• References

    De la Monte SM (2012). Contributions of brain insulin resistance and deficiency in amyloid-related neurodegeneration in Alzheimer’s disease. Drugs.  72(1):49–66.

    Gasic-Milenkovic J et al. (2003). Advanced glycation end products cause lipid peroxidation in the human neuronal cell line SH-SY5Y. J Alzheimers Dis. 5(1):25-30. 

    Jaunmuktane Z (2015). Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy. Nature 525,247–250.

    Lacor PN et al. (2007). Aß Oligomer-Induced Aberrations in Synapse Composition, Shape, and Density Provide a Molecular Basis for Loss of Connectivity in Alzheimer's Disease. The Journal of Neuroscience. 27(4):796–807.

    Laurén J et al. (2009). Cellular Prion Protein Mediates Impairment of Synaptic Plasticity by Amyloid-β Oligomers. Nature. 457(7233):1128–32.

    Li X et al. (2015). Link between type 2 diabetes and Alzheimer’s disease: from epidemiology to mechanism and treatment Clin. Interv. Aging. 10: 549–560.

    Luchsinger JA (2012). Type 2 diabetes and cognitive impairment: linking mechanisms. J Alzheimer’s Dis. 30(Suppl 2):S185–S198.

    Münch G et al. (1998) Alzheimer’s disease- synergistic effects of glucose deficit, oxidative stress and advanced glycation endproducts. J Neural Transm. 105:439-461.

    Naderali EK et al. (2009). Obesity and Alzheimer's disease: a link between body weight and cognitive function in old age. Am. J. Alzheimers. Dis. Other Demen.  24(6):445-9.

    Roberts M (2015) ‘Transmittable alzheimer’s’ concept raised. BBC News online. Available: http://www.bbc.com/news/health-34184470 [accessed 10 September 2015].

    Serban AI et al. (2015). AGEs-Induced IL-6 synthesis precedes RAGE up-regulation in HEK 293 cells: An alternative inflammatory mechanism? Int. J. Mol. Sci. 16 20100-20117.

    Singh R et al. (2001). Advanced glycation end-products: a review. Diabetologia. 44(2):129-46.

    Sjoholm A and Nystrom T (2006). Inflammation and the etiology of type 2 diabetes. Diabetes Metab Res Rev. 22(1):4–10.

    Swardfager W (2010). A meta-analysis of cytokines in Alzheimer's disease. Biol Psychiatry. 15 68(10):930-41.

    Uribarri J et al. (2010). Advanced Glycation End Products in Foods and a Practical Guide to Their Reduction in the Diet. Journal of the American Dietetic Association. 110(6):911-16.

    Von Laue S et al. (2000). Stimulation of endogenous GH and interleukin-6 receptors selectively activates different Jaks and Stats, with a Stat5 specific synergistic effect of dexamethasone. J Endocrinol.165(2):301-11.

Are you likely to develop Alzheimer’s from grilled food?

09 October, 2015
Are you likely to develop Alzheimer’s from grilled food?
A new theory has emerged, that Alzheimer’s disease could be contracted from contaminated medical instruments during certain surgeries or injections (Jaunmuktane, 2015). This is due to amyloid deposits, which are fibrous protein aggregates that can accumulate in organs in certain diseases such as Alzheimer’s. Amyloid derived toxic oligomers bind to neuron receptors which disrupt communication in the brain (Lacor et al. 2007). There is a strong link between the prion protein and Alzheimer’s disease because research shows that they act as receptors for amyloid derived toxic oligomers (Laurén et al. 2009).

This concept of transmissible Alzheimer’s gained momentum following the discovery of amyloid deposits in the brain of deceased patients who contracted Creutzfeldt-Jakob disease (CJD) from contaminated human growth hormone injections that they received as children (Jaunmuktane, 2015). These injections were discontinued in 1985 due to the links to CJD, and so the risks of contracting CJD in this way are now very low (Roberts, BBC News). The idea that Alzheimer’s could also be contracted in a similar way to CJD is a cause for concern, and further research would be needed to determine whether these concerns are valid. Although the ability to contract Alzheimer’s disease is a concerning concept, it would be very difficult for us to avoid medical treatment should we need it. It is also highly unlikely due to the measures already employed by medical staff to reduce the risk of CJD infections. 

Could changing our lifestyle reduce risk?

It therefore seems more practical to reduce our chances of developing Alzheimer’s by changing our life styles since, in addition to genetic predisposition, the development of Alzheimer’s has been strongly linked to obesity (Naderali et al. 2009) and diabetes (Li et al. 2015). Some of the proposed mechanisms of these links are: insulin resistance/deficiency, impaired insulin receptor or growth factor signaling, glucose toxicity, advanced glycation end products (AGEs), cerebrovascular injury, and vascular inflammation (Li et al. 2015, Sjoholm A and Nystrom T 2006, Luchsinger JA 2012, and De la Monte SM 2012). It would seem that most of the possible causes on this list would be difficult to avoid directly, however if you were to select one of them, AGEs would be a sensible thing to reduce in your lifestyle. 

AGEs are proteins or lipids that have been glycated or oxidized after exposure to aldose sugars (Singh et al. 2001). They have a negative effect upon the body because they can accumulate and activate the inflammatory pathway. AGEs have been found within amyloid deposits in Alzheimer’s patients (Münch et al. 1998) and cause lipid peroxidation in human neuronal cells (Gasic-Milenkovic et al. 2003). Recent studies have demonstrated a link between initial upregulation of the inflammatory cytokine IL-6 following exposure of human embryonic kidney cells (HEK 293) to AGEs (Serban et al. 2015). These findings align with research which shows that various cell types are able to produce an inflammatory response upon IL-6 detection (Von Laue et al. 2000). IL-6 stimulates inflammatory and auto immune processes in many diseases, including Alzheimer’s disease (Swardfager et al. 2010). Therefore, if AGEs can increase the levels of IL-6 for certain cell types, then this could suggest an additional link between AGEs and the development of Alzheimer’s disease.  

AGEs and heat-processed food

So you might be thinking how does this link to grilled food? Well, AGEs can be found in heat-processed foods. These are called dietary advanced glycation end products (dAGEs) and consuming them can create oxidative stress and inflammation (Uribarri et al. 2010). The levels of AGEs are significantly increased in food subjected to higher temperatures such as what you get when you use barbecues (BBQ) or grills. A full list of AGE levels in 549 different foods is available in an article for the Journal of the Academy of Nutrition and Dietetics (Uribarri et al. 2010). Below are the top 15 foods to avoid that contain high levels of AGEs: 

1. Fried bacon
2. Butter
3. Sesame oil
4. BBQ chicken
5. Margarine
6. Parmesan cheese
7. Olive oil
8. Peanut oil (Planters)
9. Beef frankfurter (broiled)
10. Pine nuts (pignolias)
11. Cream cheese
12. Diaglycerol oil
13. Beef steak
14. Extra virgin olive oil
15. Roasted cashews

 

Foods that contain high fat and protein content are more likely to contain higher concentrations of AGEs, and these increase when food is cooked at high temperatures under dry conditions, such as BBQ/grilling conditions. For example, chicken roasted and then finished on the grill was found to contain 18520 AGE kU/100g (Uribarri et al. 2010). Foods low in AGEs includes carbohydrate rich foods such as vegetables, fruit, whole grains, and milk (Uribarri et al. 2010). 

 

This pyramid diagram shows the levels of AGE kU/100g (as determined by carboxymethyllysine content) present in chicken breast after various cooking methods (Uribarri et al. 2010).

Research suggests that avoiding these dAGEs and changing the way food is cooked can help to slow down the development of diseases and aging (Uribarri et al. 2010). So if you want to reduce your chances of developing a range of diseases, including Alzheimer’s then fried, roasted and grilled food would be off the menu, but the real question is, would it be worth it?


Research into AGE induced IL-6 synthesis and its influence on inflammatory mechanisms was published by Serben et al. (2015) with the aid of our new PrecisionAb antibody NF-kB p65. We are proud that our premium antibodies are being used for such important research.

References

De la Monte SM (2012). Contributions of brain insulin resistance and deficiency in amyloid-related neurodegeneration in Alzheimer’s disease. Drugs.  72(1):49–66.

Gasic-Milenkovic J et al. (2003). Advanced glycation end products cause lipid peroxidation in the human neuronal cell line SH-SY5Y. J Alzheimers Dis. 5(1):25-30. 

Jaunmuktane Z (2015). Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy. Nature 525,247–250.

Lacor PN et al. (2007). Aß Oligomer-Induced Aberrations in Synapse Composition, Shape, and Density Provide a Molecular Basis for Loss of Connectivity in Alzheimer's Disease. The Journal of Neuroscience. 27(4):796–807.

Laurén J et al. (2009). Cellular Prion Protein Mediates Impairment of Synaptic Plasticity by Amyloid-β Oligomers. Nature. 457(7233):1128–32.

Li X et al. (2015). Link between type 2 diabetes and Alzheimer’s disease: from epidemiology to mechanism and treatment Clin. Interv. Aging. 10: 549–560.

Luchsinger JA (2012). Type 2 diabetes and cognitive impairment: linking mechanisms. J Alzheimer’s Dis. 30(Suppl 2):S185–S198.

Münch G et al. (1998) Alzheimer’s disease- synergistic effects of glucose deficit, oxidative stress and advanced glycation endproducts. J Neural Transm. 105:439-461.

Naderali EK et al. (2009). Obesity and Alzheimer's disease: a link between body weight and cognitive function in old age. Am. J. Alzheimers. Dis. Other Demen.  24(6):445-9.

Roberts M (2015) ‘Transmittable alzheimer’s’ concept raised. BBC News online. Available: http://www.bbc.com/news/health-34184470 [accessed 10 September 2015].

Serban AI et al. (2015). AGEs-Induced IL-6 synthesis precedes RAGE up-regulation in HEK 293 cells: An alternative inflammatory mechanism? Int. J. Mol. Sci. 16 20100-20117.

Singh R et al. (2001). Advanced glycation end-products: a review. Diabetologia. 44(2):129-46.

Sjoholm A and Nystrom T (2006). Inflammation and the etiology of type 2 diabetes. Diabetes Metab Res Rev. 22(1):4–10.

Swardfager W (2010). A meta-analysis of cytokines in Alzheimer's disease. Biol Psychiatry. 15 68(10):930-41.

Uribarri J et al. (2010). Advanced Glycation End Products in Foods and a Practical Guide to Their Reduction in the Diet. Journal of the American Dietetic Association. 110(6):911-16.

Von Laue S et al. (2000). Stimulation of endogenous GH and interleukin-6 receptors selectively activates different Jaks and Stats, with a Stat5 specific synergistic effect of dexamethasone. J Endocrinol.165(2):301-11.

 

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