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McCarrison Society - Delegate Contribution
Westminster Food & Nutrition Forum Keynote Seminar: Food in schools and early years settings: standards, from school meals and the future of the policy
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"It is incontrovertibly obvious deficiency of any nutrient which is essential for every tissue will eventually lead to abnormal function in every tissue."  [1]

The forum recognised obesity is a significant concern underlying the formulation of school food strategies. The government obesity strategy [2] adopts a calories in calories out perspective with a central focus on sugar intake.

Highly refined processed nutrient damaged and depleted carbohydrates including sugar, are very clearly factors in a range of Western non-infective diseases including obesity and related diabetes. Diabetes and obesity were rare in indigenous population groups prior to adoption of refined western foods.

In the 1930s East and West Africa government data for hospitals mainly attended by indigenous non-westernised patients, eating traditional diets, including coarsely milled grain /corn, record diabetes rates under 0.2%, [3]  and obesity was rarely observed. Rates of both increased greatly with introduction of western refined foods.

However, despite a 30% reduction in sugar intake since the 1930s, absence of reduction of UK obesity and diabetes rates suggests obesity and diabetes have wider causation than sugar intake alone.

1930-34 sugar consumption per head per year in the United Kingdom was 110lbs [4] , but obesity was the exception, and diabetes occurrence was very considerably lower, albeit relative mortality rates were probably higher.

In contrast current UK sugar consumption is around 75lbs per head, "nearly a third of children aged 2 to 15 are overweight or obese", and 4.5 million (3.3 million diagnosed) in the UK are estimated to have diabetes.

Arguably refined western carbohydrate related foods additional to sugar are equally or more culpable. Carbohydrate is derived from seasonal plant reproductive material, which is also rich in omega-6 linoleic acid, and sometimes accompanied by fructose glucose and sucrose in fruiting plants. Plant reproductive material availability reflects environmental fecundity, and I propose switches on and off human reproductive capacity, [5]  through oxidative stress messengering, and primarily through oxidative linoleic acid product pathways. [5]

Optimisation of successful reproductive outcomes requires fat accretion. The oxidised products of linoleic acid including 13 HODE, most common oxidised lipids in plasma, and primary endogenous activator of PPAR gamma, is often referred to as a "master regulator of adipogenous". Linoleic acid intake has risen significantly in the 20th century. [6]

Interestingly NIH USA data, suggested better correlation between chicken intake and human obesity, than for sugar intake. [7]  Chicken lipid profile has been changed by extensive grain feeding; consequently linoleic acid may represent up to 30% chicken fat. Use of biocides, bleaches, and aggressive cooking such as frying may raise oxidised linoleic acid in chicken. Excess oxidised linoleic acid arguably drives obesity by multiple pathways. Linoleic acid raises insulin, which signal for fat storage. [8]

Effects of carbohydrates and linoleic acid are synergistic. Glucose and fructose are easily oxidised driving oxidative stress pathways. Glucose raises insulin. Excess fructose is directed to fat accretion primarily. A downstream product of long chain omega-6 arachidonic acid is a primary endogenous activator of the endocannabinoid pathways, so signalling hunger. . .

Refined flour is also arguably an issue. During WWII mandatory usage of high extraction flour arguably factored in diabetes mortality reduction, and other improved health parameters including significant falls in carries rates in children. [9]  Modern wholemeal flour is disassembled and reassembled, heated and or otherwise treated, to increase shelf life, and manufacturing ease of bread, so not comparable to more traditional milling practices. Such treatment oxidises vulnerable components [10] including antioxidant factors making them non-bioavailable, also potentially increasing presence of obesogenic inflammatory oxidised linoleic acid products.

Arguably refined foods including heavily industrialised processed flours should be excluded from school diets, and use of food deep fried in vegetable oils be minimised.


[1] Dr Hugh Sinclair DM DSc FRCP (McCarrison beta-web site under development) http://mccarrison.alakmalak.org/visionaries/sinclair/

[2] Childhood obesity: a plan for action (updated Jan 2017) https://www.gov.uk/government/publications/childhood-obesity-a-plan-for-action/childhood-obesity-a-plan-for-action

[3] C.P. Donnison MD MCRP - Civilisation and Western Disease – (P. 10 -11) (McCarrison beta-web site under development) http://mccarrison.alakmalak.org/resources/other-sources-on-western-disease-on-non-western-groups/

[4] McCollum E, Orent-Keiles E, Day H. The Newer Knowledge of Nutrition (p.616) 5th. Edn. 1940 the Macmillan company

[5] Ed. Hegde M, Zanwar A, Adekar S. Omega-3 Fatty Acids Keys to Nutritional Health. The Roles of Linoleic and Alpha-linolenic Acid, Their Oxylipins and the PPAR Alpha-, Delta and Gamma-Related Peroxisomal Pathways

on Obesity in the Context of a “Western”. (Ch.27-32) Brown R. 2016 Springer 978-3-319-40456-1

[6] Blasbalg T, Hibbeln J, Ramsden C, Majchrzak S, Rawlings R. (Fig 2.) Changes in Consumption of Omega-3 and Omega-6 Fatty Acids in the United States during the 20th Century. Am J Clin Nutr. 2011 May; 93(5): 950–962. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3076650/

[7] Alvheim A, Malde M, Osei-Hyiaman D, Lin Y, Pawlosky R, Madsen L, Kristiansen K, Frøyland L, Hibbeln J. Dietary Linoleic Acid Elevates Endogenous Two-AG and Anandamide and Induces Obesity. (Fig 3 and 5) 2012; doi:10.1038/oby.2012.38. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3458187/

[8] Lai M, Teng T, Yang C. The natural PPAR agonist linoleic acid stimulated insulin release in the rat pancreas. (Fig 2 and 3). J Vet Med Sci. 2013;75(11):1449–1454. Diabetes Obes Metab. 2012;14 (11):1010–9. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3942972/

[9] Mellanby E. A Story of Nutritional Research, 1950, The Williams & Williams Company, Baltimore.

[10] Lehtinen P, KiiliaÈinen K, LehtomaÈki I, Laakso S. Effect of Heat Treatment on Lipid Stability in Processed Oats. Journal of Cereal Science 37 (2003) 215±221 http://lib.tkk.fi/Diss/2003/isbn9512265575/article5.pdf?origin%3Dpublication_detail

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