When you raise the subject of over-eating and obesity, you often see people at their worst. The comment threads discussing these issues reveal a legion of bullies, who appear to delight in other people’s problems.
When alcoholism and drug addiction are discussed, the tone tends to be sympathetic. When obesity is discussed, the conversation is dominated by mockery and blame, though the evidence suggests that it can be driven by similar forms of addiction(1,2,3,4). I suspect that much of this mockery is a coded form of snobbery: the strong association between poor diets and poverty allows people to use this issue as a cipher for something else they want to say, which is less socially acceptable.
But this problem belongs to all of us. Even if you can detach yourself from the suffering caused by diseases arising from bad diets, you will carry the cost, as a growing proportion of the health budget will be used to address them. The cost – measured in both human suffering and money – could be far greater than we imagined. A large body of evidence now suggests that Alzheimer’s is primarily a metabolic disease. Some scientists have gone so far as to rename it. They call it diabetes type 3.
New Scientist carried this story on its cover last week(5): since then I’ve been sitting in the library trying to discover whether it stands up. I’ve now read dozens of papers on the subject, testing my cognitive powers to the limit as I’ve tried to get to grips with brain chemistry. While the story is by no means complete, the evidence so far is compelling.
Around 35 million people suffer from Alzheimer’s disease worldwide(6); current projections, based on the rate at which the population ages, suggest that this will rise to 100 million by 2050(7). But if, as many scientists now believe, it is caused largely by the brain’s impaired response to insulin, the numbers could rise much further. In the US, the percentage of the population with diabetes type 2, which is strongly linked to obesity, has almost trebled in 30 years(8). If Alzheimer’s, or “diabetes type 3”, goes the same way, the potential for human suffering is incalculable.
Insulin is the hormone which prompts the liver, muscles and fat to absorb sugar from the blood. Diabetes 2 is caused by excessive blood glucose, resulting either from a deficiency of insulin produced by the pancreas, or resistance to its signals by the organs which would usually take up the glucose.
The association between Alzheimer’s and diabetes 2 is long-established: type 2 sufferers are two to three times more likely to be struck by this dementia than the general population(9). There are also associations between Alzheimer’s and obesity(10) and Alzheimer’s and metabolic syndrome (a complex of diet-related pathologies)(11).
Researchers first proposed that Alzheimer’s was another form of diabetes in 2005. The authors of the original paper investigated the brains of 54 corpses, 28 of which belonged to people who had died of the disease(12). They found that the levels of both insulin and insulin-like growth factors in the brains of Alzheimer’s patients were sharply reduced by comparison to those in the brains of people who had died of other causes. Levels were lowest in the parts of the brain most affected by the disease.
Their work led them to conclude that insulin and insulin-like growth factor are produced not only in the pancreas but also in the brain. Insulin in the brain has a host of functions: as well as glucose metabolism, it helps to regulate the transmission of signals from one nerve cell to another, and affects their growth, plasticity and survival(13,14).
Experiments conducted since then appear to support the link between diet and dementia(15,16,17,18), and researchers have begun to propose potential mechanisms. In common with all brain chemistry, these tend to be fantastically complex, involving, among other impacts, inflammation, stress caused by oxidation, the accumulation of one kind of brain protein and the transformation of another(19,20,21,22). I would need the next six pages of this paper even to begin to explain them, and would doubtless get it wrong (if you’re interested, please follow the links on my website).
Plenty of research still needs to be done. But if the current indications are correct, Alzheimer’s disease could be another catastrophic impact of the junk food industry, and the worst discovered so far. Our governments, as they are in the face of all our major crises, appear to be incapable of responding.
In this country as in many others, the government’s answer to the multiple disasters caused by the consumption of too much sugar and fat is to call on both companies and consumers to regulate themselves. Before he was replaced by someone even worse, the former health secretary, Andrew Lansley, handed much of the responsibility for improving the nation’s diet to food and drinks companies: a strategy that would work only if they volunteered to abandon much of their business(23,24).
A scarcely-regulated food industry can engineer its products – loading them with fat, salt, sugar and high fructose corn syrup – to bypass the neurological signals which would otherwise prompt people to stop eating(25). It can bombard both adults and children with advertising. It can (as we discovered yesterday) use the freedoms granted to academy schools to sell the chocolate, sweets and fizzy drinks now banned from sale in maintained schools(26). It can kill the only effective system (the traffic light label) for informing people how much fat, sugar and salt their food contains. Then it can turn to the government and blame consumers for eating the products it sells. This is class war: a war against the poor fought by the executive class in government and industry.
We cannot yet state unequivocally that poor diet is a leading cause of Alzheimer’s disease, though we can say that the evidence is strong and growing. But if ever there was a case for the precautionary principle, here it is. It’s not as if we lose anything by eating less rubbish. Averting a possible epidemic of this devastating disease means taking on the bullies: those who mock people for their pathologies and those who spread the pathologies by peddling a lethal diet.
This article was first published in the Guardian on 11 September 2012.
For more articles by George Monbiot visit: www.monbiot.com
1. Caroline Davis et al, 2011. Evidence that ‘food addiction’ is a valid phenotype of obesity. Appetite Vol. 57, pp711–717. doi:10.1016/j.appet.2011.08.017
2. Paul J. Kenny, November 2011. Common cellular and molecular mechanisms in obesity and drug addiction. Nature Neuroscience, Vol. 12, pp 638-651. doi:10.1038/nrn3105
3. Joseph Frascella et al, 2010. Shared brain vulnerabilities open the way for nonsubstance addictions: Carving addiction
at a new joint? Annals of the New York Academy of Sciences, Vol. 1187, pp294–315.
4. Ashley N. Gearhardt et al, 2010. Can food be addictive? Public health and policy implications. Addiction, 106, 1208–1212. ad. d_3301 1208..1212
5. Bijal Trivedi, 1st September 2012. Eat Your Way to Dementia. New Scientist.
6. Sónia C. Correia et al, 2011. Insulin-resistant brain state: The culprit in sporadic Alzheimer’s disease? Ageing Research Reviews Vol. 10, 264–273. doi:10.1016/j.arr.2011.01.001
7. Fabio Copped`e et al, 2012. Nutrition and Dementia. Current Gerontology and Geriatrics Research, Vol. 2012, pp1-3.
8. See the graph in Bijal Trivedi, 1st September 2012. Eat Your Way to Dementia. New Scientist.
9. Johanna Zemva and Markus Schubert, September 2011. Central Insulin and Insulin-Like Growth Factor-1 Signaling – Implications for Diabetes Associated Dementia. Current Diabetes Reviews, Vol.7, No.5, pp356-366. doi.org/10.2174/157339911797415594
10. Eg Weili Xu et al, 2011. Midlife overweight and obesity increase late life dementia risk: a population-based twin study. Neurology, Vol. 76, no. 18, pp.1568–1574.
11. M. Vanhanen et al, 2006. Association of metabolic syndrome with Alzheimer disease: A population-based study. Neurology, vol. 67, pp.843–847.
12. Eric Steen et al, 2005. Impaired insulin and insulin-like growth factor expression and signaling mechanisms in Alzheimer’s disease – is this type 3 diabetes?.
Journal of Alzheimer’s Disease, Vol. 7, pp.63–80.
13. Konrad Talbot et al, 2012. Demonstrated brain insulin resistance in Alzheimer’s disease patients is associated with IGF-1 resistance, IRS-1 dysregulation, and cognitive decline. The Journal of Clinical Investigation, Vol.122, No.4, pp.1316–1338. doi:10.1172/JCI59903.
14. Naoki Yamamoto et al, 2012. Brain insulin resistance accelerates Aβ fibrillogenesis by inducing GM1 ganglioside clustering in the presynaptic membranes. Journal of Neurochemistry, Vol. 121, 619–628. doi: 10.1111/j.1471-4159.2012.07668.x
Wei-Qin Zhao and Matthew Townsend, 2009. Insulin resistance and amyloidogenesis as common molecular foundation for type 2 diabetes and Alzheimer’s disease.
Biochimica et Biophysica Acta, Vol.1792, pp.482–496. doi.org/10.1016/j.bbadis.2008.10.014,
16. Sónia C. Correia et al, 2011. Insulin-resistant brain state: The culprit in sporadic Alzheimer’s disease? Ageing Research Reviews Vol. 10, 264–273. doi:10.1016/j.arr.2011.01.001
17. T. Ohara et al, 2011. Glucose tolerance status and risk of dementia in the community, the Hisayama study. Neurology, Vol. 77, pp.1126–1134.
18. Karen Neumann et al, 2008. Insulin resistance and Alzheimer’s disease: molecular links & clinical implications. Current Alzheimer Research, Vol.5, no.5, pp438–447.
19. Eg: Lap Ho et al, 2012. Insulin Receptor Expression and Activity in the Brains of
Nondiabetic Sporadic Alzheimer’s Disease Cases. International Journal of Alzheimer’s Disease, Volume 2012. doi:10.1155/2012/321280
20. Suzanne M. de la Monte, 2012. Contributions of Brain Insulin Resistance and Deficiency in Amyloid-Related Neurodegeneration in Alzheimer’s Disease. Drugs, Vol. 72, no.1, pp. 49-66. doi: 10.2165/11597760
21. Ying Liu et al, 2011. Deficient brain insulin signalling pathway in Alzheimer’s disease and diabetes. Journal of Pathology, Vol. 225, pp.54–62. doi: 0.1002/path.2912
22. Konrad Talbot et al, 2012. Demonstrated brain insulin resistance in Alzheimer’s disease patients is associated with IGF-1 resistance, IRS-1 dysregulation, and cognitive decline. The Journal of Clinical Investigation, Vol.122, No.4, pp.1316–1338. doi:10.1172/JCI59903.