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Effects of sugar on the brain: a peek into Alzheimer’s disease

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Between 2016-2019, adults in the UK consumed an average of 106 g added sugars every day. The Scientific Advisory Committee on Nutrition (SACN) recommends limiting added sugar intake to under 30 g per day [1]. New evidence suggests a link between sugar and Alzheimer’s disease [2]. The good news is this can be managed by good dietary practices.

Can sugar contribute to Alzheimer’s development?

Alzheimer’s disease is sometimes referred to as ‘brain diabetes’ due to the strong link between sugar and cognitive decline [3]. It is characterised by physical and behavioural changes in the brain. An important physical attribute noted in the brains of those affected is formation of plaques and tangles that can block brain cells. These are called amyloid beta and tau proteins. The accumulation of these can lead to memory loss, cognitive impairment, and loss of connections between cells [4]. Less than 1% of those diagnosed have a genetic mutation [16], and not everyone suffering from minor memory issues will get dementia or Alzheimer’s in old age. There are many actionable ways to reduce the risk of the disease. Excess sugar intake has been found to contribute to amyloid beta and tau proteins’ accumulation by disrupting metabolism of glucose. Brain regions more prone to amyloid beta and tau protein accumulation had high levels of glucose. And excess glucose in the brain was associated with higher accumulation [5]. In animal studies, when blood glucose levels were doubled, amyloid beta increased by 20%, and in those with Alzheimer’s, this increased by 40% [6].

Can sugar lead to memory loss?

Apart from contributing to production of amyloid beta, sugar decreases the production of a protein involved in producing new brain cells and connections, and is involved in memory and learning. This protein is called BDNF (brain-derived neurotrophic factor). Sugar decreases BDNF production after only 2 months on a high sugar diet [8]. A diet high in sugar and fat causes damage to the brain area that produces the majority of the BDNF, leading to poor performance on memory and learning tests [9]. There is hope because increasing physical and mental exercises can increase BDNF levels. Having higher levels of BDNF was associated with 33% lower risk of Alzheimer’s [7].

Can sugar shrink your brain?

Some studies suggest that it may. A study found that drinking sugary drinks every day, even when consumed in the form of juices which are generally seen as healthy, is associated with brain shrinkage, and decrease in size of brain areas responsible for memory, learning and cognition [10][11]. Loss of brain volume is a key characteristic of Alzheimer's-inflicted brains. Brain shrinkage can be fixed by certain dietary components and increasing physical activity levels. Improving brain cell connections by learning new skills greatly increases mental functions, regardless of brain size.  This needs to be tied in with reducing sugar intake. In diabetes, high blood glucose levels damage blood vessels. In a similar way, excess sugar damages brain cells and decreases blood flow to the brain, causing breakdown of brain structures. 

Can sugar cause brain inflammation?

Excess sugar in the brain promotes the production of inflammatory compounds [12]. Animal studies demonstrated that just 1 month on a high sugar diet was shown to cause brain inflammation, particularly in areas responsible for memory and learning [8]. 

Can the impact of a high sugar diet be reversed?

There are healthy fats that can repair damaged brains. DHA is a type of omega 3 fat that helps maintain structural integrity of brain structure. Those who consumed higher levels of omega 3 fats were found to have a large volume of brain structures involved in memory, learning and emotions [13]. In animal studies, when BDNF levels decreased after brain injury, supplementing with DHA normalised BDNF levels and restored learning skills [14]. DHA is an anti-inflammatory fat and is known to decrease activity of brain cells involved in inflammation [15]. Since prevention is better than cure, it is advisable to prevent sugar induced damage rather than fixing its damage later. There are many benefits of reducing sugar intake. Anecdotal evidence states that those who cut out sugar from their diet had more energy, were in a better mood, could focus better and slept better. There are simple ways in which you can reduce sugar in your diet:

  • Practice healthy swapping- Replace sugary cereals with whole grain cereals, soda and juices with water and tea, flavoured yoghurts with plain yoghurts, tinned fruit with fresh fruit 
  • Use ingredients like cinnamon, unsweetened applesauce, pureed dates instead of sugar to sweeten meals
  • Read food labels and watch out for terms like sucrose/high fructose corn syrup that are used to disguise sugar among ingredients. Choose low sugar/unsweetened options

References

  1. Public Health England (2020). National Diet and Nutrition Survey Rolling programme Years 9 to 11 (2016/2017 to 2018/2019). GOV.UK.
  2. Rippe, J. and Angelopoulos, T. (2016). Relationship between Added Sugars Consumption and Chronic Disease Risk Factors: Current Understanding. Nutrients, [online] 8(11), p.697. 
  3. de la Monte, S.M. and Wands, J.R. (2008). Alzheimer’s Disease is Type 3 Diabetes—Evidence Reviewed. Journal of Diabetes Science and Technology, [online] 2(6), pp.1101–1113.
  4. Bloom, G.S. (2014). Amyloid-β and tau: the trigger and bullet in Alzheimer disease pathogenesis. JAMA neurology, [online] 71(4), pp.505–8.
  5. Kubis-Kubiak, A. et al. (2020). The Interplay between Diabetes and Alzheimer’s Disease—In the Hunt for Biomarkers. International Journal of Molecular Sciences, [online] 21(8).
  6. Macauley, S.L. et al. (2015). Hyperglycemia modulates extracellular amyloid-β concentrations and neuronal activity in vivo. Journal of Clinical Investigation, 125(6), pp.2463–2467.
  7. Weinstein, G. et al. (2014). Serum Brain-Derived Neurotrophic Factor and the Risk for Dementia. JAMA Neurology, 71(1), p.55.
  8. Beilharz, J. et al. (2015). Diet-Induced Cognitive Deficits: The Role of Fat and Sugar, Potential Mechanisms and Nutritional Interventions. Nutrients, 7(8), pp.6719–6738
  9. Calvo-Ochoa, E. et al. (2014). Short-term high-fat-and-fructose feeding produces insulin signaling alterations accompanied by neurite and synaptic reduction and astroglial activation in the rat hippocampus. Journal of Cerebral Blood Flow & Metabolism, [online] 34(6), pp.1001–1008.
  10. Pase, M.P. et al. (2017). Sugary beverage intake and preclinical Alzheimer’s disease in the community. Alzheimer’s & Dementia, 13(9), pp.955–964. 
  11. Mortby, M.E. et al. (2013). High ‘Normal’ Blood Glucose Is Associated with Decreased Brain Volume and Cognitive Performance in the 60s: The PATH through Life Study. PLoS ONE, [online] 8(9), p.e73697.
  12. Park, J.-S. et al. (2021). Blocking microglial activation of reactive astrocytes is neuroprotective in models of Alzheimer’s disease. Acta Neuropathologica Communications, 9(1). 
  13. Conklin, S.M. et al. (2007). Long-chain omega-3 fatty acid intake is associated positively with corticolimbic gray matter volume in healthy adults. Neuroscience Letters, 421(3), pp.209–212.
  14. Wu, A. et al. (2004). Dietary Omega-3 Fatty Acids Normalize BDNF Levels, Reduce Oxidative Damage, and Counteract Learning Disability after Traumatic Brain Injury in Rats. Journal of Neurotrauma, 21(10), pp.1457–1467.
  15. Heras-Sandoval, D. et al. (2016). Role of docosahexaenoic acid in the modulation of glial cells in Alzheimer’s disease. Journal of Neuroinflammation, [online] 13(1).
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