Chapter 3.22
Colorectal cancer and nutrition
Rachel Lewis1 and Sorrel Burden2
1 Glangwili Hospital, Carmarthen, UK
2 Central Manchester NHS Foundation Trust, Manchester, UK
Colorectal cancer (CRC) is the third most common cancer worldwide after lung and breast cancer with an estimated 1.24 million new cases diagnosed in 2008 [1]. In 2010 there were approximately 40,695 new cases of CRC diagnosed in the UK, around two-thirds in the colon and one-third in the rectum [2].
The incidence of CRC varies between countries and the highest rates are found in Australia, New Zealand (approximately 45 cases per 10,000 population in men and 33 cases per 10,000 in women) and Western Europe, with the lowest rates reported in middle Africa (approximately four cases/10,000 in men and three cases/10,000 in women) [1]. Geographical variation in incidence across the world has been attributed to dietary variations and different levels of physical activity. Epidemiological studies report a rapid increase in risk for CRC in migrants moving from low- to high-risk countries and in countries that have had a rapid ‘Westernisation’ of diet, such as Japan [3].
Presenting symptoms include an alteration in stool output, rectal bleeding and anaemia with abdominal pain, anorexia and weight loss in more advanced tumours. Worldwide, CRC is the fourth most common cause of cancer death, estimated to be responsible for around 8% of the total (almost 610,000 deaths) in 2008 [1]. Mortality has been falling over the last decade, with the 5-year survival rates for both men and women improving considerably between the early 1970s and early 2000s [2]. Overall, 5-year survival rates average 55% in high-income countries and 39% in middle- to low-income countries [4]. Worldwide, it is estimated that there were 3.26 million CRC patients still alive in 2008, up to 5 years after their diagnosis. These changes can be attributed to screening programmes leading to earlier detection of tumours and substantial advances in treatment options.
Surgical resection with curative intent is the primary treatment for 80% of patients diagnosed with CRC [5]. The extent of intestinal resection and the presence of a stoma may affect the patient’s nutritional status.
3.22.1 Factors involved in causation
Colorectal cancer is widely considered to be an environmental disease, with diet strongly influencing risk [6]. In the UK, it has been estimated that approximately 57% of CRC cases in men and 52% in women are linked to lifestyle and environmental factors [7], with incidence of CRC generally higher in populations that consume ‘Westernised’ diets. Colorectal cancer is one of the main cancers for which modifiable causes have been identified and therefore a large proportion of disease is theoretically preventable. It has been suggested that changes in dietary habits might reduce up to 70% of this cancer burden [6].
The link between diet and cancer is multifaceted and difficult to unravel. Diet may affect GI mucosa either directly from the luminal side or indirectly through whole-body metabolism. Compounds derived from food that are constantly present in the intestine, or the blood content of nutrients, hormones and growth factors, may shift cellular balance toward harmful outcomes [8]. Variation in dietary intake and the complexity of interactions of dietary components, with each other and with metabolites, make it difficult to design studies that accurately identify dietary components that might induce or prevent CRC.
A recent report entitled Food Nutrition, Physical Activity and the Prevention of Cancer: A Global Perspective produced by the World Cancer Research Fund (WCRF) in collaboration with the American Institute for Cancer Research (AICR) provided a series of recommendations based on expert judgement, systemic reviews and case studies of the world literature [9]. Based on mainly prospective cohort studies, it was concluded that there is convincing evidence that physical activity can decrease the risk of CRC, while there is a probable reduction in cancer risk associated with foods rich in non-starch polysaccharides (NSP), garlic and calcium. Conversely, processed meat, red meat, alcohol, body fatness and in particular abdominal fatness are associated with cancer risk.
Red and processed meat
Meat consumption, most notably red and processed meat, has been described as a promoter of carcinogenesis. It has been estimated that 21% of CRC in the UK was linked to meat consumption [10], with the positive association stronger for colon cancer than rectal cancer [11]. Over the past three decades a plethora of epidemiological and prospective studies have evaluated this hypothesis. However, the possible role of this food group in CRC is equivocal.
Meta-analysis of the literature has concluded that there was a significantly increased risk of CRC in the highest category of red meat consumption when compared to the lowest category. An intake of 25–50 g/day processed meat was associated with 9–50% increased risk and a 17–30% increased risk of CRC was associated with a red meat intake of 100–120 g/day [11]. In contrast, a pooled analysis of UK case–control studies found no effect of 50 g/day red or processed meat; however, a relatively low amount of meat was consumed and the number of participants was relatively small [12].
The WCRF/AICR report concluded that consumption of red meat is a ‘convincing’ cause of CRC [9]. There has been much debate on the WCRF/AICR conclusions and a review of prospective epidemiological studies by Alexander et al. suggested that there are limitations to the available data [13]. Specifically, the epidemiological associations across the consortium of studies have been considered as being relatively weak in magnitude, most individual studies have not observed statistically significant associations, evidence of dose–response is unclear and patterns of associations vary by study characteristics. Also it is worth noting that red meat is defined and analysed heterogeneously across studies. The authors concluded that the available evidence is not sufficient to support a clear positive association between red and processed meat consumption and CRC.
Several postulated mechanisms regarding meat consumption and CRC incidence have been examined. Dietary mutagens (e.g. heterocyclic amines, polycyclic aromatic hydrocarbons) or chemical compounds that may develop during cooking at high temperatures have been most intensively studied, but associations from epidemiological analysis have been variable across several specific compounds [14]. Other mechanisms involve the potential role of nitrate and nitrite, commonly used in processed meat as preservation agents, and N-nitroso compounds, which have been shown to be carcinogenic in some laboratory animal studies. Finally, some researchers have suggested that iron may play a role in increasing CRC. However, relatively few studies have evaluated the potential role that this factor may play in cancer risk [14].
Obesity
Obesity, categorised as a Body Mass Index (BMI) >30 kg/m2, is associated with an increased risk of colon cancer. In 2010 it was estimated that 13% of CRC cases in the UK were associated with an individual being overweight or obese [10].
Meta-analyses have shown that the risk of colon cancer increases by approximately 30% per 5 kg/m2 increase in BMI for men, increasing to a 53% higher risk in obese men in comparison to healthy weight men (BMI <25 kg/m2). The data for rectal cancer show a weaker association with BMI and cancer risk; a 5 kg/m2 BMI increase is associated with a 9–12% higher risk in men, with those being obese having a 27% higher risk of developing rectal cancer [15]. The data for women are less clear with a non-significant association for colon cancer risk in one meta-analysis. It is likely that the female sex hormone oestrogen may affect the correlation between risk and BMI but the exact nature of this relationship is unclear.
Alcohol
Alcohol intake has been implicated as a risk factor for CRC, with the greatest risks associated with intakes in excess of 30 g/day. Thirteen cohort studies and 41 case–control studies reported a linear relationship with increased risk of CRC with increasing ethanol intakes. No contrary results were found with statistical significance [9].
A recent systemic review reported a 21% increase in risk for both colon and rectal cancers with an alcohol intake of 1.6–6.2 UK units (12.8–49.6 g) per day when compared to those categorised as non-drinkers or occasional drinkers [16]. Dose–response analysis within this study showed a 7% increase risk for every 10 g/day alcohol consumed. There is a suggestion of sexual dysmorphism, with evidence stronger for men. This is believed to be as a result of fewer data for women [9]. The EPIC study also found a significant positive association between alcohol consumption and CRC risk, with higher risks observed in the rectum compared to the distal colon. Several plausible mechanisms have been reported for this, including the hypothesis that individuals with habitually high alcohol intake have suboptimal intakes of essential nutrients, making them more susceptible to carcinogenesis.
Non-starch polysaccharides
It has been estimated that 12% of CRC could be attributed to poor NSP intakes <23 g/day [7]. Although the WCRF/AICR study noted foods high in NSP as being ‘probable’ in terms of decreasing the risk of CRC, it was acknowledged that the evidence is conflicting [9].
Studies have reported no correlation between CRC incidence and NSP whereas the EPIC study found a direct link, specifically in populations with low average intakes of NSP. More recently, a meta-analysis of 25 prospective studies with 2 million participants found that CRC risk was reduced by 10% for every 10 g/day total NSP [17]. Conflicting results have been attributed to possible confounding effects which include the overall amount of NSP consumed, the definition of NSP and type of fibre.
3.22.2 Nutritional status of colorectal cancer patients
Impaired nutritional status is a frequent complication in patients with CRC and can negatively affect the outcome of treatment and quality of life The consequences of underlying pathology or disease-associated symptoms such as diarrhoea, nausea or vomiting all contribute to the high incidence of protein energy malnutrition (PEM). All causes of excessive nutrient loss with or without increased metabolic needs will influence nutritional status. The undernourished cancer patient responds poorly to therapeutic interventions, such as chemotherapy, radiotherapy and surgery, with increased morbidity and mortality compared with well-nourished patients.
From early studies, the incidence of PEM in patients with CRC was cited as 37% [18]. More recently, Gupta et al. reported that PEM is observed in up to 41% of patients with advanced CRC [19]. Available data on the prevalence of PEM can vary broadly depending on evaluation criteria, for example tumour site, extension and anticancer treatment. Early identification and treatment of PEM in a patient’s cancer journey are crucial in order to achieve favourable outcomes.
Surgical treatment
It is well recognised that patients undergoing GI surgery have an increased risk of developing undernutrition secondary to inadequate nutritional intake and metabolic stress following surgery. Furthermore, undernutrition can increase the incidence of postoperative complications, such as delayed wound healing or anastomosis dehiscence [20].
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