Pancreatic cancer and nutrition

Chapter 3.8
Pancreatic cancer and nutrition

Tanya Klopper

The Royal Surrey County Hospital, Guildford, UK

Pancreatic cancer (PC) represents 2–3% of all cancers, yet it remains the fourth most common cause of death in the world, with a 5-year survival rate of 1–5% [1–4]. The presentation and onset of symptoms are non-specific so the majority of diagnoses are made once the disease is either locally or systemically advanced, thus eliminating curative disease management [5,6].

The incidence of PC has risen and plateaued over the last few decades and correlates with increasing age, peaking in 65–75 year olds. There is an uneven geographical distribution of PC with developed countries having a higher incidence than developing countries. This may be associated with differences in screening practice but also suggests that environmental factors may have a role in the development of the cancer [5,6].

Approximately 95% of tumours develop in the exocrine part of the pancreas. Ductal adenocarcinoma accounts for 80–90% of all pancreatic neoplasms, whilst neuroendocrine tumours and cystic neoplasms are less common [1,6]. Within the pancreas, approximately 75% of tumours are in the head or neck, 15–20% in the body and 5–10% in the tail [1].

As with most cancers, surgical resection is the only curative option. For a pancreatic tumour to be resectable, it must be confined to the pancreas but unfortunately this only comprises 20% of tumours at diagnosis. Successful resection, usually in conjunction with adjuvant treatment, can improve the 5-year survival rate to 10–25% [1,2,7]. For locally advanced tumours and metastatic disease, surgery is not an option so for these patients, chemotherapy and/or radiotherapy are employed. Although not curative, these options can improve symptoms and prolong survival. Median survival is currently 10–12 months [1]. Untreated metastatic and locally advanced disease has a median survival of 3–5 months and 6–10 months respectively [6].

3.8.1 Factors involved in causation

Smoking is the most significant and consistent modifiable risk factor of PC. An estimated 20–30% of cases can be directly attributed to cigarette smoking [8–11]. (The risk correlates with intensity and duration of smoking and smoking cessation does appear to reduce the risk [8,9].

Only 10% of cases result from genetic mutations [12]. Type 2 diabetes and long-standing chronic pancreatitis are associated with an increased risk of developing PC [4,5,10]. Patients with diabetes have a two-fold increased risk independent of alcohol, Body Mass Index (BMI) and smokingstatus [13].

Modifiable risk factors associated with diet and lifestyle have attracted a lot of attention for several decades. Despite alcohol being implicated in the aetiology of several other cancers and chronic pancreatitis, the consensus to date is that alcohol is not associated with PC, although one study did suggest that heavy alcohol intake may play a role [14–16].

Red meat and processed meat products have been reported to increase PC risk and preparation methods such as grilling, frying, curing and smoking have been implicated. This could suggest that polycyclic aromatic hydrocarbons, heterocyclic amines and nitrosamines produced during these cooking processes possibly play a role in the etiology of PC [17].

Studies have had varied but inconclusive results and some have attributed the risk to the fat content of the meat products. A study that specifically investigated the different types of fat and PC risk reported positive associations with total, saturated and monounsaturated fats, particularly from red meat and dairy sources, a likely mechanism being that fat promotes pancreatic carcinogenesis. There was, however, no association with fats of plant origins [18]. Other findings include no association between risk of PC and dairy products [17,19].

Several studies have reported either no association or an inverse association existing between fruit and vegetable intake and PC risk [20,22]. Possible mechanisms include antioxidant protection against free radical damage, immune-enhancing properties and inhibition of insulin-like growth factor (IGF) binding to IGF receptors [20].

Cancer-protective effects of flavonols in the prevention of PC were found to be beneficial, particularly for smokers [23]. The Netherlands Cohort Study found no association between the intake of carotenoids and vitamin supplements and PC risk [20].

Uncertainties have existed regarding an association between total sugar intake and PC risk. Previous evidence has been inconclusive, but in the NIH-AARP Diet and Health Study, no association was found between added sugars intake and PC risk [24].

Growing evidence implicates abnormal glucose metabolism and insulin resistance in the development of PC, with an increasing risk in the overweight sedentary population [25–28]. Very overweight people are 20% more likely to develop PC [10]. Further studies confirm that PC risk increases with obesity, with a significant association with central adiposity, especially in women [14,29,30]. Possible mechanisms have been linked to hormonal and inflammatory effects of adipose tissue, increased exposure to carcinogens secondary to increased dietary intake and lack of physical activity [31].

Little or no association has been found with physical activity and PC risk [14,29,30,32].

3.8.2 Dietary effects of disease and treatment

Weight loss is one of the presenting symptoms in PC. It impairs response to cancer treatment and is regarded as an important prognostic factor: the greater the weight loss, the shorter the survival [33,34]. Patients with PC lose 14.2% of their pre-illness weight, increasing to 24.5% prior to death [33].

Cancer cachexia (CC) is characterised by progressive weight loss with or without anorexia. Approximately 80% of patients with PC present with signs of CC at diagnosis and it is one of the main reasons for the decline in nutritional status [35,36].

Pancreatic exocrine insufficiency (PEI) arises from loss of pancreatic parenchyma or from obstruction of the pancreatic duct thus preventing enzymes from reaching the GI tract, causing malabsorption [12,37,38]. Pancreatic exocrine insufficiency presents in 68–92% of PC patients before surgery and in 80% after surgery. It is often overlooked as the main focus is treating the underlying disease [39].

Pancreatic exocrine insufficiency typically presents as excessive foul-smelling flatus, abdominal distension and discomfort, belching and steatorrhoea and ultimately is the other major contributor of the weight loss seen in patients with PC [37,38,40]. Approximately 65% of patients will experience fat malabsorption and 50% will experience protein malabsorption [41]. Fat absorption is further compromised by a reduction in circulating bile salts associated with obstructive jaundice [42]. Deficiencies in fat-soluble vitamins (A, D, E, K), magnesium, calcium and essential fatty and amino acids can also occur [39].

Other presenting symptoms of PC include intractable pain, jaundice, nausea, anorexia, taste changes, early satiety, gastric outlet obstruction and fatigue [35,41]. The development of complications such as glucose intolerance or overt diabetes and pancreatitis has also been reported [43,44]. Understandably these symptoms are distressing and can have an impact on the psychological well-being of patients, with 47–71% of those with PC reported as being depressed [37,41]. This is far greater than in other cancer patients and has a significant impact on morbidity [45]. The combination of these factors can further impact nutritional intake and status which may contribute to the decline in performance status and quality of life.

Standard care for patients with early-stage PC will involve surgical resection followed by adjuvant chemotherapy [43]. Surgery is precluded in those with more advanced disease; instead, these patients are treated with a range of chemotherapy regimes, radiotherapy and new emerging targeted and molecular therapies.

The standard surgical procedures performed will depend on the location and extent of the tumour. Partial pancreaticoduodenectomy with resection of the distal stomach, better known as Whipple’s procedure, is performed for tumours of the head of the pancreas. More recently, preservation of the pylorus has become the preferred option for this operation. For tumours of the body and tail of the pancreas, a distal pancreatectomy is performed and for more extensive tumours, a total pancreatectomy is undertaken [7,46].

Gastric outlet obstruction is a late complication of advanced disease that presents in 10–20% of patients, of which 3% are able to undergo a palliative gastrojejunostomy procedure [41,46].

Overall, Gupta and Ihmaidat reported that quality of life after a Whipple’s procedure can be excellent [42]. The extent of nutritional complications and their management postoperatively will depend on the procedure performed. The advantages of preserving the pylorus include fewer postgastrectomy complications, less reflux and greater improvement in postoperative nutritional status, weight gain and quality of life [7,46]. Total or partial resection of the pancreas is associated with a combination of exocrine and/or endocrine insufficiency and consequent symptoms of malabsorption and postoperative diabetes [7,47].

Chemotherapy and radiotherapy can have short- and long-term nutritional consequences. This is mainly due to the fact that these treatments cause damage to normal cells, particularly those that divide rapidly and as a result, the ability to ingest, digest and absorb nutrients becomes compromised [48]. The most common side-effects of chemotherapy that affect nutritional status include nausea, vomiting, taste and smell alterations, anorexia, food aversions, diarrhoea, mucositis and early satiety [48,49]. Radiotherapy can damage the GI mucosa, and in patients with PC presents as nausea which directly impacts nutritional intake [49].

3.8.3 Dietary management

Nutritional management of patients with PC can be complex given the myriad factors that can impact nutritional status and the aggressive nature of the disease.

The goals of nutrition support for cancer patients focus on maintaining or improving nutritional status, managing nutrition-related side-effects of treatment and disease as well as aiming to improve quality of life and prognosis [36,37,44].

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