently undergoing a medical revolution in terms of biome research, in actuality, the link between the gut and health was recognized as early as the 4th century, when a Chinese physician, Ge Hong, treated severe diarrhea using fecal microbiota transplant (except that he administered the concoction orally…which must have been special for the patient!). In terms of recognizing the relationship of these bacteria to the brain, back in 1908, a paper was published which suggested that “…health could be enhanced and ‘senility’ delayed by manipulating the intestinal microbiome with host-friendly bacteria.” Yes…unfortunately for all of us, science moves painfully slowly sometimes! Here is a cheerful statistic though: “Links between microbiota and pathophysiology triggered an explosion of interest in this field, with 85% of the over 10,000 PubMed publications on ‘intestinal microbiota’ arising in the last 5 years, currently averaging about 5 new publications per day.” It’s no wonder that I am constantly feeling overwhelmed, bringing you the latest and greatest! Sorry folks, but no…I do not have time to read and write about 35 papers every week!
Some highlights of current evidence pointing to the microbiome/mental illness connection:
In terms of our current knowledge of how to achieve and maintain the health of the biome (and thus, the brain), 4 key points that merit repeating:
In the conclusion, the authors point out that one of the many things we still don’t know all too often is what is cause and what is effect, “…when dysbiosis causes disease rather than accompanying it…” So in spite of the fact that there are five papers per day on average being published, and the evidence connecting bacterial microbiome alterations to mental illness continues to mount, we know a minute fraction of what we need to know before biome manipulation becomes the medical norm.
[i] Bruce-Keller, A, Salbaum, JM, Berthoud, H-B. Harnessing gut microbes for mental health: getting from here to there. Biological Psychiatry. 2018. 83(3):214-223. doi:10.1016/j.biopsych.2017.08.014.
A couple of weeks ago, I wrote about obesity and the concept of evolutionary mismatch. As always, I posted it up on my Biome Buzz Facebook page. A few days later, in response to a comment that the whole problem is nothing more than glyphosate, another Facebook user wrote, “Reductionism is never helpful.” Not to make a bad pun here (well…kinda to make a bad pun!): he reduced this issue to 4 perfect words.
The question of what is causing the epidemics of obesity, autism, allergy, autoimmune diseases, etc. in the industrialized world is unbelievably complicated and involves bodily processes that may not have been discovered yet, let alone, we still have no idea what outside influences might be involved or how much influence they may have. We don’t even yet know fully how our immune system works, let alone how all the trillions of organisms in and on us affect each other and our bodies, what part the foods we eat plays – and the toxins we come into contact with, the lifestyle factors, etc.
We have to accept that there is no single or simple answer to these questions. Period.
Years ago, I gave a joint talk with a medical professional who used the following 3 slides to try to express to our audience just how complex the human immune system is – let alone the entire rest of the body.
While I try to make the science I read understandable for us lay people, the reality is, there is nothing simple about it at all.
A few articles in the last few days exemplify this point. Over the weekend, as one example, I read an article on the Conversation that looks at the bad and good of antibiotics.[i] The article points out, “In the past decade, we have become more aware of the health-promoting characteristics of the microorganisms that live on and in our bodies – the microbiome. For example, a diverse and stable gut microbiome is necessary for digestion and protection against gut infections. Changing the microbiome with antibiotics can be helpful…but also harmful.” The author points out that in animal studies, antibiotics – by altering the gut bacteria – have been found to be responsible for weight gain and adverse metabolic effects; for poor immune response to cancer; and with the development of depression.
Conversely, antibiotics also save millions of lives every day and more than that, scientists have found they often do as much good as they do bad: “More than six decades ago, researchers first noticed that certain antibiotics had beneficial effects that were not explained by killing bacteria.” 60+ years ago, scientists noticed that prontosil, one of the first antibiotics, improved the functioning of immune cells responsible for killing bacteria. A recent review of 10 clinical trials of antibiotics showed that they can promote child growth in those with infectious diseases and malnutrition. Another antibiotic called cotrimoxazole promotes health and is frequently used in those with HIV to block infection and persistent inflammation. In a randomized, controlled trial conducted on children with HIV in Africa, those taking the antibiotics had improvements in systemic inflammation, including in the gut. The authors of this article, who ran this study, surmised that the antibiotic reduced inflammation in 3 ways: “One, it suppressed a group of gut bacteria called viridans group streptococci, which trigger gut inflammation. Two, it directly reduced harmful activation of blood immune cells. And, three, it blocked inflammatory signals from gut cells.” No one yet knows fully the mechanism of action but the fact remains, the medications are doing something beneficial.
The author concludes, “To guide better antibiotic choices, we need to look deeper than just their effects on infections that make us sick into the underlying body processes they can change. As antibiotic use continues to expand and change worldwide, its time we understood more fully how they work.” Well, amen to that. The fact is, how they work, what exactly they are doing in us, etc. is not even vaguely as simple as “they kill bacteria.”
A second example of the incredible complexity involved in researching chronic diseases was provided by an article I posted on Facebook from Medscape a few days ago: “New Approaches Targeting the Microbiome in CV Disease.”[ii] The article describes a review from the Journal of the American College of Cardiology on the relationship of the bacterial microbiome to the development of cardiovascular illness. “While previous studies have focused on what specific organisms are implicated, we are beginning to realize that it is their balance of the ecosystem within the body that creates an environment that protects or promotes various cardiovascular diseases…” That is, it’s the balance of the entire body and its biome that is important – not just the individual organisms that live in us.
The lead author of the review, Dr. Tang, states that “…prior studies have hypothesized that specific bacteria may directly promote pathophysiologic processes, and that by eliminating them with antibiotics, might lead to fewer adverse events. This approach has not worked because the underlying mechanisms were poorly understood, and there is an assumption of one-size-fits-all…Now we appreciate that much of our gut bacteria are likely beneficial and their compositions in our healthy gut are often difficult to alter, yet their metabolism can be modulated by dietary exposures that are unique across individuals.”
In fact, diet is one of the biggest environmental exposures humans have, but again remember that ONE SIZE DOES NOT FIT ALL! “Unique across individual.” Says Dr. Tang, “…the concept of classifying food groups or diets as ‘good’ or ‘bad’ for health is somewhat outdated, since it depends largely on how nutrients are digested and interact with the body’s gut bacteria…”
It gets even more complicated than that! To quote Dr. Tang again, “Individuals can have vastly different gut bacterial compositions, so the same food may have different short- and long-term effects in different persons…This is further complicated by the fact that we all have our own unique physiological response to nutrients and metabolites independent of our gut microbiome.” Remember a couple of years ago, when a study in Cell Metabolism found that people respond differently to white versus whole wheat bread? Some people actually had a lower glycemic response to white, shocking the scientists…who found the response was actually tied into the composition of the gut flora.[iii]
So no! We cannot reduce the discussion of “why is heart disease so much more common today than in the past” to any one factor. It is not “diet” or “toxins” or “weight.” It is complex interplay of factors many of which we probably haven’t even yet discovered.
Dr. Tang points out that this why studies so often have contrasting results: we have not as yet learned out to account for individual microbiomes and individual physiological responses. In the future though, as we learn more, we can hope that personalized therapies in terms of diet, probiotics, prebiotics and on will become the norm.
So please: do not think that because becoming vegan, or following a paleo diet, or giving up carbs, etc. has made you feel like a million bucks that it is right for everyone. Do not think that toxins are THE answer, or that a probiotic that has worked for you is right for everyone. There is no such thing as one truth.
I’ve written a fair amount lately about the association of obesity to bacterial microbiome alterations, but have thus far, only had the chance to write a few times about the relationship of dysbiosis to anorexia nervosa (AN). In my frenzy of reading these last couple of weeks, I came across an incredibly interesting article on the subject, which suggested something I had never read before: many researchers now believe that, “…AN is an autoimmune disease caused by delayed exposure to common microorganisms (hygiene hypothesis) in which autoABS [auto antibodies] to appetite-regulating neuropeptides, neurotransmitters, and hypothalamic neurons, disturb appetite and result in decreased intake of food.”[i] Is biome depletion once again rearing its ugly head?
In my first ever post about AN, I wrote about the relationship of other autoimmune diseases to the development of eating disorders: “The researchers found ‘…significantly higher hazards of eating disorders for children and adolescents with autoimmune or autoinflammatory diseases: 36% higher hazard for anorexia nervosa, 73% for bulimia nervosa, and 72% for an eating disorder not otherwise specified.’” I go on to mention that there is a growing body of literature associating eating disorders to alterations in the microbiome. The second time I wrote about it, I went into these alterations in much more detail: “Specifically, the authors of this paper note that there seems to be a general pattern found in those with anorexia: ‘…a depletion of Lactobacillus and butyrate-producing Roseburia. In contrast, the relative abundance of Bifidobacteria, Proteobacteria, Akkermansia muciniphila and archaeon Methanobrevibacter smithii increases.’”
Now before you snap at me, “Judy, isn’t anorexia a cultural issue? Isn’t it brought about by girls wanting to emulate the airbrushed, Photoshopped super models they see everywhere, in the media?” let’s take a big step back and remember that the human body is a whole – that the mind and body are one organism, and not separate entities. Just as you get butterflies in your stomach when nervous or upset (the mind affects the body), remember too that it works both ways. You get the flu, for example, and your body will engage in what is known as “sickness behavior” which is “…characterized by loss of appetite, reduction in activity and social interactions, depressed mood, and loss of libido.” The communication between body and mind is bi-directional. So the answer is YES – stress and anxiety brought about by attempting to emulate the fictional perfection of these models most certainly may play a part in the development of eating disorders: “Genetic factors contribute to the etiology of AN based on various genetic studies. Moreover, psychological risk factors as well as sociocultural influences and biological factors contribute to the risk of AN development.”
Remember: stress and anxiety affect your microbiome, just as your microbiome affects your mind and behavior. You have all read about this over and over on my blog.
So back now to AN and highlights from this article:
These authors restate what I have written about in the past regarding known microbiome alterations, including the archaea, Methanobrevibacter smithii. And whoa…would you look at that! I wrote about that too, in this post on archaea from earlier this month: “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]”
Biome Buzz readers really are up to date with all the latest!
These researchers state, “It was reported that AN patients possess greater concentrations of the archaeon Methanobrevibacter smithii in the gut. This increase of a methane producing archaeon can result in the optimization of food transformation in a very low-calorie diet.” That is, this particular archaea helps maximize the body’s ability to get energy from food, which is pretty critical when you’re barely eating. They go on to say, “AN is associated intestinal microbial dysbiosis marked by lower microbial diversity and taxonomic differences in comparison with healthy controls. This dysbiosis is also associated with depression and eating disorder psychopathology.”
Back to the autoimmune connection for a moment: the intestinal bacterial play a crucial role in the “…increased permeability of tight junctions to macromolecules…This so called ‘leaky gut’ is associated with the development of inflammation, chronic diseases, sepsis, and also with some neurological and psychiatric disease. The increased intestinal permeability enables the transport of microbial metabolites into the peripheral circulation….A ’leaky gut’ can be provoked by starvation…”
Bacterial metabolites, crossing through the leaky gut, look like invaders to the immune system, which then produces antibodies to them. These cross-reacting autoABS have been observed and documented by researchers, who have found they react with chemicals in the body that stimulate appetite. In fact, in both humans and animals, antibodies to a hormone called alpha-melanocyte stimulating hormone (α-MSH), which, as the name suggests, stimulates appetite, are generated in response to a protein produced by some gut bacteria including E.coli. In fact, “The levels of α-MSH autoABS correlate with core psychobehavioral abnormalities in patients with eating disorders.”
To sum that up: metabolites from gut bacteria, like E.coli, cross the permeable gut barrier into the blood stream. In response, the body produces antibodies to those metabolites, which also unfortunately, attack and destroy the α-MSH, which stimulates appetite. And of course, the worse your appetite, the less you eat…and the leakier the gut becomes. A vicious cycle is born.
Just a couple more items of interest:
As you may know, the bacteria of the gut produce many of our neurotransmitters. It always surprises people when I tell them that 90% of the serotonin in their bodies is actually in the gut. This article points this out, and goes on to state: “The production of serotonin in the gut is affected by diet and regulates the motility of the gut as well as mood, appetite, sleep, and the cognitive functions of the individual.” Dopamine, GABA, acetylcholine, etc., are also products of the gut flora. Thus, anything that affects these microbes also affects the central nervous system. Of course, decreased food intake also affects the immune system: “Decreased food intake may have an impact on the interactions among the immune system and the CNS. The impaired communication between these systems may be responsible for several associated psychiatric symptoms, such as stress, anxiety, and depression.” So back to where I started this post: psychological stress affects the microbiome…and the microbiome affects the emotional well-being and behavior of the person, including feeding behaviors.
The conclusion of the paper: “Evidence has been published that behavioral disorders including eating disorders are accompanied by significant perturbations in the composition of the gut microbiota…The presence of antibodies primarily aimed against the compounds of the gut microbiota and cross reacting with neuroregulatory peptides in AN patients leads to a hypothesis that autoimmune mechanisms play an important role in the pathogenesis of AN.”
It will be incredibly interesting to see where this research leads. I remember a few years ago, a doctor friend of mine went to a conference on complex inflammatory diseases. The keynote speaker made a bold statement that really resonated with both my friend and me: “Until proven otherwise, assume that all chronic illness is autoimmune.” He may well turn out to be right!
[i] Roubalova, R, et. al. Anorexia nervosa: gut microbiota-immune-brain interactions. Clinical Nutrition. 2019. https://doi.org/10.1016/j.clnu.2019.03.023
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:
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. https://doi.org/10.1007/s00284-019-01679-8
[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.