September 2012, Week 2


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Tue, 11 Sep 2012 20:30:57 -0400
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The Mind Thieves

The evidence linking Alzheimer’s disease to the food industry
is strong and growing.

By George Monbiot
September 11, 2012


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

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

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

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

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

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.


1. Caroline Davis et al, 2011. Evidence that ‘food addiction’
is a valid phenotype of obesity. Appetite Vol. 57, pp711-717.

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. doi: 10.1111/j.1749-6632.2009.05420.x

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.

7. Fabio Copped`e et al, 2012. Nutrition and Dementia.
Current Gerontology and Geriatrics Research, Vol. 2012,
pp1-3. doi:10.1155/2012/926082

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.

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 Aß fibrillogenesis by inducing GM1 ganglioside
clustering in the presynaptic membranes. Journal of
Neurochemistry, Vol. 121, 619-628. doi:

15. Eg: 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.

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.

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.






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