Purple fruit health claims are premature
Eating purple-coloured fruit such as blueberries “could help ward off Alzheimer’s, Multiple Sclerosis and Parkinson’s”, The Daily Telegraph has reported. The newspaper says the foods act by soaking up harmful iron compounds.
This theory is based on a scientific paper that looked at the chemical and biological actions of iron and chemicals that bind to it. The author summarises a body of evidence that suggests that a form of iron may play a role in many different diseases, also providing a number of simple predictions of how this might occur.
Crucially, this paper only presents a theory, and we do not yet know if the theory is true. Foods that might react with iron, such as blueberries, are also only mentioned in passing in this paper. Stronger evidence is needed to see whether iron plays a role in the development of diseases such as Alzheimer’s disease. If it does, this could be followed by studies looking at how food might intervene in the actions of iron.
Where did the story come from?
The review article was written by Professor Douglas B Kell of The University of Manchester’s School of Chemistry and Manchester Interdisciplinary Biocentre. Previous work that has led to this review was funded by the Biotechnology and Biological Sciences Research Council, the Engineering and Physical Sciences Research Council and the Medical Research Council.
The study was published in the peer-reviewed journal Archives of Toxicology.
The Daily Telegraph has reported this review in brief and provided balancing quotes from Alzheimer’s organisations. However, the headline “Eating purple fruit could fend off Alzheimer's Disease and Multiple Sclerosis” is misleading, as this is only a theory at this stage. Some other unproven theories raised in the review, such as the possibility that “toxins, called hydroxyl radicals, cause degenerative diseases of many kinds in different parts of the body”, are presented as definite fact in the newspaper article.
What kind of research was this?
This was a review article that proposes a theory that some cellular death is caused by a particular chemical form of iron called ‘poorly liganded iron’. The author summarises a vast amount of research literature in this area, including 43 papers authored or co-authored by himself.
The topic is comprehensively addressed from multiple angles. The field of study involved, known as systems biology, aims to look at the interactions between all the individual parts of biological systems. This includes the toxicology and biochemistry of metabolic pathways as well as their potential to cause disease. The author also discussed some of the future implications of the theory and suggested some ways in which the theory might be researched in the future. One topic focused on was chelators, which are chemicals that bind to metal ions, such as iron, and inactivate the positive charge they carry.
Dietary sources of chelators are briefly mentioned in a small part of this review. These include polyphenols and anthocyanins (pigments found in blueberries and other fruits and vegetables), along with the components of green tea and curry powder. This brief mention of dietary sources appears to have been given undue prominence in the media.
What did the research involve?
This review article introduces the topic by describing the chemical properties of iron and the fact that it is an essential part of the oxygen-carrying blood pigment haemoglobin and many enzymes. The ferric form of iron, which has three positive charges (Fe+++), behaves differently from the ferrous form, which has two positive charges (Fe++). Different ways they can safely bind (respectively either liganded or chelated) are described by the author. An iron ion contains up to six individual chelation sites where other atoms can bind, and chelation is considered to occur when these sites are all bound to other molecules in a way that prevents them reacting with hydrogen peroxide to form toxic hydroxyl radicals. When not all of these sites are bound, the iron is referred to as being “poorly liganded”. The author says that poorly liganded ferrous ions change the “comparatively harmless hydrogen peroxide into the deadly hydroxyl radical”.
The author goes on to list a number of neurodegenerative diseases where research has examined a possible causal link with poorly liganded iron, including:
- stroke
- Huntington’s disease
- Parkinson’s disease
- Alzheimer’s disease
- multiple sclerosis
The review also discusses the roles of poorly liganded iron and chelation in the body, detailing:
- how blood and urine tests can be used as measures of the oxidised form of iron or stores of the substance in the body
- the effect of poorly liganded iron in causing bacteria and virus death
- chemical toxins and their relationship to poorly liganded iron
- the effect of poorly liganded iron on inflammation
- dietary and pharmaceutical treatment of iron toxicity (which is the section where the role of chemicals found in purple fruit is briefly discussed)
What were the basic results?
The author describes several types of iron-chelating natural products found in foodstuffs for which he says no full pharmaceutical regulatory controls are required and which are classed as nutritional substances. These include polyphenols and the pigment anthocyanin found in some fruits, which
he says has proved chemoprotective against cancer in mice. Polyphenols found in green tea and curcumin (a constituent of turmeric) are also referenced.
The theory is that many of the protective effects observed from these chemicals are probably due to the iron chelating, as well as directly antioxidative properties of the molecules.
How did the researchers interpret the results?
The author concludes that a substantial amount of science involves finding patterns he calls “laws” that can be seen in observable data, even when some of these “observables” or their presumed causes seem to have little in common. He acknowledges that the exact molecular mechanisms, cascading actions and networks involved depend on many other factors, but argues that the extensive evidence for iron’s involvement in these diseases is very hard to ignore.
Conclusion
This interesting theory of the role of poorly liganded iron may add to the understanding of the complex metabolic pathways that underlie a number of nerve diseases. However, it is too soon to say that there is a definite role for iron chelation in all these diseases, whether achieved through chemical, pharmaceutical or dietary means. The research has also suggested a number of related theories regarding chelation that appear to be interesting candidates for future research.
Crucially, though, there is still a need for more proof that food can have a meaningful effect on these specific pathways in humans. It would appear that the next steps in the exploration of this theory would be to establish the action of the individual compounds found in foods such as purple fruit and to test whether candidate foods affect either health outcomes or iron chelation in humans. Such research is likely to be long and complex.
