ABSTRACT
Personalised and precision nutrition uses information on individual characteristics and responses to nutrients, foods and dietary patterns to develop targeted nutritional advice that is more effective in improving the diet and health of each individual. Moving away from the conventional 'one size fits all', such targeted intervention approaches may pave the way to better population health, including lower burden of non-communicable diseases. To date, most personalised and precision nutrition approaches have been focussed on tackling obesity and cardiometabolic diseases with limited efforts directed to cancer prevention and for cancer survivors. Advances in understanding the biological basis of cancer and of the role played by diet in cancer prevention and in survival after cancer diagnosis, mean that it is timely to test and to apply such personalised and precision nutrition approaches in the cancer area. This endeavour can take advantage of the enhanced understanding of interactions between dietary factors, individual genotype and the gut microbiome that impact on risk of, and survival after, cancer diagnosis. Translation of these basic research into public health action should include real-time acquisition of nutrigenomic and related data and use of AI-based data integration methods in systems approaches that can be scaled up using mobile devices.
Subject(s)
Cancer Survivors , Neoplasms , Humans , Nutrigenomics , Precision Medicine , Diet , Genotype , Neoplasms/genetics , Neoplasms/prevention & controlABSTRACT
BACKGROUND: Colorectal cancer (CRC) is the third most common cancer worldwide. Age is the strongest non-modifiable risk factor but it is estimated that over half of CRC cases are linked with lifestyle factors such as diet. The Biomarkers Of RIsk of Colorectal Cancer (BORICC) Study recruited 363 participants in 2005 to investigate the effects of lifestyle factors on biomarkers of CRC risk. AIM: In the present BORICC Follow-Up (BFU) Study, we are using a longitudinal study design to investigate the effects of ageing (12+ years) and lifestyle factors on biomarkers of CRC risk and on healthy ageing. METHODS: BFU Study participants attended a study visit at North Tyneside General Hospital (UK) for collection of biological samples, including blood and rectal biopsies, and information collected included anthropometric measurements, a Health & Medications Questionnaire, physical activity and sedentary behaviour, and habitual diet. Furthermore, musculoskeletal function was assessed by heel bone densitometry, timed up and go and hand grip strength as markers of healthy ageing. The BFU Study outcomes will be similar to those measured at baseline in the BORICC Study, such as DNA methylation and mitochondrial function, with additional measurements including the gut microbiome, faecal short-chain fatty acid concentrations and expression of genes associated with CRC. RESULTS: Participants' recruitment to BFU Study and all sample and data collection have been completed. Forty-seven of the original BORICC participants were re-recruited to the BFU Study (mean age 67 years, 51% female). The recruits included 37 initially healthy participants and 10 participants who had adenomatous polyps at baseline. Approximately 70% of participants were over-weight or obese. CONCLUSION: Ultimately, identifying lifestyle factors that can reduce CRC risk, and understanding the underlying mechanisms for the effects of lifestyle and ageing on CRC risk, could lead to early prevention strategies.
Subject(s)
Colorectal Neoplasms/epidemiology , Age Factors , Aged , Biomarkers , Diet/methods , Diet/statistics & numerical data , Female , Follow-Up Studies , Humans , Life Style , Longitudinal Studies , Male , Middle Aged , Risk Factors , Surveys and Questionnaires , United Kingdom/epidemiologyABSTRACT
Colorectal cancer (CRC) is the third most common cancer globally. CRC risk is increased by obesity, and by its lifestyle determinants notably physical inactivity and poor nutrition. Obesity results in increased inflammation and oxidative stress which cause genomic damage and contribute to mitochondrial dysregulation and CRC risk. The mitochondrial dysfunction associated with obesity includes abnormal mitochondrial size, morphology and reduced autophagy, mitochondrial biogenesis and expression of key mitochondrial regulators. Although there is strong evidence that increased adiposity increases CRC risk, evidence for the effects of intentional weight loss on CRC risk is much more limited. In model systems, energy depletion leads to enhanced mitochondrial integrity, capacity, function and biogenesis but the effects of obesity and weight loss on mitochondria in the human colon are not known. We are using weight loss following bariatric surgery to investigate the effects of altered adiposity on mitochondrial structure and function in human colonocytes. In summary, there is strong and consistent evidence in model systems and more limited evidence in human subjects that over-feeding and/or obesity result in mitochondrial dysfunction and that weight loss might mitigate or reverse some of these effects.