Wednesday 25 September 2013

Is public health the food industry's responsibility? (part 1 of 3)

This series of posts make up a piece I wrote while doing the excellent "Diet Quality and Health" module, run by the Food Advance Training Partnership last year. It discusses the role of the food industry and what it should or should not do regarding responsibility for public health and non-communicable diseases.
I've cut the piece into 3 parts, since the whole thing is pretty big. If you want a copy of the whole thing, email me at I hope you find it interesting, and that it will perhaps spark some debate.


The role of the food industry in today’s society is multi-factoral. It provides variety, choice and information to their consumers, while being (at least morally-) bound to provide fair prices to their suppliers, sustainability and husbandry for the environment and profit to their shareholders. The issue of whether the industry should also be responsible for the wellbeing of the public, above and beyond basic provision of nutrition, is contentious for two reasons. Firstly this is typically seen as the remit of government rather than business, and secondly there is the issue of whether consumer choice should be the ultimate decider of the individual’s health. If this latter is the case, it suggests that the industry need only provide this choice, and can leave responsibility for public health to the government and the consumer.

Diet and Disease

There is a wealth of evidence as to the connection between consumption of certain foods and/or nutrients, and non-communicable chronic disease. The correlation between consumption of fat, particularly saturated fat, and coronary heart disease (CHD) is well-supported. The mechanism behind this is that an increase in blood cholesterol can be brought about by increased fat consumption (particularly saturated fat). This in turn can lead to the laying down of atherosclerotic plaques in the arteries, leading ultimately to blockage and therefore heart attack.
Furthermore it has been shown that reduction or replacement of such fats in the diet can help to reduce CHD risk 1. Increased alcohol consumption has been also correlated with greater CHD risk2, while overconsumption has been shown to cause chronic liver diseases3 and has been implicated in certain types of cancer 4. Similarly, increased levels of dietary salt have been shown to cause hypertension5, a leading cause of death by myocardial infarction and stroke and a strong association has been made between high consumption of red meat and the risk of colo-rectal cancer.6
Despite reduced consumption of overall energy, and dietary fat, epidemiological evidence points to a continued increase in overweight, partly due to an increasingly sedentary lifestyle brought about by labour-saving devices, the overuse of motorised transport and the reduced need for professions requiring manual labour7. Consequent to increased bodyweight is Metabolic Syndrome, comprising increased risk of various conditions such as Type II Diabetes Mellitus, elevated LDL cholesterol, coronary artery disease and stroke. These conditions are in part due to genetic predisposition, but also due to modifiable risk factors such as smoking, physical activity and, crucially, diet. The key to weight control is to maintain energy balance – if energy intake exceeds usage then energy is conserved in the form of body-fat stores, while if demand exceeds intake then energy in the form of body fat is used up. Since this is the case, it follows that despite our reduced energy intake mentioned above, the trend is still towards overconsumption of energy relative to the needs of our lifestyle, suggesting that this is at least partially due to the easy availability of energy-dense foods. One example of this is the prevalence of childhood obesity. Currently in the UK 30.3% of children (aged 2-15) are overweight or obese8, which can be partially attributed to a reduction in physical activity due to the increased popularity of screen-based entertainment such as video games, but is also contributed to by the availability of high-energy foods from vending machines in schools.
Given this situation, it is logical that reduced consumption of overall energy might be an effective risk-reduction strategy, as well as reduced consumption of fat, salt, and sugar. However, these ingredients are often added to convenience foods by the manufacturers, either as preservatives, flavour- or texture-enhancers, or in the case of sugar to replace the mouthfeel of fat in “diet” products. Given this last fact, it is logical to suggest that the food industry is partly responsible for the increase in the conditions mentioned above. In this case, it follows that the food industry could play a role in addressing it.

Beneficial effects of certain nutrients

In contrast, consumption of certain foods or nutrients has been seen to have beneficial effects in humans, often offering protection against various diseases. High consumption of fruit and vegetables has been shown to reduce risk of coronary heart disease by 30% and stroke by 20%9, while regular consumption of fish, particularly oily fish, can have a cardio-protective effect via lowering of plasma triglyceride levels10. Further benefits of fish oil appear to include augmentation of immune function via modulation of metabolic pathways which normally produce inflammatory cytokines11 and possible reduction of  cancer risk  in men12.
Similarly, there is an emerging trend of evidence regarding the health benefits of certain compounds derived from plants. Stilbenes, found in wine and nut skins have been associated with anti-cancer effects such as the initiation of apoptosis to control unregulated cell replication and therefore tumour formation13, as do glucosinolates, derived from cruciferous vegetables14. Carotenoids found in vegetables such as peppers and tomatoes, appear to be protective against cardiovascular disease and some forms of cancer15. Even some components of foods typically regarded as “unhealthy” have been identified as beneficial. One such compound is flavanols found in cocoa, high intake of which has been associated with protection against hypertension, ischemic heart disease, stroke, diabetes mellitus, and cancer in certain populations.16


1.         Jakobsen MU, O'Reilly EJ, Heitmann BL et al. Major types of dietary fat and risk of coronary heart disease: a pooled analysis of 11 cohort studies. Am J Clin Nutr 2009; 89: 1425-32.
2.         Ronksley PE, Brien SE, Turner BJ et al. Association of alcohol consumption with selected cardiovascular disease outcomes: a systematic review and meta-analysis. BMJ 2011; 342: d671.
3.         Lee M, Kowdley KV. Alcohol's Effect on Other Chronic Liver Diseases. Clin Liver Dis 2012; 16: 827-37.
4.         Jung EJ, Shin A, Park SK et al. Alcohol Consumption and Mortality in the Korean Multi-center Cancer Cohort Study. J Prev Med Public Health 2012; 45: 301-8.
5.         Elliott P, Marmot M, Dyer A et al. The INTERSALT study: main results, conclusions and some implications. Clin Exp Hypertens A 1989; 11: 1025-34.
6.         Vargas AJ, Thompson PA. Diet and nutrient factors in colorectal cancer risk. Nutr Clin Pract 2012; 27: 613-23.
7.         NICE. Walking and Cycling Should Become the Norm for Short Journeys. (28th November 2012.
8.         Health D.O. Facts and Figures on Obesity.
9.         Hu FB. Plant-based foods and prevention of cardiovascular disease: an overview. Am J Clin Nutr 2003; 78: 544S-51S.
10.       Mozaffarian D, Appel LJ, Van Horn L. Components of a cardioprotective diet: new insights. Circulation 2011; 123: 2870-91.
11.       Gray P, Gabriel B, Thies F et al. Fish oil supplementation augments post-exercise immune function in young males. Brain Behav Immun 2012; 26: 1265-72.
12.       Augustsson K, Michaud DS, Rimm EB et al. A prospective study of intake of fish and marine fatty acids and prostate cancer. Cancer Epidemiol Biomarkers Prev 2003; 12: 64-7.
13.       Rimando AM, Suh N. Biological/chemopreventive activity of stilbenes and their effect on colon cancer. Planta Med 2008; 74: 1635-43.
14.       Shapiro TA, Fahey JW, Wade KL et al. Human metabolism and excretion of cancer chemoprotective glucosinolates and isothiocyanates of cruciferous vegetables. Cancer Epidemiol Biomarkers Prev 1998; 7: 1091-100.
15.       Nishino H, Murakosh M, Ii T et al. Carotenoids in cancer chemoprevention. Cancer Metastasis Rev 2002; 21: 257-64.

16.       Hollenberg NK, Fisher ND, McCullough ML. Flavanols, the Kuna, cocoa consumption, and nitric oxide. J Am Soc Hypertens 2009; 3: 105-12.

That's part 1.Part 2 should be with you towards the end of this week.

No comments:

Post a Comment