In this post, I’d like to go over some environmental risk factors associated with IBD.
Table of Contents
While discussing diet in relation to health isn’t easy, I’m hoping these other risk factors are easier to deal with, without anyone becoming defensive, offended, aggressive and just plain insulting by the research.
It seems that after the post on Diet and IBD, many people felt that it was wrong to suggest that people have caused their own illness through their prior dietary choices.
Not that I’ve seen anyone actually say that someone had CAUSED their own illness, we simply can’t keep ignoring the research. What’s the point of raising millions of dollars, bringing about IBD awareness and spending countless, sleepless nights trying to support the community if we’re all just going to get upset and ignore the data?
I find it shocking, to say the least, that such a denial of the evidence exists, but I hope that by continuing to show what the current research tells us, we can spare future generations the suffering and devastation caused by Crohn’s disease and Ulcerative Colitis.
Without sounding like a broken record, I have to point out that these are POTENTIAL RISK FACTORS, not sole causes, not 100% guarantees, not the silver bullet we’re searching for. Some of these risk factors, as you’ll later see, are things we have control over.
And while many of us tend to think that our genetics guarantee that we will eventually get IBD in our lifetime, the World Health Organization suggests that environmental risks play a role in over 80% of reported diseases [SOURCE] (including non-IBD), which indicates that even “bad genes” are likely being triggered by something we have control over.
This point is crucial to understand because it means that we don’t have to concede to illness or give up because “it runs in the family”. There’s also evidence to suggest that immigrant populations that had low rates of IBD seemed to increase their rates when they move to countries with higher rates (i.e. Canada), which further supports the idea of environmental triggers [SOURCE].
If you’re new to reading statistics, here’s a quick explanation on how the odds ratio works: Epidemiology – Odds Ratio (OR)
Let’s start by defining what “environmental risk factor” means. An environmental risk factor is something outside our body that has an influence on our health. The air we breathe, the water we drink, the chemicals we put on our skin, our exposure to infectious disease, UV radiation, and food quality are some examples of environmental factors which can impact our health (both positively and negatively).
Many of these environmental risk factors also overlap with behavioral risk factors. Smoking, for example, is something we can choose to do (behavioral), but it’s an environmental factor (breathing chemicals) as well.
For IBD, researchers have identified several environmental risk factors which can also be modified through behavior.
While avoiding these risk factors will not guarantee that you’ll be immune to IBD, they are things to consider if you want to minimize your risks.
Here are a handful of studies, which cover a range of factors which have been implicated in IBD. It’s interesting to note that some factors which seem to affect Crohn’s disease don’t necessarily affect Ulcerative Colitis (and vice versa). There’s speculation about why this happens, but the research is still ongoing.
Tobacco use is widely known as one of the leading causes of death and disease. It’s been implicated in everything from heart disease to cancer to stroke, yet 1/5th of the US population smokes [SOURCE].
I was a heavy smoker in my teens and early 20s (up to a pack a day of non-filtered cigarettes), so it’s possible that my prior habit was a contributing factor to my own Crohn’s disease.
Of course, I may never know for sure, but it’s important to know what the risks are in relation to IBD. Now the research on smoking and IBD is quite fascinating; we may view Crohn’s and Ulcerative Colitis as similar illnesses, but as we can see in the following studies, smoking affects them very differently.
In this meta-analysis (pooling a number of studies in order to combine the data with the hopes of finding a pattern), we can see some pretty strange results:
“We found evidence of an association between current smoking and CD (OR, 1.76; 95% confidence interval [CI], 1.40-2.22) and former smoking and UC (OR, 1.79; 95% CI, 1.37-2.34). Current smoking had a protective effect on the development of UC when compared with controls (OR, 0.58; 95% CI, 0.45-0.75).” [SOURCE]
A protective effect against Ulcerative Colitis? What? Pretty wild, but that’s what researchers have found over and over again.
“Cigarette smoking is protective against developing UC at any age, but is not associated with the development of CD in Korean population. Former smoking is not the high risk factor in developing UC.” [SOURCE]
“Smoking was more frequent in male patients and was associated with an increased risk of CD (odds ratio, 1.96; 95% confidence interval, 1.63-2.37; P < 0.001). In contrast, current smoking was protective against UC (odds ratio, 0.33; 95% confidence interval, 0.27-0.41).” [SOURCE]
There are researchers who are trying to find out why this contradiction occurs, and I’ve come across THIS and THIS if you’re interested in digging deeper into those theories. Nobody is suggesting that you take up smoking if you want to prevent Ulcerative Colitis since it increases the risks of other diseases quite significantly, but knowing these risk factors are important, especially when second-hand smoke can be a potential trigger for IBD in children:
” Passive smoking exposure at birth was significantly associated with the development of IBD (odds ratio 3.02, 95% confidence interval 1.28-7.06). The effect was greater in Crohn’s disease (odds ratio 5.32) than in ulcerative colitis (odds ratio 2.19). Maternal smoking at birth also was significantly associated with the development of IBD (odds ratio 2.09, 95% confidence interval 1.02-4.29), an effect that also was greater in Crohn’s disease than in ulcerative colitis. There was a dose-response relationship between packs smoked per day and IBD, and packs smoked at home per day and IBD. ” [SOURCE]
Arguably one of the greatest medical advances in the past 50 years has been the discovery of antibiotics. Unfortunately, it’s use (overuse) has also been the source of drug-resistant bacteria and has been implicated as a possible risk factor for IBD.
In this study, published in 2004, it was found that:
“…a statistically significant association between Crohn’s disease and prior antibiotic use [was found]. This cannot be explained by recall bias, but due to lack of specificity it is unclear whether it is causal.” [SOURCE]
Another study, which focuses on kids with IBD, the authors wrote in their conclusion that:
“Antibiotic use is common in childhood and its potential as an environmental risk factor for IBD warrants scrutiny. This is the first prospective study to show a strong association between antibiotic use and CD in childhood. However, as with any observational study, causality cannot be inferred from our results and confounding by indication—in particular, prescribing of antibiotics to children with intestinal symptoms of as yet undiagnosed CD—should also be considered as a possible explanation.” [SOURCE]
Yet another study, which focused on pediatric IBD wrote:
“Subjects diagnosed with IBD in childhood are more likely to have used antibiotics in their first year of life.” [SOURCE]
You’ll notice that the first two studies acknowledge that it’s difficult to conclude a causal association, but knowing that a risk is there means that we should ask our doctor’s if any antibiotic they prescribe is absolutely necessary before taking it. Sometimes we may be prescribed antibiotics as a precaution, rather than necessity, although I believe this practice is quickly coming to an end as the overuse of antibiotics has been in the spotlight over the years.
In this meta-analysis, published in 2008, it was concluded that:
“This study provides evidence of an association between the use of oral contraceptive agents and development of IBD, in particular CD. The study also suggests that the risk for patients who stop using the OCP reverts to that of the nonexposed population.” [SOURCE]
And here’s a 2013 study which includes two, large prospective cohort’s (follows a group of people over a period of time to see if any patterns are found) over a span of over 30 years and also found that:
“… oral contraceptive use was associated with risk of CD.” [SOURCE]
So it seems that oral contraceptive use has an influence on Crohn’s disease rates. I find it interesting that in the first study, it was found that discontinuing the use of oral birth control brought the risks down to the same level as seen in women who never took them. Considering there are many other options for birth control, this is a risk that women don’t have to expose themselves to.
As I already covered in my previous post Diet and IBD: What the research says, there are several dietary links to IBD. Along with the dietary factors which increase risks, there are numerous which cut risks too. As a benefit, these specific dietary patterns have also been found to reduce the risk of other illnesses too.
Fiber, which tends to be an enemy for anyone with active IBD, is protective against Crohn’s Disease and cancers of the colon. One interesting find is that the type of fiber makes all the difference.
“Compared with the lowest quintile of energy-adjusted cumulative average intake of dietary fiber, intake of the highest quintile (median of 24.3 g/day) was associated with a 40% reduction in risk of CD (multivariate HR for CD, 0.59; 95% confidence interval, 0.39-0.90). This apparent reduction appeared to be greatest for fiber derived from fruits; fiber from cereals, whole grains, or legumes did not modify risk. In contrast, neither total intake of dietary fiber (multivariate HR, 0.82; 95% confidence interval, 0.58-1.17) nor intake of fiber from specific sources appeared to be significantly associated with risk of UC.” [SOURCE]
Wow. There’re a couple of things I’d like to point out. First, it seems like that risk reduction for Crohn’s disease seemed to only be related to fiber coming from fruit. UC didn’t benefit from the fiber, but as colon cancer risks are high in those with UC [SOURCE] compared with the general population, eating fiber should be a long-term, preventative strategy that can begin during childhood.
I’d also like to point out that the highest quintile group had a median fiber intake of only 24.3g/day. I say “only”, because plant-based diets can offer an abundance of fiber-rich foods; I often top 40g/day without even trying, and that’s with an ileostomy too. If 24.3g/day was able to reduce risks by 40%, it would have been very interesting to see what 40 or 50g/day would get.
For reference sake, the Dietitians of Canada recommend between 25-38g per day (most Canadians get 14g on average), so even the highest quintile group was below the recommended minimum.
So while fiber doesn’t reduce the risk of UC, what does? Vegetables! While none of the studies in this meta-analysis found a statistically significant reduction in UC risk, they still found that high vegetable consumption reduced the risk of UC overall. I do want to point out that, like the previous note on fiber, “high” consumption may not actually mean adequate consumption or ideal consumption.
In some studies eating fruit or veg four times a day would be considered “high”, despite the calls for a minimum of 9+ servings per day.
If you haven’t seen my Food Gallery, then you might not realize how easy it is to get all those plants on your plate.
Vitamin D, while not strictly obtained through diet alone, has been the source of much research. While we haven’t uncovered the full benefits of this amazing vitamin (actually, it’s a hormone), there’s evidence to suggest that having low vitamin D levels can increase your risks of developing IBD. This could explain why cases of IBD are more prominent in the northern hemisphere, where access to adequate UV from the sun is often impossible all-year-round.
In this study, Vitamin D levels obtained through a 25-hydroxy vitamin D score were used to predict Crohn’s disease. The authors concluded that:
“Higher predicted plasma levels of 25(OH)D significantly reduce the risk for incident CD and nonsignificantly reduce the risk for UC in women.” [SOURCE]
Not only do adequate vitamin D levels help to reduce IBD, but it also reduces the risk of surgery and hospitalizations for those who already have it. [SOURCE]
As with most of the other environmental risk factors, diet is one that we have complete control over and making changes to optimize our diets should be a priority.
Non-steroidal anti-inflammatory drugs (NSAID’s)
Aspirin, Advil, Motrin, Aleve. Chances are, you’ve heard of at least one of those brands of popular NSAID’s, you might have taken them at some point for pain caused by inflammation, but did you know that they are also a risk factor in the development of IBD? The FDA has already stated that NSAID’s come with an increased risk of “serious adverse cardiovascular events”, so there are now warnings included in all drug packaging. And some of these drugs, like Vioxx, have already been pulled from the market.
These same drugs also harm our stomach lining, which can cause ulcers to form. In studies specific to IBD, there seems to be a consensus that NSAID’s should be avoided in those with Crohn’s or Ulcerative Colitis. This can obviously make pain management more challenging, but your doctor has other options at their disposal.
This study, which goes all the way back to 1988 found that:
“Subjects taking NSAID medications appear to be five times more likely to develop colonic inflammation than the general population.” [SOURCE]
A more recent study, published in 2011 found that regular aspirin use was strongly associated with Crohn’s disease, but not UC. Stating that “Our main findings were: over a six times greater risk of developing CD in those taking regular aspirin, but none for UC.” [SOURCE]
Aspirin, however, was not found to be associated with either Crohn’s or UC in the study “Aspirin, Nonsteroidal Anti-inflammatory Drug Use, and Risk for Crohn Disease Ulcerative Colitis”, for which the researchers went on to explain that:
“Although aspirin and NSAIDs share the potential for gastrointestinal toxicity, aspirin was notably not associated with CD or UC in our study. There are a few potential explanations for this finding. There are established differences in the action of aspirin and NSAIDs on the COX isoenzymes.” [SOURCE]
While this blog post is aimed at the risks which have been known to cause IBD, it should be noted that the use of NSAID’s while in remission, may also cause a relapse. It’s best to discuss their use with your GI before taking them.
If you’re still interested in reading more about the environmental risk factors or triggers for IBD, I invite you to read up on the latest research (I like PubMed). Below, you will find more in-depth analysis of the current research.
This 2013 publication from the journal Gastroenterology & Hepatology, aptly titled “Environmental Risk Factors for Inflammatory Bowel Disease” [SOURCE] reviews the data researchers have found in relation to IBD and environmental risk factors.
I really like the diagram in this 2013 clinical review, which gives a nice overview of the many risk factors suspected for IBD. [SOURCE]
Here’s a European study which aims to investigate the changes in IBD rates by exploring environmental factors. [SOURCE]
One of the more fascinating studies I’ve come across deals with twins. It’s pretty obvious after reading it that environmental risk factors likely have more to do with IBD than straight up genetics since you can see that:
“Comparing diseased and non-diseased twins regarding their alimentary habits, high consumption of sausages and other processed meat, red meat, nuts, soft drink and antibiotic use showed significant increases in several twin groups. This effect was also observed in some of the non-twin IBD controls. These data suggest that dietary ingredients and antibiotics, potentially directly or via an alteration of the gut microbiota, may contribute to the pathogenesis of IBD. ” [SOURCE]
This study is interesting as it includes factors such as breast feeding and contact with animals as part of their risk model. It even concluded that:
“CD and UC associated with infrequent childhood sports activities and short breastfeeding. Furthermore, CD associated with smoking and infrequent contact with animals in childhood. UC associated with a smaller family size in childhood.”[SOURCE]
If you’re still reading this, thank you! Hopefully, I haven’t bored you with this information. Since my diagnosis in 2008, I made myself a promise to always be informed about Crohn’s disease and where the research is taking us.
- Preventing disease through healthy environments: Towards an estimate of the environmental burden of disease
- Foster A, Jacobson K. Changing Incidence of Inflammatory Bowel Disease: Environmental Influences and Lessons Learnt from the South Asian Population. Front Pediatr. 2013 Nov 6;1:34. eCollection 2013. Review. PubMed PMID: 24400280; PubMed Central PMCID: PMC3864265.
- [Environmental Risk Factors for Inflammatory Bowel Disease], Ashwin N. Ananthakrishnan
- Gastroenterol Hepatol (N Y) 2013 June; 9(6): 367–374. PMCID: PMC3736793
- Smoking & Tobacco Use FACT SHEET – CDC
- Mahid SS, Minor KS, Soto RE, Hornung CA, Galandiuk S. Smoking and inflammatory bowel disease: a meta-analysis. Mayo Clin Proc. 2006 Nov;81(11):1462-71. Erratum in: Mayo Clin Proc. 2007 Jul;82(7):890. PubMed PMID: 17120402.
- Jang JY, Kim HJ, Jung JH, Chae MJ, Kim NH, Lee SK, Joo KR, Dong SH, Kim BH, Chang YW, Lee JI, Chang R. [The role of smoking as a risk factor in inflammatory bowel diseases: single center study in Korea]. Korean J Gastroenterol. 2006 Mar;47(3):198-204. Korean. PubMed PMID: 16554673.
- Lakatos PL, Vegh Z, Lovasz BD, David G, Pandur T, Erdelyi Z, Szita I, Mester G, Balogh M, Szipocs I, Molnar C, Komaromi E, Golovics PA, Mandel M, Horvath A, Szathmari M, Kiss LS, Lakatos L. Is current smoking still an important environmental factor in inflammatory bowel diseases? Results from a population-based incident cohort. Inflamm Bowel Dis. 2013 Apr;19(5):1010-7. doi: 10.1097/MIB.0b013e3182802b3e. PubMed PMID: 23399739.
- Ueno A, Jijon H, Traves S, Chan R, Ford K, Beck PL, Iacucci M, Fort Gasia M, Barkema HW, Panaccione R, Kaplan GG, Proud D, Ghosh S. Opposing effects of smoking in ulcerative colitis and Crohn’s disease may be explained by differential effects on dendritic cells. Inflamm Bowel Dis. 2014 May;20(5):800-10. doi: 10.1097/MIB.0000000000000018. PubMed PMID: 24691114.
- Bergeron V, Grondin V, Rajca S, Maubert MA, Pigneur B, Thomas G, Trugnan G, Beaugerie L, Cosnes J, Masliah J, Sokol H, Seksik P, Bachelet M. Current smoking differentially affects blood mononuclear cells from patients with Crohn’s disease and ulcerative colitis: relevance to its adverse role in the disease. Inflamm Bowel Dis. 2012 Jun;18(6):1101-11. doi: 10.1002/ibd.21889. Epub 2011 Oct 10. PubMed PMID: 21987436.
- Lashner BA, Shaheen NJ, Hanauer SB, Kirschner BS. Passive smoking is associated with an increased risk of developing inflammatory bowel disease in children. Am J Gastroenterol. 1993 Mar;88(3):356-9. PubMed PMID: 8438840.
- Card T, Logan RF, Rodrigues LC, Wheeler JG. Antibiotic use and the development of Crohn’s disease. Gut. 2004 Feb;53(2):246-50. PubMed PMID: 14724158; PubMed Central PMCID: PMC1774910.
- Hviid A, Svanström H, Frisch M. Antibiotic use and inflammatory bowel diseases in childhood. Gut. 2011 Jan;60(1):49-54. doi: 10.1136/gut.2010.219683. Epub 2010 Oct 21. PubMed PMID: 20966024.
- Shaw SY, Blanchard JF, Bernstein CN. Association between the use of antibiotics in the first year of life and pediatric inflammatory bowel disease. Am J Gastroenterol. 2010 Dec;105(12):2687-92. doi: 10.1038/ajg.2010.398. Epub 2010 Oct 12. PubMed PMID: 20940708.
- Antimicrobial Resistance – Factsheet from the World Health Organization
- J.A Cornish, E Tan, C Simillis, S K Clark, J Teare and Paris P Tekkis [The Risk of Oral Contraceptives in the Etiology of Inflammatory Bowel Disease: A Meta-Analysis], The American Journal of Gastroenterology 103, 2394-2400 (September 2008) | doi:10.1111/j.1572-0241.2008.02064.x
- Khalili H, Higuchi LM, Ananthakrishnan AN, Richter JM, Feskanich D, Fuchs CS, Chan AT. Oral contraceptives, reproductive factors and risk of inflammatory bowel disease. Gut. 2013 Aug;62(8):1153-9. doi: 10.1136/gutjnl-2012-302362. Epub 2012 May 22. PubMed PMID: 22619368; PubMed Central PMCID: PMC3465475.
- Information for Healthcare Professionals: Non-Selective Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)
- Tanner AR, Raghunath AS. Colonic inflammation and nonsteroidal anti-inflammatory drug administration. An assessment of the frequency of the problem. Digestion. 1988;41(2):116-20. PubMed PMID: 3265394.
- Chan SS, Luben R, Bergmann MM, Boeing H, Olsen A, Tjonneland A, Overvad K, Kaaks R, Kennedy H, Khaw KT, Riboli E, Hart AR. Aspirin in the aetiology of Crohn’s disease and ulcerative colitis: a European prospective cohort study. Aliment Pharmacol Ther. 2011 Sep;34(6):649-55. doi: 10.1111/j.1365-2036.2011.04784.x. Epub 2011 Jul 26. PubMed PMID: 21790683.
- Ananthakrishnan AN, Higuchi LM, Huang ES, Khalili H, Richter JM, Fuchs CS, Chan AT. Aspirin, nonsteroidal anti-inflammatory drug use, and risk for Crohn disease and ulcerative colitis: a cohort study. Ann Intern Med. 2012 Mar 6;156(5):350-9. doi: 10.7326/0003-4819-156-5-201203060-00007. PubMed PMID: 22393130; PubMed Central PMCID: PMC3369539.
- Ananthakrishnan AN, Khalili H, Konijeti GG, Higuchi LM, de Silva P, Korzenik JR, Fuchs CS, Willett WC, Richter JM, Chan AT. A prospective study of long-term intake of dietary fiber and risk of Crohn’s disease and ulcerative colitis. Gastroenterology. 2013 Nov;145(5):970-7. doi: 10.1053/j.gastro.2013.07.050. Epub 2013 Aug 2. PubMed PMID: 23912083; PubMed Central PMCID: PMC3805714.
- Lukas M. Inflammatory bowel disease as a risk factor for colorectal cancer. Dig Dis. 2010;28(4-5):619-24. doi: 10.1159/000320276. Epub 2010 Nov 18. PubMed PMID: 21088413.
- Ananthakrishnan AN, Khalili H, Higuchi LM, Bao Y, Korzenik JR, Giovannucci EL, Richter JM, Fuchs CS, Chan AT. Higher predicted vitamin D status is associated with reduced risk of Crohn’s disease. Gastroenterology. 2012 Mar;142(3):482-9. doi: 10.1053/j.gastro.2011.11.040. Epub 2011 Dec 9. PubMed PMID: 22155183; PubMed Central PMCID: PMC3367959.
- Ananthakrishnan AN, Cagan A, Gainer VS, Cai T, Cheng SC, Savova G, Chen P, Szolovits P, Xia Z, De Jager PL, Shaw SY, Churchill S, Karlson EW, Kohane I, Plenge RM, Murphy SN, Liao KP. Normalization of plasma 25-hydroxy vitamin D is associated with reduced risk of surgery in Crohn’s disease. Inflamm Bowel Dis. 2013 Aug;19(9):1921-7. doi: 10.1097/MIB.0b013e3182902ad9. PubMed PMID: 23751398; PubMed Central PMCID: PMC3720838.
- Ponder A, Long MD. A clinical review of recent findings in the epidemiology of inflammatory bowel disease. Clin Epidemiol. 2013 Jul 25;5:237-47. doi: 10.2147/CLEP.S33961. Print 2013. PubMed PMID: 23922506; PubMed Central PMCID: PMC3728155.
- Burisch J, Pedersen N, Cukovic-Cavka S, Turk N, Kaimakliotis I, Duricova D, Bortlik M, Shonová O, Vind I, Avnstrøm S, Thorsgaard N, Krabbe S, Andersen V, Dahlerup JF, Kjeldsen J, Salupere R, Olsen J, Nielsen KR, Manninen P, Collin P, Katsanos KH, Tsianos EV, Ladefoged K, Lakatos L, Ragnarsson G, Björnsson E, Bailey Y, O’Morain C, Schwartz D, Odes S, Giannotta M, Girardin G, Kiudelis G, Kupcinskas L, Turcan S, Barros L, Magro F, Lazar D, Goldis A, Nikulina I, Belousova E, Martinez-Ares D, Hernandez V, Almer S, Zhulina Y, Halfvarson J, Arebi N, Tsai HH, Sebastian S, Lakatos PL, Langholz E, Munkholm P; EpiCom-group. Environmental factors in a population-based inception cohort of inflammatory bowel disease patients in Europe – An ECCO-EpiCom study. J Crohns Colitis. 2014 Jul 1;8(7):607-16. doi: 10.1016/j.crohns.2013.11.021. Epub 2013 Dec 7. PubMed PMID: 24315795.
- Hlavaty T, Toth J, Koller T, Krajcovicova A, Oravcova S, Zelinkova Z, Huorka M. Smoking, breastfeeding, physical inactivity, contact with animals, and size of the family influence the risk of inflammatory bowel disease: A Slovak case-control study. United European Gastroenterol J. 2013 Apr;1(2):109-19. doi: 10.1177/2050640613478011. PubMed PMID: 24917948; PubMed Central PMCID: PMC4040732.
- Spehlmann ME, Begun AZ, Saroglou E, Hinrichs F, Tiemann U, Raedler A, Schreiber S. Risk factors in German twins with inflammatory bowel disease: results of a questionnaire-based survey. J Crohns Colitis. 2012 Feb;6(1):29-42. doi: 10.1016/j.crohns.2011.06.007. PubMed PMID: 22261525.