nutrition and cancer Flashcards
dietary factors: obesity
- chronic low level inflammation
- adipose tissue increased oestrogen
- changes in circulation of certain adipokines- increased leptin (promotes cell proliferation, decrease in adiponectin (antiproliferative effects)
- increased circulating insulin- insulin signalling through insulin receptor A, has direct oncogenic effects on cancer cells
- ↑ insulin-like growth factor (IGF) 1 - a survival agent and growth factor for a diverse range of normal and malignant cells.
dietary factors: red and processed meat
intake of red and processed meat associated with increased risk of colorectal and gastrointestinal cancers.
- nitrosamines (potent carcinogens) are formed in cured meats
- nitrates can be converted into N-nitroso compounds (NOCs)- carcinogenic
- haem iron (in high levels in red meat) has been shown to promote colorectal tumorigenesis by stimulating the endogenous formation of carcinogenic N-nitroso compounds.
- Processed meatsare often cooked at high temperatures which can lead to formation of heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs) both of which have been linked tocolorectal cancerdevelopment
dietary factors: saturated fat
Increased risk of lung, colorectal, prostate & breast cancer
The mechanisms by which fats promote tumorigenesis are not fully understood
High fat intake results in increased production of bile acid, which is converted by intestinal bacteria into secondary bile acid and cytotoxic compounds.
These compounds may enhance the proliferative activity of the colonic epithelium
High fat diets often associated with obesity
High-fat-diet-induced obesity can lead to a chronic state of low-grade inflammation
High dietary SFA intake often synonymous with high intake of processed and red meat
Dietary intake of certain types of fat (e.g. Omega 3 PUFAs) is inversely correlated with development of certain cancers
dietary factors: alcohol
Alcohol has been identified as a contributory factor for several types of cancer including: upper aerodigestive tract, liver & breast
Mechanisms not fully understood, but include:
Acetaldehyde
Acetaldehyde is the first metabolite of ethanol oxidation. Acetaldehyde has been shown to be mutagenic and carcinogenic in animal experiments
Oestrogen
Alcohol can increase the circulating levels oestrogen, which is linked to breast cancer
Folate and other nutrients
Epidemiologic studies have indicated a negative association between folateintakeand risk of breast cancer,
as well as a negative association between vitamin B12statusand risk of breast cancer
Postulated that the lower folate and B12 levels in individuals consuming alcohol increase cancer risk
Alcohol + smoking has a synergistic effect
High alcohol consumption can also cause cirrhosis of the liver, which can then lead to cancer
dietary factors: fruit and vegetables
Epidemiological studies have consistently shown that regular consumption of fruits and vegetables is strongly associated with reduced risk of developing chronic diseases, such as cancer
Antioxidants interact with and neutralizefree radicals (aka ROS – reactive oxygen species)
Widely believed that the actions of the antioxidant nutrients alone do not explain the observed health benefits of diets rich in fruits and vegetables
- Because in isolation, the individual antioxidants studied in clinical trials do not appear to have consistent preventive effects
Glucosinolates & isothiocyanates - increase elimination/metabolism of carcinogens (Nitrosamines)
dietary factors: fibre
Dietary fibre is thought to protect against colorectal cancer
Results from EPIC study concluded that “In populations with low average intake of dietary fibre, an approximate doubling of total fibre intake from foods could reduce the risk of colorectal cancer by 40%”
Proposed mechanisms include:
Formation of short-chain fatty acids from fermentation by colonic bacteria These SCFAs (e.g. butyrate) can inhibit the development of colorectal cancer
Reduction in intestinal transit time
undernutrition in cancer patients
At the time of diagnosis approximately 75% of cancer patients are undernourished, with a significantly lower fat-free mass than healthy controls.
Patients with highest weight loss are those with cancer of oesophagus, stomach, and larynx (when nutrient intake is impaired).
Patients with stage III/IV disease have reduced energy and protein intakes, due to factors including: Anorexia Taste changes Dysphagia Nausea, Vomiting, Diarrhoea Other disease/treatment related factors
cachexia
Definition: Chronic hypermetabolic state characterised by rapid weight loss and anorexia.
Generally seen in cancer patients, certain infectious diseases (e.g. malaria, TB, HIV, cystic fibrosis), and chronic alcoholics.
Prevalence depends on type of malignancy. Seen in up to 85% of gastrointestinal, pancreatic, colorectal & lung cancer patients at diagnosis.
Duration, malignancy (pancreatic & lung), and number of anatomic sites tend to cause hypermetabolism (Resting Energy Expenditure >20% predicted).
nutrition therapy for cancer patients
Essential to increase the likelihood of completion of cancer treatment and improve quality of life
Support adequate energy and nutrient intake with the aim to:
Reverse undernutrition and weight loss that have already occurred
Prevent weight loss and promote weight gain
Enhance immune function
Reduce mental and physical fatigue
Sufficient protein should be provided (1-1.5 g/kg/day)
Carbohydrate should be the primary source of energy
Fat should represent ~25% of energy intake (including adequate intake of omega-3 fatty acids)
Adequate dietary fibre and fluid (including electrolytes)
enteral nutrition support
Provided when patients are expected to (or have) not received adequate nutrition for 7 days
Small bowel feeding administered with pump over 8-20 hours
Formulas come in a variety of energy densities (0.8 to 2.0 kcal/ml)
Most patients with standard fluid requirements will tolerate 1 to 1.2 kcal/ml
parenteral nutrition support
Used when GI tract is not functional, accessible, or safe to use e.g. colon cancer
Central (total Parenteral Nutrition, TPN) or peripheral (peripheralparenteral nutrition, PPN) vein
Energy requirement predicted from estimated daily energy expenditure (using appropriate equations)
