Alzheimer’s disease is one of those conditions where genetics is known to play a profound role but is not the sole factor in disease development and progression. The evidence is mounting that the environment has a great deal to do with the development of this neurodegenerative disorder. Moreover, it is now known that the right kind of nutrition and lifestyle may play preventive role in many cases.
Certain environmental factors, like exposure to toxic chemicals and brain injury, have long been known to increase the risk of Alzheimer’s, dementia, and Parkinsonism. However, the intricacies of this interaction between the environment and genetics is poorly understood. What we know for sure is that the environment does play an important role in the diseases’ development and that certain genes can be predisposing factors.
For instance, a gene called APOE4 is considered to be one of the major risk factors in developing familial Alzheimer’s disease. However, studies have shown the much lower prevalence of Alzheimer’s in sub-Saharan Africans as compared to Africans living in Western societies, where pollution, industrial food, stress, and a sedentary lifestyle render people more susceptible to the disease. There have been very few studies comparing the prevalence of Alzheimer’s among genetically similar populations living in completely different environments. One such study compared the residents of a small Nigerian town with African Americans and found the incidence of Alzheimer’s much higher among those living in the USA.
Let us look at the factors that have been strongly linked with neurodegeneration, dementia, and Alzheimer’s disease.
Acute exposure to and poisoning with heavy metals and pesticides has been well studied and documented. However, neurodegeneration occurs due to chronic low-level exposure to these toxic elements. The long term accumulativeexposure to lead has been shown to cause a decrease in memory and progressive decline in mental functions. In contrast to lead, the role of aluminium has long been overlooked. This metal is present in many medications (like antacid suspensions). Aluminium is an additive in various commercially available food products, food colorants, and is even used to purify water. There is increasing evidence that it may be playing a role in the development of Alzheimer’s disease.
Air pollution is something to that many of us are exposed to from a very young age, and in most cases, we do not have much choice. Polluted air in large cities contains a toxic cocktail of organic and non-organic compounds, metals, and gases. Evidence of a link between neurodegeneration and air pollution is growing.
Unlike in developing nations, non-infectious diseases are the main health threat in Western societies, and an unhealthy lifestyle is the main causative factor in the development of serious chronic conditions. Some estimates suggest that obesity and a sedentary lifestyle are now killing more people than any other disease. Research data show that the risk of developing Alzheimer’s disease increases by as much as 6-fold in obese people with high blood pressure and high cholesterol level.
Physical activity decreases the risk of almost any disease, thus having a direct and indirect effect on the development of Alzheimer’s as well. Apart from physical exercise, it is also important to stay mentally active. Older people who continue to participate in mental activities, such as learning new things, reading, or even listening to music have a lower chance of declines in brain function. Social participation may also help to stay mentally active. Many people tend to become isolated as they grow old. However, maintaining a high level of social activity not only decreases stress and improves mood but may also prevent or delays Alzheimer’s disease and dementia.
Psychological stress results in an increased level of stress hormones that have been shown to be damaging for brain functionality. Emotional distress like depression and anxiety in young people and middle-aged adults is thought to increase the risk of developing dementia and Alzheimer’s later in life. Some researchers think that emotional distress could be considered an early symptom of neurodegeneration. There is now a wide consensus that emotional distress is a risk factor for dementia and mental decline.
Nutrition is perhaps the single most important factor that can either prevent or aggregate mental decline. A balanced diet rich in fruits and vegetables is a preventive factor, due to the high content of vitamins, microelements, and antioxidants. Diets with a high saturated fat and cholesterol content are harmful, as these fats block blood vessels and are the reason for stroke and cardiac diseases. As the brain is mostly made of fats, it is important to have a balanced diet. Omega-3 has been shown to be neuroprotective, and products like fish oil, soya oil, and walnuts, are a rich source of this compound.
The familial genetic history of neurodegenerative diseases does not necessarily mean that a person will develop mental decline. Neurodegenerative diseases are still highly preventable. By avoiding triggers in the environment and living a healthy, active life, one may expect to remain mentally alert until ripe old age.
Bazan, N.G., 2007. Omega-3 fatty acids, pro-inflammatory signaling and…?: Current Opinion in Clinical Nutrition & Metabolic Care. Curr. Opin. Clin. Nutr. Metab. Care 10, 136–141. doi: 10.1097/MCO.0b013e32802b7030.
Castillo-Fernandez, J.E., Spector, T.D., Bell, J.T., 2014. Epigenetics of discordant monozygotic twins: implications for disease. Genome Med. 6. doi: 10.1186/s13073-014-0060-z.
Corbo, R.M., Scacchi, R., 1999. Apolipoprotein E (APOE) allele distribution in the world. Is APOE*4 a ‘thrifty’ allele? Ann. Hum. Genet. 63, 301–310. doi: 10.1046/j.1469-1809.1999.6340301.x.
Fleminger, S., Oliver, D.L., Lovestone, S., Rabe-Hesketh, S., Giora, A., 2003. Head injury as a risk factor for Alzheimer’s disease: the evidence 10 years on; a partial replication. J. Neurol. Neurosurg. Psychiatry 74, 857–862. doi: 10.1136/jnnp.74.7.857.
Fratiglioni, L., Paillard-Borg, S., Winblad, B., 2004. An active and socially integrated lifestyle in late life might protect against dementia. Lancet Neurol. 3, 343–353. doi: 10.1016/S1474-4422(04)00767-7.
González-Maciel, A., Reynoso-Robles, R., Torres-Jardón, R., Mukherjee, P.S., Calderón-Garcidueñas, L., 2017. Combustion-Derived Nanoparticles in Key Brain Target Cells and Organelles in Young Urbanites: Culprit Hidden in Plain Sight in Alzheimer’s Disease Development. J. Alzheimers Dis. 59, 189–208. doi: 10.3233/JAD-170012.
Grant, W.B., Campbell, A., Itzhaki, R.F., Savory, J., 2002. The significance of environmental factors in the etiology of Alzheimer’s disease. J. Alzheimers Dis. 4, 179–189. doi: 10.3233/JAD-2002-4308.
Hendrie, H.C., Ogunniyi, A., Hall, K.S., Baiyewu, O., Unverzagt, F.W., Gureje, O., Gao, S., Evans, R.M., Ogunseyinde, A.O., Adeyinka, A.O., Musick, B., Hui, S.L., 2001. Incidence of Dementia and Alzheimer Disease in 2 Communities: Yoruba Residing in Ibadan, Nigeria, and African Americans Residing in Indianapolis, Indiana. JAMA 285, 739–747. doi: 10.1001/jama.285.6.739.
Jorm, A.F., 2000. Is Depression a Risk Factor for Dementia or Cognitive Decline? Gerontology 46, 219–227. doi: 10.1159/000022163.
Kivipelto, M., Ngandu, T., Fratiglioni, L., Viitanen, M., Kåreholt, I., Winblad, B., Helkala, E.-L., Tuomilehto, J., Soininen, H., Nissinen, A., 2005. Obesity and Vascular Risk Factors at Midlife and the Risk of Dementia and Alzheimer Disease. Arch. Neurol. 62, 1556–1560. doi: 10.1001/archneur.62.10.1556.
Liu, C.-C., Kanekiyo, T., Xu, H., Bu, G., 2013. Apolipoprotein E and Alzheimer disease: risk, mechanisms, and therapy. Nat. Rev. Neurol. 9, 106–118. doi: 10.1038/nrneurol.2012.263.
Stewart, W.F., Schwartz, B.S., Davatzikos, C., Shen, D., Liu, D., Wu, X., Todd, A.C., Shi, W., Bassett, S., Youssem, D., 2006. Past adult lead exposure is linked to neurodegeneration measured by brain MRI. Neurology 66, 1476–1484. doi: 10.1212/01.wnl.0000216138.69777.15.
Thompson, N.P., Driscoll, R., Pounder, R.E., Wakefield, A.J., 1996. Genetics versus environment in inflammatory bowel disease: results of a British twin study. BMJ 312, 95–96. doi: 10.1136/bmj.312.7023.95.
Wilson, R.S., Leon, C.F.M. de, Barnes, L.L., Schneider, J.A., Bienias, J.L., Evans, D.A., Bennett, D.A., 2002. Participation in Cognitively Stimulating Activities and Risk of Incident Alzheimer Disease. JAMA 287, 742–748. doi: 10.1001/jama.287.6.742.
Vía Brain Blogger http://ift.tt/2jw6kT3
via WordPress http://ift.tt/2wgrMRU