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cancer risk factors

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Incorporating genetic and environmental risk factors in to risk prediction for colorectal cancer


Cancer Epidemiology HomeFrom: Incorporating non-genetic risk factors and behavioural modifications into risk prediction models for colorectal cancer

Yarnall, Crouch & Lewis (Division of Genetics and Molecular Medicine, King’s College London, United Kingdom.). Cancer Epidemiology 2013 Jan 29

Abstract

Background: Epidemiological studies have identified potentially modifiable risks for colorectal cancer, including alcohol intake, diet and a sedentary lifestyle. Modelling these environmental factors alongside genetic risk is critical in obtaining accurate estimates of disease risk and improving our understanding of behavioural modifications. Methods: 14 independent single nucleotide polymorphisms identified though GWAS studies and reported on by the international consortium COGENT were used to model genetic disease risk at a population level. Six well validated environmental risks were selected for modelling together with the genetic risk factors (alcohol intake; smoking; exercise levels; BMI; fibre intake and consumption of red and processed meat). Through a simulation study using risk modelling software, we assessed the potential impact of behavioural modifications on disease risk. Results: Modelling the genetic data alone leads to 24% of the population being classified as reduced risk; 60% average risk; 10% elevated risk and 6% high risk for colorectal cancer. Adding alcohol consumption to the model reduced the elevated and high risk categories to 9% and 5% respectively. The simulation study suggests that a substantial proportion of individuals could reduce their disease risk profile by altering their behaviour, including reclassification of over 62% of heavy drinkers. Conclusion: Modelling lifestyle factors alongside genetic risk can provide useful strategies to select individuals for screening for colorectal cancer risk. Impact: Quantifying the impact of moderating behaviour, particularly related to alcohol intake and obesity levels, is beneficial for informing health campaigns and tailoring prevention strategies.

Risk factors

Low risk (Green), average risk (blue), moderate risk (yellow) and high risk (red)using combined genetic and environmental risk factors

Discussion

Over the last 30 years the lifetime risk of colorectal cancer (CRC) for men has almost doubled, from 3.5% to 6.9% in the UK in 2008. For women the increase is more than a quarter, rising from 3.9% to 5.4%.  Since both genetic and environmental factors contribute to the susceptibility to colorectal cancer, this trend may be due to a change in the dietary and lifestyle factors of the general population leading to higher levels of obesity and more sedentary pastimes.

The major risk factor for colorectal cancer is age and over 85% of colorectal cancer occurs in people over the age of 60.  Other risk factors include the presence of polyps and people having an Ashkenazi Jewish genetic heritage. The use of non-steroidal anti-inflammatory drugs (NSAIDs), hormone replacement therapy and aspirin use have also been associated with disease risk. However, it is estimated that between 52 and 57% of colorectal cancers are associated with lifestyle and environmental factors.  Many risk factors for colorectal cancer may be modified by intervention, ranging from known risks, such as increased risk from a sedentary lifestyle and dietary changes. The evidence for dietary factors indicates possible increased risk from diets low in fibre, garlic, calcium, fruit, vegetables and fish and high in red and processed meat. In addition to alcohol, BMI, smoking and exercise, we chose to model the most consistent and well validated dietary findings, which suggest that low levels of fibre and high levels of red and processed meat are both significant risk factors.

The international consortium COGENT (COlorectal cancer GENeTics) have identified many of the known genetic variants that predispose to CRC with the 14 single nucleotide polymorphisms (SNPs) found to be convincingly associated with CRC risk from GWA studies summarized in Houlston et al.’s recent update.  Of these 14 SNPs, the mean odds ratio per allele is 1.14, with the highest odds ratio reported for SNP rs16892766 near the EIF3H gene (OR 1.28).

The identification of SNPs that contribute to susceptibility for CRC has raised the prospect of genetic screening. Companies such as DeCODEme and 24andme include panels of SNPs for CRC in their genetic testing panels, yet research suggests that the genetic risk prediction alone is of questionable utility.  In this research study, we combined the known genetic risk with data on the environmental risks for CRC, enabling more complete risk prediction. We applied a statistical risk model and to determine the impact of modelling environmental factors alongside the 14 genetic susceptibility loci identified by the COGENT consortium.

Early screening for colorectal cancer can be extremely helpful in identifying individuals with polyps and nonpolypoid lesions and preventing the development of cancer. Regular faecal occult blood tests (FOBT) in the over 50 s for example have been found to reduce the number of deaths due to CRC by 15–33%.  In the UK, screening is offered to all men and women aged between 60 and 69 at a cost of £77.3 million and this will be extended to 74 year olds. However, it has been suggested that if individuals are provided with a personalized disease risk assessment from their combined genetic and environmental profile, they are likely to be more motivated to alter their lifestyle as a preventative measure, which would increase the effectiveness of health campaigns. In this study we develop predictions of CRC risk in different sub populations and assess the impact of modifying lifestyle factors on risk levels. By providing predictions of disease risk both before and after a lifestyle change for a given genetic profile, the study illustrates the potential benefits for both selection of candidates for screening programmes and the tailored promotion of healthier lifestyle choices, in high risk groups.

There are several modifiable risk factors for colorectal cancer and building predictive models encompassing both genetic and environmental factors enables us to move in the direction of a complete assessment of disease risk. This paper describes a predictive model which takes account of the known genetic contribution as well as the modifiable risks. There is considerable evidence to suggest that detecting polyps in the early stages can reduce mortality rates for colorectal cancer and whilst the interactions between the genetic and environmental elements are undeniably complex, separating out the inherited risk from the lifestyle factors using this model helps to illustrate the potential gains from modifying lifestyle behaviour and could usefully inform healthy lifestyle campaigns.

Our findings indicate that that cessation of alcohol consumption and reducing obesity levels lead to the most significant changes to the proportion of the population reducing their disease risk category. Whilst this could have been predicted to some extent by the higher odds ratios for these factors, it is the combination of relative risk, together with the prevalence of the factor within the population that determines the overall impact. In addition, being able to create personalized risk predictions in this way, has the potential to motivate greater behavioural change, showing for example, that it is possible to significantly reduce disease risk by moving from a high risk category to an average risk category though increasing fibre levels; cessation of alcohol consumption or weight management, given a particular genetic profile. Further research is required to increase understanding of how individuals respond to risk assessment based on genetic information.  This may increases their motivation since the results are personal, or decrease their motivation because they consider that their genetic risk cannot be modified.

Our focus has been on risk categorization, and not on the absolute level of risk estimated from the combination of genetic and environmental risk factors, which is modest for most categories. There are two advantages to this strategy. Firstly it moves away from the strategy used, for example, by direct-to-consumer genetic testing companies such as 23andme and deCODEme (who provide a single figure of risk with no confidence intervals) towards the strategy deployed in genetic counselling of using a qualitative risk level, which can be more easily interpreted for the purpose of risk prediction. Secondly, it puts a stronger statistical framework on the risk model: an assignment to elevated risk implies that the risk is statistically distinct from the risk of the average, baseline, individual, given the uncertainty of the parameters used in the model.

There are several limitations of the model. Firstly, the model is built from estimates in the literature extracted from different studies. This enables researchers to select the best study to capture information on each risk factor, but assumes that information is directly comparable between studies. This limits the precision with which risk estimates can be calculated. A further limitation is that the model assumes all risk factors entered are independent. For known gene and environment interactions, this can be overcome by either modelling the interaction explicitly as an environmental risk factor, or by omitting known genetic loci to prevent over-representation of a risk factor (such as SNPs on the FTO gene which are associated with BMI). Within the genetic component, linkage disequilibrium between SNPs can be tested to confirm no correlation at a population level; few interactions of risk between genetic loci have been identified, so the assumption of independence should not be a major problem. For the environmental component, assumptions of independence are more difficult to assess. Lack of independence may lead to inaccuracies in the population frequencies estimated, but the contribution of environmental factors to the model is based on relative risks that are estimated in the presence of relevant covariates, so levels of risk should not be inflated. Increasing our understanding of the association between lifestyle factors, as well as between genes and the environment, will be important in obtaining more accurate assessments of risk. In addition, the accuracy could be further improved by more specific modelling of the population being targeted. Applying data with relative risks by sex, by population group, or for individuals with a first degree relative with CRC for example, would provide more accurate estimations of disease risk specific to those populations.

Colorectal cancer screening programmes are widespread, but are age-targeted and look for signs of cancer in early development. In contrast, the methods described here can be used to target lifestyle factors, and are relevant for younger age-groups. The approach could encourage behavioural changes and help to reduce CRC rates. Although the model indicates that certain individuals can reduce their CRC risk by changing their behaviour, the time taken for changes in environmental risk factors to have an effect on risk is unknown, and will differ by factor. Additional research is needed to further elucidate the genetic and environmental contributions to disease risk and to measure the longer term impact of behavioural change on disease outcomes.

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Using food as medicine: The fibre challenge from Channel 4’s food hospital


 

The Fibre Challenge


If there’s one thing most of us don’t like talking about, it’s our bowel movements. However, your stools (that’s poo to you and me) can be a clear indicator of how healthy your insides are, particularly problems with your digestive system. Many of us are too embarrassed to talk about discomfort of going to the toilet. But even short-term problems can indicate longer-term health risks that can go undiagnosed if you don’t do anything about them.
The Food Hospital Fibre Challenge aims to tackle the toilet taboo and encourage people to make simple changes in their diet that could have significant benefits to their bowel and overall health.
Find out more about our approach.

Fresh vegetables are important components of a...

Fresh vegetables are important components of a healthy diet. (Photo credit: Wikipedia)

Take the Fibre Challenge

The Fibre Challenge has been devised by specialist dietitians and is a mass participation initiative to assess the effect of fibre on the nation’s bowel health. For 21 days, you’ll eat extra dietary fibre and send information about your bowel movements (anonymously) to our expert team for analysis. The results will help us to better understand whether a high fibre diet significantly improves short-term bowel health and general well-being. There are some people who shouldn’t take part for health reasons, but the rest of you can download the app, check out the assortment of fibre foods to add to your diet, print-out our stool chart and monitor the effects of eating extra fibre over the next few weeks. Find out more about the challenge.

http://foodhospital.channel4.com/fibre-challenge

 

Study to test spice curcumin’s ability to fight bowel cancer


Cancer Research UK

Cancer Research UK (Photo credit: Wikipedia)

A UK trial is investigating whether a curry ingredient can improve the treatment of patients with advanced bowel cancer.

Scientists will supplement standard chemotherapy with pills containing curcumin, a compound found in the yellow curry spice turmeric.

Laboratory tests have suggested that curcumin can boost the ability of chemotherapy drugs to kill bowel cancer cells. The compound is known to have powerful anti-inflammatory properties and also acts as an antioxidant.

Turmeric powder 薑黃粉

Turmeric powder 薑黃粉 (Photo credit: Wikipedia)

Some studies have indicated it may slow the spread of cancer, improve the effectiveness of chemotherapy and protect healthy cells from the effects of radiotherapy. However, hard evidence from properly conducted scientific trials is lacking.

The two-year trial, by scientists from Cancer Research UK and the University of Leicester, aims to recruit about 40 patients with bowel cancer that has spread to the liver.

Trial leader Professor William Steward, director of the Experimental Cancer Medicine Centre at the University of Leicester, said: “The prospect that curcumin might increase the sensitivity of cancer cells to chemotherapy is exciting because it could mean giving lower doses, so patients have fewer side-effects and can keep having treatment for longer.”

Read more here

http://scienceblog.cancerresearchuk.org/2012/05/07/new-trial-to-test-spice-extract-curcumin-against-bowel-cancer/

Lifestyle and Reducing Your Risk of Bowel Cancer


Lifestyle Risk factors – how to reduce your risk of bowel cancer?

Risk factors other than family history can play a more important role in the development of bowel cancer.  The main risk factor for bowel cancer is increasing age. Only 7% of bowel cancer occurs before the age of 50 years.  However, even if you have a family history or other genetic risk of bowel cancer, this risk can be reduced by leading a healthy lifestyle.   This kind of healthy lifestyle can also reduce your risk of heart disease, stroke and other cancers.  It has been recently estimated that approximately 70% of colorectal cancer could be avoided by changes in lifestyle in Western countries.

A good further source of information about dietary and other lifestyle related risk factors is available from Cancer Research UK at http://www.cancerresearchuk.org/cancer-info/cancerstats/types/bowel/riskfactors/bowel-cancer-risk-factors

Diet 

Summary: A diet high in red meat and animal fat and low in fruit and vegetables increases your risk of bowel cancer.  So if you want to reduce your risk of bowel cancer, whether or not you have a genetic risk, eat 5 pieces of fruit or vegetables daily, plenty of fibre, and don’t eat too much processed or red meat.

Dietary Fibre

Putative anti-carcinogenic mechanisms of dietary fibre within the bowel include: the formation of short-chain fatty acids from fermentation by colonic bacteria; the reduction of secondary bile acid production; the reduction in intestinal transit time and increase of faecal bulk; and a reduction in insulin resistance. In the European Prospective Investigation into Cancer and Nutrition (EPIC) study after an average 6.2 years of follow-up, and 1,721 colorectal cancer cases, a 21% reduced risk amongst participants in the highest intake quintile was observed when compared against the lowest intake group. These results support our previous conclusion, of the potential of reducing colorectal cancer incidence by increasing fibre intake from cereal, fruit, and vegetable food sources.

Figure 5.2: The number of portions of fruit and vegetables eaten per day by adults aged 16 and over, England, 2009
Red and processed meat

In the EPIC study high intake of red or processed meat may increase risk by 71%.  The mechanisms underlying the association between colorectal cancer risk and high intake of red and processed meat are uncertain. Controlled human intervention studies have raised the possibility that the endogenous nitrosation that arises from ingestion of heme iron but not of inorganic iron or protein may account for the increased risk associated with red and processed meat consumption.  Heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAH) in diet may pose a potential risk of cancer to humans, depending on the extent to which the compounds are activated in vivo by metabolic enzymes. HCAs are formed as a byproduct of reactions during the cooking of meat, poultry, and fish at high temperatures, such as pan-frying or grilling with charcoal or on a gas grill; PAHs are formed in grilled and barbecued meat and in cured, processed foods. It has been suggested that processed meat intake has a stronger association with colorectal cancer than red meat intake.

Folate and selenium

Ball-and-stick model of the folic acid molecul...

Ball-and-stick model of the folic acid molecule, a B vitamin and an important compound in cell division. This image shows it as an anion (folate). Colour code (click to show) : Black: Carbon, C : White: Hydrogen, H : Red: Oxygen, O : Blue: Nitrogen, N (Photo credit: Wikipedia)

Folate (a water-soluble B vitamin) appears to protect against bowel cancer, but it remains unclear whether the same level of benefit is derived from dietary folate (from food, particularly fruit and vegetables) and synthetic folate (folic acid supplements).  Selenium can be obtained in food (particularly brazil nuts) and supplements; evidence for its effect on bowel cancer risk is mixed. The WCRF/AICR 2010 Report concluded that “Evidence for foods containing folate… and selenium… is less consistent and no conclusion could be drawn”.

Some experts have proposed that folate plays a dual role in bowel cancer in which moderate dietary intake before development of pre-cancerous adenomas reduces risk of adenoma development, but increased folate intake once adenomas have developed increases risk of cancer. Data from interventional studies indicate that folate supplementation decreases colonic mucosal cell proliferation .  A large prospective study showing a 31% reduction in bowel cancer risk for people with the highest overall folate intake 12-16 years before diagnosis, but no effect of intakes in the more recent past.

The US Government was sufficiently convinced of the health benefits (and absence of risk) from folic acid that it introduced mandatory folic acid fortification of grain products in 1997, and a recent large cohort study found that 8.5 years on, higher total folate intake (including intake specifically from supplements) was associated with a decreased bowel cancer risk.  There is some evidence that it is better to take folic acid in its natural form rather than as supplements i.e. tablets.

A 2011 meta analysis found men with the highest concentrations of selenium in the blood had 32% lower bowel cancer risk compared with men with the lowest concentrations, but found no association between selenium level and bowel cancer risk in women.3A 2004 pooled analysis found a similar level of risk reduction for both sexes combined.

Body weight and Obesity

Body mass index (BMI) values

Body mass index (BMI) values (Photo credit: Wikipedia)

Obesity is associated with an increased risk of colon cancer, particularly for men. Meta analyses show the risk of colon cancer increases by an estimated 24-30% per 5kg/m2 increase in body mass index (BMI) for men. In comparison to healthy-weight men (BMI less than 25 kg/m2), overweight men (BMI 25-29.9kg/m2) have a 23% higher risk of colon cancer, and obese men (BMI 30kg/m2 or more) have a 53% higher risk. The association is weaker in women, with colon cancer risk increasing by 9-12% per 5kg/m2 BMI increase, and the association proving non-significant in one meta analysis.

Larger waist size has been associated with increases in colon cancer risk in men (33% risk increase per 10cm waist circumference increase) and women (16% risk increase per 10cm waist circumference increase), as has increasing waist-to-hip ratio in both men (43% risk increase per 0.1-unit increase in ratio) and women (20% risk increase per 0.1 unit increase in ratio).

Higher BMI is linked less strongly to higher rectal cancer risk: a 5kg/m2 BMI increase is associated with a 9-12% higher rectal cancer risk for men (obese men have a 27% higher rectal cancer risk than healthy-weight men), but with no effect on rectal cancer risk in women

Regular exercise

Regular physical activity can reduce your risk of bowel cancer, this is clearly shown in many studies.  We would recommend 2-3 30 minute sessions per week of dedicated exercise (rather than more ‘passive’ exercise such as being busy at work!).

The relationship between physical activity and a reduced risk is one of the most consistent findings in epidemiologic literature.

Other risk factors

Not smoking and drinking less than the upper recommended limit of normal (less than 21 units for men and less than 14 units for women) may also be helpful in reducing risk.

 

Halving red meat consumption would slash heart disease and bowel cancer… and cut our carbon footprint!


BMJ

BMJ (Photo credit: Wikipedia)

Cutting back on the amount of red meat people eat would reduce the risk of chronic disease and also slash Britain’s carbon footprint, according to a study published in the BMJ.

Reducing red and processed meat consumption would not only prompt a fall in chronic disease incidence of between three per cent and 12 per cent in the UK, but our carbon footprint would shrink by 28 million tonnes a year, researchers said.

Food and drink account for a third of all greenhouse gas emissions attributable to British consumers, with livestock farming accounting for around half of the proportion, owing to the large quantity of cereals and soy imported for animal feed.

Even when imported foods are taken out of the equation, the Government’s 2050 target for an 80 per cent cut in the UK’s carbon footprint will be ‘unattainable’ without a substantial reduction in greenhouse gas emissions from livestock farming, say the researchers, citing the Committee on Climate Change.

Previously published evidence shows that the risks of coronary heart disease, type 2 diabetes, and bowel cancer rise by 42 per cent, 19 per cent, and 18 per cent respectively, with every additional 50 grams of red and processed meat eaten daily.

The researchers used responses to the 2000-2001 British National Diet and Nutrition Survey to estimate red and processed meat intake across the UK population and published data from life cycle analyses to quantify average greenhouse gas emissions for 45 different food categories.

They then devised a feasible ‘counter-factual’ alternative, based on a doubling of the proportion of survey respondents who said they were vegetarian – to 4.7 per cent of men and 12.3 per cent of women – and the remainder adopting the same diet as those in the bottom fifth of red and processed meat consumption.

Those in the top fifth of consumption ate 2.5 times as much as those in the bottom fifth, the survey responses showed.

Therefore, adopting the diet of those eating the least red and processed meat would mean cutting average consumption from 91g to 53g a day for men, and from 54g to 30g for women.

The calculations showed that this would significantly cut the risk of coronary artery disease, diabetes, and bowel cancer by between three per cent and 12 per cent across the population as a whole.

And this reduction in risk would be more than twice as much as the population averages for those at the top end of consumption who moved to the bottom end.

The expected reduction in greenhouse gas emissions would amount to 0.45 tonnes per person per year, or just short of 28million tonnes of the equivalent of CO2 a year.

The researchers acknowledge that their data, published in the online journal BMJ Open, is a decade old, but the most recent nutrition survey (2008/9) indicates broadly similar and even slightly higher figures for red and processed meat consumption.

Dr Louise Aston, of the Institute of Public Health at the University of Cambridge, said: ‘This indicates that our estimates remain relevant and may even be conservative, highlighting the need for action to prevent further increases in intake in the UK population.’

Se below

Se below (Photo credit: Wikipedia)

She said while it may be harder for people to understand the direct impact that climate change has on them, it is much easier to understand the impact on their health.

Dr Aston added: ‘Health benefits provide near term rewards to individuals for climate friendly changes and may thus “nudge” humanity towards a sustainable future.

‘Dietary recommendations should no longer be based on direct health effects alone.’
Read more: http://www.dailymail.co.uk/health/article-2201458/Halving-red-meat-consumption-slash-heart-disease-bowel-cancer–cut-carbon-footprint.html#ixzz26cZH4CzR

Poor people are at a higher risk of colorectal cancer


 

Journal of the National Cancer Institute

Journal of the National Cancer Institute (Photo credit: Wikipedia)

http://m.jnci.oxfordjournals.org/content/early/2012/09/03/jnci.djs346.abstract

September 5, 2012 — People with a relatively low socioeconomic status account for a disproportionate number of colorectal cancers in the United States. Now, for the first time, a large prospective, observational study has shed light on the degree to which behavior and body mass contribute to this disparity.

Over one third of the excess risk…could be explained by differences in…behavioral risk factors.

“This study showed that over one third of the excess risk of invasive adenocarcinoma of the colon and rectum resulting from low [socioeconomic status] could be explained by differences in…behavioral risk factors, particularly in an unhealthy diet,” conclude the authors, led by Chyke A. Doubeni, MD, MPH, from the Department of Family Medicine and Community Health at the University of Pennsylvania Perelman School of Medicine in Philadelphia.

In addition to diet, Dr. Doubeni and colleagues found that physical inactivity, smoking, and being overweight are likely contributors to this risk.

In their study, published online September 5 in the Journal of the National Cancer Institute, the authors looked at health behaviors, obesity, and colorectal cancer risk among Americans of all socioeconomic statuses.

They used the National Institutes of Health-AARP Diet and Health Study as their data source. Specifically, they looked at middle-aged and elderly people from 6 states (California, Florida, Louisiana, New Jersey, North Carolina, and Pennsylvania) and 2 metropolitan areas (Atlanta, Georgia and Detroit, Michigan). All of the participants enrolled in the study in 1995/96 and were followed through 2006. Health behaviors of the participants were determined using questionnaires.

Of the 506,488 study participants, 7676 developed colorectal cancer during the 10-year follow-up period.

How Class and Behavior/Body Mass Are Related

The authors evaluated the socioeconomic status of the participants in 2 ways: by census-tract data, which revealed “neighborhood socioeconomic status,” and by self-reported educational level (less than high school vs high school and more than high school).

On the basis of data from other studies on colorectal cancer and behavior, Dr. Doubeni and his team used statistical modeling to estimate the likely percentage of colorectal cancers mediated by behavioral risk factors.

They found that differences in socioeconomic status in the reported levels of physical inactivity, unhealthy diet, smoking, and unhealthy weight each explained between 11.3% and 21.6% of the association between education and risk for colorectal cancer, and between 8.6% and 15.3% of the association between neighborhood status and risk for colorectal cancer. Diet was found to have the biggest impact of all the health behaviors.

Overall, the combination of health behaviors and body mass index (BMI) explained approximately 43.9% (95% confidence interval [CI], 35.1% to 57.9%) of the association between risk for colorectal cancer and education and 36.2% (95% CI, 28.0% to 51.2%) of the association between the risk and neighborhood socioeconomic status.

In short, somewhere between one third and nearly one half of colorectal cancers among either low-income or less-than-high-school-educated Americans might be attributable to obesity and unhealthy behaviors.

However, a pair of experts not involved with the study do not find these results to be a cause for despair.

Instead, the study “demonstrates the intricate interplay” of socioeconomic and behavioral factors affecting colorectal cancer risk, write John Z. Ayanian, MD, and John M. Carethers, MD, in an accompanying editorial. Dr. Ayanian is from the Department of Health Care Policy at Harvard Medical School in Boston, Massachusetts, and Dr. Carethers is from the Department of Internal Medicine at the University of Michigan in Ann Arbor.

Public health practitioners can learn from these results, they believe. The study “underscores the need for more effective public health strategies to improve nutrition and physical activity in the United States and thereby curb the rising tide of obesity, particularly for those with less education and in disadvantaged communities,” the editorialists write.

Colon Cancer by Location

The study accounted for the anatomic location of the participants’ cancers (proximal colon, distal colon, or rectum), which resulted in one of the study’s “key findings,” according to the editorialists.

The health behaviors and BMI explained 95% of the association between education and the incidence of proximal colon cancer, but only 38% of the association between education and distal cancer and 24% of that between education and rectal cancer, Dr. Ayanian and Dr. Carethers point out.

That is a dramatic difference, they note. However, the editorialists think that these contrasting results for proximal and more distal cancers might “reflect the impact of an important omitted variable — colorectal cancer screening by socioeconomic status.”

Colorectal cancer screening has been shown to be more effective in reducing cancer incidence and mortality in the distal colon and rectum than in the proximal colon, the editorialists explain. Thus, this finding might have an easy explanation, they note.

“Because adults who are less educated and from less affluent communities are less likely to be screened, the greater effectiveness of screening for distal colorectal cancer may explain why socioeconomic gradients were much steeper for these anatomic sites than for proximal cancer,” they write.

The study was funded in part by the National Cancer Institute. The study authors and editorialists have disclosed no relevant financial relationships.

Logo of the United States National Cancer Inst...

Logo of the United States National Cancer Institute, part of the National Institutes of Health. (Photo credit: Wikipedia)

J Natl Cancer Inst. Published online September 5, 2012. Abstract, Editorial

 

Lifestyle and Reducing your Risk


 

Lifestyle Risk factors – how to reduce your risk of bowel cancer?

Risk factors other than family history can play a more important role in the development of bowel cancer.  The main risk factor for bowel cancer is increasing age. Only 7% of bowel cancer occurs before the age of 50 years.  However, even if you have a family history or other genetic risk of bowel cancer, this risk can be reduced by leading a healthy lifestyle.   This kind of healthy lifestyle can also reduce your risk of heart disease, stroke and other cancers.  It has been recently estimated that approximately 70% of colorectal cancer could be avoided by changes in lifestyle in Western countries.

A good further source of information about dietary and other lifestyle related risk factors is available from Cancer Research UK at http://www.cancerresearchuk.org/cancer-info/cancerstats/types/bowel/riskfactors/bowel-cancer-risk-factors

Diet 

Summary: A diet high in red meat and animal fat and low in fruit and vegetables increases your risk of bowel cancer.  So if you want to reduce your risk of bowel cancer, whether or not you have a genetic risk, eat 5 pieces of fruit or vegetables daily, plenty of fibre, and don’t eat too much processed or red meat.

Dietary Fibre

Putative anti-carcinogenic mechanisms of dietary fibre within the bowel include: the formation of short-chain fatty acids from fermentation by colonic bacteria; the reduction of secondary bile acid production; the reduction in intestinal transit time and increase of faecal bulk; and a reduction in insulin resistance. In the European Prospective Investigation into Cancer and Nutrition (EPIC) study after an average 6.2 years of follow-up, and 1,721 colorectal cancer cases, a 21% reduced risk amongst participants in the highest intake quintile was observed when compared against the lowest intake group. These results support our previous conclusion, of the potential of reducing colorectal cancer incidence by increasing fibre intake from cereal, fruit, and vegetable food sources.

Figure 5.2: The number of portions of fruit and vegetables eaten per day by adults aged 16 and over, England, 2009
Red and processed meat

In the EPIC study high intake of red or processed meat may increase risk by 71%.  The mechanisms underlying the association between colorectal cancer risk and high intake of red and processed meat are uncertain. Controlled human intervention studies have raised the possibility that the endogenous nitrosation that arises from ingestion of heme iron but not of inorganic iron or protein may account for the increased risk associated with red and processed meat consumption.  Heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAH) in diet may pose a potential risk of cancer to humans, depending on the extent to which the compounds are activated in vivo by metabolic enzymes. HCAs are formed as a byproduct of reactions during the cooking of meat, poultry, and fish at high temperatures, such as pan-frying or grilling with charcoal or on a gas grill; PAHs are formed in grilled and barbecued meat and in cured, processed foods. It has been suggested that processed meat intake has a stronger association with colorectal cancer than red meat intake.

Folate and selenium

Ball-and-stick model of the folic acid molecul...

Ball-and-stick model of the folic acid molecule, a B vitamin and an important compound in cell division. This image shows it as an anion (folate). Colour code (click to show) : Black: Carbon, C : White: Hydrogen, H : Red: Oxygen, O : Blue: Nitrogen, N (Photo credit: Wikipedia)

Folate (a water-soluble B vitamin) appears to protect against bowel cancer, but it remains unclear whether the same level of benefit is derived from dietary folate (from food, particularly fruit and vegetables) and synthetic folate (folic acid supplements).  Selenium can be obtained in food (particularly brazil nuts) and supplements; evidence for its effect on bowel cancer risk is mixed. The WCRF/AICR 2010 Report concluded that “Evidence for foods containing folate… and selenium… is less consistent and no conclusion could be drawn”.

Some experts have proposed that folate plays a dual role in bowel cancer in which moderate dietary intake before development of pre-cancerous adenomas reduces risk of adenoma development, but increased folate intake once adenomas have developed increases risk of cancer. Data from interventional studies indicate that folate supplementation decreases colonic mucosal cell proliferation .  A large prospective study showing a 31% reduction in bowel cancer risk for people with the highest overall folate intake 12-16 years before diagnosis, but no effect of intakes in the more recent past.

The US Government was sufficiently convinced of the health benefits (and absence of risk) from folic acid that it introduced mandatory folic acid fortification of grain products in 1997, and a recent large cohort study found that 8.5 years on, higher total folate intake (including intake specifically from supplements) was associated with a decreased bowel cancer risk.  There is some evidence that it is better to take folic acid in its natural form rather than as supplements i.e. tablets.

A 2011 meta analysis found men with the highest concentrations of selenium in the blood had 32% lower bowel cancer risk compared with men with the lowest concentrations, but found no association between selenium level and bowel cancer risk in women.3A 2004 pooled analysis found a similar level of risk reduction for both sexes combined.

Body weight and Obesity

Body mass index (BMI) values

Body mass index (BMI) values (Photo credit: Wikipedia)

Obesity is associated with an increased risk of colon cancer, particularly for men. Meta analyses show the risk of colon cancer increases by an estimated 24-30% per 5kg/m2 increase in body mass index (BMI) for men. In comparison to healthy-weight men (BMI less than 25 kg/m2), overweight men (BMI 25-29.9kg/m2) have a 23% higher risk of colon cancer, and obese men (BMI 30kg/m2 or more) have a 53% higher risk. The association is weaker in women, with colon cancer risk increasing by 9-12% per 5kg/m2 BMI increase, and the association proving non-significant in one meta analysis.

Larger waist size has been associated with increases in colon cancer risk in men (33% risk increase per 10cm waist circumference increase) and women (16% risk increase per 10cm waist circumference increase), as has increasing waist-to-hip ratio in both men (43% risk increase per 0.1-unit increase in ratio) and women (20% risk increase per 0.1 unit increase in ratio).

Higher BMI is linked less strongly to higher rectal cancer risk: a 5kg/m2 BMI increase is associated with a 9-12% higher rectal cancer risk for men (obese men have a 27% higher rectal cancer risk than healthy-weight men), but with no effect on rectal cancer risk in women

Regular exercise

Regular physical activity can reduce your risk of bowel cancer, this is clearly shown in many studies.  We would recommend 2-3 30 minute sessions per week of dedicated exercise (rather than more ‘passive’ exercise such as being busy at work!).

The relationship between physical activity and a reduced risk is one of the most consistent findings in epidemiologic literature.

Other risk factors

Not smoking and drinking less than the upper recommended limit of normal (less than 21 units for men and less than 14 units for women) may also be helpful.

 

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