A big leap ahead for science this week: for the first time ever, scientists from a variety of major universities (University of Chicago, the University of California San Diego, Children’s Hospital of Philadelphia/University of Pennsylvania, etc.) have directly connected specific alterations in gut bacteria to a neurovascular disease: “This is the first demonstration of a sensitive and specific diagnostic microbiome in a human neurovascular disease.”[i]
The disease they studied specifically is called carvernous angioma (CA), which had I never heard of, as it is quite rare. I checked it out on the UCLA website to learn more: “A cavernous angioma is a blood vessel abnormality characterized by large, adjacent capillaries with little or no intervening brain. The blood flow through these vessels is slow. Cavernous angiomas can occur anywhere in the central nervous system. The disease occurs in 0.4 percent of the population, and 18.7 percent of these patients have multiple lesions.” The symptoms can include seizures, headaches, hemorrhages, compression of the surrounding brain tissue, weakness, numbness, double vision, visual disturbances or language difficulties.
While this particular bit of research is on a rare condition, the lessons learned from it will likely have vast implications for a number of “brain diseases.” They chose carvernous angioma because there was already a strong animal model, which suggested that there was a distinct association between the development of this illness and an altered gut biome. Did this same gut-brain association exist in humans?If so, says the senior author, from the University of Chicago, “”The implications of that were very big…”[ii] Remember that other vascular brain diseases include stroke, various kinds of stenosis, aneurysms, and so forth. So we are talking help/treatment for a lot of people before devastating illness strikes. (I wonder too, if this won’t also apply to vascular dementia?)
The scientists sampled fecal samples from more than 100 people with CA and these were compared with 250 samples from non-affected controls. There was a clear and distinct difference: those with CA had a predominance of gram-negative bacteria, no matter where they were from, regardless of the number of lesions they have, regardless of how often lesions appear. In fact, the researchers were able to identify the 3 species that made all the difference and could completely reliably be used to identify those with CA from those without: “Those with greater amounts of a gram negative species called Odoribacter splanchnicus, lower numbers of gram positives Faecalibacterium prausnitzii and Bifidobacterium adolescentis.”
Lipopolysaccharides (LPS), metabolites produced by bacteria, seems to drive the formation of these brain lesions. The data also suggest that “…microbiome and inflammation together drive CA disease severity…” which, of course, makes sense since the more aberrant the microbiome, the more severe the disease
The question then becomes, of course, can a regimen be constructed – perhaps a combination of diet, probiotics, prebiotics and potentially antibiotics of some sort – that can stop such a process in its tracks, now that science knows the exact culprits? I’m watching and waiting for that next step because the implications for so many diseases is absolutely vast.
[i] Polster, SP, et. al. Permissive microbiome characterizes human subjects with a neurovascular disease carvernous angioma. Nature Communications. 2020;11:2. https://doi.org/10.1038/s41467-020-16436-w
Last week, an interesting biome story came out about research out of the University of California, San Francisco, in which scientists looked at the specific microbiome effects of a ketogenic diet.[i] As many of you may know, this diet – very low in carbohydrates and proteins in comparison to fats – has been used for over a hundred years to treat childhood epilepsy. In recent years, it has also become popular for weight loss, with many people believing in its health benefits. Although its use in the non-seizure population for dieting is still controversial, that it does have significant effects upon health is inarguable. (I spent a lot of time these past few weeks reading about its use in treating cancer, for example.)
How it works: when faced with a lack of carbohydrates, which your body ordinarily breaks down into the glucose used to feed every cell of your body, your liver will instead create ketone bodies from fat, which can be used as fuel instead. It turns out that ketones have a pretty dramatic effect upon the composition of the bacterial microbiome, and are ultimately highly anti-inflammatory and a potential way of treating autoimmune disorders of the gut, like Crohn’s or ulcerative colitis. (I would imagine, it might be used someday to treat other autoimmune diseases as well.)
In this study, 17 overweight or obese men (without diabetes) spent 2 months as inpatients in a metabolic ward, where diet and exercise were carefully controlled. For the first 4 weeks of the study, the men were fed either a standard diet (50% carbs, 15% protein, 35% fat) or a ketogenic diet (5% carbs, 15% protein, 80% fat). After 4 weeks, the two groups switched. Their microbiomes were analyzed from stool samples: “Actinobacteria, Bacteroidetes, and Firmicutes in participants’ guts, including significant changes in 19 different bacterial genera. The researchers focused in on a particular bacterial genus—the common probiotic Bifidobacteria—which showed the greatest decrease on the ketogenic diet.”[ii] The paper itself states: “Our data support the contribution of select gut bacterial changes, specifically Bifidobacterium, in modulating the intestinal Th17 cell population, consistent with previous work that showed that Bifidobacterium robustly induced intestinal Th17 cells.”
The scientists then took the microbiomes of those on the ketogenic diet and introduced them to mice. They discovered that this altered microbiome reduced the number of Th17 immune cells, which are well known to be involved in autoimmune inflammation. (Remember that inflammation is not bad! It’s necessary to fight pathogens. It’s only too MUCH inflammation, or inflammation that doesn’t turn off when no longer necssary, that is problematic.)
In further experiments, the researchers gradually shifted mice’ diets between low-fat, high-fat and low-carb keto diets, which confirmed that a high-fat diet and a keto diet (in spite of this also being high fat) have opposite effects on the gut biome. That is, it is the presence of carbohydrates or lack thereof in the diet that make the major difference. Simply reducing carbs in animals on a high-fat diet showed the start of this same shift, correlating with a slow rise in ketones.
The last part of their research is particularly fascinating. By feeding actual ketones to mice, they found that even those animals eating normal amounts of carbohydrates began to have the beneficial microbial shift seen in a keto diet. Maintaining a strict ketogenic diet is incredibly difficult for many people; this research suggests though that this may not actually be necessary. Simply feeding people ketones in the future may turn out to be a really effective way of manipulating the gut bacteria into a less inflammatory composition.
They conclude that their research provides “…evidence that the impact of diet on the gut microbiota is not only translatable from animal models to humans, but also appears to play a causal role in mediating host immune responses to diet. Continued progress in elucidating the mechanistic basis for these observations could help inform more personalized approaches to utilize dietary interventions for the prevention and treatment of human disease.”
[i] Ang, Q. Y., Alexander, M., Newman, J. C., Tian, Y., Cai, J., Upadhyay, V., … Turnbaugh, P. J. (2020). Ketogenic Diets Alter the Gut Microbiome Resulting in Decreased Intestinal Th17 Cells. Cell. doi:10.1016/j.cell.2020.04.027
As you all know, I am always on the look out for good news on the “what can we do about it now” front – or at least meaningful progress toward a solution. I very much enjoyed an article yesterday in Scientific American on manipulating the bacterial microbiome to treat food allergy. It was a summary of some recent research and findings, but what I found almost most interesting, was the summary of some new companies and the products they are testing.[i]
The article starts by describing the research of Dr. Cathryn Nagler, at the University of Chicago, who is attempting to isolate the bacteria that can prevent allergic response. Last year, she demonstrated that giving fecal transplants of microbes from healthy, non-allergic human babies, can stop severe allergy in mice prone to such reactions. Her “ah ha” moment came in 2000, when she read an article about how peanut-allergic mice had a genetic glitch which lead to damage to a receptor (TLR4) that appears on immune cells, and recognizes microbes. The immune cells of these allergic mice then lacked the ability to “talk” to microbes in the gut. Dr. Nagler realized then that those trillions of bacteria have the ability to suppress immune response by stimulating TLR4, and thus, alterations to the microbiome may lead to a lack of that communication…and allergy. And of course, with our shifts in lifestyle (i.e. the biome depletion paradigm, caused by our lack of exposure to our old friends in our industrialized, modern societies), these alterations are all too ubiquitous.
In 2004, Dr. Nagler showed that indeed, mice with defective TLR4 receptors went on to develop severe peanut allergy (anaphylaxis); those with normal receptors did not. But when gut bacteria were wiped out with antibiotics, even the “normal” mice went on to develop the allergy.
In recent work, Dr. Nagler and her team have discovered that Clostridia prevent food allergy in germ-free mice, she believes by stimulating the production of regulatory T-cells (which modulate inflammation) and the production of IL-22, a molecule well-documented to protect the gut epithelial lining. She theorizes that if protective bacteria are missing, the integrity of the gut barrier is compromised, which (by letting food particles into the blood stream), triggers allergic response. It turns out that top food allergens (casein (dairy protein), eggs, peanuts, tree nuts, soy, wheat, fish and shellfish) have something in common: they are resistant to digestion. Says Dr. Nagler: “’That seems to be what makes peanut the champion—its ability to resist degradation in the gut…’”
Other researchers have shown, by comparing babies with allergy to those without, consistent alterations in the gut bacteria in the former. One study tracked 226 children with milk allergy from infancy until they were 8 years old. The scientists found that certain bacteria, including Clostridia, were enriched in the stool of 3-6 month old babies who outgrew their allergy, as compared to those who did not outgrow it. This difference though did not exist in older children. The conclusion: “…allergy-protective microbes may only act early in life.”
Back to the work of Dr. Nagler then: her team has isolated the Clostridia species, Anaerostipes caccae. Another team of scientists at Boston Children’s Hospital found that the species Subdoligranulum variabile and a set of Clostridia species prevented allergy.
So where is all this going, in terms of actual products that can help actual people?
So…perhaps help is on the way. Considering that the prevalence of food allergy – which is already frighteningly common – is growing yearly, that is a really good thing. I’ll watch for the results of these trials over the next year or two!
Today’s post is about an amazing piece of research out of the University of Pittsburgh, published in the Proceedings of the National Academy of Sciences.[i]
We’re all familiar with “gut feelings” and know that our brain can influence our digestive system. Think of those butterflies in your stomach when you’re nervous. At this point, I’m sure all of you are also familiar with the fact that the gut can influence the brain – I talk about it all the time.
There are a lot of questions though about how this all works. What exact neural pathways are involved in connecting the brain to the gut?
To figure this out, these researchers injected a strain of rabies virus into the stomach of rats. They then traced the progress of the virus, as it made its way to the brain. It jumped from neuron to neuron, thereby eventually revealing the pathway from the stomach to the brain. They found that the parasymptathic nervous system (the “rest and digest” side) goes from the stomach to a brain area called the rostral insula, which is responsible for visceral sensation and emotion regulation. Says one of the authors of the paper, “The stomach sends sensory information to the cortex, which sends instructions back to the gut…That means our ‘gut feelings’ are constructed not only from signals derived from the stomach, but also from all the other influences on the rostral insula, such as past experiences and contextual knowledge.”[ii]
The sympathetic nervous system pathways, those that regulate our “fight or flight” response which kick in when we are stressed, trace from the stomach to the primary motor cortex, which directs the movements of the muscles. That makes sense, actually: when you are about to be eaten by a tiger, your body does not waste energy on digestion (which actually takes a huge amount of energy). Often, in fact, under acute dire circumstances, people evacuate food through either vomiting or defecation. (Scaring the sh-t out of someone is an expression for a reason.) Energy is directed to the muscles, to run or fight.
Why is this particularly interesting? “Our results suggest that the gut–brain axis should also be viewed from another perspective; that is, how signals from the brain influence the gut microbiome. As we noted here, the balance of activation in the two autonomic drives to the stomach can tune the gastric microenvironment. Stomach content has a strong influence on the composition of the microbiome that is passed on to more distal regions of the gastrointestinal tract.”
For example, stress is a primary cause of gastritis (inflammation of the lining of the stomach) and stomach ulcers. The latter, we’ve known for many years, is associated with the growth of the bacteria, Helicobacter pylori (H. pylori). This is a remarkable paragraph from the paper:
“Ulcer formation provides one concrete example of the interaction between central signals and the stomach’s microbiome. For more than a century, every increase in unemployment and its associated stress was accompanied by an increase in death rates from stomach ulcers. We now know that a proximal cause of ulcer formation is often infection by Helicobacter pylori. However, the growth conditions for this bacterium can be influenced by parasympathetic command signals communicated by the vagus nerve…Our current finding of direct cerebral control over parasympathetic output to the stomach elucidates a mechanism for a significant psychosomatic contribution to this problematic disease.”
That is, signals from the brain’s cerebral cortex (higher thinking) may “…influence the bacteria’s growth by adjusting gastric secretions to make the stomach more or less hospitable to invaders.”
As much as stress can cause disease then, controlling it can be a cure. As these researchers say (highlights added by me), “Our results provide cortical targets for brain-based therapies for functional gastrointestinal disorders. This could involve altering stomach function and/or the microbiome through the engagement of specific cortical areas, using noninvasive transcranial stimulation alone or combined with cognitive-, behavioral-, and movement-based therapies.” Considering the potential side effects of so many of the medications used to treat GI issues, that sounds awfully good to me. And I’ll tell you the other thought that occurs to me: the next time I “feel it in my gut,” I will forever more know that this means that I am really registering something in my brain, even if I haven’t yet consciously processed it.
[i] Levinthal, DJ and Strick, PL. Multiple areas of the cerebral cortex influence the stomach. Proceedings of the National Academy of Sciences of the United States of America. 2020. https://doi.org/10.1073/pnas.2002737117
Those who read this blog regularly know that there are some topics that particularly interest me: autism, Parkinson’s, the obesity epidemic, so-called mental illnesses, dementia, to name just a few. Another obsession of mine is ALS (amyotrophic lateral sclerosis) which, for all my life up – until 5 years ago or so – I mistakenly thought was unbelievably rare. Thus, I am always exceptionally happy to read of any progress being made as it seems there’s precious little.
Today, I’m reporting to you that new research out of Harvard provides yet more “compelling evidence” of a link between the gut biome and the development of ALS.[i] I have written a little about this before (here, for example), but the latest news is, I believe, a big leap forward.
The gene C9orf72 is the most common genetic variant leading to familial ALS. To date, the development of ALS is thought to be a combination of genes and environment. After all, not everyone who carries the genetic marker develops the disease – they are just more prone to do so. In this research, genetically identical mice with C9orf72 mutations, raised in two different facilities (one group at Harvard, one group at separate location), showed radically different outcomes. The latter group lived to a ripe and healthy old age. The Harvard mice did not. Why?
The scientists looked at many variables that could have led to the different outcomes, and ended up zeroing in on the gut microbes (no surprise!) of the two groups: “At institutions hundreds of miles apart, very similar gut microbes correlated with the extent of disease in these mice.” What they were able to ascertain is that the mice housed in the remote facility had fewer pro-inflammatory species of gut bacteria: “Here we report that an environment with reduced abundance of immune-stimulating bacteria protects C9orf72-mutant mice from premature mortality and significantly ameliorates their underlying systemic inflammation and autoimmunity.” [ii]
Once they recognized this, they tested to see if altering the microbiota of the Harvard mice would change their health outcomes. Antibiotics and fecal transplants from healthy mice did indeed improve their immune status and increase their lifespans.
They conclude, “…our studies suggests that the microbiome may be an important governor of the onset and progression of neurological disease in patients with C9ORF72 mutations, including those experiencing autoimmune and inflammatory conditions before a diagnosis of ALS…” The next step in their research is to look at the gut microbiomes of humans within families carrying this genetic mutation to see whether or not “… the gut microbiota differs between individuals that remain healthy and those that acquire the conditions.”
By the way, I want to remind you that a study done last year by the Weizmann Institute, looked at specific species that seem to be associated with the development of ALS. I wrote about this at the time the paper came out. (These mice had a different gene variant, also linked with familial ALS.) The two suspect species are Ruminococcus torques and Parabacteroides distasonis which rapidly exacerbated ALS development. As I wrote about in that post, Akkermansia muciniphila, markedly slowed the development of symptoms.[iii]
I’ve written many times about potential ways to promote the growth of Akkermansia, which unfortunately is still not available as an OTC probiotic. To name just a few: prebiotics, like FOS; other probiotic species, like L. rhamnosus and B. animalis; cranberries, black tea, grape extract; the medicine, Metformin, which I have written about before; and caloric restriction. Some day soon, I suspect, we’ll also be able to supplement with it as a store-bought probiotic. Oh, yeah! – and add Akkermansia research to that list of my personal obsessions!
As you know, I’ve been closely following developments in the field of Parkinson’s disease (PD) research as I already have multiple friends diagnosed, and that, in their 40s and 50s. (Here are just a couple of the many, many posts I’ve written over the years, on this subject: here and here.)
Research out of Australia was presented at a conference for the American Academy of Neurology Science, describing findings from a multi-center study of 167 patients with PD, compared to 100 controls.[i] All individuals in the study completed a rating scale of 15 gastrointestinal symptoms, and donated stool samples for analysis. Compared to the controls, those with PD reported significantly more GI symptoms including heartburn, acid reflux, nausea/vomiting, rumbling/gurgling ( which is called borborygmus), increased flatulence, decreased passing of stool/constipation, feeling of incomplete evacuation, hard stools. Constipation is the GI symptom that appears most in the medical literature, often preceding the actual symptoms of PD by many years. To date, other GI symptoms have not really been explored much.
The microbial analysis showed markedly reduced microbial diversity overall in those with PD. It also showed increased Firmicutes and Proteobacteria, with somewhat increased Verrucomicrobia. Proteobacteria and Verrrucomicrobia are pro-inflammatory families of bacteria. Other kinds of bacteria that were found at low levels in the PD patients are known to produce the short chain fatty acid, butyrate, which – as you’ve read many times before on this blog – is a known anti-inflammatory and improves the integrity of the gut epithelial barrier.
To boot, this research showed that as PD and GI symptoms increase in severity, microbiota diversity decreases. Says the presenter of this data: “As reduced diversity is associated with increased intestinal inflammation, this indicates that the altered microbiome we saw in [individuals with Parkinson’s disease] may be instigating the increase in incidence and severity of GI symptoms.”
Another paper on this very subject was published a few months back. This looked at association between gut microbiota and the inflammatory bacterial metabolite, lipopolysaccharide (LPS), which is often used to induce inflammation in laboratory experiments. Like the Australian study above, an increase in Verrocomicrobiae was also found in those with PD, as well as LPS-producing Gammaproteobacteria. In a mouse model of PD, exposure to LPS resulted in the development of PD symptoms by 10 weeks, as opposed to untreated mice who, after 10 weeks, were still asymptomatic. They conclude that, “This study reaffirms that an altered microbiome exists in patients with PD, and supports the notion of a proinflammatory gut microbiome environment as a trigger for PD pathogenesis.”[ii]
By the way, just a week ago, a paper came out providing more support for PD as an autoimmune disease: “The team discovered that a protein called alpha-synuclein acts like a beacon for the immune system’s T cells, causing them to attack brain cells, and thus contributing to the progression of Parkinson’s.”[iii] This autoimmune activity can be seen at least 10 years before the actual development of any PD symptoms – I’m sure not coincidentally, at the same time that early GI symptoms are often experienced, like the constipation mentioned above.
It’s fascinating, having watched this space for several years now, to watch the evidence continue to mount for the gut origins of Parkinson’s disease. And it’s exciting to contemplate the possibilities for the not-very-distant future. By the time symptoms are seen, it’s likely too late to reverse things as the dopamine-producing cells are already lost. But hopefully soon, we’ll be able to stop the symptoms of PD from developing in the first place and, at the very least, stop the progression for those already affected.
[ii] Gorecki AM, Preskey L, Bakeberg MC, et al. Altered Gut Microbiome in Parkinson’s Disease and the Influence of Lipopolysaccharide in a Human α-Synuclein Over-Expressing Mouse Model. Front Neurosci. 2019;13:839. Published 2019 Aug 7. doi:10.3389/fnins.2019.00839
Almost 2 years ago, I first wrote about the gut health benefits of honey bee products in a post about research into why queen bees live so much longer than their workers. It turned out that they are fed exclusively with royal jelly, the bee equivalent of breast milk, which keeps their microbiomes robust and diverse; whereas workers rely upon pollen, and like aging humans, over time their microbiomes become less diverse and have higher and higher levels of pathogenic bacteria.
A few months later I wrote about honey bee products again, in a post about autism and boosting levels of Akkermansia and other good, probiotic species of bacteria: “…studies show that propolis (another polyphenol), produced by honey bees, reduces bacterioides, alleviating colitis and intestinal inflammation.”
Well, interestingly, yesterday I read a paper about using honey bee products to improve brain inflammation and dysbiosis induced by none other than our old friend, propionic acid (PPA).[i] Remember that excessive PPA is considered an-almost-certain cause of some cases of autism. (I have written extensively over the years about the work of Dr. Derrick MacFabe, who has studied the effect of excess PPA for almost 2 decades now. You can read more about that here, here and here, as just 3 example of many.) As these scientists likewise state, “PPA, which is a metabolic end product of clostridia species and is known to be 10-fold higher in individuals with autism, can be regarded as a stressor for both the immune and nervous systems.” As I’ve talked about in my previous posts on bee products, they are rich in flavonoids and many other healthy components, and have been shown to have many amazing health benefits: they are antioxidants, anti-inflammatory, and even anti-allergy.
To test the efficacy of bee products, they put hamsters into 4 different groups: the first was control; the 2nd was were treated with propionic acid for 3 day; the third was treated with bee pollen for 4 weeks after the administration of PPA; and the last group was treated with propolis for 4 weeks after the administration of PPA. The animals’ neuroinflammatory responses were evaluated.
As expected, when treated with PPA the major regulatory cytokine, IL-10, which modulates the inflammatory response, went way down and pro-inflammatory cytokine levels went up. To boot, “…the neurotoxic effects of PPA was clearly presented…” But there was good news to report: “Both bee pollen and propolis were effective in ameliorating the neurotoxic effects of PPA….”
Their conclusion is potentially heartening: “The present study demonstrates the immune variation of the neurotoxic properties of PPA and the remarkable ameliorating effects of bee pollen and propolis as prebiotics because they can induce the growth of healthy bacteria and reduce the overgrown of pathogenic C. difficile.” That is, not only do these bee products directly improve inflammatory status; they also do so indirectly by promoting acting as probiotics, improving the quality of the gut bacteria, reducing pathogens.
One more really important point. The scientists point out that glutamate (an excitatory neurotransmitter that causes the firing of brain neurons) and neuroinflammation are “…well-known etiological mechanism of several neuro-developmental disorders, including autism…” Local inflammation in the brain causes decreased uptake of glutamate, resulting in too much being available to cause the over-stimulation of brain neurons. The increase in pro-inflammatory cytokines, and the decrease in regulatory ones (like IL-10), are known to be involved in creating this issue, and in decreasing GABA transmission (the counter-neurotransmitter to glutamate, which calms the brain neurons down). Thus, part of the effectiveness of bee products, as shown by both this and their previous studies, is that “bee pollen was effective in ameliorating the glutamate excitotoxicity…” caused by PPA toxicity.
Of course this needs to be tested in actual humans. However, to me this is one of those “can’t hurt, could help” scenarios. I got lazy with testing the bee products 2 years ago: I’ve already placed an order to get more to give it a fair shot for both my son Alex, who has autism, and myself.
[i] Aabed K, Bhat RS, Al-Dbass A, et al. Bee pollen and propolis improve neuroinflammation and dysbiosis induced by propionic acid, a short chain fatty acid in a rodent model of autism. Lipids Health Dis. 2019;18(1):200. Published 2019 Nov 16. doi:10.1186/s12944-019-1150-0
A friend of mine who is a neurologist recently pointed out to me that while we are all very familiar with diseases associated with the loss of memory, ie. Alzheimer’s, there are others that are associated with hyper-memory, including PTSD. In these latter cases, the person continually relives a memory over and over, and cannot stop. OCD, he explained to me, is another illness of hyper-memory. You know me: I brooded (pondered, contemplated, ruminated…dare I say, obsessed?) on this for several days afterwards, and did some outside reading. Hyperthymesia, which is the name for the anomaly wherein someone has highly superior autobiographical memory (HSAM) – i.e. they can remember an “exceptional number of experiences, and the dates on which they occurred, over many years” – was recently associated with a rare form of OCD. In a study, 20 people with HSAM had their extraordinary memories tested and the researchers noted a common behavioral pattern: “…they discovered the participants tended to display obsessive behavior, not unlike people with OCD.” Their conclusion completely confirmed what my friend had told me: “…their obsessive-compulsive behaviors leads them to constantly reflect on and order memories from their past.”[i]
As you know from my post of a week ago, there are distinct differences in the gut bacteria of those with OCD, according to recent findings. It was really interesting for me, then to read a recent article on New Atlas about a newly published study showing how the gut bacteria interact with genes to influence memory, as memory seems to closely tied in to OCD behaviors.[ii] These researchers used a mouse model called the Collaborative Cross, which involves 29 different strains of mice which is used as a model to reflect the genetic variations that occur in human populations. The scientists discovered that 2 particular sets of genes appeared to be linked to memory in mice. They then looked at the gut bacteria of the different mouse strains and found that Lactobacillus is the most common family of bacteria associated with better memory – specifically, our old friend, L. reuteri. That is, L. reuteri seems to improve memory and low levels are linked to poor memory.
I was really surprised. After all, almost exactly 3 years ago, on May 10, 2017, I wrote about L. reuteri being used to treat PTSD, a hyper-memory disorder. I described an article in Scientific American where L. reuteri was to be administered to veterans with PTSD in a clinical study. (I thought the results would have been reported by now, but taking a look at clinicaltrials.gov[iii] shows that the study was only completed a year ago, and apparently, the paper is not yet published. I’ll continue to watch out for those results.) That the same bacteria may potentially be used to treat both hyper- and hypo-memory disorders is kind of amazing and very strange.
Back to today’s study: further experiments done on germ-free mice confirmed that Lactobacillus improved memory. The researchers could therefore conclude that genes, as well as the composition of the microbiome, independently affect memory. They believe this has to do with the lactate (lactic acid) produced by Lactobacillus bacteria. When they gave mice with poor memory lactate, their memories improved. This has apparently been shown in previous research. (We know that lactic acid can cross the blood-brain barrier, and that too much of it can cause I kind of intoxication. Remember my post on that back in August, 2018? All this shows, yet again, that too much of something is as bad as not enough…and yes, you can have too much of a good thing…)
The conclusion is that this work needs to be replicated in humans, i.e. that Lactobacillus can improve memory. As I mentioned above, I’m also still waiting for the results of that study on veterans to be released. Stay tuned for the exciting conclusions to this exciting biome story!