Posts Tagged ‘disease’

As my last post started to explore, different types of dietary fats have different effects on the progression of alcoholic liver disease. This post will further explore the protective effects of saturated fats in the liver.


For many, the phrase “heart healthy whole grains” rolls off the tongue just as easily as “artery clogging saturated fats”. Yet where is the evidence for these claims? In the past few decades saturated fats have been demonized, without significant evidence to suggest that natural saturated fats cause disease (outside of a few well touted epidemiological studies). Indeed, most of the hypothesis-driven science behind the demonization of saturated fats is flawed by the conflation of saturated fats with artificial trans fats (a la partially hydrogenated soybean oil).


In the face of a lack of any significant scientific evidence that clearly shows that unadulterated-saturated fats play a significant role in heart disease (and without a reasonable mechanism suggesting why they might), I think the fear-mongering “artery clogging” accusations against saturated fats should be dropped. On the contrary, there is significant evidence that saturated fats are actually a health promoting dietary agent- all be it in another (though incredibly important) organ.


Again (from my last post), here is a quick primer on lipids (skip it if you’re already a pro). For the purpose of this post, there are two important ways to classify fatty acids. The first is length. Here I will discuss both medium chain fatty acids (MCFA), which are 6-12 carbons long, and long chain fatty acids (LCFA), which are greater than 12 carbons in length (usually 14-22; most have 18). Secondly, fatty acids can have varying amounts of saturation (how many hydrogens are bound to the carbons). A fatty acid that has the maximal number of hydrogens is a saturated fatty acid (SAFA), while one lacking two of this full complement, has a single double bond and is called  monounsaturated (MUFA) while one lacking more (four, six, eight etc.) has more double bonds (two, three, four, etc.) and is called a polyunsaturated fatty acid (PUFA).


Next time you eat a good fatty (preferably grass-fed) steak, or relish something cooked in coconut or palm oil, I hope you will feel good about the benefits you are giving your liver, rather than some ill-placed guilt about what others say you are doing to your arteries. From now on, I hope you think of saturated fats as “liver saving (and also intestine preserving) lipids”. Here’s why:


In 1985, a multi-national study showed that increased SAFA consumption was inversely correlated with the development of liver cirrhosis, while PUFA consumption was positively correlated with cirrhosis [1].  You might think it is a bit rich that I blasted the epidemiological SAFA-heart disease connection and then embrace the SAFA-liver love connection, but the proof is in the pudding- or in this case the experiments that first recreated this phenomenon in the lab, and then offered evidence for a mechanism (or in this case many mechanisms) for the benefits of SAFA.


The first significant piece of support for SAFA consumption came in 1989, when it was shown in a rat model that animals fed an alcohol-containing diet with 25% of the calories from tallow (beef fat, which by their analysis is 78.9% SAFA, 20% MUFA, and 1% PUFA) developed none of the features of alcoholic liver disease, while those fed an alcohol-containing diet with 25% of the calories from corn oil (which by their analysis is 19.6% SAFA, 23.6% MUFA, and 56.9% PUFA) developed severe fatty liver disease [2].


More recent studies have somewhat complicated the picture by feeding a saturated fatty-acid diet that combines beef tallow with MCT (medium chain triglycerides- the triglyceride version of MCFAs). This creates a diet that is more highly saturated than a diet reliant on pure-tallow, but it complicates the picture as MCFA are significantly different from LCFA in how they are absorbed and metabolized. MCFA also lead to different cellular responses (such as altered gene transcription and protein translation). Nonetheless, these diets are useful for those further exploring the role of dietary SAFA in health and disease.


These more recent studies continue to show the protective effects of SAFA, as well as offer evidence for the mechanisms by which SAFA are protective.


Before we explore the mechanisms, here is a bit more evidence that SAFAs are ‘liver saving’.



A 2004 paper by Ronis et al confirmed that increased SAFA content in the diet decreased the pathology of fatty liver disease in rats, including decreased steatosis (fat accumulation), decreased inflammation, and decreased necrosis.  Increasing dietary SAFA also protected against increased serum ALT (alanine transaminase), an enzymatic marker of liver damage that is seen with alcohol consumption [3].  These findings were confirmed in a 2012 paper studying alcohol-fed mice. Furthermore, these researchers showed that SAFA consumption protected against an alcohol-induced increase in liver triglycerides [4].  Impressively, dietary SAFA (this time as MCT or palm-oil) can even reverse inflammatory and fibrotic changes in rat livers in the face of continued alcohol consumption [5].


But how does this all happen?


Before I can explain how SAFA protect against alcoholic liver disease, it is important to understand the pathogenesis of ALD. Alas, as I briefly discussed in my last post, there are a number of mechanisms by which disease occurs, and the relative importance of each mechanism varies based on factors such as the style of consumption (binge or chronic) and confounding dietary and environmental factors (and in animals models, the mechanism of dosing). SAFA is protective against a number of mechanisms of disease progression- I’ll expound on those that are currently known.


In my opinion, the most interesting (and perhaps most important) aspect of this story starts outside the liver, in the intestines.


In a perfect (healthy) world, the cells of the intestine are held together by a number of proteins that together make sure that what’s inside the intestines stays in the lumen of the intestine, with nutrients and minerals making their way into the blood by passing through the cells instead of around them. Unfortunately, this is not a perfect world, and many factors have been shown to cause a dysfunction of the proteins gluing the cells together, leading to the infamous “leaky gut”. (I feel it is only fair to admit that when I first heard about “leaky gut” my response was “hah- yeah right”. Needless to say, mountains of peer-reviewed evidence have made me believe this is a very real phenomenon).


Intestinal permeability can be assessed in a number of ways.  One way is to administer a pair of molecular probes (there are a number of types, but usually a monosaccharide and a disaccharide), one which is normally absorbed across the intestinal lining and one that is not. In a healthy gut, you would only see the urinary excretion of the absorbable probe, while in a leaky gut you would see both [6]. Alternatively, you can look in the blood for compounds such as lipopolysaccharide (LPS-a product of the bacteria that live in the intestine) in the blood. (Personally, I would love to see some test for intestinal permeation become a diagnostic test available to clinicians.)


Increased levels of LPS have been found in patients with different stages of alcoholic disease, and are also seen in animal models of alcoholic liver disease.  Increased levels of this compound have been associated with an increased inflammatory reaction that leads to disease progression.  Experimental models that combine alcohol consumption and PUFA show a marked increase in plasma LPS, while diets high in SAFA do not.



But why? (Warning- things get increasingly “sciencey” at this point. For those less interested in the nitty-gritty, please skip forward to my conclusions)


Cells from the small intestine of mice maintained on a diet high in SAFA, in comparison to those maintained on a diet high in PUFA, have significantly higher levels of mRNA coding for a number of the proteins that are important for intestinal integrity such as Tight Junction Protein ZO-1, Intestine Claudin 1, and Intestine Occludin.  Furthermore, alcohol consumption further decreases the mRNA levels of most of these genes in animals fed a high-PUFA containing diet, while alcohol has no effect on levels in SAFA-fed animals.  Changes in mRNA level do not necessarily mean changes in protein levels, however the same study showed an increase in intestinal permeability in mice fed PUFA and ethanol in comparison to control when measured by an ex-vivo fluorescent assay. This shows that PUFA alone can disturb the expression of proteins that maintain gut integrity, and that alcohol further diminishes integrity. In combination with a SAFA diet, however, alcohol does not affect intestinal permeability [4].


Improved gut integrity is no doubt a key aspect of the protective effects of SAFA. Increased gut integrity leads to decreased inflammatory compounds in the blood, which in turn means there will be decreased inflammatory interactions in the liver.  Indeed, in comparison to animals fed alcohol and PUFA, animals fed alcohol with a SAFA diet had significantly lower levels of the inflammatory cytokine TNF-a and the marker of macrophage infiltration MCP-1 [4].  Decreased inflammation, both systemically and in the liver, is undoubtedly a key element of the protective effects of dietary SAFA.


This post is already becoming dangerously long, so without going into too much detail, it is worth mentioning that there are other mechanisms by which SAFA appear to protect against alcoholic liver disease. Increased SAFA appear to increase liver membrane resistance to oxidative stress, and also reduces fatty acid synthesis while increasing fatty acid oxidation [3]. Also, a diet high in SAFA is associated with reduced lipid peroxidation, which in turn decreases a number of elements of inflammatory cascades [5]. Finally- and this is something I will expand on in a future post- MCFAs (which are also SAFA) have a number of unique protective elements.


I realize that this post has gotten rather lengthy and has brought up a number of complex mechanisms likely well beyond the level of interest of most of my readers…


If all else fails- please consider this:


The “evidence” that saturated fats are detrimental to cardiac health is largely based on epidemiological and experimental studies that combined saturated fats with truly-problematic artificial trans-fats. Despite the permeation of the phrase “artery clogging saturated fats”, I have yet to see the evidence nor be convinced of a proposed mechanism by which saturated fats could lead to decreased coronary health.




There is significant evidence, founded in epidemiological observations, confirmed in the lab, and explored in great detail that shows that saturated fats are protective for the liver. While I have focused here on the protective effects when SAFA are combined with alcohol, they offer protection to the liver under other circumstances, such as when combined with the particularly liver-toxic pain-killer Acetaminophen [7].


Next time you eat a steak, chow down on coconut oil, or perhaps most importantly turn up your nose at all things associated with “vegetable oils” (cottonseed? soybean? Those are “vegetables”?), know that your liver appreciates your efforts!



1.            Nanji, A.A. and S.W. French, Dietary factors and alcoholic cirrhosis. Alcohol Clin Exp Res, 1986. 10(3): p. 271-3.

2.            Nanji, A.A., C.L. Mendenhall, and S.W. French, Beef fat prevents alcoholic liver disease in the rat. Alcohol Clin Exp Res, 1989. 13(1): p. 15-9.

3.            Ronis, M.J., S. Korourian, M. Zipperman, R. Hakkak, and T.M. Badger, Dietary saturated fat reduces alcoholic hepatotoxicity in rats by altering fatty acid metabolism and membrane composition. J Nutr, 2004. 134(4): p. 904-12.

4.            Kirpich, I.A., W. Feng, Y. Wang, Y. Liu, D.F. Barker, S.S. Barve, and C.J. McClain, The type of dietary fat modulates intestinal tight junction integrity, gut permeability, and hepatic toll-like receptor expression in a mouse model of alcoholic liver disease. Alcohol Clin Exp Res, 2012. 36(5): p. 835-46.

5.            Nanji, A.A., K. Jokelainen, G.L. Tipoe, A. Rahemtulla, and A.J. Dannenberg, Dietary saturated fatty acids reverse inflammatory and fibrotic changes in rat liver despite continued ethanol administration. J Pharmacol Exp Ther, 2001. 299(2): p. 638-44.

6.            DeMeo, M.T., E.A. Mutlu, A. Keshavarzian, and M.C. Tobin, Intestinal permeation and gastrointestinal disease. J Clin Gastroenterol, 2002. 34(4): p. 385-96.

7.            Hwang, J., Y.H. Chang, J.H. Park, S.Y. Kim, H. Chung, E. Shim, and H.J. Hwang, Dietary saturated and monounsaturated fats protect against acute acetaminophen hepatotoxicity by altering fatty acid composition of liver microsomal membrane in rats. Lipids Health Dis, 2011. 10: p. 184.

What is “Fatty Liver”? Well here’s a slide from my research showing a slice of liver from a control-fed rat on the left and an alcohol-fed rat on the right. Arrows mark macrovesicular lipid accumulations (other models can show much more impressive lipid accumulations).


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As the popularity of an evolutionary approach to wellness grows, the belief that everything can be fixed with an appropriate diet and exercise plan seems to diminish. While eliminating Neolithic components of the diet that humans don’t thrive on and participating in physical activities that challenge and benefit our bodies are vital elements of wellness, it’s becoming increasingly obvious that food and movement alone do not a healthy body make.

One of the big topics du jour in the paleosphere and in scientific research is the role of an appropriate gut microbiome in health and wellness. I’ve written about it a bit in some of my past posts on the appendix and breast-feeding, and it seems like you can’t surf too far on the paleo interwebz without seeing something about how to feed, nurture, or modify your microbiome. Having the right little guys inhabit your gut is important as commensal bacteria are capable of utilizing molecules that we can’t otherwise metabolize (turning them into compounds we can use), are capable of making vitamin K which we need to thrive, and they outcompete nasty bacteria that cause disease. Also, as mentioned in one of my posts on the appendix, a healthy and appropriate gut microbiome is probably essential in keeping the immune system appropriately occupied so that it doesn’t get bored and start attacking our own body.

But there’s more to a healthy human biome than bacteria. If we imagine out large intestines as something akin to the Great Plains, I imagine our bacteria as the diverse species of rodents that run around and occupy their little niches. Mice, voles, prairie dogs and beavers- they all play their part in keeping that ecosystem healthy. There is another creature, however, one much larger that once roamed those grassy prairies. The Bison were a keystone species of the Great Plains: their grazing and migration helped maintain the native prairie and shape the environment. Much as the buffalo were almost eradicated by modern civilization, the keystone species of our intestine- parasites such as helminths- have all but disappeared in the modern world.

In my first year of medical school I attended a seminar by one of the faculty in our immunology department where he discussed the role of intestinal parasites in appropriately priming the immune system. The human body did not evolve in a sterile bubble; it coevolved with bacteria and intestinal parasites. This means that our immune system has been selected to function in (and indeed is optimized for) an environment where we interact with parasites. Similarly, while there are definitely situations where parasites are problematic (when in the wrong host, or when infections occurs on top of other disease or malnutrition, and when the parasite burden is too high), parasites have not evolved to be overly harmful to their host. A parasite that kills its host is an evolutionary dead end.

It turns out that internal parasites significantly modulate our immune system. The gut is especially rich in immune tissue, specifically GALT (gut-associated lymphoid tissue) as mentioned in previous posts. Helminths secrete a multitude of molecules, including protease inhibitors, cytokine homologues, and a number of other compounds that alter T-cell function. These molecules down-regulate the host’s immune system. While the idea of down-regulating our immune system may make some wary, remember that this is a relationship that our immune system (indeed, probably the immune system of all mammals) evolved to handle. In fact, our rather unique modern environment, in which our immune system is no longer occupied with intestinal parasites, might be considered as something of an evolutionary arms race that has suddenly gone unopposed.

This theory is supported by a number of interesting findings, both in people living in pre-industrial cultures who are chronically exposed to parasites, and in those of us living in the hygienic modern world where our immune systems have become a bit out of whack. In Africa, children living in rural communities carrying chronic parasite infection have a shorter course of asthma (a condition caused by inflammation of the respiratory tract) [1]. Similarly, a study in children in Gabon demonstrated that chronic parasite infection decreased the immune response to common allergens such as dust mites [2, 3]. In these situations, carrying parasites appears to mitigate or prevent an abnormal immune response.

In the developed world, where hygiene and pharmaceuticals have all but eliminated human parasites, we are starting to recognize conditions that may occur as a result of an immune system with a well-developed arsenal and no enemy to use it on. One interesting and promising example of this was an experimental trial where individuals with Crohn’s disease were infected with porcine whip worms (used because they are self-limiting and do not leave the intestine) in an attempt to otherwise occupy an immune system that had turned on its host. While the trial was limited in size, the results were resounding. Almost 80% of participants saw a decrease in disease severity, with 72% seeing a remission of disease [4]. In another study, patient with multiple sclerosis who were also infected with intestinal parasites had significantly fewer adverse events and diminished disease progression in comparison to those free of parasites [5]. Furthermore, experiments utilizing animal models of immune-regulated diseases such as colitis, type 1 diabetes, arthritis, and allergies also show promising results that appropriate parasitic infection may prevent these conditions.

Principle into Practice

Reconstituting the human biome in order to control the epidemics of allergic and autoimmune diseases has been suggested. Much like some other things I’ve written about, there’s a certain ‘gross factor’ that some people find uncomfortable when you start to suggest that everyone should have a domestic helminth residing within them. Perhaps the idea of reconstituting the cocktail of secreted compounds that helminths produce to modulate our immune system is a little more appealing, but the problem here, as with so many other aspects of biology, is that we are only just starting to understand the complex interaction between our immune system and the parasites they were ‘designed’ to control. With only a limited understanding, how can we hope to fully and correctly mimic biology? Furthermore, the understanding that normal parasites, which we evolved with over hundreds of thousands of years, actively alter the functioning of our immune system makes us realize that almost all our research on the immune system has thus far focused on the very evolutionary-novel depopulated gut.

There is a fantastic paper that was published last year in ‘Medical Hypotheses’ (it’s probably time for me to admit that “Publish in ‘Medical Hypotheses’” is one of the few items on my bucket list) entitled Reconstitution of the human biome as the most reasonable solution for epidemics of allergic and autoimmune diseases [6]. If you’re interested in this subject, I highly recommend you give this paper a look. I particularly like their statement that:

“Just as we have the option of safely utilizing proper diet and exercise regimens to give our cardiovascular system what it has evolved to require, it is expected that, far more effortlessly, we can safely utilize selected organisms to give our immune system what it is evolved to require”.

Parasites are definitely not something to be ignored or downplayed. While I’ve focused here on the role these interesting creatures can play in health and wellness, parasites can also be the source of illness and disease. For the most part, a low or moderate burden of normal human parasites in an otherwise healthy individual seems to be benign, if not helpful. Problems arise, however, with some non-human parasites and in unwell individuals. Porcine whipworms are a useful model for studying the effects of parasites in humans because they elicit an immune response, are limited to the intestines, and are self-limiting (you have to keep dosing yourself every 2-weeks if you want to sustain an infection). On the other hand, some parasites that did not evolve with humans as their host are not always so well behaved. Perhaps the best-known pathogenic parasite infections are those that occur with non-human parasites that exit the intestines. Parasites evolved with their host, and as such have a bit of a built in road map as to where they should migrate within their normal host. Unfortunately, in the wrong host, this road map can take parasites very seriously off course. Cysticercosis is a condition that occurs when humans are infected with pork tapeworm that encyst in different parts of the body, including the brain in a condition known as neuro cysticercosis. Similarly, if humans pick up the raccoon roundworm Baylisascaris procyonis, the course is frequently fatal because of damage caused during the parasites’ migration throughout the body. A good parasite does not want to kill its host- doing so would be self-destructive- but in the wrong host parasites can go awry. Nonetheless, ‘domestication’ of appropriate human parasites and their prophylactic or therapeutic use may one day be an important and normal part of modern wellness.

1.            Medeiros, M., Jr., J.P. Figueiredo, M.C. Almeida, M.A. Matos, M.I. Araujo, A.A. Cruz, A.M. Atta, M.A. Rego, A.R. de Jesus, E.A. Taketomi, and E.M. Carvalho, Schistosoma mansoni infection is associated with a reduced course of asthma. J Allergy Clin Immunol, 2003. 111(5): p. 947-51.

2.            van den Biggelaar, A.H., C. Lopuhaa, R. van Ree, J.S. van der Zee, J. Jans, A. Hoek, B. Migombet, S. Borrmann, D. Luckner, P.G. Kremsner, and M. Yazdanbakhsh, The prevalence of parasite infestation and house dust mite sensitization in Gabonese schoolchildren. Int Arch Allergy Immunol, 2001. 126(3): p. 231-8.

3.            van den Biggelaar, A.H., R. van Ree, L.C. Rodrigues, B. Lell, A.M. Deelder, P.G. Kremsner, and M. Yazdanbakhsh, Decreased atopy in children infected with Schistosoma haematobium: a role for parasite-induced interleukin-10. Lancet, 2000. 356(9243): p. 1723-7.

4.            Summers, R.W., D.E. Elliott, J.F. Urban, Jr., R. Thompson, and J.V. Weinstock, Trichuris suis therapy in Crohn’s disease. Gut, 2005. 54(1): p. 87-90.

5.            Correale, J. and M. Farez, Association between parasite infection and immune responses in multiple sclerosis. Ann Neurol, 2007. 61(2): p. 97-108.

6.            Bilbo, S.D., G.A. Wray, S.E. Perkins, and W. Parker, Reconstitution of the human biome as the most reasonable solution for epidemics of allergic and autoimmune diseases. Med Hypotheses, 2011. 77(4): p. 494-504.

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I hope that my last post persuaded you that the appendix is not the pathetic remains of our forbearers’ large cecum, but is in fact a nifty piece of anatomy that maintains a safe house for the normal micro flora of our gut (If you’re interested in gut micro flora, Melissa wrote a great post here). While this little organ seems to work well in developing countries where there are frequent outbreaks of enteric pathogens and minimal hygiene, something seems to have gone awry in the developing world. While appendicitis is exceedingly rare in developing countries, it has been reported that up to 6% of the population in industrialized countries develop appendicitis necessitating appendectomy [1]. Why has our bacterial safe house turned into a ticking time bomb?

As early as 1505, Leonardo da Vinci identified the appendix and recognized that it sometimes became inflamed and burst. Much of his medical knowledge was lost, and it wasn’t recognized again until 1705 when the (then very young) father of clinical case reports, Giovanni Battista Morgagni, dissected a man who had died of appendicitis and subsequent peritonitis. That case actually revolutionized the understanding of medicine, with Morgagni and his mentor Valsalva recognizing that a specific disease was caused by a specific condition in a specific part of the body. This showed that illness was not caused by an imbalance of humors or a generalized malaise, but rather a specific cause. This one case led Morgagni and Valsalva to perform autopsies on all their deceased patients, and their detailed notes of over 700 cases were analyzed and published in the book On the Seats and Causes of Disease as Indicated by Anatomy. This book, and the idea that disease is caused by specific disorders, revolutionized medicine.

While appendicitis was one of the first diseases for which the anatomical source was recognized, we still don’t clearly understand why the condition occurs. It is generally believed that appendicitis occurs when the appendix is obstructed (by obstruction of the opening into the cecum by feces or swelling of the appendix due to proliferation of the tissue of the appendix itself), and the mucinous products of the appendix build up, leading to increased pressure and eventually tissue death. This dead tissue encourages bacterial proliferation (and we’re no longer talking about the friendly house-keeping type). Acute appendicitis is a medical emergency, and one that must be diagnosed and handled quickly. The removal of an inflamed, but intact, appendix is a much easier and neater procedure than trying to manage the aftermath of a ruptured appendix and subsequent peritonitis. If you think you might have appendicitis- get thee to the emergency department!

But why has appendicitis become so common? Appendectomy is sometimes referred to as ‘bread and butter’ for a general surgeon, but in developing countries this condition is almost unheard of. The rate of appendicitis is reported to be about 35-fold higher in the United States than in areas of African unaffected by modern health care and sanitation. Additionally, as communities adopt Western sanitation and hygiene practices, the rate of appendicitis increases [2]. Could appendicitis be another result of the “hygiene hypothesis”- the idea that modern medicine and sanitation can lead to an under-stimulated and over-active immune system?

As discussed in my first post, the appendix is associated with a large amount of gut-associated lymphoid tissue (GALT). While I pointed out that the appendix does secrete some substances that actively encourage the formation of biofilms for friendly bacteria, GALT also plays a role in the more typically recognized ‘keep the bad guys out’ aspect of the immune system. It’s that part of the system that tends to go awry with our modern hygienic world. Our immune system evolved to handle and control a number of different pathogens, including unfriendly bacteria and parasites. In the absence of pathogens, however, the system can go amiss The immune system is primed and looking for a fight, and if nothing appropriate comes along to take a beating, the immune system can start getting self-destructive, going after the body in which it is housed. It’s a classic case of ‘idle hands’ (or an active teenager with no good way to get the energy out!). This may well play a role in the prevalence of appendicitis in the developed world: overactive GALT tissue causes the appendix to swell, plugging the appendix, stopping the secretions from exiting into the cecum, and leading to increased pressure and subsequent necrosis and disease. (This is the condition that tends to occur in young people. In older people, appendicitis tends to be caused by the physical blockage of the appendix by a coprolith).

So is that it? In the past, and in the developing world, the appendix operated as a safe house for commensal bacteria. In the modern/hygienic world the appendix isn’t really needed, and can in fact get a bit out of whack because it doesn’t have anything to direct it’s immune-related functions towards. It definitely seems as though this might be the case, and unfortunately the problem appears to extend beyond the appendix. It turns out that an overactive appendix may also play a role in ulcerative colitis- an inflammatory condition of the large intestine. In some people with ulcerative colitis, an appendectomy improves the symptoms of ulcerative colitis, and in others it can completely cure the condition. The intended purpose of the appendix may shed light on why this pathology occurs. First- in a hyper-immune state, the appendix may house bacteria that the immune system aberrantly attacks. Alternatively (or additionally), the GALT tissue may drive the gut into a hyper-immune state. In either case- understanding the evolutionary purpose of the appendix can help understand and treat the conditions that occur in our modern hygienic world. Furthermore, it offers evidence that we should think about the impact of our uber-hygienic world, and consider how we might best handle the mismatch between our immune system that evolved to keep us safe in a dirty world and our modern clean environment.

(If you’re looking for a scholarly discussion of this topic, I highly recommend The cecal appendix: one more immune component with a function disturbed by post-industrial culture [2].)

1.            Bollinger, R.R., A.S. Barbas, E.L. Bush, S.S. Lin, and W. Parker, Biofilms in the normal human large bowel: fact rather than fiction. Gut, 2007. 56(10): p. 1481-2.

2.            Laurin, M., M.L. Everett, and W. Parker, The cecal appendix: one more immune component with a function disturbed by post-industrial culture. Anat Rec (Hoboken), 2011. 294(4): p. 567-79.

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