Assessing the economic costs of unhealthy diets and low physical activity: an evidence review and proposed framework
Unhealthy diets and low physical activity contribute to many chronic diseases and disability; they are responsible for some 2 in 5 deaths worldwide and for about 30% of the global disease burden. Yet surprisingly little is known about the economic costs that these risk factors cause, both for health care and society more widely.
This study pulls together the evidence about the economic burden that can be linked to unhealthy diets and low physical activity and explores
- How definitions vary and why this matters
- The complexity of estimating the economic burden and
- How we can arrive at a better way to estimate the costs of an unhealthy diet and low physical activity, using diabetes as an example
The study also tests the feasibility of using a disease-based approach to estimate the costs of unhealthy diets and low physical activity in Europe, projecting the total economic burden associated with these two risk factors as manifested in new type 2 diabetes cases at €883 million in 2020 for France, Germany, Italy, Spain and the United Kingdom alone. The ‘true’ costs will be higher, as unhealthy diets and low physical activity are linked to many more diseases.
The study’s findings are a step towards a better understanding of the economic burden that can be associated with two key risk factors for ill health and they will help policymakers in setting priorities and to more effectively promoting healthy diets and physical activity.
Candari, C. J., Cylus J. & Nolte, E. (2017). European Observatory on Health Systems and Policies.
Cancer, obesity, diabetes, and antidiabetic drugs: is the fog clearing?
The prevalence of obesity, of type 2 diabetes mellitus (T2DM), and of cancer are all increasing globally. The relationships between these diseases are complex, and thus difficult to elucidate; nevertheless, evidence supports the hypothesis that obesity increases the risks of both T2DM and certain cancers. Further complexity arises from controversial evidence that specific drugs used in the treatment of T2DM increase or decrease cancer risk or influence cancer prognosis. Herein, we review the current evidence from studies that have addressed these relationships, and summarize the methodological challenges that are frequently encountered in such research. We also outline the physiology that links obesity, T2DM, and neoplasia. Finally, we outline the practical principles relevant to the increasingly common challenge of managing patients who have been diagnosed with both diabetes and cancer.
Klil-Drori, A. J., Azoulay, L., & Pollak, M. N. (2016). Cancer, obesity, diabetes, and antidiabetic drugs: is the fog clearing?. Nature Reviews Clinical Oncology.
High-fat diet enhances stemness and tumorigenicity of intestinal progenitors
Little is known about how pro-obesity diets regulate tissue stem and progenitor cell function. Here we show that high-fat diet (HFD)-induced obesity augments the numbers and function of Lgr5+ intestinal stem cells of the mammalian intestine. Mechanistically, a HFD induces a robust peroxisome proliferator-activated receptor delta (PPAR-δ) signature in intestinal stem cells and progenitor cells (non-intestinal stem cells), and pharmacological activation of PPAR-δ recapitulates the effects of a HFD on these cells. Like a HFD, ex vivo treatment of intestinal organoid cultures with fatty acid constituents of the HFD enhances the self-renewal potential of these organoid bodies in a PPAR-δ-dependent manner. Notably, HFD- and agonist-activated PPAR-δ signalling endow organoid-initiating capacity to progenitors, and enforced PPAR-δ signalling permits these progenitors to form in vivo tumours after loss of the tumour suppressor Apc. These findings highlight how diet-modulated PPAR-δ activation alters not only the function of intestinal stem and progenitor cells, but also their capacity to initiate tumours.
Beyaz, S., Mana, M. D., Roper, J., Kedrin, D., Saadatpour, A., Hong, S. J., ... & Pinello, L. (2016). High-fat diet enhances stemness and tumorigenicity of intestinal progenitors. Nature, 531(7592), 53-58.
European Code against Cancer 4th Edition: Diet and cancer
Lifestyle factors, including diet, have long been recognized as potentially important determinants of cancer risk. In addition to the significant role diet plays in affecting body fatness, a risk factor for several cancers, experimental studies have indicated that diet may influence the cancer process in several ways. Prospective studies have shown that dietary patterns characterised by higher intakes of fruits, vegetables, and whole-grain foods, and lower intakes of red and processed meats and salt, are related to reduced risks of death and cancer, and that a healthy diet can improve overall survival after diagnosis of breast and colorectal cancers. There is evidence that high intakes of fruit and vegetables may reduce the risk of cancers of the aerodigestive tract, and the evidence that dietary fibre protects against colorectal cancer is convincing. Red and processed meats increase the risk of colorectal cancer. Diets rich in high-calorie foods, such as fatty and sugary foods, may lead to increased calorie intake, thereby promoting obesity and leading to an increased risk of cancer. There is some evidence that sugary drinks are related to an increased risk of pancreatic cancer.
Taking this evidence into account, the 4th edition of the European Code against Cancer recommends that people have a healthy diet to reduce their risk of cancer: they should eat plenty of whole grains, pulses, vegetables and fruits; limit high-calorie foods (foods high in sugar or fat); avoid sugary drinks and processed meat; and limit red meat and foods high in salt.
Norat, T., Scoccianti, C., Boutron-Ruault, M. C., Anderson, A., Berrino, F., Cecchini, M., ... & Wiseman, M. (2015). European Code against Cancer 4th Edition: diet and cancer. Cancer epidemiology, 39, S56-S66.
Impact of the Obesity Epidemic on Cancer
There is growing appreciation that the current obesity epidemic is associated with increases in cancer incidence at a population level and may lead to poor cancer outcomes; concurrent decreases in cancer mortality at a population level may represent a paradox, i.e., they may also reflect improvements in the diagnosis and treatment of cancer that mask obesity effects. An association of obesity with cancer is biologically plausible because adipose tissue is biologically active, secreting estrogens, adipokines, and cytokines. In obesity, adipose tissue reprogramming may lead to insulin resistance, with or without diabetes, and it may contribute to cancer growth and progression locally or through systemic effects. Obesity-associated changes impact cancer in a complex fashion, potentially acting directly on cells through pathways, such as the phosphoinositide 3-kinase (PI3K) and Janus kinase–signal transducer and activator of transcription (JAK-STAT) pathways, or indirectly via changes in the tumor microenvironment. Approaches to obesity management are discussed, and the potential for pharmacologic interventions that target the obesity–cancer link is addressed.
Goodwin, P. J., & Stambolic, V. (2015). Impact of the Obesity Epidemic on Cancer. Annual review of medicine, 66, 281-296.
Concordance with World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) guidelines for cancer prevention and obesity-related cancer risk in the Framingham Offspring cohort (1991–2008)
Purpose: This prospective cohort study evaluates associations between healthful behaviors consistent with WCRF/AICR cancer prevention guidelines and obesity-related cancer risk, as a third of cancers are estimated to be preventable.
Methods: The study sample consisted of adults from the Framingham Offspring cohort (n = 2,983). From 1991 to 2008, 480 incident doctor-diagnosed obesity-related cancers were identified. Data on diet, measured by a food frequency questionnaire, anthropometric measures, and self-reported physical activity, collected in 1991 was used to construct a 7-component score based on recommendations for body fatness, physical activity, foods that promote weight gain, plant foods, animal foods, alcohol, and food preservation, processing, and preparation. Multivariable Cox regression models were used to estimate associations between the computed score, its components, and subcomponents in relation to obesity-related cancer risk.
Results: The overall score was not associated with obesity-related cancer risk after adjusting for age, sex, smoking, energy, and preexisting conditions (HR 0.94, 95 % CI 0.86–1.02). When score components were evaluated separately, for every unit increment in the alcohol score, there was 29 % lower risk of obesity-related cancers (HR 0.71, 95 % CI 0.51–0.99) and 49–71 % reduced risk of breast, prostate, and colorectal cancers. Every unit increment in the subcomponent score for non-starchy plant foods (fruits, vegetables, and legumes) among participants who consume starchy vegetables was associated with 66 % reduced risk of colorectal cancer (HR 0.44, 95 % CI 0.22–0.88).
Conclusions: Lower alcohol consumption and a plant-based diet consistent with the cancer prevention guidelines were associated with reduced risk of obesity-related cancers in this population.
Makarem, N., Lin, Y., Bandera, E. V., Jacques, P. F., & Parekh, N. (2015). Concordance with World Cancer Research Fund/American Institute for Cancer Research (WCRF/AICR) guidelines for cancer prevention and obesity-related cancer risk in the Framingham Offspring cohort (1991–2008). Cancer Causes & Control, 26(2), 277-286.
Obesity and Cancer
original article in German
The incidence of obesity in the western world has increased dramatically during recent decades. Epidemiological data suggest that obesity is associated with an increased risk of several but not all types of cancers, with clear sex-specific differences. The underlying mechanisms are still a matter of debate. This review focuses on the potential factors linking obesity to cancer. Current experimental evidence suggests that insulin resistance and a chronic, subclinical inflammation in the visceral fat are the major metabolic events causing alterations in the levels of insulin, glucose, free fatty acids, insulin-like growth factor 1 (IGF-1) and 2, adipose tissue-derived proinflammatory cytokines and other bioactive molecules, such as adipokines (e.g. leptin and adiponectin), vascular endothelial growth factor (VEGF), sex hormones, gut microbiota and secondary bile acids. All these factors may act directly or indirectly on the tumor microenvironment to drive tumor progression via stimulation of cell survival/antiapoptosis, cell proliferation, angiogenesis and invasion/metastasis of the cancer cells. Therapeutic strategies that target dysfunctional or inflamed fat and have been shown to benefit patients include bariatric surgery, while other cell or hormone-directed interventions, such as conversion of visceral fat macrophages to an anti-inflammatory M2 phenotype or the pharmacological modulation of serum adipokine levels are still theoretical and need to be clinically evaluated for their ability to successfully treat or prevent obesity-related cancers.
Gieseler, F., & Lehnert, H. (2015). Adipositas und Krebs. Der Internist, 56(2), 127-136.
Body-mass index and risk of 22 specific cancers: a population-based cohort study of 5.24 million UK adults
Background: High body-mass index (BMI) predisposes to several site-specific cancers, but a large-scale systematic and detailed characterisation of patterns of risk across all common cancers adjusted for potential confounders has not previously been undertaken. We aimed to investigate the links between BMI and the most common site-specific cancers.
Methods: With primary care data from individuals in the Clinical Practice Research Datalink with BMI data, we fitted Cox models to investigate associations between BMI and 22 of the most common cancers, adjusting for potential confounders. We fitted linear then non-linear (spline) models; investigated effect modification by sex, menopausal status, smoking, and age; and calculated population effects.
Findings: 5·24 million individuals were included; 166 955 developed cancers of interest. BMI was associated with 17 of 22 cancers, but effects varied substantially by site. Each 5 kg/m2 increase in BMI was roughly linearly associated with cancers of the uterus (hazard ratio [HR] 1·62, 99% CI 1·56–1·69; p<0·0001), gallbladder (1·31, 1·12–1·52; p<0·0001), kidney (1·25, 1·17–1·33; p<0·0001), cervix (1·10, 1·03–1·17; p=0·00035), thyroid (1·09, 1·00–1·19; p=0·0088), and leukaemia (1·09, 1·05–1·13; p≤0·0001). BMI was positively associated with liver (1·19, 1·12–1·27), colon (1·10, 1·07–1·13), ovarian (1·09, 1.04–1.14), and postmenopausal breast cancers (1·05, 1·03–1·07) overall (all p<0·0001), but these effects varied by underlying BMI or individual-level characteristics. We estimated inverse associations with prostate and premenopausal breast cancer risk, both overall (prostate 0·98, 0·95–1·00; premenopausal breast cancer 0·89, 0·86–0·92) and in never-smokers (prostate 0·96, 0·93–0·99; premenopausal breast cancer 0·89, 0·85–0·94). By contrast, for lung and oral cavity cancer, we observed no association in never smokers (lung 0·99, 0·93–1·05; oral cavity 1·07, 0·91–1·26): inverse associations overall were driven by current smokers and ex-smokers, probably because of residual confounding by smoking amount. Assuming causality, 41% of uterine and 10% or more of gallbladder, kidney, liver, and colon cancers could be attributable to excess weight. We estimated that a 1 kg/m2 population-wide increase in BMI would result in 3790 additional annual UK patients developing one of the ten cancers positively associated with BMI.
Interpretation: BMI is associated with cancer risk, with substantial population-level effects. The heterogeneity in the effects suggests that different mechanisms are associated with different cancer sites and different patient subgroups.
Bhaskaran, K., Douglas, I., Forbes, H., dos-Santos-Silva, I., Leon, D. A., & Smeeth, L. (2014). Body-mass index and risk of 22 specific cancers: a population-based cohort study of 5.24 million UK adults. The Lancet, 384(9945), 755-765.
A systematic review and meta-analysis of social cognitive theory-based physical activity and/or nutrition behavior change interventions for cancer survivors
Purpose: Theory-based approaches are now recommended to design and enact dietary interventions, but their use in cancer trials is unknown. This systematic review examined application of behavior theory to dietary interventions aimed at preventing cancer to improve the design and interpretation of trials.
Methods: Electronic databases were searched (inception-July 2011). Data were synthesized and a theory coding scheme (TCS) used to describe and assess how behavior theory informed interventions. Studies not reporting a dietary behavior intervention informed by a specified behavior change model(s) were excluded.
Results: Of 237 potentially eligible studies, only 40 (16.9 %) were relevant, mostly RCTs (34, 85.0 %). Twenty-one interventions targeted diet alone (52.5 %) or integrated diet into a lifestyle intervention (19, 47.5 %). Most (24, 60.0 %) invoked several behavior change models, but only 10 (25.0 %) interventions were reported as explicitly theory-informed and none comprehensively targeted or measured theoretical constructs or tested theoretical assumptions. The 10 theory-informed interventions were more effective at improving diet.
Conclusions: Dietary interventions for cancer prevention improved diet more effectively if they were informed by behavior theory. While behavior theory was often applied to these dietary interventions, they were rarely implemented or described thoroughly. Accurate intervention reporting is essential to assess theoretical quality and facilitate implementation effective behavior change techniques. Guidelines regarding the application and reporting of behavior theory for complex interventions, for example, proposed by the National Institutes of Health and Medical Research Council, should be revised accordingly. Failure to adequately ground dietary interventions in behavior theory may hinder establishing their effectiveness and relationships between diet and cancer.
Avery, K. N., Donovan, J. L., Horwood, J., & Lane, J. A. (2013). Behavior theory for dietary interventions for cancer prevention: a systematic review of utilization and effectiveness in creating behavior change. Cancer Causes & Control, 24(3), 409-420.
A systematic review of the impact of weight loss on cancer incidence and mortality
Obesity is well recognized as a significant risk factor for certain cancers; however, a corresponding risk reduction with weight loss is not yet clearly defined. This review aims to examine the literature investigating the effect of all types of weight loss on cancer incidence and mortality, and to more clearly describe the relationship between these two factors. A literature search identified 34 publications reporting weight loss data in relation to cancer incidence or mortality. All except one were observational studies and the majority used self-reported weights and did not define intentionality of weight loss. 16/34 studies found a significant inverse association between weight loss and cancer incidence or mortality. The remainder returned null findings. The observed association was more consistently seen in studies that investigated the effect of intentional weight loss (5/6 studies) and the risk reduction was greatest for obesity-related cancers and in women. In conclusion, intentional weight loss does result in a decreased incidence of cancer, particularly female obesity-related cancers. However, there is a need for further evaluation of sustained intentional weight loss in the obese with less reliance on self-reported weight data and more focus on male populations.
Birks, S., Peeters, A., Backholer, K., O'Brien, P., & Brown, W. (2012). A systematic review of the impact of weight loss on cancer incidence and mortality. Obesity Reviews, 13(10), 868-891.
Diet, nutrition and the prevention of cancer
Objective: To assess the epidemiological evidence on diet and cancer and make public health recommendations.
Conclusions and recommendations: Overweight/obesity increases the risk for cancers of the oesophagus (adenocarcinoma), colorectum, breast (postmenopausal), endometrium and kidney; body weight should be maintained in the body mass index range of 18.5-25 kg/m2 , and weight gain in adulthood avoided. Alcohol causes cancers of the oral cavity, pharynx, oesophagus and liver, and a small increase in the risk for breast cancer; if consumed, alcohol intake should not exceed 2 units/d. Aflatoxin in foods causes liver cancer, although its importance in the absence of hepatitis virus infections is not clear; exposure to aflatoxin in foods should be minimised. Chinese-style salted fish increases the risk for nasopharyngeal cancer, particularly if eaten during childhood, and should be eaten only in moderation. Fruits and vegetables probably reduce the risk for cancers of the oral cavity, oesophagus, stomach and colorectum, and diets should include at least 400 g/d of total fruits and vegetables. Preserved meat and red meat probably increase the risk for colorectal cancer; if eaten, consumption of these foods should be moderate. Salt preserved foods and high salt intake probably increase the risk for stomach cancer; overall consumption of salt preserved foods and salt should be moderate. Very hot drinks and foods probably increase the risk for cancers of the oral cavity, pharynx and oesophagus; drinks and foods should not be consumed when they are scalding hot. Physical activity, the main determinant of energy expenditure, reduces the risk for colorectal cancer and probably reduces the risk for breast cancer; regular physical activity should be taken.
Key, T. J., Schatzkin, A., Willett, W. C., Allen, N. E., Spencer, E. A., & Travis, R. C. (2004). Diet, nutrition and the prevention of cancer. Public health nutrition, 7(1a), 187-200.