Archive for April, 2012

Some may be aware of a NYT contest that asked people to submit a brief essay on why it is ethical to eat meat.  Because I have an opinion on the topic (and because I occasionally enjoy exercises in futility) I applied myself to the task and wrote a response. Those of you that read my blog might appreciate that constraining myself to 600 words was difficult, but I managed! I was alerted by a post of Melissa’s over at Hunt Gather Love that the finalists had been announced, which meant it was time for me to publish my entry here!  I hope you enjoy…

Composing a convincing argument on why it is ethical to eat meat in less than 600 words is challenging, and by no means can such an argument be comprehensive. But few aspects of moral philosophy can be described with such brevity, and contemplating an issue as provocative as meat-eating under such auspices would take even longer. That’s not to say, however, that a brief and compelling case for the ethical eating of animals cannot be made, and I shall attempt to do so here, positing the (arguably utilitarian or hedonic) case that the appropriate consumption of well-raised and well-managed livestock maximizes benefits for humans, the environment, and animals. Considering the evolutionary context of the different components further strengthens the case.

Despite the occasional media hysteria over epidemiological studies, the argument that humans evolved to eat and thrive on meat is irrefutable. Anthropological evidence suggests that when our ancestors started to eat meat, our brains grew and our intestines shrank, starting the long road to making us human. As a result of millions of years of evolution, humans are “designed” to thrive on meat, and that is what modern research continues to show. While epidemiological dietary studies are notoriously difficult to interpret, the fact that meat is rich in compounds that the human body needs to survive and thrive is irrefutable. While humans can survive on a vegetarian diet (and, with supplementation of B12, a vegan one), we thrive on a diet that includes meat. The consumption of meat, in order for humans to prosper, is an ethical pursuit.

While eating meat has arguable benefits for human prosperity, there are also numerable ethical implications for the environment. Correct management of livestock can benefit the environment dramatically. Much as humans evolved to thrive on meat, our environment thrives when appropriately utilized by animals. Animals raised outside, on the products of the land on which they walk, give back to the environment by fertilizing the land with their manure and shaping the land with their habits. The (usually small-scale) farms that appropriately raise livestock are able to nurture (and often heal) the land that they manage. Furthermore, the purchase of local farm products greatly increases the economic health of the local community. These implications bolster an ethical argument based on maximizing benefits.

Perhaps the hardest aspect of an ethical argument for the consumption of meat is the argument in favor of the animals. Unlikely though this may seem, I believe this is the strongest component of this argument. My family raises beef cattle. I have raised broiler chickens, and I continue to have a laying flock. These animals have good lives. Seeing a chicken enjoy a dust bath, watching a steer peacefully graze- it is hard to deny the inherent ‘goodness’ of seeing an animal thrive in their environment. The reality, of course, is that these animals would not exist if we did not eat them. Killing animals is not pleasant, but when done correctly can be less stressful and painful than common procedures we perform on pets and ourselves. Furthermore, the net benefit of allowing animals to enjoy life in their natural environment is, from my perspective, an ethical ‘win’.

In our modern world we have the luxury to argue about the ethics of eating meat. In the past, and in many communities today, such arguments would be frivolous. Nonetheless, when the evidence is considered under the auspices of the ‘the greatest good’, one can ethically argue that the consumption of meat leads to benefits for humans, the environment, and the animals that are consumed.

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Pop a squat

I lied.


I said I was going to take a break from writing about bowels and microbiota (I was, I really was), but then my awesome chief resident (the head of my surgery team) distracted me with bowels again.  After I revealed my interest in evolutionary medicine (followed by a brief rant on the appendix, gut microbiota, and the general tenets of evolutionary medicine) he said “Cool- let’s see what kinds of patients I can find for you”.  He then assigned me a few patients with some thoughts of things I should look up and get back to the team on.  I was thrilled.  The patients were interesting and the things he suggested I look up were spot-on… He totally ‘gets it’.


Diverticula are out-pouches of the colon, and can either be “true” diverticula, consisting of all layers of the bowel wall, or “false” (AKA pseudodiverticula), where the thin layers of the bowel balloon out through gaps in the muscular layer.  Diverticula can occur on the right side of the colon (the part closest to the small intestine) but are much more common (at least in the Western world) on the left side, particularly in the sigmoid colon (the last bit of the colon before the rectum).  These are almost always “pseudodiverticula” though are generally referred to as “diverticula” and are the type I will discuss in this post.


Diverticula were once considered so rare that surgical textbooks from the early 1900s didn’t even mention them.  It is now thought to be one of the most common colonic conditions in the developed world, though the prevalence is difficult to determine as most cases are asymptomatic.  Current estimates, however, are that more than 40% of people in industrialized nations develop diverticula by the age of 60, and more than 60% develop them by the age of 80.  As I mentioned, diverticula are frequently asymptomatic, but we become aware of them when they become inflamed, infected, or abscessed, leading to a condition known as diverticulitis (interestingly, diverticula on the right are more prone to bleed, while the ones on the left are more likely to become infected).


The pathogenesis of diverticula is generally believed to be dependent on the intraluminal pressure of the colon, specifically increased pressure during defecation.  While straining to ‘perform’, the pressure in the colon greatly increases, especially in the areas closest to the rectum.  Exaggerated contractions with spasmodic bowel movements cause increases in bowel pressure that may lead to diverticula.  Conventional wisdom would have you believe that increased peristaltic activity is caused by our industrialized low-fiber diet, which leads to low-bulk stool, which cause our colon to work extra hard to expel their payload.  You might suspect, however, that I am a little skeptical of conventional wisdom (refreshingly, so is my chief resident!).


The thought process that led to a ‘fiber-deficiency’ model of diverticular disease is actually rather encouraging for those of us who appreciate an ancestral approach to health.  The argument was initially made by Burkitt and Painter [1] who in 1975 compared the stool transit time and volume of native Ugandans (a population virtually devoid of diverticula) with that of native Britons (importantly, while native Africans do not develop diverticula, those of African descent living in the developed world do).  Burkitt and Painter realized that Ugandans had much larger (450g/day vs. 110g/day) stools and a much shorter transit time (34 hours vs. 80 hours) than UK natives.  It was reasoned that these differences were caused by decreased fiber consumption in the developed world.


Alas, while this argument has gained substantial credence through years of reinforcement, the case for diverticula being a disease of a fiber deficiency fails to hold up.  In fact, a paper recently published in the Journal of Gastroenterology is just the most recent take down of the fiber-based model of disease [2].  This paper adds to the library of references that have failed to show a link between low-fiber diets and diverticula.  In fact, this paper actually suggests that the inverse is true, with those that consumed the most fiber having the highest incidence of diverticula.  This paper also took a look at other factors often implicated in diverticular disease, specifically infrequent bowel movements, high-fat diets, diets with a lot of red meat, and physical inactivity.  None of these factors were associated with diverticulosis (indeed, people with few bowel movements had fewer diverticula than those with many!).


So if a lack of fiber doesn’t cause diverticula, what does? In their 1975 paper, Burkitt and Painter focused on the fiber content of the native diet of Ugandans.  Their focus on diet, I fear, has led astray those who seek to prevent diverticular disease.  While it is true that native Ugandans ate an evolutionary-appropriate diet, they ALSO utilized evolutionary appropriate behavior… For lack of a more tactful explanation- they squat to defecate and only go when they feel the need!  Shocking, I know.


The hypothesis that diverticula could be prevented by squatting and urge-driven bowel habits was put forth in a 1988 paper (in one of my favorite journals, Medical Hypotheses), which pointed out that underdeveloped nations (which have an exceptionally low prevalence of left sided diverticular disease) utilize latrine pits.  They went on to point out that bowel emptying in a sitting position, as caused by a western toilet, requires multiple straining efforts, while bowel empting upon urge in a squatting position usually only requires one [3].  This suggestion has been followed up with a couple of recent studies that show that straining to defecate is greatest in the standing or lying position and minimized in the squatting position [4, 5].  Anatomically, this is explained by the change in the recto-anal angle, which becomes aligned in the squatting position and is obstructed as the flexion of the hips is decreased.


An interesting aside at this juncture is a quick look at the prevalence of diverticular disease in Japan.  As an Asian country, Japan used to have a higher prevalence of right-sided diverticular disease, with left-sided being fairly uncommon.  This trend, however, started to change with the westernization of Japan.  Following Burkitt and Painter, the increase in left sided diverticular disease has been attributed to a decrease in fiber in the westernized Japanese diet [6], but is the blame duly placed?  My brother has lived in Japan for many years and I’ve visited a number of times, and I’ve often been impressed by the spectrum of toilets available in Japan.  They range from the  ‘traditional’ Japanese squatting toilet (a ceramic latrine set in the ground) through to the modern toilet which is an amazing feat of engineering (perhaps you’ve seen one on TV somewhere- they come complete with jets that direct warm water and warm air at various body parts, play music to hide unwanted sound effects, and may, in fact, be able to tell you the answer to the ultimate question of life, the universe, and everything).  Is it fair to blame a lack of fiber on the increase in diverticular disease in Japan?  Or might it actually be due to a conversion from the traditional squatting toilets to westernized seated ones?


“Seated-stooling” has also been implicated in other conditions of the bowel.  There’s another Medical Hypotheses paper that names sitting as a mechanism underlying primary constipation [7], and another communication from the Israel Medical Journal describing a neat little trial conducted on patients with hemorrhoids [8].  This small trial, consisting of only 20 patients, showed interesting results.  Of the 20 patients, 17 had tried (with minimal success) conservative treatment for hemorrhoids, including the ‘all-curing’ high-fiber diet, as well as suppositories, salves, and laxative preparations.  The remaining 3 patients had undergone ligation for severe hemorroids.  Throughout the course of this study (conducted over 1 year) the patients were asked to defecate in a squatting position only and to defecate only in response to a strong urge (no straining to perform!).  The result of these interventions was alleviation of symptoms in most patients.  Alas, 2 of the 3 who had undergone ligation did not experience significant improvement, which may have been a result of fibrous tissue development at the site of ligation.


The conclusion of this last paper seems particularly fitting in consideration of the overlying evolutionary-based interests of this blog: “that a program may be needed to reacquaint man with his natural habits.”[8](No, you don’t need a pit latrine- there are little stools available designed to fit around toilets that allow you to squat over the pot! (Here’s an example, with the option to ‘build your own’)



1.            Painter, N.S. and D.P. Burkitt, Diverticular disease of the colon, a 20th century problem. Clin Gastroenterol, 1975. 4(1): p. 3-21.

2.            Peery, A.F., P.R. Barrett, D. Park, A.J. Rogers, J.A. Galanko, C.F. Martin, and R.S. Sandler, A high-fiber diet does not protect against asymptomatic diverticulosis. Gastroenterology, 2012. 142(2): p. 266-72 e1.

3.            Sikirov, B.A., Etiology and pathogenesis of diverticulosis coli: a new approach. Med Hypotheses, 1988. 26(1): p. 17-20.

4.            Sikirov, D., Comparison of straining during defecation in three positions: results and implications for human health. Dig Dis Sci, 2003. 48(7): p. 1201-5.

5.            Rao, S.S., R. Kavlock, and S. Rao, Influence of body position and stool characteristics on defecation in humans. Am J Gastroenterol, 2006. 101(12): p. 2790-6.

6.            Nakaji, S., K. Sugawara, D. Saito, Y. Yoshioka, D. MacAuley, T. Bradley, G. Kernohan, and D. Baxter, Trends in dietary fiber intake in Japan over the last century. Eur J Nutr, 2002. 41(5): p. 222-7.

7.            Sikirov, B.A., Primary constipation: an underlying mechanism. Med Hypotheses, 1989. 28(2): p. 71-3.

8.            Sikirov, B.A., Management of hemorrhoids: a new approach. Isr J Med Sci, 1987. 23(4): p. 284-6.

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Sorry there’s been a delay in getting anything new out. I’ve had some exams, a quick trip to Colorado, and am now just finding my feet on my surgery clerkship. I have a bunch of things I intend to write about soon, but this paper popped up the other day and it ties in really nicely to some of the things I’ve already written about. I just had to write about it! I promise that in my upcoming posts I will get away from bowels and microbiota (though these subjects are incredibly important!).

You may remember Clostridium difficile from one of my previous posts on the appendix. C. diff is an anaerobic bacterium that frequently resides in the large intestine. After a course of antibiotics, when other gut-inhabitants have been killed, an overgrowth of C. diff can lead to a very nasty spectrum of symptoms ranging from mild diarrhea to death. Because of the frequent use of antibiotics and because of new hyper-virulent strains of C. diff, infection with this bacterium has reached epidemic levels. Alas, this is one of the most common infections found in hospitals, nursing homes, and other medical facilities.

The incidence of C. diff is on the rise, with both the number of cases and the mortality from infection recently doubling. There are approximately 3 million cases of C. diff infection in the US each year, and it’s estimated that care for these cases is in excess of $3.2 billion. C. diff infection leads to a number of discomforts, including abdominal pain, diarrhea, fatigue, and flu-like symptoms. Alas, treatment can be difficult, and symptoms can persist for months or even years.

As I mentioned in a previous post, the usual treatment for C. diff is further antibiotic treatment. C. diff infection usually occurs after all the normal gut flora has been eliminated and further antibiotics (sometimes given with probiotics to encourage the return of commensal bacteria) are targeted at eliminating C. diff (there’s even a new antibiotic (Dificid) specifically targeted at C. diff). The problem, of course, is that IF these antibiotics are effective, you now have a relatively unpopulated gut that is barren and ready for the taking by whatever stray bacteria have survived the courses of antibiotics or whatever quick growing bacteria happens to make their way to the intestines to claim the empty territory- unfortunately C. diff is frequently the victor in this foot race!

Recurrent rates of C. diff infection range from 15-30%, and once you’ve had one recurrence, you’re more likely to have another: a 40% chance of having a second, and a 65% chance of having a third. Obviously antibiotics are of limited efficacy here, so what is an appropriate course of action?

In my previous post, I discussed a paper that showed that having an appendix (and thus having a safe house for normal commensal bacteria that can repopulate your gut after infection or antibiotic treatment), is protective against a recurrence of C. diff [1]. But what if you don’t have that safe house, or if you get a recurrence despite having an appendix? Again, as mentioned in a previous post, a Fecal Microbiota Transplant (FMT) seems to do the trick.

A paper published at the end of March [2], combined data from 5 sites and showed that FMT can provide RESOUNDING cure rates in people suffering from recurrent C. diff infections. Here’s a quick review: 77 patients, with average symptom duration of 11 months (range 1-28) underwent FMT at 1 of 5 medical centers in an attempt to cure their chronic infection. On average, these patients had already undergone 5 treatment regimes to try and cure their infection. FMT (most donors were family members, spouses, partners, or friends) was infused by colonoscopy into the terminal ileum, cecum, and (depending on the site) parts of the colon. Resolution of a number of symptoms- abdominal pain, fatigue, and diarrhea, were recorded.

In 70% of patients, pain resolved with FMT, while it improved in an additional 23%. 42% of patients saw a resolution of fatigue, with an additional 51% reporting an improvement. An astounding 82% saw a resolution of diarrhea and 17% saw an improvement within 5 days of FMT. These are patients, remember, that have been suffering from symptoms for an average of 11 months.

Alas, 7 patients (just under 10%) experienced an early recurrence (less than 90 days after FMT), and required a secondary treatment (either antibiotics targeted at C. diff or another FMT), which successfully treated the recurrence. Thus, the “primary cure rate” (resolution of diarrhea within 90 days of FMT) was 91%, and the “secondary cure rate” (resolution of infection after a further course of antibiotics or a second FMT), brought the cure rate to 98%. (It is worth noting that the one not “cured” patient died in hospice and was not re-treated after failure of a primary cure).

Some patients did have late recurrent infections of C. diff. Not surprisingly, these cases all occurred in patients that took a course (or multiple courses) of antibiotics to treat an unrelated infection. Recurrence occurred in 8 of the 30 patients that took a course of antibiotics. Interestingly, recurrence may also be associated with the use of proton-pump inhibitors (perhaps not a surprise, as PPIs inadvertently affect our microbiota [3])

This paper is excellent evidence to support FMT becoming a first-line therapy for the treatment of C. diff infection (and I will add especially for those that lack an appendix). FMT restores a natural biodiversity to the intestine of someone who has had their own microbiota disturbed by disease and/or antibiotics. For many people (those that experienced a primary cure), the restoration of the biodiversity was enough to overcome C. diff infection. For others, the restored biodiversity gave them the edge to overcome infection with a further targeted antibiotic or a second transplant. Remember- these are patients that had failed MULTIPLE treatments for C. diff and had been experiencing symptoms for an average of 11 months.

While there are definitely risks to FMT (it is important that donors be screened to rule out dangerous transmissible infections such as HIV, hepatitis, and parasitic infections), there are arguably additional benefits. One patient in this study reported a significant decrease in allergic sinusitis and another reported an improvement in arthritis. Both associated the improvement of symptoms with FMT. Indeed, FMT has been reported as a successful treatment for a number of conditions including inflammatory bowel disease (such as ulcerative colitis), irritable bowel disease, idiopathic constipation and insulin resistance [2].

It is important to recognize that some of the patients in this trial did suffer from subsequent disorders that should be further explored. While the conditions were not apparently associated with FMT, 4 patients that received this therapy later developed conditions including peripheral neuropathy, Sjogren’s disease, rheumatoid arthritis, and idiopathic thrombocytopenic purpura. Further studies need to determine if there is an association between FMT and autoimmune or rheumatologic disorders. If associations are found, I would expect that this would call into question the appropriate selection of donors for individual patients.

It is becoming increasingly obvious that an appropriate and diverse microbiome is important for health. When this microbiome is thrown out of whack, be it by an evolutionary-novel lifestyle, infection, or antibiotic treatment, the restoration of this environment should be the focus of medical treatment. Fecal Microbiota Transplant is a rational and effective method of restoring a healthy and diverse intestinal microbiome.

(It is worth mentioning that 97% of the patients in this study stated that they would undergo another FMT if they experienced a recurrence of C. diff, and 53% would choose FMT as their first treatment option before a trial of antibiotics. Yes, the idea of FMT may seem gross, but it is effective. For those that have suffered for upwards of a year, this treatment truly is a life-changing option.).

1.            Im, G.Y., R.J. Modayil, C.T. Lin, S.J. Geier, D.S. Katz, M. Feuerman, and J.H. Grendell, The appendix may protect against Clostridium difficile recurrence. Clin Gastroenterol Hepatol, 2011. 9(12): p. 1072-7.

2.            Brandt, L.J., O.C. Aroniadis, M. Mellow, A. Kanatzar, C. Kelly, T. Park, N. Stollman, F. Rohlke, and C. Surawicz, Long-Term Follow-Up of Colonoscopic Fecal Microbiota Transplant for Recurrent Clostridium difficile Infection. Am J Gastroenterol, 2012.

3.            Vesper, B.J., A. Jawdi, K.W. Altman, G.K. Haines, 3rd, L. Tao, and J.A. Radosevich, The effect of proton pump inhibitors on the human microbiota. Curr Drug Metab, 2009. 10(1): p. 84-9.

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