The Impact Of Ultra-Processed Foods On Your Brain

Ultra-processed foods have become a significant part of the modern diet, often characterized by their high levels of added sugars and unhealthy fats, as well as artificial additives and preservatives. These foods, which include soft drinks, packaged snacks, instant meals, and fast food, have been associated with various health issues, including obesity, type 2 diabetes, and cardiovascular disease.

The impact of ultra-processed foods on brain health is a growing area of research, and emerging evidence suggests that the consumption of these foods may have negative effects on cognitive function, mental health, and neurodegenerative diseases. In this article we will discuss the potential impact of ultra-processed foods on brain health, highlighting key scientific findings.

Cognitive Function
The consumption of ultra-processed foods has been linked to poorer cognitive function, particularly in children and adolescents [1,2]. These foods often contain high levels of added sugars, unhealthy fats, and sodium, which may contribute to adverse effects on brain health [3]. For example, high sugar intake has been associated with impaired memory and learning abilities, as well as decreased hippocampal neurogenesis [4,5]. Similarly, diets high in unhealthy fats, such as trans and saturated fats, have been linked to cognitive decline and an increased risk of dementia [6]. Moreover, high sodium intake may negatively impact cognitive function by increasing blood pressure and impairing cerebrovascular function [7].

Mental Health
The consumption of ultra-processed foods has also been linked to an increased risk of mental health issues, such as depression and anxiety. Several large-scale observational studies have found that higher intakes of ultra-processed foods are associated with a higher risk of depression [8,9]. One potential explanation for this relationship is the influence of diet on inflammation and oxidative stress, which are known to contribute to the development of depression [10]. Ultra-processed foods are typically high in added sugars, unhealthy fats, and artificial additives, which can promote inflammation and oxidative stress in the body [11,12].

Another possible mechanism is the impact of ultra-processed foods on the gut microbiome. The gut-brain axis plays a critical role in maintaining mental health, and a healthy gut microbiome is essential for the production of neurotransmitters and the regulation of the immune system [13]. Diets high in ultra-processed foods, which are often low in fiber and rich in artificial additives, may disrupt the balance of the gut microbiome and contribute to the development of mental health disorders [14,15].

Neurodegenerative Diseases
Emerging evidence suggests that the consumption of ultra-processed foods may be associated with an increased risk of neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease [16]. These conditions are characterized by the progressive deterioration of brain function, often resulting from the accumulation of toxic proteins and the loss of neuronal connections. The high levels of added sugars, unhealthy fats, and sodium in ultra-processed foods may contribute to the development of these diseases through various mechanisms, such as promoting inflammation, oxidative stress, and insulin resistance [17,18].

For example, diets high in added sugars have been linked to the production of advanced glycation end products (AGEs), which can accumulate in the brain and contribute to the pathogenesis of Alzheimer's disease [19]. Similarly, high intakes of unhealthy fats, such as trans and saturated fats, may increase the risk of neurodegenerative diseases by promoting the aggregation of amyloid-beta plaques and exacerbating neuronal dysfunction [20]. Finally, high sodium intake has been associated with an increased risk of stroke, which can lead to vascular dementia and cognitive decline [21].

Food Addiction
Ultra-processed foods are often designed to be highly palatable, with specific combinations of sugar, fat, and salt that can stimulate the brain's reward system [22]. This can lead to overeating and the development of food addiction, a phenomenon characterized by compulsive consumption of specific foods despite negative consequences [23]. Food addiction has been linked to alterations in the brain's reward and stress systems, which can contribute to the development of mental health issues, such as depression and anxiety [24].

Additionally, food addiction may exacerbate cognitive decline by promoting overeating and obesity, both of which are risk factors for dementia and other neurodegenerative diseases [25]. Furthermore, the constant exposure to highly palatable, ultra-processed foods can lead to habituation and reduced sensitivity to the rewarding properties of food, which may promote further overconsumption and the development of obesity [26].

Impact on Sleep
The consumption of ultra-processed foods may also have indirect effects on brain health through its impact on sleep quality. Diets high in sugar and unhealthy fats have been associated with poor sleep quality and an increased risk of sleep disorders, such as insomnia and sleep apnea [27,28]. Poor sleep can negatively affect cognitive function, memory consolidation, and emotional regulation, as well as increase the risk of mental health disorders [29]. Moreover, sleep disturbances have been linked to an increased risk of neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease [30].

In summary, the consumption of ultra-processed foods has been associated with various negative effects on brain health, including impaired cognitive function, increased risk of mental health issues, and a heightened risk of neurodegenerative diseases. By making informed dietary choices and reducing the intake of ultra-processed foods, we can promote overall brain health and potentially decrease our risk of developing these conditions.

References
[1] Li, Y., Lv, M. R., Wei, Y. J., Sun, L., Zhang, J. X., Zhang, H. G., & Li, B. (2017). Dietary patterns and depression risk: a meta-analysis. Psychiatry research, 253, 373-382.
[2] Jacka, F. N., Cherbuin, N., Anstey, K. J., & Butterworth, P. (2014). Dietary patterns and depressive symptoms over time: examining the relationships with socioeconomic position, health behaviours and cardiovascular risk. PloS one, 9(1), e87657.
[3] Micha, R., Peñalvo, J. L., Cudhea, F., Imamura, F., Rehm, C. D., & Mozaffarian, D. (2017). Association between dietary factors and mortality from heart disease, stroke, and type 2 diabetes in the United States. JAMA, 317(9), 912-924.
[4] Beilharz, J. E., Maniam, J., & Morris, M. J. (2015). Diet-induced cognitive deficits: the role of fat and sugar, potential mechanisms and nutritional interventions. Nutrients, 7(8), 6719-6738.
[5] Noble, E. E., Hsu, T. M., & Kanoski, S. E. (2017). Gut to brain dysbiosis: mechanisms linking western diet consumption, the microbiome, and cognitive impairment. Frontiers in behavioral neuroscience, 11, 9.
[6] Morris, M. C., Evans, D. A., Bienias, J. L., Tangney, C. C., Bennett, D. A., Aggarwal, N., ... & Wilson, R. S. (2003). Dietary fats and the risk of incident Alzheimer's disease. Archives of neurology, 60(2), 194-200.
[7] Gardener, H., Rundek, T., Wright, C. B., Elkind, M. S., & Sacco, R. L. (2012). Dietary sodium and risk of stroke in the Northern Manhattan study. Stroke, 43(5), 1200-1205.
[8] Molendijk, M., Molero, P., Sánchez-Pedreño, F. O., Van der Does, W., & Martínez-González, M. A. (2018). Diet quality and depression risk: a systematic review and dose-response meta-analysis of prospective studies. Journal of affective disorders, 226, 346-354.
[9] Adjibade, M., Assmann, K. E., Andreeva, V. A., Lemogne, C., Hercberg, S., Galan, P., ... & Kesse-Guyot, E. (2017). Prospective association between adherence to the French nutritional guidelines, the alternaive healthy eating index-2010, and the risk of depression in the NutriNet-Santé cohort. The Journal of nutrition, 147(12), 2352-2361.
[10] Berk, M., Williams, L. J., Jacka, F. N., O'Neil, A., Pasco, J. A., Moylan, S., ... & Maes, M. (2013). So depression is an inflammatory disease, but where does the inflammation come from?. BMC medicine, 11(1), 1-16.
[11] Fritsche, K. L. (2015). The science of fatty acids and inflammation. Advances in Nutrition, 6(3), 293S-301S.
[12] Francischetti, E. A., Tibirica, E., & da Silva, E. G. (2015). The link between the consumption of ultra-processed foods, the nutritional status and the risk of cardiovascular diseases. Current atherosclerosis reports, 17(11), 64.
[13] Dinan, T. G., & Cryan, J. F. (2017). The microbiome-gut-brain axis in health and disease. Gastroenterology clinics of North America, 46(1), 77-89.
[14] Suez, J., Korem, T., Zeevi, D., Zilberman-Schapira, G., Thaiss, C. A., Maza, O., ... & Kuperman, Y. (2014). Artificial sweeteners induce glucose intolerance by altering the gut microbiota. Nature, 514(7521), 181-186.
[15] Sonnenburg, J. L., & Bäckhed, F. (2016). Diet-microbiota interactions as moderators of human metabolism. Nature, 535(7610), 56-64.
[16] Grant, W. B. (2016). Using multicountry ecological and observational studies to determine dietary risk factors for Alzheimer's disease. Journal of the American College of Nutrition, 35(5), 476-489.
[17] De la Monte, S. M., & Wands, J. R. (2008). Alzheimer's disease is type 3 diabetes-evidence reviewed. Journal of diabetes science and technology, 2(6), 1101-1113.
[18] Kivipelto, M., Ngandu, T., Fratiglioni, L., Viitanen, M., Kå reholt, I., Winblad, B., ... & Nissinen, A. (2005). Obesity and vascular risk factors at midlife and the risk of dementia and Alzheimer disease. Archives of neurology, 62(10), 1556-1560.
[19] Srikanth, V., Maczurek, A., Phan, T., Steele, M., Westcott, B., Juskiw, D., & Münch, G. (2011). Advanced glycation endproducts and their receptor RAGE in Alzheimer's disease. Neurobiology of aging, 32(5), 763-777.
[20] Julien, C., Tremblay, C., Phivilay, A., Berthiaume, L., Emond, V., Julien, P., & Calon, F. (2010). High-fat diet aggravates amyloid-beta and tau pathologies in the 3xTg-AD mouse model. Neurobiology of aging, 31(9), 1516-1531.
[21] Pendlebury, S. T., & Rothwell, P. M. (2009). Prevalence, incidence, and factors associated with pre-stroke and post-stroke dementia: a systematic review and meta-analysis. The Lancet Neurology, 8(11), 1006-1018.
[22] Kessler, D. A. (2009). The end of overeating: Taking control of the insatiable American appetite. Rodale Books.
[23] Gearhardt, A. N., Grilo, C. M., DiLeone, R. J., Brownell, K. D., & Potenza, M. N. (2011). Can food be addictive? Public health and policy implications. Addiction, 106(7), 1208-1212.
[24] Davis, C. (2013). From passive overeating to “food addiction”: A spectrum of compulsion and severity. ISRN Obesity, 2013, 435027.
[25] Whitmer, R. A., Gunderson, E. P., Quesenberry, C. P., Zhou, J., & Yaffe, K. (2007). Body mass index in midlife and risk of Alzheimer disease and vascular dementia. Current Alzheimer research, 4(2), 103-109.
[26] Stice, E., Yokum, S., Burger, K. S., Epstein, L. H., & Small, D. M. (2011). Youth at risk for obesity show greater activation of striatal and somatosensory regions to food. The Journal of neuroscience, 31(12), 4360-4366.
[27] St-Onge, M. P., Roberts, A., Shechter, A., & Choudhury, A. R. (2016). Fiber and saturated fat are associated with sleep arousals and slow wave sleep. Journal of clinical sleep medicine, 12(1), 19-24.
[28] Cao, Y., Wittert, G., Taylor, A. W., Adams, R., Shi, Z., & Appleton, S. (2016). Nutrient patterns and chronic inflammation in a cohort of community-dwelling middle-aged men. Clinical nutrition, 35(5), 1207-1213.
[29] Alhola, P., & Polo-Kantola, P. (2007). Sleep deprivation: Impact on cognitive performance. Neuropsychiatric disease and treatment, 3(5), 553-567.
[30] Ju, Y. E., Lucey, B. P., & Holtzman, D. M. (2014). Sleep and Alzheimer disease pathology—a bidirectional relationship. Nature Reviews Neurology, 10(2), 115-119.