Treat yo’ self…
After doing much research on the gut brain axis for the end of the year project, it is obvious that our gut microflora plays a pivotal part in our mental health. In this blog post I wanted to take a further look into the possible treatment of disorders such as depression and bi-polar disorder with the use of probiotics.In doing some research regarding autism Ryne and I found an NPR article that stated that a trial patient who was a college student with bipolar disorder was taking a probiotic regimen as a way to help treat her symptoms, and while the research being done on this topic is still in its infancy the young lady participating in the study noted that she felt better than she had ever felt and was in a very good place.
This one example of success into probiotic treatment warranted more research on the topic, and after doing a little digging I discovered that the field of Bio psychology is expanding and doing more research into what may be the an answer to the mechanism of depression. many patients with depression suffer from inflammation in the body. Most people with depression feel often feel sore and experience slight swelling throughout their bodies. The cause of this is not well understood, but a similar thing occurs in patients with syphilis and Lyme disease, which can also produce depressive states.
Studies indicate that this problem may be alleviated by immune activation via probiotics. However, the studies and research of the psychobiotics is limited do to a lack of participation in studies. Evidence suggest that of all current known probiotics, only a select few contain the specific bacteria that could classify them as psychobiotics. None the less, it is exciting to speculate what the future of the treatment of these mental disorders will look like as further research is done in this field. For more information read the article I did at:
http://www.sciencedaily.com/releases/2013/11/131114094754.htm
Typhoid Mary
In this blog post, i wanted to respond to the NOVA video we watched the other day in class about Typhoid Mary. I know by the end of the video the class consensus of Mary Mallon was not sympathetic, but I would disagree with general view. I believe that Mary was the victim of unreasonable prejudice in this era. If Mary Mallon had not had a lower socioeconomic status I believe the events that occured would look completely different.
in this era, the discovery of pathogenic bacteria was in its infancy. There were no antibiotics, and the information of how disease was spread was only scarcely discovered. The investigator that went to go obtain samples from Marry Mallon was not a people person to say the least. George Soper did not give Mary Mallon, a women who likely had no idea of how disease was spread, any information on the subject. She saw only threatening persecution that would have not only affected her lively hood, but further stigmatization of her character.
The civil engineer should have done all he could not to victimize the woman who was completely naive of her situation, and made it his goal to help her to understand the situation at hand. The fact that she was a woman and was Irish, was likely a factor, and I can easily see how the further deaths Marry caused by returning to a cooking position could have been avoided.
For more information on the subject take a look at the article posted on:
Are the choices we make really ours?
After doing some more research for our end of the year presentation, I wanted to go back and examine the effects that our gut micrbiome plays on our personality. The more research Ryne and I did on our topic of the gut brain axis, the more I came to realize just how much the bacteria in our gut can affect who we are as a person. The gut microbiota can have effects on behaviors like anxiety, boldness, aggression, depression, and even despair.
The fact that this much information has been discovered about all that the gut microbiome is able to do, makes me wonder how much control we actually have over who we are. Our gut bacteria develop from the time we are born all the way through adulthood, however, it is in our youth that the bacteria in our gut are established. The food we eat, the environment we are raised in, and several other factors go into the development of our microbiomes.
If this is all true, then several of our behaviors and even our how much we weigh, could be much further out of our control that we might expect. Our microbes play such a key role in these behaviors, and our microbes are developed when we have extremely limited control of our lives. The question that I want to know, is to what degree our personality is affected by these behaviors.
If you want to read more on this topic, I recommend you take a look at this article:
Dynamic Consent
In class today we discussed the ethical problems that both the patient and the researchers face in the studies done on samples kept in biobanks. It is obvious that the rules and regulations for clinical trials do not apply to the research done on sample of biobanks, due to the nature of the studies being done on these samples. Informed consent was the biggest issue discussed in that of clinical research, and right now, most biobanks instead of having true informed consent from those submitting sample, use a broad consent. This broad consent approach allows less hindered research and lots of readily available samples for the researchers, but this approach leaves the patients very much so in the dark.
In an article I read in the European Journal of Human Genetics, a group of researches has proposed a compromise to this ethical issue by way of dynamic consent, With the modern advances in technology, dynamic consent involves an interactive response in which the patients are kept up to date on the research being done to their samples. This interactive involvement of the patient in the research being done, allows the consent to be much more informed and allows the patient to remove consent if the research being done is not to their ethical approval.
This creates a slight time inconvenience for the researcher and a more time involved commitment for those who have donated samples. However, these shortcomings solve the ethical issues seen in that of broad consent. If this method proves effective on a trial based study, it could completely revolutionize biobank research. To read more on this subject, take a look at the article I read at:
http://www.nature.com/ejhg/journal/v21/n9/full/ejhg2012282a.html
Stop, drop, shut ’em down, and open up shop!
As we have mentioned previously in class, there is a serious problem that we have created for ourselves in the department of antibiotics. Bacterial life forms are amazing. They have inhabited this planet far longer that we have, and because of such, have gained the ability to live just about anywhere. Even the bacteria that infect us, due to their genetic make up, have the ability to adapt to the antibiotics we have created to battle pathogenesis. This of course has created the world wide problem of antibiotic resistant bacteria, and in turn enables infection with limited treatment.
So what are we to do? We cannot sit idly by and let once treatable infections continue to claim human lives, but how in the world do we treat these infections without furthering the problem. One possibility as stated in a Ted Talk given by Bonnie Bassler, is not to kill the bacteria that are killing us, enabling further mutation, but rather to stop the mechanism by which these bacteria go about infecting their hosts.
A single bacteria has no effect whatsoever on the human body. Much like DMX needed the Ruff Riders, bacteria require a community to open up shop in our body. Bacteria of several different varieties live in a great community, and can communicate with one another. Bacteria of the same species have an enzyme in there body that secretes a chemical, much like our cells secrete hormones, and this chemical in the environment reaches a set concentration in which receptors on the outside of the bacteria connect with the chemical much like a lock and key. With this increase in concentration, bacteria can communicate with one another, let each other know of their presence, and then act as a community.
This method also occurs across all species of bacteria. By way of the same mechanism, all bacteria possess the same enzyme that secretes the same chemical. When all the bacteria present recognize this community, they can act together and take over their host. The answer that scientist have proposed to our antibiotic dependence, is to create interference of this signaling preventing bacteria of the same species, as well as all bacteria present from communicating with one another. In a study done with mice infected with a harmful bacteria population, the introduction of this interfering chemical, prevents infection and spreading of the disease.
The implications of this finding our huge, and may enable us to resolve the momentous problem we have created with antibiotic resistance. These findings may also shed light on how the eucharyotic cells in our body communicate with one another, which could lead to the further discovery of preventing several other diseases. My worry with this finding is that what affect does this blanketed interference have on our own microbiota?
If any of this tickles your fancy, I encourage you to watch the Ted Talk I watched at
I’m Mike O’Malley, and this is GUTS
As we continue to dive deeper into all that our human microbiome is able to do in our bodies, my interest in the subject continues to build. After doing lots of research on all that our gut microbiota does to play a role in our mental heath, I wanted to do a little research on the mechanisms by which these microorganisms are able to affect things like anxiety, boldness and even conditions like bipolar disorder and autism. In the research I had previously done, the source of this connection appears to be the Vagus nerve, but I was still baffeled by how this exactly happened.
Naturally, in lieu of reading more articles on the subject I went to Youtube to find a Ted Talk on the subject, because honestly, why read when you can watch. I was not disappointed by my search, and found a great little video of a post grad student from Caltech giving a Ted Talk on the subject. As it turns out, the Vagus nerve is not the only way that our gut communicates with our brain. When done by way of the Vagus nerve, our gut microbiota uses the bacteria Lactobacillus rhamnosus to metabolically produce a chemical that activates the nerve. This sends signals to our brain and when done by this particular bacteria reduces depression like symptoms.
The gut microbiota are also able to activate immune cells in the gut. In one mechanism, the bacteria Bacterioides fragilis prevents a form of Multiple Sclerosis in mice, meaning that when treated with this bacteria the mice are much less susceptible to the disease. This finding, to me, was absolutely incredible, and is baffling when you think of the medical implications it may hold for the future of MS. The gut microbiome can also activate our endocrine system, producing various neuropeptides and neurotransmitters which are actually used to treat the autism like symptoms in mice.
If your as interested as I am in this stuff, I urge you to check out this Ted Talk on Youtube at
Your Brain’s Sidekick
Before having taken this class, I would have never thought it was possible that our mental processes are affected by factors other than our brain. I can tell beyond a shadow of a doubt that my general psych class never mentioned that our brain had a partner in crime, but as we have discussed in class, our gut microbiota play a role in our mental processes. Our gut microbiome play a role in our anxiety, aggression, and even our boldness. One day in class Dr. Duffin mentioned the connection between our guts and autism. I found this tidbit of information absolutely fascinating, and it compelled me to do a little more research.
Upon further investigation, I found several papers and scholarly research on this topic as well as an article done by NPR that was really well written. This article discussed the connection between anxiety and the other behaviors I listed, and how the gut plays a role in communicating with the brain by way of the vagus nerve. In the second portion, the author focused specifically on autism and the experiments and correlation found between the two.
As it turns out, many people diagnosed with autism also have gastrointestinal problems. As recent studies have shown a much less diverse community of microbiota in the guts of people with autism, scientist furthered this research by experimenting with mice. Scientist infected pregnant lab mice with a virus that left the baby mice with social symptoms very similar to what would be seen in people. These mice were very antisocial and presented severe anxiety, and in these mice the scientist found similar GI problems seen in humans with autism. The next step of this experiment was to implant the gut microbiota of nice that expressed more bold and aggressive behaviors into these mice that presented autistic behaviors, and the results were absolutely amazing. The autistic mice began to behave in a more normal fashion, with much less anxiety and social withdrawal.
Hopefully, with these results in mind, we can further experimental treatment in humans to make autism a much less severe disability. To read more on this issue, look at the NPR article I referenced at
Diversity- an old wooden ship
In our class we have discussed the correlation between the microbiome in ones gut and a persons relative size. Studies have shown that the abundance of Firmicutes in the gut are seen in more obese individuals, whilst the abundance of Bacteriodetes are seen in leaner individuals. This of course is an oversimplification of a complex relationship and after doing some more research on the topic I came across an article that offered more insight into the correlation.
In the study done, sets of twins in which one twin was lean and the other twin was heavy had the microbiota from their gut implanted into mice that had been raised in a sterile environment. Twins were used in the study so that genetic implications would be as limited as possible, and the findings of this experiment showed that mice that received microbes from the obese twin gained weight, whereas mice who received microbes from the lean twins retained a slimmer body type. The study showed that the thinner mice had a much more diverse microbiome in their guts than that of their obese counterparts. What is more interesting is that when the two mice were place together in the same cage, the microbes from the thin mice were transferred to the heavier mice, and the heavy mice began to loose weight.
This was an extraordinary finding to me, but the study probed the issue further by changing the diet of the mice. In America, the diet that we consume is one that contains more saturated fats and less lean protein. When the diet of the mice was shifted to reflect our common diet, the transfer of microbes between the two mice did not occur.
This study show that it is not microbe alone that control obesity, but the diet we consume as well. Whilst this finding might be rather obvious to some it would appear that the end goal of a healthy gut is not a dominance of one type of bacteria, but a diverse colony, coupled with (or brought about about by the means of) a healthy diet. All in all, diversity is key, sorry Ron Burgundy…
To read more on this study, you can find the article I referenced at
http://nih.gov/researchmatters/september2013/09162013obesity.htm
Eyeball hard in the paint
My first post on the subject of microbial life on the ocular surface was a response to the study done by the Ocular Biome Project and their findings that the ocular surface was indeed home to the its own ecosystem of bacteria and other microscopic life. However, this established fact left me with more questions to follow up on. Some of the responses I received from this first post led me to question this presence of pathogenic bacteria on the surface that has the potential to cause infection of the eye, and how it can exist despite the antibacterial tears naturally produced by the eye.One would naturally expect the eye to be a sterile surface that is infected with bacteria from an outside source, but given the findings from the article published by the Ocular Biome Project, we now know that the infections of the ocular surface occur when the bacteria already home to the eye undergo pathenogenesis.
After doing some further research on this topic I came across an article that proposed some answers tot his problem. According to the article Of Biomes, Biofilm and The Ocular Surface written by Mark B. Abelson, MD, CM, FRCS, FARVO, and James McLaughlin, PhD, Andover, Mass. I found that the mucus of the eye and the bacteria that reside on the eye coexist and work together. According to the article…
” The mucins of the ocular surface exist in both soluble and membrane-associated forms, and one of their key functions is to act as anti-adhesives, preventing bacteria from establishing a foothold. Soluble mucins also have antimicrobial properties that contribute to the tear film’s bacteriostatic role. In addition, some bacteria produce enzymes that cleave membrane-associated mucins from the epithelial surface. It’s possible that this process is part of the ecosystem of the ocular surface: Both mucins and their bacterial guests have been coevolving for millions of years.”
This shows that the mucus of the eye prevents the bacteria that exist there from forming a biofilm on the ocular surface which would cause infection while the bacteria, in turn, break down the mucus preventing completely coating the epithelial surface, enabling the continued production of this mucus.
I’ve worked in an optometrist office for four years now, and more often that not, infection occurs along with the presence of over warn or improperly cared for contact lenses. The article written by Abelson and McLaughlin attributes the formation of this biofilm to the bacterial pathenogenesis, and the contact lens provides the perfect surface for the formation of this bacterial film. They even state that, “In their native habitat, microbes most often live in ultra-thin layers coating any and all available surfaces, from catheters to contact lenses.”
The further study of the microbial ecology is necessary to further the protection and treatment of bacterial infection of the eye. These finding are a huge step to the health of the eye, and I am very excited to see how this research develops.
Abelson, Mark B. “Newsletters.” Review of Ophthalmology® Of Biomes, Biofilm and The Ocular Surface. N.p., 6 Sept. 2012. Web. 28 Apr. 2014.
Eyeball so Hard
See as how this is my first post, and my first attempt at blogging, I thought I would keep it relatively short and sweet. After graduating from Transylvania University I would like to pursue a career as an Optometrist, and as such, my interests when studying the diversity of microbiomes in my May term class was to look into what kind of microbial life, if any, exists in our eyes.
I was not overly optimistic, seeing as how our eyes produce tears and moisture to keep the eyeball a sterile environment. However, after doing a little poking around on the internet I discovered that not only was this presumption of mine a false one, but that there was in fact a group of scientist from Miami, Seattle, North Texas, and Indiana working on this exact field of research. Their project is called the Ocular Microbiome Project (not the most creative name in the world, I know) and in 2011 the scientists from Miami published some of the work the had done in the Investigative Ophthalmology and Visual Science Journal. The research done by the project continues to this day, but this article that they published back in 2011 demonstrates just how groundbreaking their research is.
According to their paper, before this study, ” Comprehensive analysis of microbial diversity at the OS has been impossible because of the limitations of conventional cultivation techniques (Dong).” The pilot study done by these scientist however was able to implement the technique we discussed in class know as 16S rRNA analysis and view the gene expression of the microbial life seen. The findings were astonishing, and according to the article, “a total of 115,003 quality DNA reads, corresponding to 221 species-level phylotypes per subject (Dong).” The study concluded that the surface of the eye contains many gernera of microscopic life that are commonly identified as pathogens to the ocular surface (Dong).
This study confirms that the pathogens seen when the eye becomes infected our not merely visitors to the ocular surface but exist in their own biome right on the surface. The study will continue by doing further analysis across population groups, but the ultimate goal of this project would be to understand the role that these indigenous bacteria play in the heath and disease of the eyeball (Dong).
Hopefully after reading this you learned a little something new about your eyes. If you are as curious as I am about this topic, the paper I read can be found at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3176057/#__ffn_sectitle , and although it is a little dry, the leaps being made in the scientific knowledge of ocular biomes is truly impressive.
Dong, Q., J. M. Brulc, A. Iovieno, B. Bates, A. Garoutte, D. Miller, K. V. Revanna, X. Gao, D. A. Antonopoulos, V. Z. Slepak, and V. I. Shestopalov. “Diversity of Bacteria at Healthy Human Conjunctiva.”Investigative Ophthalmology & Visual Science 52.8 (2011): 5408-413. Print.
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