Eating purple fruits such as blueberries and drinking green tea can help ward off diseases including Alzheimer’s, Multiple Sclerosis and Parkinson’s, a University of Manchester report claims. New research from Professor Douglas Kell, published in the journal Archives of Toxicology, has found that the majority of debilitating illnesses are in part caused by poorly-bound iron which causes the production of dangerous toxins that can react with the components of living systems. These toxins, called hydroxyl radicals, cause degenerative diseases of many kinds in different parts of the body. In order to protect the body from these dangerous varieties of poorly-bound iron, it is vital to take on nutrients, known as iron chelators, which can bind the iron tightly.
Brightly-coloured fruits and vegetables are excellent sources of chelators, as is green tea, with purple fruits considered to have the best chance of binding the iron effectively. However, despite conflicting reports, the widely-publicised benefits of red wine seem to work in a different way, and have no similar benefits, Professor Kell’s paper noted.
This new paper is the first time the link has been made between so many different diseases and the presence of the wrong form of iron, and gives a crucial clue as to how to prevent them or at least slow them down. Professor Kell argues that the means by which poorly-liganded iron accelerates the onset of debilitating diseases shows up areas in which current, traditional thinking is flawed and can be dangerous. For instance, Vitamin C is thought to be of great benefit to the body’s ability to defend itself against toxins and diseases. However Professor Kell, who is Professor of Bioanalytical Science at the University, indicates that excess vitamin C can in fact have the opposite effect to that intended if unliganded iron is present.
Only when iron is suitably and safely bound (“chelated”) will vitamin C work effectively. Professor Kell said: “Much of modern biology has been concerned with the role of different genes in human disease. “The importance of iron may have been missed because there is no gene for iron as such. What I have highlighted in this work is therefore a crucial area for further investigation, as many simple predictions follow from my analysis.
“If true they might change greatly the means by which we seek to prevent and even cure such diseases.”
The paper directly compared findings from two separate studies: 'The Diets of British Schoolchildren' conducted by the Department of health (DH) in 1983 (Department of Health 1989); and the National Diet and Nutrition Survey (NDNS) from 1997 (Gregory & Lowe, 2000).
Gibson's analysis found that total sugar intake averaged at 115g/day in 1983, compared with 113g/day in 1997. Allowing for exclusions of low and high energy reporters, intake levels were 122g/day (1983) and 127g/day (1997), showing a marginal and insignificant increase over the study period. Contrastingly, mean body weight increased significantly during the period of the DH and NDNS surveys, showing a rise of 1.9kg for 10-11 year olds and 3.4kg among 14-15 year olds. BMI increased from 17.9 to 18.6 units in the younger group, and 20.2 to 21.3 units in the older group. According to these calculations, the prevalence of being overweight (plus obesity), as defined by the International Obesity Taskforce (IOTF) cut-offs (91st percentile) rose from 13% to 21-22% between surveys. Gibson concluded that the slight increase in consumption of total sugars did not account for the significant increase in BMI, equivalent to 2-3 kg over the review period.
During the same period, Gibson found that mean energy intake (EI) was 3% lower in 1997 than in 1983, mainly as a result of lower fat intake. This change in overall energy consumption meant that sugars represented a higher proportion of daily energy intake in 1997 (23.6% versus 22.3%), despite total sugar consumption remaining relatively static in comparison. The review surmises that the most likely cause for the increased BMI is a decline in energy expenditure.
In addition, Gibson's paper found that basal metabolic rate (BMR) increased by approximately 3% between surveys as a result of higher body weights, and it is estimated that EI in relation to basal requirements was even lower at 6%. Gibson found that the paradox of rising BMI, despite a 2-3% rise in BMR and an EI that is static or falling, pointed to declining energy expenditure as an important factor in the change.
The Gibson analysis showed that the key sources of sugars in the diet have changed with a marked shift away from table sugar and smaller falls in consumption of sugars through milk, biscuits and cakes, counterbalanced by a significant increase in sugars consumed in soft drinks and, to a lesser extent, fruit juice and breakfast cereals.
A conclusion of Gibson's reanalysis of data from the DH and NDNS studies, that consumption of total sugars remained relatively static during the period, providing an estimated 22% of energy, is supported by findings from a repeated cross sectional study of children's food and drink intake, conducted in Northumberland in 1989, 1990 and 2000 which looked at trends in children's food and drink intake.
Sigrid Gibson, the paper's author, said: “There are very few studies that have assessed trends in sugar intake over time and particularly over such an extended period. The findings of the reanalysis strongly contradict widespread assumptions that sugar levels in the diet are responsible for rising obesity levels. With dietary sugar intakes relatively static, and overall energy consumption showing decline, increased BMI levels cannot be attributed to sugar consumption.”