March is Colorectal Cancer Awareness Month, so I made this infographic to highlight the key facts that everyone should know about colorectal cancer!
For much more about this and other important health topics, please visit my informational site Retroflexions.com!
Bowel prep, or that stuff you need to drink to get cleaned out for your colonoscopy, is never something that one looks forward to doing. You knew that drinking the prep was a necessary evil to ensure a high-quality colonoscopy, but what do you do if you followed all the instructions but the prep simply didn’t work?
If you’re reading this while in the midst of a potentially failed bowel prep don’t despair! There are many ways to salvage a bowel prep and still have a safe, high-quality colonoscopy the next day. It all depends on what time you take action; If you wait until 2 hours before the procedure is scheduled than yes, it’s probably too late to do much. However, if you’re already having issues the night before you can totally recover from this and be fine. This is what I usually recommend, based on the issue at hand:
“I drank the first dose of the prep and nothing happened.” I usually tell patients to wait several hours before panicking. If you have waited 6 hours and there is no bowel activity whatsoever then at that point I would recommend taking either 10 mg of bisacodyl by mouth, or giving yourself an enema. If you’ve done all that and still nothing happens, then it’s probably time to call your doctor and ask for suggestions.
“I drank the first dose of the prep but vomited most of it up.” Unfortunately, you will need more prep then. This usually requires a phone call to the doctor explaining the issue and often an alternative prep is recommended. In selected patients, I would usually recommend Miralax prep or using magnesium citrate instead–both of which can be purchased over the counter.
“I can’t drink the first dose of the prep because it tastes horrible! Yuck!” Try putting the prep in the refrigerator and making it as cold as you can tolerate. Much of the taste disappears when you really chill the prep. You can also call your doctor to see if an alternative prep is an option for you. Ultimately this is also a case of mind-over-matter…it’s unpleasant but sometimes you just have to do it anyway!
“I drank both doses of the prep and my bowels are still not clear” This is a common issues with some bowel preps. It really depends on what time this happens. If you did all the prep the night before, then there is plenty of time to follow the prep with a bottle of magnesium citrate and a large volume of clear liquids. If you notice that you are not clear the morning of the procedure, you can still drink magnesium citrate but really need to finish drinking it about 4-5 hours before the procedure is scheduled to start. This gives it enough time to have an effect, and also keeps you well within the 2 hours safety window for ingestion of clear liquids with respect to receiving anesthesia. However, if the procedure time is close (2-3 hours away) and you’re still not clear, then the only real option is to give yourself an enema or two. You can always reschedule the procedure if you have to, but realize that you already completed the bowel prep and will therefore have to do the entire prep again if you need to reschedule!
Happy prepping!
Fermented dairy sounds rather disgusting, as the name suggests something akin to spoiled milk, but in reality most fermented milk products are actually quite delicious! Fermented dairy products are foods like yogurt, cheese, sour cream, and kefir among others. The process of fermentation is usually done by bacteria such as Lactobacillus species, and results in a product that is more shelf-stable than milk, while retaining all of the protein and other substances that give milk its healthy reputation. Fermented dairy has been enjoyed by people dating back to about 10,000 B.C., so that trendy kefir stuff you are now seeing at the local food store is really nothing new…
Please click here to read the full article on my informational site ‘Retroflexions.’
On May 30, 2018, the American Cancer Society (ACS) released new guidelines regarding colorectal cancer screening for the average-risk individual. The big news is that they now recommend that screening for colorectal cancer begin at age 45 rather than age 50. This reduction in the starting age was in reaction to recent data showing that colon cancer is increasing in younger Americans for unclear reasons. By screening people at a younger age, the hope is that we can detect and prevent colon cancer in more people.
The ACS states that 20% of new cases of colorectal cancer occur in the younger-than-55 crowd. Furthermore, despite a general downward trend in colorectal cancer in the over-50 population, the risk is actually rising slightly in the subgroup of people aged 50-54. These are the cases of cancer the new guidelines are trying to prevent. The ACS is pragmatic in acknowledging that people don’t typically sign up for a colonoscopy exactly on their fiftieth birthday…in fact many wait a few years or more after age 50 to get screened. By pushing the starting age up by 5 years there will likely be a benefit to these patients who would otherwise be late to the colonoscopy party.
The consequences of these recommendations are potentially huge. If these guidelines are followed, an estimated twenty million additional people are now eligible for colon cancer screening. However, the ACS does not specify any one best choice for colorectal cancer screening and states that colonoscopy, stool DNA testing (Cologuard), virtual colonoscopy, and stool testing for occult blood with Guaiac-based tests or FIT testing are all equivalent. I think that by now we know that all tests are not really equivalent, with colonoscopy being the gold-standard test, but with millions of people not getting any type of screening at all, any test is better than nothing.
A few caveats about these new recommendations:
I’ll just start out by letting you know that I had mixed feelings about posting this. Not because I’m embarrassed to publicly discuss my colonoscopy experience (weirdly enough, I am OK with that part), but because I don’t want to be responsible for people interpreting what I’m about to disclose far too liberally and ruining their pre-colonoscopy cleanout. So please read on, but don’t push the limits too much. Failing to achieve a good bowel prep will require you to repeat the exam and prep again, and nobody wants that to happen!
For the past year or so I have been having minor IBS-type symptoms on and off, mostly related to stress or periods of poor diet. As a gastroenterologist, I started getting into my own head and worrying that I had some rare or catastrophic disease (the availability heuristic is real!) Part of me knew that if the test was normal, I would probably feel better just with that knowledge alone. I’d also be lying if I said that I wasn’t just a little curious about the whole process too. I either talk to people about colonoscopies or perform them for most of my waking hours; shouldn’t I also have some first-hand experience to reference for my patients?
So I scheduled a colonoscopy and requested Suprep bowel prep. I choose Suprep because it is what I usually give out to patients…I’ve noticed that most people seem to complain the least about the taste of Suprep when compared to most other preps. That’s not to say that the other preps are inferior…I use them interchangeably. However, I wasn’t about to get two or three more colonoscopies just to test out all the preps, so the Suprep experience is what you get to hear about!
I was given the usual instructions for split-dose bowel prep: 1) Clear liquids only the entire day prior to the procedure; 2) Take the first dose of prep at 5 PM and the second dose of prep 5 hours before the procedure start time; 3) Nothing to eat or drink after the second dose of prep. Pretty standard stuff, these are the instructions I usually give to my patients. Following this will lead to a good or excellent bowel prep in the vast majority of people. But what if I told you that I did something different but still achieved an excellent clean-out?
I cheated on the prep. I ate solid food the day before. Now before anybody gets too excited, I ate a very limited and small amount of food, but it made a huge difference in the ability to tolerate the entire process. The following is my “justification” for my cheating, other than the obvious reason of “I was hungry.” I wake up around 5:00 AM or earlier every day. I usually wake up starving and if I don’t eat something within an hour or so of waking I usually feel weak and like my head is spinning. I’ve been this way as far as I can remember, even back in elementary school. I had a long day ahead of me at work, and knew that without some calories in me I would crash in the mid-morning while doing procedures and not be able to function well. “It’s for the patients,” is what I told myself. I almost believed it, too!
So that morning I ate a good-sized bowl of plain vanilla yogurt (no toppings, nuts, fruit, etc.) I also had a few pieces of white toast with butter. We usually don’t have white bread in the house, but we were lucky to have an unseeded loaf of Italian bread from the night before that I toasted in the toaster and buttered up. For lunch, I had a huge gelato without any nuts or toppings. Throughout the day I drank black coffee and plenty of clear liquids.
I got home around 6PM that day (a little later that the recommended 5PM start time) and began drinking the prep. I mixed the first part of the prep with water as recommended and took a sip. Thinking that I’d be really slick, I used a straw to try and bypass my taste buds. “Not terrible,” I thought to myself, relieved that this process wasn’t going to be as bad as many patients made it sound. The prep tasted like a mixture of seawater, dish soap, and grape cough syrup…yum! A few sips later and I was rethinking this whole thing…the cumulative effect of drinking the prep made each sip taste grosser than the last. After drinking about one-quarter of the first 16 ounces of the stuff, I put the container in the fridge and took a 10-minute break to pace around the house and rethink my strategy.
Going back to the prep in the fridge, I took a few more sips through the straw. Why was it taking so long to drink this stuff? If this were water I could have drank the whole thing in five minutes. I think the straw is actually slowing the process down. I ditched the straw and was able to drink the prep much faster. A few gulps later I was half-way done with the first round. I put the container back in the fridge since the colder the prep was the less bad it tasted. It’s now about 6:20 PM and I suddenly felt a strange grumbling in my lower abdomen.
I was surprised at how fast this stuff works! I figured it would take an hour or so to have any effect, or at least give me some warning first. I was wrong on both counts! With 8 oz. of the nasty stuff down so-far, I was lucky that my bathroom was only a few steps away! Immediate watery diarrhea was the result. The thing I wasn’t expecting was the total lack of pain, cramps, or any discomfort whatsoever. It was as someone just opened the faucet, then closed it again. Magic!
I finished the rest of that evening’s prep over the following 20-30 minutes in between several other sprints to the bathroom. The prep was definitely easier to drink when cold straight out of the fridge. It was about 7PM and the bowel movements were coming fast and furious now. I also noticed that I was incredibly thirsty all of a sudden. I chugged 32 ounces of room temperature Gatorade in about five minutes flat. I wanted more, but only had tomorrow’s ration in the house. Therefore I drank a glass or two of water. By 9PM, all was quiet. I mixed tomorrow morning’s prep and put it in the fridge to chill overnight. I woke from sleep around 1AM for one more small bowel movement, but it was no big deal. I actually got decent sleep.
The next morning, I woke up at my usual time of 5AM. I drank 2 cups of black coffee as soon as I woke up. This was followed by another 16 oz. of Suprep over the next 45 minutes. I would gulp down about 4 oz. at a time, then rest for 10-15 minutes and repeat until done. This time, the bowel movements started immediately after taking the first bit of the prep and were mainly yellowish water. Another 32 oz. of Gatorade down the hatch and the process was complete. The last 2-3 bowel movements were literally clear water, like as clear as the water that comes out of the faucet. Cool, I did it!
Now would be a good time to talk about a study from a few years back. Thinking that improving the tolerance of the prep would remove one of the classic barriers for some people to do colonoscopy as well as decrease the number of broken appointments and inadequate preps, researchers randomized patients into two groups: One group received a clear liquid diet the entire day prior, and the other was able to eat a light breakfast and lunch with several food restrictions the day prior. Both groups then completed the standard bowel prep. The study showed exactly what we would expect: The people who starved all day were miserable, the people who ate a little were less miserable, and the quality of the bowel preps achieved were the same between the groups! The most interesting finding was that the group of patients who were restricted to only having clear liquids cancelled their appointments more than twice as frequently as the patients that were allowed to eat just a little. Hunger is a powerful force to compete with!
Now before you eat a bacon cheeseburger with fries, corn on the cob, and a salad the day before your colonoscopy, it’s very important to understand that these subjects (and yours truly) ate a very limited diet the day before the colonoscopy. Fibrous foods such as any fruits or vegetables are not allowed. Seeds, nuts, whole grains, fresh or dried herbs/seasonings, popcorn, and the like are definitely not allowed. Corn is probably the worst thing one can eat the day before having a colonoscopy!
What kind of foods are OK to eat the day before the colonoscopy? Low residue foods (low roughage) are ideal; these are processed flours (white bread, etc.), white rice, pasta, yogurt, gelato, and related snacks, eggs, lean meats, and other foods. A light breakfast is fine. A light snack around lunch time is OK too, but after that it’s clear liquids only. That means “dinner” is clears only: You don’t want food and bowel prep in your stomach at the same time, trust me.
So back to the title of this article: A gastroenterologist cheats on the colonoscopy prep and wins! Did I really cheat? I guess not, since it seems that research backs up what I did! But did I win? Can you ever call getting a colonoscopy “winning?” I guess it depends on the findings. I did, however, have an excellent bowel prep!
When it comes to colon cancer prevention, the polyp is the key player to know. Colon polyps, called adenomas, are precancerous growths originating from the inner lining of the colon wall. There are other types of polyps in the colon which are not considered precancerous, but for our purposes in this article we will consider the terms colon polyp and adenoma to be one and the same.
Polyps are important to know about because they are the precursors to colon cancer. That is, virtually all cases of colon cancer began many years earlier as a small polyp growing in the colon. For the average person, it takes many years for these small polyps to appear on the scene, which is why we don’t usually recommend colonoscopy until a person is 50 years old. However, it’s not totally uncommon to find significant-sized polyps in younger people in their 30s or 40s (and even in their 20s!) From the time a polyp starts growing, it is thought to take more than 10 years for the polyp to grow into cancer…and not all adenomatous polyps grow larger or turn into cancer at all. However, many polyps will continue to have cellular changes such as mutations that will promote growth of the polyp and eventually transformation into colon cancer.
By understanding what causes colon polyps, we can understand what causes colon cancer. Here are some risks factors for getting colon cancer/polyps that an individual cannot change:
However, roughly half of all cases of colon cancer (and by extension, colon polyps) are a result of modifiable risk factors. These are the things that you can control. If we know what these risk factors are, maybe we can make better choices for ourselves and our families. The following is a list of the known risk factors for developing colon cancer/polyps:
And let’s not forget the final factor that leads to colon polyps and cancer in many individuals:
It’s March, which means it’s Colorectal Cancer Awareness Month!
Preventing colon cancer is one of the most important things that we gastroenterologists get to do. Even if you’re not particularly interested in colon cancer, there will still be some interesting stuff for you to read this here as I will cover a little bit about nutrition, exercise, and healthy lifestyle choices as they relate to colon cancer prevention. I also look forward to sharing a somewhat humorous and true story about bowel prep from the perspective of a patient, and that patient is me!
First, I’d like to review some basic facts about colorectal cancer for any new readers out there:
Cancer, in general, is when your own cells develop DNA mutations and eventually stop obeying the normal control signals from the body that function to tell the cells when to stop dividing and where not to grow (obviously this is a gross oversimplification). These rebellious cancer cells multiply and form a tumor, which is just a mass of cancerous cells. Tumors can grow into other organs and cause damage, blockages, bleeding, and other types of badness. The cells inside the tumor can also spread through the bloodstream or lymphatic system and land in other locations in the body, a process known as metastasis.
Colorectal cancer is when this process happens in the colon (or the rectum, which is the end portion of the colon). The cells that transform into the typical type of colon cancer originate from the inner lining of the colon and turn into a type of cancer called adenocarcinoma.
Colorectal cancer occurs when a precancerous polyp (known as an adenoma) forms inside the colon and slowly accumulates additional genetic mutations, causing the polyp to grow larger and act more aggressively, eventually invading into the muscle layer of the colon wall and becoming full-blown cancer. We think this process takes about 10-20 years to occur, which is a very important fact when it comes to colorectal cancer prevention. This long sequence, from adenoma to cancer, is the reason why screening can prevent colon cancer—we can intervene during the long precancerous stage and change the natural history of the disease. Stated more simply, we can remove the precancerous polyp before it actually turns into colon cancer, therefore preventing colon cancer from developing at all!
All professional gastrointestinal societies recommend starting to screen most people for colorectal cancer starting at fifty years old. However, true prevention really starts many years before most people have to worry about getting a colonoscopy! Diet, exercise, and many lifestyle choices can increase or decrease the risk of developing colorectal cancer. We will cover this important topic in more detail later this month.
As far as screening goes, there are various tests available to look for both colorectal cancer and adenomatous polyps. I have covered these topics in more detail in past articles, so I will invite new readers to peruse the links below for more info:
However, if you are in a hurry and don’t want to read those older articles, we can boil down the testing recommendations for most individuals as follows: To prevent colorectal cancer, the average-risk man or woman should have a colonoscopy starting at age 50, and then every 10 years thereafter, until about 75-85 years of age. If polyps are found, they are removed during the colonoscopy, and the next exam is scheduled sooner than 10 years later.
Most cases of colon cancer are diagnosed in people in their late sixties and early seventies, with rectal cancer being diagnosed somewhat earlier (early sixties). The good news is that colorectal cancer rates in the over-fifty population are on the decline! This may be due to several factors such as the increase in effective colorectal cancer screening programs and a decline in the popularity of smoking. However, new data is showing that the rate of colorectal cancer in young people is actually on the rise! Although it is still relatively rare, the rate of colorectal cancer is increasing in the 30- and 40-year-old age group.
We are not quite sure why colorectal cancer is increasingly developing in the younger population. Various theories exist, including the influence of obesity, inactivity, food additives, poor diet, and even antibiotic exposure. All we can conclude at this point in time is that symptoms that could be consistent with colorectal cancer should not be ignored just because a patient is relatively young.
Well, that about wraps up the basics on colorectal cancer. I am going to hit this topic from all angles this month, so be sure to keep reading!
For a quick reference on colorectal cancer, see the American Cancer Society’s publication Colorectal cancer facts and figures 2017-2019.
I think it’s safe to say that most people already know that eating “junk food” is probably not really a good thing to do. You can show the average five-year-old a bunch of broccoli and a candy bar, and ask her which food is healthier, and she’ll regrettably pick the broccoli (and then take the candy bar out of your hand, run away, and eat it!)
But just how bad is junk food for you really? Do we even know what happens to the body after eating too much junk? A study published in the BMJ just last week aims to answer some of our questions about the harmful effects of a poor diet with some shocking, but not entirely unexpected, results. In order to understand the data, we first need to define the concept of “junk food” as it was used by the authors. This study looked at the worst types of junk that we can eat, the so-called ultra-processed foods. Ultra-processed foods are usually pretty easy to spot…they almost always come in a package of some sort, usually have a long shelf-life, and are often made in a factory.
More specifically, ultra-processed foods are defined in this study as mass-produced packaged breads, snacks, confectionary, desserts, sodas and sweetened drinks; meat products such as chicken nuggets, meat balls, fish sticks and the like; instant noodles/soups, frozen ready-to-eat meals, and other food products made mostly of sugar, hydrogenated oils, fats, modified starches, and protein isolates. Often processed foods are deeply chemically processed and have flavoring agents, artificial coloring, and emulsifiers added.
Now that we have defined the problem, let’s take a second to realize just how much of this stuff most of us eat on a daily basis. How many of these “treats” do we open for ourselves or our children? Look in your pantry or freezer today and I bet there are a bunch of packages of snacks, cakes, muffins, frozen meatballs, chicken nuggets, and desserts in there looking right back at you. How many “foods” do we eat that were shaped by a machine into some pleasing shape and injected with modified fats and preservatives before being deep-fried, flash frozen and shipped out from a factory somewhere?
The study that we are talking about basically followed over 100,000 people (78% women) in France over an eight-year period and monitored their dietary intake of ultra-processed foods amongst other things. They followed these people for the development of cancer until the study period ended in 2017. It’s important to note that they calculated the amount of ultra-processed foods that were consumed by weight (not by calories), which allowed diet sodas and other artificially-sweetened products to still be counted in the overall intake of junk food. The study results were also statistically adjusted for other lifestyle factors such as smoking, alcohol intake, obesity, exercise, and others in an attempt to correct for any confounding variables.
Yes, soda is an ultra-processed food. Diet soda and juices were also counted as junk in the study.
Here is what they found: A 10% increase in the proportion of ultra-processed foods in the diet was associated with a 12% increased risk of developing any cancer. The risk of breast cancer was increased by 11%. For colon cancer (a particular concern to us gastroenterologists), there was a nonsignificant trend towards increased risk with eating ultra-processed foods. Is this conclusion a big surprise? Not really, but this study was the first to actually put some numbers on the risk. I, for one, like numbers when it comes to nutritional advice…it keeps us in the realm of science and hopefully away from veering into pseudoscience territory.
Alright, we get it…eating garbage is bad for your health. Now we know that eating 10% more garbage is associated with increasing your risk of developing cancer by more than 10%. But how might ultra-processed junk foods cause cancer in people? The study authors have a few thoughts on that:
So what is the bottom line? If we want to take care of our bodies the best we can, we should avoid these ultra-processed foods as much as possible. They are associated not only with high cholesterol, obesity, and high blood pressure, but now also with many different cancers. We should view these “foods” of convenience as what they really are, a shortcut to bad health at the sake of saving a little time. Eating junk food treats our taste buds to a temporary high at the cost of our long-term health. Knowing this, you can still enjoy the occasional doughnut or packaged snack, but this really should be a rare indulgence, not a daily or weekly occurrence.
Alcohol has been enjoyed by people throughout the world from the beginning of recorded history up until present day. It is an important part of many cultures and social gatherings, but because alcohol is available almost everywhere it is also easily misused and abused. By now, it is pretty much common knowledge that drinking a lot of alcohol is not really great for your liver. But how does alcohol actually cause liver damage?
To understand how alcohol causes damage, we need to understand what happens in the body when alcohol is ingested. After alcohol is consumed it is absorbed by the stomach and small intestine and delivered to the liver through the portal vein. The liver now has to deal with the alcohol by metabolizing it into something less toxic for the body.
The liver detoxifies alcohol in two main ways: First, there is an enzyme called alcohol dehydrogenase which is present in the liver cells with the main job of breaking down alcohol into something called acetaldehyde. The only problem is that acetaldehyde is kind of toxic too, and can cause damage to the normal proteins in the liver. If too much acetaldehyde forms, one can experience flushing, nausea, vomiting, palpitations…hopefully this doesn’t sound too familiar! Acetaldehyde is then broken down by an enzyme called aldehyde dehydrogenase to a substance called acetate, which is released from the liver cells and can be turned into energy by the heart and muscles.
Alcohol is also broken down by a family of liver enzymes (called cytochrome P450 enzymes) which also convert alcohol to acetaldehyde. However, not only is acetaldehyde toxic in its own right, but the cytochrome P450 enzyme system also causes the formation of nasty reactive oxygen species as a byproduct. (Reactive oxygen species are also called “free radicals” and are unstable molecules that cause damage by oxidizing critical proteins and other materials in cells. Think of pouring hydrogen peroxide on an open wound…that is what free radical damage looks like, only on a smaller cellular level.
This is a huge oversimplification and there are many other ways that alcohol a) gets metabolized, and b) causes liver damage. However, since this is not a textbook we will move on to the fun stuff next.
Alcoholic liver disease (ALD) is the general term used for liver problems related to excess alcohol ingestion. There is a spectrum of liver disease seen with alcohol use, which usually occurs in a continuum from mild and reversible, to severe and irreversible.
The first manifestation of ALD is alcoholic fatty liver. The alcohol-induced inflammation described above alters metabolism of triglycerides and fatty acids in the liver favoring accumulation of these substances in the liver cells. The liver becomes swollen and inflamed, leading to the leakage of liver enzymes into the blood. Blood tests may show high levels of these liver enzymes (called AST and ALT). Ultimately, fatty liver is reversible once excess drinking is stopped.
However, if the patient with alcoholic fatty liver continues to drink, one of two things will usually happen depending on the patient’s sex, genetic predispositions, nutritional state, the time course of the drinking, the sheer amount of alcohol consumed, and many other factors: Alcoholic hepatitis or alcoholic cirrhosis.
If someone drinks a large amount of alcohol in a relative short period of time, they are at risk of developing alcoholic hepatitis. In alcoholic hepatitis, the inflammation in the liver goes into overdrive causing liver swelling, abdominal pain, fever, jaundice (yellow skin), and often ascites (fluid in the abdominal cavity) and/or encephalopathy (confusion). Left untreated, alcoholic hepatitis is often fatal, and unfortunately even with the best medical care the outcome remains rather grim. Once activated, the massive levels of liver inflammation seen in alcoholic hepatitis can continue to worsen even after the patient quits drinking alcohol entirely.
Most patients who survive the experience of alcoholic hepatitis eventually find out that underneath all that liver inflammation is cirrhosis. Cirrhosis is when the liver becomes fibrotic (filled with scar tissue) and functions poorly, causing a host of problems. Cirrhosis also can occur slowly and quietly without having to progress through alcoholic hepatitis; this is often seen in the “heavy social drinker” who never really drinks that much in any one sitting. However, over the course of a week or so, the heavy social drinker consumes quite a bit of alcohol and as we know, weeks lead to months, which lead to years. Just like interest in a retirement account, the slow progressive damage adds-up over the years of “social drinking” and causes cirrhosis just the same as if the person binge-drank their way there in only a few years of heavy alcoholism. At least when someone drinks with fury the liver damage is expected: The slow silent damage is more insidious since there are no great ways to tell that liver damage is happening until the damage is done. In fact, liver function blood tests may be normal despite the presence of cirrhosis.
There is an old adage that states “The dose makes the poison.” That is, anything can be a poison in sufficient quantity (think water, potassium, or oxygen for example), and if you take a real poison like cyanide and dilute it down so it’s barely detectable than it ceases to cause damage. In that same vein, alcohol is basically poison that people ingest willingly for pleasure, but just how much alcohol does it take to poison your liver? How many drinks separate safe social drinking from “heavy” social drinking, from a full blown bender? Well, that is an excellent topic for a future post, so stay tuned!
Diverticulitis is a common and sometimes serious problem that affects several hundred thousand people each year. Diverticulitis is the condition where small outpouchings or “pockets” in the wall of the large intestine called diverticula become inflamed and infected, and typically presents as a constant lower abdominal pain, associated with fever or chills, and often bloating or constipation symptoms. Despite becoming even more common in recent years, not much is understood about why diverticulitis occurs.
Diet has long been implicated in the formation of these diverticula which can eventually become inflamed leading to diverticulitis (the condition of just having the pockets without an associated infection/inflammation is called diverticulosis). We know that diverticular disease is rare in countries where fiber intake is high, and we know that when populations change to a more westernized diet (poor in fiber/rich in protein, fat and processed sugars) the rate of diverticular disease rises accordingly. So if fiber is protective against developing diverticular disease in the first place, does it stand to reason that supplementing fiber when one already has diverticulosis will help prevent future complications?
The answer to the above question is unknown, but because fiber is a mostly harmless supplement and has other health benefits, we often recommend fiber supplementation to patients after they are diagnosed with diverticulosis or diverticulitis. But what about the common advice of avoiding seeds, nuts, corn, and popcorn that is readily doled out by some doctors and most family members/friends as soon as they hear the words diverticulosis or diverticulitis? One can reason that it makes common sense to try to avoid having sharp, hard, indigestible seeds getting stuck in a diverticulum and causing an abrasion or perforation which may lead to infection and other nastiness. But does this recommendation have any valid scientific reasoning behind it?
While I’m not sure when or where this recommendation started, it probably belongs more under the category of “old wives’ tale” rather than scientific fact. Let me explain my reasoning for this:
It is very commonly observed during colonoscopy that patients with diverticulosis are found to have a small ball of stool impacted in each and every diverticulum. Presumably, this is the natural state of affairs in the colon of the patient with diverticulosis. So if small hard pellets of stool (mostly composed of indigestible waste and bacterial mass) do not cause an infection, why would a small seed or nut cause a problem? Nevertheless, people still take great pains to avoid seeds, nuts, and corn, causing themselves a fair amount of grief when it comes to meal options. Is this all worth it?
I would reason that it is not necessary to avoid seed and nuts if you have diverticular disease. Probably the best evidence we have that seeds, nuts, corn, and popcorn do not cause complications in patients with diverticular disease comes from a study published in JAMA in 2008 showing that not only was intake of nuts, seeds, popcorn, and corn NOT associated with developing diverticulitis, but in fact the opposite was true. Eating more seeds, nuts, corn, and popcorn actually seemed to be associated with LESS of a chance of developing diverticulitis! These foods are thought to be somewhat anti-inflammatory, and therefore may protect against diverticulitis.
So what is the ideal diet to prevent development of diverticular disease? I think it is pretty obvious that a high-fiber diet is king in preventing the development of diverticulosis. But what if you are late to the high-fiber party but still want to make some changes to prevent that next attack of diverticulitis? Starting a high-fiber diet later in life may still help to reduce the progression of more diverticula, but unfortunately there is no way to reverse the existing diverticula (besides surgical resection of the diseased segment of colon). However, there are still diet changes you can make that might help.
It seems that diets high in red meat are also associated with the development of diverticulitis. This is independent of the effect of fiber, as red-meat eaters develop diverticulitis more often than their vegetarian counterparts even after controlling for fiber intake between the groups. What is more interesting is that researchers found that the recent diet for the past 1-4 years before developing diverticulitis seemed to shape the risk more than the lifelong diet habits. That means that changing to a high-fiber, low-red-meat diet now can still lessen your chance of developing diverticulitis in the near future. But look at the bright side–at least you can eat all the seeds, nuts, corn, and popcorn you want!