Category Archives: Science and Nerd Stuff

Blogs about my thoughts on various scientific topics and other nerdy non-physically active things. See the “Making Science Accessible” tab for a complete list.

Covid-19; Testing, Drugs, Vaccines and Seasonality 3/25/20

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It’s been a week since my first Covid-19 blog on 3/18/20, and I will have to admit how amazed I am at the feedback and attention it got. A LOT has happened since that day, and not all of it has not been so positive. Here in Colorado Governor Jared Polis officially announced today (3/25/20) that ALL residents of Colorado are under a ‘Stay at Home’ order. Meaning we’re supposed to stay in our place of residence with the exception of essential trips (medical, food, work for us exempt jobs) and exercise, all the while maintaining social distancing from anyone not in our immediate household (which is just me and my cat). For many of us this isn’t too much of a change, but for those who didn’t think this was serious it’s probably a bit of a rude awakening. Since my post LAST WEEK (now 3/26/20) the number of worldwide confirmed cases has more than doubled to 530,000 (from 219,243), the number of deaths has increased to over 24,000 (from 8,968) and on 3/26/20 the United States confirmed over 17,000 NEW cases, making us the country with the most confirmed cases in the world (go us?) (worldometers.com, washingtonpost.com).

I’m hoping by now that most people realize how serious this is, and that there is definite need to slow the spread; both to allow our medical care teams to keep up and to allow scientist to keep working (please no arguments on the political actions or economic impact, yes it’s going to be bad). My goal in this blog write up is to outline the things that help us bring this pandemic to an end (or at least slow it down). I’ll be focusing on the status of testing in the US (what those tests are), the current drug pipeline and what is being tested, the process and timeline for a vaccine and whether there’s anything to the claim of seasonality with the infection. So here we go, Round 2, diving back into the Science!

Testing

So in my last post I wrote about how much of a mess the Covid-19 testing and surveillance were in the United States, well sadly that has not improved a whole lot. While we’ve definitely tested a lot more people, I’ve been hearing from providers and hospitals all over the country that they’re only testing people who are in high risk populations or have advanced/severe cases of disease. Very recently a rash of new tests have become available to providers and hospitals, meaning the surveillance is starting to grow and hopefully this will continue. There is definitely hope as we are soon to have two different types of tests available, the PCR based tests that we’re currently using for diagnosing active disease and an Antibody based test.

The PCR based test is the one I spoke about previously where labs are able to look for pieces of the viral genome in human samples (usually a nasopharyngeal swab). This test can be quite sensitive and is used to identify infected patients even during the early stage of disease. Though, being such a sensitive test it is more prone to errors and false positives (though they are still very well validated), hence why the original CDC test failed. The other issue right now is that because there’s not a lot of top down coordination in the United States we have dozens of different labs who have created PCR based tests that are being used in different parts of the country. Here are a few of the companies/hospitals who have created PCR based tests; ThermoFisher, Roche, Cepheid, Mayo Clinic, Stanford University, University of Pittsburgh, Atrium Health and the list goes on and on. The CDC even setup a website to allow researchers to develop their own tests and to provide some general guidelines. While on the surface this seems smart, it also means we don’t have any national coordination in our Covid-19 testing on the ground.

The second type of test that is just now being release is a test to look for IgM and IgG antibodies in the blood of patients. You might remember in the previous post where I talked about us building immunity to the virus? Well, antibodies are one of the hallmarks of immunity, and we can test for them, even after we’re no longer infected. A simple prick of the finger (a little blood) on a indicator strip and we have a positive or negative for SARS-CoV-2 antibodies in minutes rather than hours or days, think of it like a pregnancy test for Coronavirus (United Biomedical, Aytu Bioscience). The problem with these tests is that SARS antibodies may not be detectable until 7-14 days after onset of symptoms (Chan et al 2005), so there’s a good chance they won’t identify people who are in the early stages of disease. They WILL help us dramatically as we attend to understand the true prevalence of the disease and how many people are now immune. Once a person is immune and recovered you’re very unlikely to pickup or spread the disease.

Drugs and Clinical Trials

Much to the chagrin of many of us in the biomedical research sciences and healthcare, Donald Trump touted hydroxychloronquine as a ‘game changer’….wow wow, let’s pump the breaks for a second, back it up, and talk about the process by which drugs are created, rigorously tested and finally produced for mass distribution (if they even make it there). The first step is identifying potential drugs and targets then testing them in a laboratory to see if they actually work like you hoped and they’re not excessively toxic. This usually involves some mix of cell culture and animals models. If a candidate is lucky enough to make it through the lab testing phase (known as pre-clinical trials, only 1 in 1000 do) then the company can apply to the FDA to move it’s drug on to a multi-stage Clinical trial in human subjects. Phase I of the clinical trials process involves taking healthy individuals and dosing them with the new drug (usually starting low and escalating). They have to look for safety, effects on the body, toxicity, side effects, maximum tolerate dose, tissue distribution, half-life and on and on. IF the drug makes it through this initial phase then it’s on to Phase II where the drug is tested in a medium size group of diseased individuals (in this case Covid-19 positive). All of this under careful supervision of doctors who are specially trained to assess dosing and efficacy. If the drug proves efficacious in this Phase II study it will move on to a larger Phase III randomized double blind study where the drug being tested is compared to a placebo control (sugar pill) to ensure that it’s really the drug having an effect. These large studies can include 1000s of people and take many years depending on the nature of the disease being tested. Finally, once a drug survives Phase III; proving safe, efficacious and with the dosing amount and regimen worked out, the company can file for approval from the FDA (1 in 5000 make it this far)(medicine.net). This whole process can take up to 12 years for chronic diseases, but of course right now things are moving much more rapidly, and a lot of the regulations and paperwork are being modified to speed up the process.

So what about all the drugs that are being tested against Covid-19 right now? There are several drugs that were identified as being potential therapeutics, and thankfully they had already passed Pre-clinical testing and Phase I trials, so this dramatically expedites the process of testing. The most promising seem to be Remdesivir (from Gilead), Favipiravir (anti-viral), and the previously mentioned hydroxychloroquine (cdc.gov, Dong et al, Wang et al). Even though all of these drugs have successfully completed varying levels of clinical trials, using them against a new disease requires a new round of efficacy, dosing and safety testing. Patients with different diseases respond to drugs differently, dosing needs to be adjusted for the new disease and of course the drug needs to be thoroughly tested to ensure that the differences seen in early studies weren’t simply because of patient selection, population bias or other factors that were not controlled for with the small sample set. In short, all these drugs, while promising, are many months away from being approved for safe use in a wide array of Covid-19 patients, if they get there at all. See the comment below from my college friend Aileen, who’s a pharmacist in the San Francisco Bay Area in response to the small test of hydroxychloroquine in patients in France (Gautret et al)….

More PSA from a pharmacist….to detail out certain claims Hydroxychloroquine used in this case is in particular HIGH DOSE (usual dose of the drug is 200-400mg daily, in this case…600mg daily and we only use that dose in Q Fever patients). When the hydroxychloroquine in high dose and azithromycin are taken together, there are risks for GI side effects…and most importantly…POTENTIAL ARRHYTHMIA. First azithromycin is a known QT prolonging agent…but also…hydroxychloroquine can either cause direct mycocardial toxicity or exacerbate underlying mycocardial dysfunction. This is a RISK that must be weighed by physicians and healthcare professionals vs. the unproven benefits.
Is there promise? potentially….but we NEED MORE EVIDENCE TO EVALUATE SAFETY AND EFFICACY.
Please…do not demand for it….leave it to healthcare professionals to make that decision and do our jobs….

The next question is in regards to a vaccine against Covid-19. Unfortunately, the process I outlines above for drugs, also applies to vaccines, but we’re starting from ground zero. Prior to this pandemic there were no coronavirus vaccines available (though plenty of background research), so companies have gone into serious overdrive trying to develop something, and amazingly in just two months Moderna, in collaboration with the NIH, took the first vaccine candidate to Phase I clinical trials this month (March 2020) (nih.gov). A process that usually takes 6-12 months took them 2, let that sink in for a moment. And they’re not the only company working hard on creating a vaccine, as there are numerous others with vaccine designs being tested in Pre-Clinical trials as we speak. But, this bring us back to question of time. Before a vaccine can be deployed to the general public it has many hurdles to pass, and only if it successfully passes those hurdles can it be mass produced and distributed. So, as Dr Fauci has explained many times, we’re looking at best case 12-18months for a vaccine. Guess we’re going to have to hang tight and weather this storm for a bit longer.

Seasonality

Most people have probably heard the claim at one point or another that this thing (Covid-19) is like the flu and it’ll go away when the weather warms up. Even our President claimed “…you know, a lot of people think that (the virus) goes away in April with the heat — as the heat comes in. Typically, that will go away in April.” Is there any logic or scientific evidence to support this claim? The short answer is, no, but it’s definitely more complicated than that.

The idea of seasonality was brought up because the influenza virus does see a very seasonal pattern of spread and retraction. During the cooler winter months in the Northern Hemisphere we see a dramatic rise in influenza infection rates, then a drop as the weather warms in April, as Trump suggested. There are many reasons for this; reduced contact time between people (stuck inside, schools) as weather improves, improvements in immune responses due to people being outside more and increases in Vitamin D, potential increase in duration of infection during winter months, and decreased survival of some pathogens in warmer environments (Fisman et al). While we do have the first three things going for us as they are environmental changes that aren’t pathogen specific, what about the survival time of different viruses? It’s been well documented that influenza viruses survive and transmit best at lower environmental temperatures in the range of 5C and 20C. Though starting at 20C, depending on humidity, influenza virus transmission becomes much more variable, and at 30C a dramatic decrease is seen in viral transmission (Lowen et al). Unfortunately, coronaviruses don’t seem to have the same susceptibility profile. Testing on the original SARS-CoV-1 virus showed that it was fairly stable at environmental temperatures as high as 33C (91F), and only when temperature was increase to 38C (100F) did the virus infectivity begin to dramatically drop (Chan et al 2010). SARS-CoV-2, the causative agent of Covid-19 seems to be more temperature resistant than the influenza viruses that we commonly associate with having seasonal cycles. So with the virus currently spreading in the Southern Hemisphere and in several warm weather countries we shouldn’t expect too much help with the virus from Mother Nature’s change of seasons.

But not all hope is lost! I’ve heard recently that the extreme measures taken by many states have allowed the hospitals in the US a little breathing room. Even if this is short lived it means that staff and supplies can be replenished and that buys more time for widespread testing to come on line. Countries like Germany and South Korea are good case studies for how excellent testing and surveillance can lead to minimizing the number of fatalities (testing large percentages of their populations, and doing so quickly). Even though cases and number of deaths are still increasing, we’re slowly catching up on testing, and keeping our death rate low, but the fact that we have 2,122 serious or critical Covid-19 cases is still a little scary. For now, we’re all going to have to sacrifice a bit, be more compassionate to our fellow humans and just realize that we’re living through unprecedented times, that we will get through, though it’s going to take some time. If you’re interested in reading about some potential scenarios on how the pandemic plays out in the next 3-12months this article from the Atlantic outlines them pretty well in my opinion.

Citations
aytubio.com/covid-19/
cdc.gov/coronavirus/2019-ncov/hcp/therapeutic-options.html
Chan et al. The Effects of Temperature and Relative Humidity on the Viability of the SARS Coronavirus. Advances in Virology, 2011.
Chan et al. Serological response in patients with Severe Acute Respiratory Syndrome Coronavirus infection and Cross-Reactivity with Human Coronavirus 229E, OC43, and NL63. Clinical and Diagnostic Laboratory Immunology, 2005.
Dong et al. Discovering Drugs to treat Coronavirus disease 2019 (Covid-19). Drug Discoveries and Therapeutics, 2020.
Fisman et al. Seasonality of Viral Infections: mechanisms and unknown. European Society of Clinical Microbiology and Infectious Diseases, 2012.
Gautret et al. Hydroxychloroquine and azithromycin as a treatment for Covid-19: results of an open-label non-randomized clinical trial. Journal of Antimicrobial Agents, 2020.
Lowen et al. Roles of Humidity and Temperature in Shaping Influenza Seasonality. Journal of Virology, 2014.
nih.gov/news-events/news-releases/nih-clinical-trial-investigational-vaccine-covid-19-begins
unitedbiomedical.com/COVID-19/
Vincent et al. Chloroquine is a potent inhibitor of SARS coronavirus infection and spread. Virology Journal, 2005.
Wang et al. Remdesivir and chloroquine effectively inhibit the recently emerged novel coronavirus (2019-nCov) in vitro. Cell Research, 2020.
washingtonpost.com/world/2020/03/24/coronavirus-latest-news/
worldometers.info/coronavirus/

Chaos and COVID-19

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Society is in some state of chaos at the moment, and there’s so much misinformation and misunderstanding floating around. So in this blog I’m hoping to provide some of the scientific knowledge based on the research and observations. First, here are my credentials; Masters of Science in Immunology and Infectious Diseases, I’ve spent 14 years in the laboratory doing research (HIV, Tuberculosis, West Nile, Autoimmune diseases, cancer) and worked in a BSL3 laboratory. So with that out of the way, I’m going to try and stay away from giving too many opinions, talking about the politics or debating the models because there’s just too much speculation there. So if you’re interested just in the scientific research about the virus, the immune system and the current case study numbers hang on, this is going to be a long one (all references cited will be at the end).

Background

In early December 2019 a cluster of pneumonia cases appeared in Wuhan, China with clinical characteristics similar to SARS-CoV-1. Of the initial patients studied the mortality rate was extremely high (10-15%, now estimated closer to 2-3.5%), which gave rise to great concern that this virus would be a serious health issue. Sampling from the initial patients and sequencing identified the causative agent as a novel (new) coronavirus that was originally named 2019-nCoV (Huang C et al). Subsequent sequencing and analysis of the virus from those original cases showed that the founding virus has similar characteristics to coronaviruses found in bats, but is also related to those found in pangolins. There are currently two sub-strains of the virus circulating in the population; S-type and L-type. The S-type is thought to be the founding strain, while the L-type is a slightly altered variant that is now the predominant virus circulating in the population (70% of cases), though the consensus sequence for both strains only differ by a few base pairs (Tang et al). As of now (3/18/20) there is no evidence that SARS-CoV-2 can sustain infection and spread through any other animals other than humans. As of 3/18/20 China has experienced 80,894 confirmed cases on COVID-19 (disease caused by the virus SARS-CoV-2 formerly 2019-nCoV) and 3,237 deaths from the virus (worldometers.info). While daily number of new cases in China has significantly waned in recent weeks, it has spread to the rest of the world and is currently spreading rapidly throughout Europe, the Middle East and the United States.

How the Virus Spreads

Viruses can spread by either direct (touching, kissing, sex) and indirect (coughing, sneezing, aerosols) methods. Early on during the epidemic of SARS-CoV-2 it was realized that the virus was capable of spreading by indirect contact and possibly survived in aerosols. Though the primary route of transmission is still thought to be direct or close contact with an infected individual. Studies showed that aerosolized liquids containing SARS-CoV-2 could survive on surfaces (specifically plastic and steel) as long as 72 hours in a controlled laboratory setting (Doremalen et al). Though the half-life of the virus on all surfaces was 16 hours or less. Meaning that while the virus can be detected up to 3 days after deposition most of it dies much earlier, though we don’t know exactly what the survival time in a natural environment is. The main take home from this should be, the virus can be transferred from one host to another fairly easily and surface contamination can be an issue if an infected person sneezes/coughs, so cover your mouth and clean common areas! One thing that has made the virus especially difficult to track and control is the presence of what are known as asymptomatic carriers. These are individuals who become infected with the SARS-CoV-2 virus and are contagious without showing any symptoms (Bai et al). Thus, while they appear fully healthy, they are in fact vectors for the disease without even knowing it. Additionally there can be long incubation times between becoming infected and showing symptoms, thus allowing people to spread the viruses unknowingly.

Preventative Measures (WHO.int)

Standard hygiene rules apply for SARS-CoV-19;
Wash your hands frequently.
Clean common surfaces in shared areas.
Cover coughs and sneezes with an elbow or arm.
Do not touch your nose, eyes and mouth (this is how the virus gains access to the body).
Social distancing (the practice of staying 2m away from potential contacts).
Stay home if you’re sick and self-quarantine. This one is very important and something Americans do not do well.

The question of using masks and gloves has come up numerous times, so I’m going to try and dispel some of the rumors and misinformation. These items are known as PPE (Personal Protective Equipment) to those in healthcare and the medical sciences. They are used to protect one’s self from infectious and hazardous materials when used properly. Both N95 masks (fitted and tested, designed to filter out 95% of microparticles) and surgical masks (loose fitting masks that cover your mouth, no seal) are designed to create a barrier between the user and the surrounding environment. N95 masks when worn properly will filter out most particulate and infectious matter, protecting the wearer, when USED PROPERLY. Proper use does not include wearing it around your chin, pulling it off your nose to breath or touching the mask with unwashed hands, in short most of the public is not trained well enough to properly use these and thus negates a lot of the benefits they can provide. Surgical masks on the other hand are designed to protect those surrounding the user by blocking some of the aerosolization of material, they ARE NOT designed to protect the user from inhaling microparticles (same goes for cloth masks) (Balazy et al). The reason the government does not want the public using and hoarding these disposable masks is that there is a HUGE shortage for our healthcare workers, the people who have to take care of the sick and injured on a daily basis (which may be you). They come into contact with the infectious and at risk at levels exponentially higher than the average person and if they don’t have these protective equipment then it’s almost a certainty they’ll get infected, and then either be forced to take time off (leaving our hospitals understaffed) or infect those around them such as patients who are at risk. If you’ve been hoarding masks or bought a bunch think of donating them to your nearby hospital, every nurse or doctor I’ve spoken with says they are rationing and running very low on these supplies. If you need to wear a mask buy a cloth reusable mask (and wash it regularly) in order to protect those around you from anything you might be carrying. As with the N95s above, disposable latex and nitrile gloves are not very practical or helpful for most people. Every time you touch your body, your cell phone, your hair, your mask on your face, you contaminate the gloves and spread that contamination around. Save yourself the waste and trouble and just regularly wash your hands.

Symptoms and Testing

The main symptoms as outlined by the Center for Disease Control (CDC) are; fever, cough and shortness of breath along with a host of other minor symptoms (CDC.gov). What sets SARS-CoV-2 apart from influenza or the common cold is the lower respiratory involvement. Symptoms usually appear in 2-7days, but there have been cases where symptoms are very delayed (beyond a week). The state of Colorado recommends that if you have these symptoms or are concerned due to exposure to a positive case to call your primary care doctor first, do not go to an ER unless it’s an Emergency.

Once the virus enters the body it binds to ACE2 (Angiotensin-Converting Enzyme 2) receptors on vascular endothelial cells and uses these cells as a host to replicate. ACE2 receptors are also found in the lungs, kidney and GI tract, all locations known to harbor coronaviruses (Jia et al). In addition to the more general symptoms, in moderate to severe cases pulmonary inflammation and damage are seen and these are considered the more critical issues when looking at long term prognosis. CT scans of the lungs were found helpful in diagnosing patients with more advanced disease (Zhu et al). Patients over the age of 65 and those having a host of other chronic disorders (hypertension, diabetes, auto-immune diseases, immunocompromised) are more likely to progress to severe COVID-19 disease than those without (Zhou et al). Though recently it has been seen that even younger patients can have lasting pulmonary damage beyond disease resolution.

Which brings us to the next issue, testing…oh testing….. When the epidemic first began in China researchers isolated and sequenced the viral genome (this is an RNA virus). Allowing them to identify unique sequences in the virus that they could use as a genetic finger print. In January of 2020 a group at the Charité University Hospital in Berlin released information on an assay that would guide the creation of the first large scale PCR testing to be adopted by the WHO (Corman et al). Since then several other countries have released different versions of the test. Since January over 1million tests have been run around the world, with China (320,000), South Korea (286,000) and Italy (148,000) leading the way (ourworldindata.org). Sadly the estimates in the United States are that only 41,000 people have been tested. I say ‘estimates’ because right now we have no National testing strategy or centralized facility monitoring our testing. Tests are being run by government labs, hospitals, private diagnostic labs and even some private biotech companies have created their own tests, but the short of it is there’s no central coordinated effort as of 3/18/20. If you’re interested in reading more about what went wrong with our testing, check this article from the New Yorker.

Which brings us to how can you get tested? Well, the short answer is most people can’t. Because of testing shortages the guidelines on who can get tested vary wildly from state to state and county to county. The standard criteria in Colorado as of 3/18/20 is that you must have an order from your healthcare provider, stating known contact with another infected patient and/or presenting with symptoms. Even if you do meet that criteria there’s no guarantee you can or will get tested right now, I personally know several people who fit the criteria but have been turned away to self-quarantine and monitor. So how do you know if you are infected with the virus? Well, in the United States right now you really don’t, and in lieu of broader testing to identify the spread of the virus social distancing and limitations on group gatherings (including concerts, bars, restaurants) have been put in place.

Treatment Options

Right now there’s no fully validated and approved treatments for COVID-19 (SARS-CoV-2). For those with more mild forms of the disease the CDC recommends; quarantine, rest, monitor your symptoms and continue with the preventative measures listed above. For those with more severe symptoms go to the hospital for care.

As of 3/18/20 there are numerous companies in the early stage of testing vaccines against COVID-19, one has even begun Phase I human trials, which simply looks at whether or not the vaccine is safe in humans, it’s a long way from mass production though. There are also several approved medications that are being tested in Phase II and III clinical trials in patients suffering from COVID-19; Remdesivir, Chloroquine and Favipiravir appear to be the most promising. All three were originally developed for other diseases (Ebola, malaria, influenza) but are being repurposed to fight COVID-19 and have shown promise in early patient testing. It’s quite common for drugs to be tested and used for numerous different indications, because this expedites testing as the safety has already been proven in previous studies. EDIT:
Because Trump and the FDA made specific announcements about Hydroxychloroquine today (3/19/20) I’ll add an extra note here. Hydroxychloroquine has been been used as an anti-malarial (parasite) for almost 70 years, and is also used to treat Lupus and rheumatoid arthritis, so you might ask, how does this drug help us fight a virus??? The drug alters the pH inside special compartments inside our cells (for the scientist; lysosomes, endosomes and the Golgi) having an affect on several pathways. One such pathway is the process of breaking down antigens and presenting them to immune cells (Fox et al). For autoimmune diseases this means the drug helps slow the immune response to your own body, but this is counter productive to fighting a virus that we want to kill, so what gives? Ah, but there’s an alternate pathway that the drug affects, modification of proteins in the Golgi. These modifications are essential for viruses to replicate and produce more functional virion! So the drug does function to slow down some parts of the immune system (not all) BUT it also serves to reduce viral replication (in experiments with HIV showed modest reduction, SARS-CoV-2 specifically has not been tested yet) (Romanelli et al).

Immunity?

With most infections, your body has two stages of response. First is the non-specific innate immune response where our body recognizes that there’s a foreign invader (bacteria, virus, parasite, etc) and attempts to kill it. Sometimes the number of the microbe is too great and they infect and spread in the body causing disease. All infectious organisms have a minimum infectious dose that’s required to get a person sick, though this exact amount varies from person to person, for route of entry and is different for each microbe. Once the initial non-specific response fails our body goes into overdrive to try and kill off the rapidly replicating organism. This includes running a fever to burn the pathogen out and creating a pathogen specific memory response via T-cells and B-cells selection. These specific memory responses are the backbone of what is known as pathogen specific immunity, or our ability to fight off a disease. As of now (3/18/20) it appears as though people who survive and recover from COVID-19 are immune to the virus. Recently there have been news articles about how several recovered COVID-19 patients have retested positive for the virus, these cases most likely fall into one of two categories; first that the patients were released prematurely from the hospital and thus still had low levels of virus remaining in their system, second the recovered patient came into contact with another infectious patient who transferred the virus to them allowing them to retest positive. Being immune does not mean that another person who is infected can not transfer the virus to us, it simply means our body is able to destroy the invading pathogen before it causes disease, this is how a vaccine works. Note that in both cases the affected individuals did not get sick a second time (as far as we know) and for those who become immune it is not believed they can further spread the virus once fully recovered.

Current Statistics (3/18/20)

As of 10pm on 3/18/20 there have been 219,243 people who have tested positive for COVID-19, 124,530 cases are still active (6,814 are in serious/critical condition), 85,745 have recovered (mostly in China) and 8,968 have died (worldometers.info). The current world wide mortality rate stands at 4.09% but as many have and will point out that is a flawed number because of the lack of testing and the lack of understanding what the actual case load is. COVID-19 is different than other viral infections we have because it does seem to be killing patients at a higher rate than other viruses currently in circulation. On Wednesday March 18^th alone 976 people worldwide died from COVID-19, that’s a pretty astounding number, especially considering the pandemic is still spreading in many countries. In the United States we had 2,848 NEW cases on March 18^th, and that’s with our testing infrastructure greatly lagging and many people not being tested. What makes the potential for this virus so scary is that it has a disproportionately negative effect on those who are elderly, immunocompromised and those who have a number of specific risk factors that depress the body’s normal immune responses. The pandemic is far from over and while none of us know exactly what will happen, it’s not looking good in the short term.

Cited Literature and Sources
Bai et al, Presumed Asymptomatic Carrier Transmission of COVID-19. JAMA Network, Feb 2020.
Balazy et al, Do N95 respirators provide 95% protection level against airborne viruses, and how adequate are surgical masks? American Journal of Infectious Control, March 2006.
cdc.gov/coronavirus/2019-nCoV/index.html
Chiang et al. Inhibition of HIV-1 replication by hydroxychloroquine: mechanism of action and comparison with zidovudine. Clinical Therapeutics, November 1996.
Corman et al, Detection of 2019 novel coronavirus (2019-nCoV) by real-time RT-PCR. Eurosurveillance, Jan 2020.
Doremalen et al, Aerosol and surface stability of HCoV-19 (SARS-CoV-2) compared to SARS-CoV-1. New England Journal of Medicine, March 2020.
Fox et al, Mechanism of action of hydroxychloroquine as an antirheumatic drug. Seminars in Arthritis and Rheumatism, Oct 1993.
Huang et al, Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet, Jan 2020.
Jia et al, ACE2 Receptor expression and severe acute respiratory syndrome coronavirus infection depends on differentiation of human airway epithelia. Journal of Virology, Dec 2005.
Newyorker.com/news/news-desk/what-went-wrong-with-coronavirus-testing-in-the-us
Ourworldindata.org/covid-testing
Romanelli et al. Chloroquine and Hydroxychloroquine as Inhibitors of Human Immunodeficiency Virus (HIV-1) Activity. Clinical Pharmaceutical Design, 2004.
Smith et al, Effectiveness of N95 respirators versus surgical masks in protecting healthcare workers from acute respiratory infection: a systematic review and meta-analysis. Canadian Medical Association Journal, Dec 2015.
Tang et al, On the origin and continuing evolution of SARS-CoV-2. National Science Review, March 2020.
Wang et al, Establishment of a reference sequences of SARS-CoV-2 and variation analysis. Journal of Medical Virology, March 2020.
Who.int/emergencies/diseases/novel-coronavirus-2019
Worldometers.info/coronavirus/
Zhou et al, A pneumonia outbreak associated with a new coronavirus of probable bat origin. Nature, Feb 2020.
Zhou et al. Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study. Lancet, March 2020.
Zhu et al, Initial clinical features of a suspected Coronavirus disease 2019 in two emergency departments outside Hubei, China. Journal of Medical Virology, March 2020.

Navigating Medical help in Chile

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Morning stroll through the Plaza de Armas on my way to the clinic.

First off, I’m fine nothing major, but I contracted a nasty case of poison oak in California a week ago which has spread to all my lower extremities and has my left leg swollen as if I’d run 100 miles. I’m quite allergic and since it wasn’t improving I made the venture into the wide world of Chilean healthcare for a little assistance.

My swollen and rash covered leg, hard to appreciate my cankle and giant calf.

First off I was relieved to learn that the Chilean healthcare system is quite good. The network of pharmacies is wide, but while one can get many things over the counter, corticosteriods are not one. So my choice was a ‘hospital’ or a ‘clinica’ to get a prescription. Hospitals are government subsidized facilities while clinics are privately run (and often better), so I opted for the Clinica Davila near downtown Santiago. My traveler insurance doesn’t cover small medical visits, so that was of no use, so it was all going to be out of pocket.

Entry to the Clinica Davila, looks legit.

I walked in the main doors of the clinic and up to the front desk, where it became apparent I’d be doing my transactions in Spanish, I wanted to practice and what a way to learn. I was sent to a check-in desk where I was able to get my name on the list for a doctor consult, then came the fun adventure of getting my information in the system as a foreigner without insurance. The guy at the payment desk had a little trouble, but we figured it out, $45 later, then came the wait to be called in to see the doctor. An hour later I was called in; the doctora examined me, we navigated my issues with my limited Spanish, she looked at my leg and prescribed an antibiotic and a steroid and off I went.

Bottom is my appointment form, top my prescription, mmm steroids.

I stopped in at the local Ahunada farmacia and picked up my meds without issue ($18). In total the process took about 3h, but if I didn’t speak any Spanish I’m not sure how I would have done it. So just a word of warning, that while the healthcare in Chile is wonderful and very available, finding English speakers is a tough task and be ready to fumble your way through the process if you don’t speak Spanish. Here’s to hoping the swelling goes down quickly and I can get back to normal. It’s been a rough start to 2017, full of all kinds of learning experiences.

When is it too much?

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As endurance athletes we make our living (recreationally for most) off pushing ourselves to and beyond our limits. But in the past several years many of us have become all too familiar with terms such at OTS (OverTraining Syndrome) and Adrenal Fatigue, many of us even know someone who may have struggled with this in the recent past (or present). There are countless good articles discussing these issues, so that’s not my purpose here, rather my intention is to discuss the culture that leads many down this nasty spiral of over training and into months, if not years of recovery.

Finish line of the Gorge Waterfalls 100k, 12:54

11 days ago I ran and finished the Gorge Waterfalls 100k race in Oregon, I was tired, a bit sore, but no worse for the wear. I’ve found over the past several years that my body seems to recover pretty well from long distance races, so wasn’t too surprised when the following Tuesday (3days later) I was back on the trail headed up the second flatiron for a jog/hike. The legs felt ok so I got out again Wednesday, then Thursday and when the weekend rolled around plans for a mellow ski snowballed into a possibly epic ski mountaineering route around Longs Peak; including some 5.4 climbing, lots of rock hopping with ski gear, and possibly 7500ft of vertical gain, oy.

Headed toward Longs Peak, 4/9/16.

We started skinning up the Longs Peak trail just after sunrise on 4/9/16 (one week after running a 100k race). I felt alright, but as we climbed higher and higher my legs began to feel like lead, my stabilizers were shot and I felt wobbly on the rocky terrain hiking in ski boots. The entire day was a slog for me, extremely fatigued, barely managing 1mph much of the time, and just feeling like crap. It was pretty apparent that I was not recovered from Gorge Waterfalls, but had no choice but to finish the route, so 13hours later (note, 14mi took longer than my 100k) I staggered back into the Longs Peak parking lot, completely wasted, so much so that over the next two days all I did was sleep and walk 3miles quite slowly. Special thanks to Jason, Andy and Dana for sticking out this long slog with me.

Sunset as we descend away from Longs and Chasm Lake back to the TH, 4/9/16.

So the endurance athletes out there might be saying, “so what, you had a bad day” and that’s what our sport(s) is built on, but at what point is it more than a bad day, and really just a bad idea? In ultra distance running the mental ability to push through pain, to weather the highs and lows and to keep yourself going when most in this world would quit is really what separates many finishers from DNFs. But it is also this incessant drive to fight, struggle and suffer that gets so many in trouble. Terms such as FOMO (Fear of Missing Out), YOLO (You Only Live Once), ‘pain is temporary, glory last forever’, and ‘sufferfest’ are often thrown around by well meaning friends and training partners to help motivate others to get out and push through the pain. While this encouragement is a necessary part of success, especially in 100milers, I argue it’s also what leads many into over training territory. Combined with the fact that many of us know only one thing…physical activity, you have a ticking time bomb just waiting to go off.

When you need a nap, you need a nap. 2010 Wasatch 100 Pete decided 500 yards from the Ant Knoll AS he was sleeping, 10 seconds later he was snoring.

But the real question is, when does pushing your body no longer become beneficial, but rather detrimental. This is exactly what I was asking myself the day after my Longs Peak debacle, and trying to understand if the signs were simply indicating short term fatigue, or if there was a larger underlying issue creeping in. Sadly the answer is, I don’t really know. There are various metrics such as heart rate, blood work, sleep patterns, etc that can help address fatigue, but what it comes down to is you really just need to listen to your body, and do so very carefully. Building in rest week (40+miles/wk is NOT rest) during big training cycles, rest months (or two) during the off season where you do limited cardiovascular activity, and really taking the time to take care of your body during those harder training weeks are probably the key. As the scientific community learns more about over training, we may have our magic biomarker to indicate when it’s happening, but for now the endurance athlete (me included) needs to remember to take a break every now and then, you’ll be better off in the long run.

Inaugural Salomon Run Club group run, 4/5/16.

Last week’s training cycle was supposed to be for rest post-Gorge Waterfalls, but does 19hours on my feet with 12000ft of vertical gain sound restful…I didn’t think so. Thankfully after several days of hard rest and recovery I’m feeling much more normal, but as I ramp into bigger training cycles there will definitely be this seed in the back of my mind…don’t overdo it. In the ten years since I started ultra distance running, 12 years of competing in ultra distance events, I’ve managed to avoid over training issues (plenty of aches and pains though), but have also watched many a friend fall down this rabbit hole. Sorry I can’t provide you any definitive answers, but maybe the ramblings of my brain will sound familiar to your personal struggles or your friend’s. So I hope everyone has a wonderful rest of the week, get in some great trail/rock time, but also listen to your body about what it truly needs, sometimes that’s activity, sometimes it’s a good acupuncture session, sometimes it’s a soak in the hot tub, but sometimes it’s simply rest. Thanks to Vfuel for helping to keep me energized throughout training, and all my friends in the Rocky Mountain Runners and Boulder Trail Runners for sharing many a long day with me. Run fast, run healthy, but mostly run happy.

A few articles for further reading on the topic if you so desire…

Dark side of Fitness, 5280

Overtraining Syndrome, Sports Health

Are you overtraining?, Runners World

You Are What You Eat?

Ebola; Zombie Apocalypse or Just Another Infection?

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Just in case know the rules of Zombieland…

In the past several weeks the world has seen the horrible images of what the Ebolavirus can do to a human thrust into the public eye. Understandably there has been a lot of discussion, fear and misunderstanding in regards to Ebola. I’m hoping to lay out some information about the disease, assuage some fears, correct some of the misunderstanding and give the non-scientific public (or at least people I know) a glimpse into what is known about the disease.

First off, I have a Masters in Cell Biology/Immunology with a special emphasis in Infectious Disease Research. I currently do mucosal HIV research, looking at the dynamics of how HIV and the gut microbiome interact and how these interactions affect disease progression and pathogenesis. My Masters Thesis focused on the recognition of Mycobacterium tuberculosis by Dendritic Cells (a key piece of our immune system) and how the bacteria are able to corrupt our own host responses in order to avoid recognition and survive. So, in short, I have a fairly strong background in working with various infectious diseases, including Level 3 pathogens, though I am by no means an expert on Ebolavirus specifically. The thoughts below are merely my interpretations of the literature which I have read, the discussions I’ve had with others in the field, and observations on how our hospital (University of Colorado Anschutz) is preparing for this threat.

Images of Ebolavirus (top) with a schematic of its structure below.

What is Ebola?

The Ebolavirus is part of the Filoviridae family, a group of single-stranded negative sense RNA viruses. What the hell does that mean, basically it’s a virus. They are tiny structures of RNA with an envelope wrapped around the outside, they have a very basic genome, are able to form multi-virion strands (up to 6), but require the full intact structure to replicate (the RNA itself is non-infectious). There are 5 different subtypes of Ebola, each one slightly different in how virulent (infectious and deadly) it is, the current outbreak in Guinea, Sierra Leone and Liberia is caused by a variant of Zaire Ebolavirus. In most people the virus causes what’s know as hemorrhagic fever, a not so fun complex process by which the immune system is hyperactivated to such an extent that the virus literally destroys you from the inside, causing massive blood vessel leakage and organ damage. This is not a new disease, first officially discovered in 1976 in the Democratic Republic of the Congo (Zaire strain), and it has flared up numerous times in the past 40years, though the previous flare ups have all burned themselves out in more rural areas. The current outbreak has spread to the urban areas in West Africa and continues to spread uncontrolled as of this moment (10/21/14). Below I will discuss the general pathology (what happens with disease), the current state of Ebolavirus research, and what all of this means for both the US and the World (in my opinion). (Ansari AA et al 2014, Feldman H et al 2011)

A map showing the location of the 2014 Ebolavirus outbreak. As of Oct 21st there have been over 9000 cases and 4500 confirmed deaths. Making this the largest Ebola outbreak in history.

Infection and Symptoms

The Ebolavirus, like other filoviruses, survives in and is transmitted through contact with bodily fluids such as; blood, vomit, stool, saliva, semen, urine, puss, etc. The current research and epidemiology show no evidence for generalized aersole transmission (unlike flu or cold viruses), though Ebolavirus has been shown to survive in body fluids outside of the host for several hours on surfaces, making it much easier to contract than a virus like HIV. Infection occurs when infectious materials/fluids come into contact with the mucus membranes or open wounds of a new individual (eyes, mouth, throat, nose, cuts/scrapes, etc). After infection there is what is known as an incubation period (average 4-10days), in which the virus is replicating in the individual but they don’t show any obvious signs of being sick, during this stage the new individual is not known to be infectious. During this latter part of this incubation period the initial symptoms are very general and include; fever, chills, malaise and myalgia. During the later stages of disease (typically 6-16 days) the disease takes on its more severe form in which excessive immune activation leads to coagulation disorders, blood vessel leakage, multiorgan failure and shock, often leading to death. The current Ebolavirus strain (Zaire) has a 60-90% fatality rate, though some do recover from the disease back to (apparently) full health. We still do not know exactly what leads to Ebolavirus immunity, but high levels of specific neutralizing antibodies seem to be one of the leading candidates. (Ansari AA et al 2014, Feldman H et al 2011, Hoenen T et al 2012)

Treatment Options

There are not currently any officially FDA approved vaccines or treatment options available to the general public, though there are many strong candidates in the works. Several different vaccine candidates are in development, but none have gone beyond animal trials as of this writing (Oct 2014). Several have shown very strong abilities to protect Non-Human Primates (monkeys) from infection and thus may also work in humans, TBD. Post exposure treatments are in a similar state, with several treatments having shown to be effective in animal models, but none have been extensively tested in humans. The two most common experimental treatments are the use of serum from previously immune (recovered patients) and a synthetic antibody cocktail known as ZMAPP. Both are based on the premise that specific antibodies against Ebolavirus can help the patient neutralize the infection and thus recover. All of these treatments are experimental and have NOT been extensively tested for safety and efficacy in humans, but due to the high mortality rate of Ebolavirus infection they are being used in a life saving experimental fashion. NOTE: The makers of ZMAPP are now working with Amgen to see if it would be possible to scale up its production in order to have larger quantities of this therapeutic on hand in case its needed. (Ansari AA et al 2014, Feldman H et al 2011, Hoenen T et al 2012)

Why All the Confusion?

Ebolavirus research lags behind many other disease for several reasons. One, there is not as much funding for Ebolavirus as there is for HIV, TB, and many other more prominent diseases. Two, since Ebolavirus is a Biosafety Level 4 pathogen there are only a dozen or so research laboratories that have the facilities to properly and safely study this virus. Even though the Ebolavirus research is in its infancy, it is much further along than HIV research was when the initial HIV outbreak happened in the 80s and 90s, thus there is much more promise for containing its spread.

A lot of the current fear instilled in populations of the developed world revolves around several health care workers becoming infected, and thus the concern that the virus may easily spread throughout the world. Note that just as in Africa, those becoming infected are people who have direct contact with highly infectious patients, and not simple casual bystanders. What these secondary infections in health care workers do highlight is the need for a more coordinated plan on how to deal with isolated patients in order to properly protect the care givers from the infectious virus. Many hospitals (Emory and Nebraska are two exceptions) don’t have the proper containment wards setup and Personal Protective Equipment (PPE) protocols in place to deal with an Ebolavirus infected patient if they were to walk into their facilities today. This is very disconcerting for healthcare workers who would be at high risk for transmission as they treat the patient. After the transmissions in Dallas many hospitals have implemented procedures and specific protocols on how to identify and deal with a potentially infected patient (UC Denver Anschtuz is working on this now). This is where I feel the CDC has dropped the ball the most, in not implementing an extremely detailed Nation wide protocol for hospitals on how to identify and deal with a potential Ebola case, their hospital guidelines were initially very general and in my opinion not adequate for something that is so deadly.

Evolution of the CDC recommended Personal Protective Equipment (PPE) for those treating Ebola patients. http://www.nytimes.com/interactive/2014/10/15/us/changes-to-ebola-protection-worn-by-us-hospital-workers.html

What Does This Mean For Me?

For most of us (me included) this outbreak in West Africa, while tragic, does not pose a direct threat to us individually. It is definitely something worth watching to see how well the CDC and WHO are able to help control the spread of the disease in the impoverished countries, but spread in the developed world has been halted by simple containment protocols and proper handling. I wouldn’t go traveling to West Africa any time soon though. If you are a healthcare worker, specifically one who works in a hospital, ER or ICU I would be more concerned until I knew my facility had the proper protocols, PPE and containment facilities in place to handle a patient potentially infected with Ebolavirus. These are the people who are at high risk because they are asked to care for the highly infectious and to put themselves directly in harms way. For now, unless you are a healthcare worker there are many more things to worry about, Ebola being quite a ways down the list. Information on the current status of the West African Outbreak, where the disease has been treated outside West Africa, and the state of the current coordinated effort on the CDCs website.

If all else fails, just remember the rules of Zombieland…

References

CDC website, http://www.cdc.gov/vhf/ebola/outbreaks/2014-west-africa/index.html

Ansari AA, Clinical features and pathobiology of Ebolavirus infection, Journal of Autoimmunity (2014), http://dx.doi.org/10.1016/j.jaut.2014.09.001

Feldman H et al, Ebola haemorrhagic fever, Lancet. 2011 March 5; 377(9768): 849–862.

Hoenen T, Current Ebola vaccines, Expert Opin Biol Ther. 2012 July; 12(7): 859–872.

Gatherer D, The 2014 Ebola virus disease outbreak in West Africa, Journal of General Virology (2014), 95, 1619–1624.

Shhhh….Don’t Talk to Me

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As a long distance runner who often runs solo one question I often get asked is, ‘Don’t you get bored?’ While I’d be lying if I said I never got bored, it’s more the exception than the rule. What I’ve learned during my seven year foray into Ultrarunning is that I personally possess two traits that make Ultrarunning, especially in the mountains, a good fit. The first is I have a strong ability to disassociate from situations, think ‘zoning out’, and secondly I’m an Introvert. DISCLAIMER: I am not an expert in either field, the text below merely represents my opinions based upon my own reading, observation and personal understanding of these topics.

QEEG brain scans from two different Ultrarunners (top/middle) and one normal (bottom). The more orange and red indicate increases above normal.

The first topic is still something that is not too well understood, but was highlighted by a study performed by Dr Aharon Shulimson using QEEG to look at the brain wave patterns of Ultrarunners who had finished 100mile races. In Ultrarunning Magazine (“This is Your Brain on the Wasatch 100”) Dr Shulimson published his preliminary findings that all of the Ultrarunners he tested showed increased Theta and/or increased Beta brain wave activity above the ‘normal’ population. In total, one possible significance of this data is that many of us have a higher than normal ability to ‘zone out’ or to spend our many miles on the trail just lost in our own thoughts. These results are just preliminary, and while they don’t prove whether this phenomenon was the chicken or the egg, it’s definitely a beneficial trait for those of us who compete in 50mile and 100mile events. Now for part 2…..

Contemplating my tough race year while on a solo recovery hike/run high above Zermatt, 9/4/13.

Hello my name is Eric; I enjoy long walks (runs) on the beach, watching sunrise, star gazing and long solo runs in the mountains, basically what I’m saying is that I am an introvert. Many of you may be familiar with the terms introvert and extrovert, many of you may even have a very strong understanding of what those two terms mean and how they interact, but for the sake of discussion I’ll start from scratch. An introvert is one who gathers energy from individual and reflective time, while an extrovert is one who gathers energy from social interaction and from external stimulation. An introvert is NOT inherently antisocial, shy or quiet, but that doesn’t mean there aren’t introverts who are, it’s just not the rule. Introversion-Extroversion is also not a black and white distinction, but rather a whole gray scale in between. Some have a stronger need for social interaction or quiet time to recharge, while others need more of a mix of the two to feel balanced, I fall somewhere near 70%/30% Introvert. As you can imagine, long solo miles on the trails and in the mountains better serve an introvert’s needs than an extrovert’s, advantage us.

Hanging with a few friends this past weekend in the North Cascades, 1/21/14. The introvert’s preferred social scene. Photo by Ben S.

You may ask, “but Eric, you’re fairly social and friendly, shouldn’t that tire you out?”, and the answer is yes it does, but I’m also fortunate enough to have a job where I get to work alone much of the day and I spend quite a bit of my running/training time solo recharging. It’s not that us introverts don’t enjoy social interaction, it just requires more energy from us. So the next time you see me at a social event sneak off to the side to observe the crowd, give me a moment to relax and recharge, I promise everything is ok.

Part of the misunderstanding and condemnation of introverts comes from an American society based around the thought that constant action, speaking your mind and being a ‘go getter’ are sought after traits. While the quiet and more thoughtful personality types are deemed weaker and often don’t get their voices heard (general stereotypes, thus not always true). An introvert doesn’t have fewer ideas or less conviction, they just contemplate and evaluate each thought more thoroughly before speaking, hence why many of us don’t do well with the conventional ‘small talk’, especially in large groups. Now if there is a topic an introvert is very passionate about we can talk your ear off, but that’s only because the ideas are often already well formulated and contemplated. Even the most introverted person can appear extroverted at times, but in the end they’ll need that individual reflective time to recharge their batteries.

Self portrait in front of Mt Rainier, part of a 2 month solo road trip in 2004.

I’m not saying don’t talk to me or other introverts, just to be aware that when I say I want to stay home and watch a movie by myself or I need to go for a run solo, its not you, it really is ME. Every introvert and extrovert finds their own ways to recharge, just be conscious that different personality types require differing levels of interaction. Whether they are your regular running partner or your significant other, an introvert will need some time to themselves, just give them a hug and let them do their thing. If you’re interested in reading more about the topic there are a couple of fantastic books out; “The Introvert Advantage” by Marti Olsen Laney and “Quite” by Susan Cain. Or if you’re interested in finding out your Meyers-Briggs personality type, here is one of many free tests you can take (I’m an INTJ). Of course I’m always happy to share my thoughts and insight over a beer or on a run, as long as I get some time to recharge. Special thanks to Misti for sharing her thoughts and insight on these topics. I’m also excited to announce that in 2014 I’ll be continuing my sponsorships with Hind and Vfuel! Run fast, run healthy, but mostly run happy.

The Dirty Truth; Bacteria at Home

Guts and Bugs; The Human Microbiome

A topic I’ve often brushed aside or been very curt on to date is what my lab research deals with, there is more to me than just running 🙂 The overall focus of my group is mucosal and intestinal HIV infection, but one of the largest areas of focus is the relationship between bacteria and HIV infection, specifically one’s commensal bacteria. Within each and every one of us lives a diverse microbiome, consisting of hundreds of different bacterial species. Each one colonizing a specific niche within us, many having beneficial and symbiotic roles, and yes some pathogenic species we’d be better off without. In the past several years technological advancements have allowed for rapid and very thorough analysis of these bacterial species that reside within the various compartments of the human body; leading to a better understanding of the complexity of the human microbiome and many more questions yet to be answered. In the past several months I’ve received a flurry of questions from friends about the human microbiome, personal microbiome sequencing and fecal transplants. I’ll avoid the latter for now, but know that I am familiar with them and I do know Dr’s that I can recommend if people want a recommendation.

In the past year I’ve read dozens of articles about the human microbiome and probiotics and attended several talks on the subjects as well, but most of these have been in science papers relegated to the small community of scientist who study the topic. This past week I was sent a link to an article published in the New York Times on May 15th by Michael Pollan entitled “Some of My Best Friends are Germs” (click link for the article). It was one of the first articles on the Human Microbiome I’ve read that was not only written for the general audience, but where the author not only did his homework, but did a very comprehensive job discussing many of the reasons why we should ALL care about our microbiome just as much as we do our diet. In fact you’ll see that in many instances these two items (diet and the microbiome) are very intimately related.

In the article Pollan participates in a microbiome sequencing project based at CU Boulder and interviews some of the biggest players in the microbiome world, people at CU Boulder and CU Denver with whom I’ve worked, collaborated and interacted with. I won’t summarize the article, as I strongly encourage all readers to take 15-20min to read it on their own, but I will respond to and comment about a few of the points made in the article. If you want to discuss the specifics or have science questions feel free to ask me and I’ll do my best to answer.

Humane Microbiome sequencing data generated by Eric Lee.

I think one of the most critical discussions the article brings up is the ongoing ‘cleansing’ of the Western microbiome. Through our diet and daily practice we’re slowly killing off much of the diversity within our microbiome, something that may be associated with a lot of our immune disorders, obesity issues and digestive troubles that ail an increasing number of people in the ‘developed’ world. The shift in our diets away from a more plant based diet toward large amounts of meat consumption and our overuse of antibiotics and antimicrobial agents may be slowly depleting our guts of the diversity that is hypothesized to be necessary for optimal gut health.

In addition to the affects one’s microbiome has on digestive health is the lesser known idea that all the bacteria that make up our gut microbiome also play a key role in creating and modulating our immune system. Bacteria from the gut are constantly translocating across the gut wall and into our circulatory system, I can corroborate this from my personal studies looking at human gut tissue. As these bacteria move from your intestine into your body, the body is forced to respond and either identify the microbe as ‘friend’ or ‘foe’. One might think, ‘well if I have bacteria inside me, isn’t that a bad thing?’, not necessarily. Many of the commensal bacteria that live in our gut want nothing to do with colonizing the rest of us, thus simply die off and do no harm to the rest of the body, it’s our immune system’s job to recognize these and to realize that they pose no threat. Then there are the pathogenic bacteria that once they are released into our tissue want to colonize, reproduce and spread, here it’s the immune system’s job to recognize these and kill them off before one get’s a full blown infection (ie salmonella and pathogenic E.coli).

If the body isn’t trained properly and simply tries to attack EVERY BACTERIA that enters the tissue we’d be in a constant state of inflammation, ie many of the autoimmune and inflammatory bowel disorders seen in the Western world today. Alternatively if our gut isn’t properly colonized by the good comensals this creates a niche for all those bad bacteria and pathogenic bacteria (the weeds) to grow up and do damage to our body, without the benefits of good bacteria. Just like the “Hygeine Hypothesis” that was made popular in the 90s and early 2000s, we’re starting to realize that bacteria might not be so bad, in fact it appears they are necessary for us to live a healthy life.

As Pollan says in the article we are no where near having a complete understanding of all the nuances of the Human Microbiome, and what a healthy microbiome might be. Every bacterial species plays a unique role, but what these roles are is not fully understood. Probiotics and Prebiotics may be beneficial, but we don’t yet know enough to say there is a ‘best’ formula for people to take for optimum gut health. What we as scientist do know is that the health and diversity of our microbiomes is critical for many aspects of our lives, not just digestion and these are affected by many factors starting as early as birth. The goal of my ramblings isn’t to tell you to eat less meat, to go guzzle gallons and gallons of probiotic yougart or to stop sanitizing your house. All I want is for you to think about the consequences that many of your actions have on the health of those little microscopic organisisms that colonize the various niches of our body, you know, the one’s that outnumber your human cells 10 to 1. Next time you are thinking about taking antibiotics because you just don’t feel well, rub that hand sanitizer all over your child because she/he was crawling on the floor or the you pick up that big steak for dinner; remember the bacteria.

MtnRunner_ELee

"Adventure is out there"

Category Archives: Science and Nerd Stuff

Covid-19; Testing, Drugs, Vaccines and Seasonality 3/25/20

Chaos and COVID-19

Navigating Medical help in Chile

When is it too much?

You Are What You Eat?

Ebola; Zombie Apocalypse or Just Another Infection?

Shhhh….Don’t Talk to Me

The Dirty Truth; Bacteria at Home

Guts and Bugs; The Human Microbiome