Monthly Archives: January 2021

Sugar and the Brain

Excerpted from Natural Brain Health by Michael Edson, MS, L.Ac.

With consumption of soft drinks and candy, Americans consume an enormous amount of sugar, the equivalent of more than seven tablespoons daily. This amount of sugar is about 355 calories. We are in the midst of a crisis of obesity in the U.S. and the consumption of sweet foods is part of the problem.

The brain uses more energy than any other organ in the human body and glucose is its source of fuel.  In the adult brain, neurons have the highest energy demand,[i] requiring continuous delivery of glucose from blood. The main process by which this is accomplished is called glycolysis. Glucose provides precursors for neurotransmitter synthesis and ATP to fuel their actions. Glucose is also required for the brain’s energy demands unrelated to signaling.[ii]

However, too much glucose is toxic to brain cells. This is a problem worsened by the fact that regular intake of sugar has drug-like effects in the reward center of the brain, creating a desire for more sugar. High blood glucose levels can negatively affect the brain in a number of ways:

  1. It reduces functional connectivity of the default mode network, that system of the brain which links the individual with the outside world.[iii] Such altered functionality is associated with cognitive impairments.
  2. It can cause the brain to atrophy or shrink[iv] as does deteriorating brain glucose metabolism[v]
  3. It can lead to cerebral small vessel disease which restricts blood flow in the brain which can result in cognitive difficulties and, if severe enough, can cause vascular dementia.[vi]

High Blood Sugar

The body needs insulin to carry glucose into the brain. Excess sugar (and refined carbohydrate intake) over time can result in insulin insensitivity (requiring the body to make more insulin) contributing the type-2 diabetes. The effects of glucose and other forms of sugar on the brain may be the most profound in diabetes.

Research strongly supports the fact that people without diabetes but with above normal blood sugar levels have an increased risk of developing dementia.[vii] There is a relationship between the breakdown of glycolysis and Alzheimer’s disease,[viii] the severity of which is linked to the severity of Alzheimer’s pathology. Lower rates of glycolysis and higher brain glucose levels correlate to more severe plaques and tangles in the brains of people with the disease. Enzymes, amino acids serine, glycine, and alanine are essential parts of glycolysis, and are lower in Alzheimer’s cases compared to normal brain tissue samples.[ix] In addition, lower enzyme activity is associated with more severe Alzheimer’s pathology in the brain and the development of symptoms.

Hypoglycemia is a common complication of diabetes caused by low glucose levels in the blood. This can lead to loss of energy for brain function and is linked to poor attention and cognitive function.

Inflammation

Sweeteners of all kinds contribute to inflammation. Sugar is one of the most acidic foods, and excess sugar in one’s diet is considered a leading contributor to disease, such as type-2 diabetes, cardiovascular disease, high blood pressure (hypertension), cancer, and dementia.[x]

Why Reduce Sugar

There are many reasons to reduce sugar intake.

  • Metabolic stability. When you eat or drink something sweet, it gives a quick surge of energy. However, the consequence of glucose entering the bloodstream so quickly is that the body’s ability to maintain stability is compromised.
  • Stable blood sugar levels. With some attention to our diet, we can help balance blood sugar. This is especially true in type-2 diabetes (adult onset), which sometimes can be managed by diet alone. It is rarely true of type 1 diabetes (juvenile onset).
  • Stronger immune system. Individuals with higher sugar consumption had shorter telomeres in their white blood cells as compared to those with lower sugar consumption (telomeres are the caps at the end of each strand of DNA that protect our chromosomes, like the plastic tips at the end of shoelaces).[xi]

Reduced glycation. Glycation is the binding of sugar and protein molecules in one’s body, and is part of the natural aging process. When the sugar molecule binds inappropriately to a protein, it forms a new compound called “advanced glycation end-products (AGE’s).” AGE’s cause ongoing inflammation and react with body tissues to produce free radicals and reactive oxygen species that damage healthy cells if not neutralized.

Recommended

Limit your sweets and avoid sugary drinks and sodas. In general, an alkaline diet will be a low sugar diet and will be anti-inflammatory. Avoid high glycemic index foods. Stevia is a great alternative to sugar and has been shown to be very safe.[i] It is an herb that is not sugar (has zero calories) and works by stimulating the sugar receptors in the tongue. Stevia is two-hundred times sweeter than sugar taken in the same dosages, so a small amount (even 3-5 drops in plain yogurt for example) goes a long way. Too much stevia gives food a bitter taste.

Reduce AGE’s. In addition to the above, avoid grilled and charred foods, fried foods, and slow cook your food or lightly steam your vegetables. Avoid vegetable oils for cooking in high heat. Olive oil is fine in low heat, saturated fats such as butter and coconuts oil have high heat tolerance which means that these oils when used in cooking maintain stability whereas oils such as vegetable oils have poor heat tolerance and can be quickly turned into an unhealthy oil high in free radicals when used in cooking. Complex carbohydrates and high fiber foods reduce the production of AGE’s in the body. Foods that help clear one’s body of AGE’s include kale, collard greens, spinach, broccoli, cauliflower, citrus fruits, peaches, most berries, tomatoes, carrots, as well as green tea, grapeseed extract, carnosine, and vitamin B6.

Avoid artificial sweeteners. Sugar and artificially sweetened beverage intake have been linked to cardiometabolic risk factors, which increase the risk of cerebrovascular disease and dementia. Artificially-sweetened soft drinks are associated with an increased risk of ischemic stroke, all-cause dementia, and AD dementia.[ii] [iii] Some of the adverse effects on the central nervous system caused by the intake of aspartame are headaches, mood changes, insomnia and seizures.[iv] Other effects include confusion, personality disorders, dizziness and visual difficulty.[v] In mice studies, chronic aspartame consumption resulted in a longer time for the mice to locate the reward within the T-maze, which showed impaired long-term memory retention.[vi] [vii] [viii]

Ironically, although people consume artificial sweeteners in an attempt to reduce caloric intake and control or lose weight, studies actually show that consumption results in increased weight and has been attributed to obesity.[ix] [x] One reason may be that consumption of foods and fluids containing high-potency sweeteners interfered with the ability to detect sweet taste, thereby affecting energy regulation (and possibly increasing the desire for more sweets, or stimulating the desire for sugar).[xi]


[i] Ashwell M. (2015). Stevia, Nature’s Zero-Calorie Sustainable Sweetner: A New Player in the Fight Against Obesity. Nutr Today. May; 50(3):129–134.

[ii]Pass MP, Himali JJ, Beiser AS, Aparicio HJ, Satizabal CL, et al. (2017). Sugar- and Artificially Sweetened Beverages and the Risks of Incident Stroke and Dementia: A Prospective Cohort Study. Stroke. May;48(5):1139–1146.

[iii] Gorelick PB, Scuteri A, Black SE, Decarli C, Greenberg SM, et al. (2011). Vascular contributions to cognitive impairment and dementia: a statement for healthcare professionals from the american heart association/american stroke association. Stroke. Sep; 42(9):2672-713.

[iv] Romano M, Diomede L, Guiso G, Caccia S, Perego C, et al. (1990). Plasma and brain kenetics of large neutral amino acids and striatum monoamines in rats given aspartame. Food Chem Toxicol. May;28(5):317-321.

[v] Pepino MY. (2015). Metabois effects of non-nutritive sweeteners. Physio Behav. Dec 1;152(Pt B):450-5.

[vi] Christian B, McConnaughey K, Bethea E, Brantley S, Coffey A , et al. (2004). Chronic aspartame affects T-maze performance, brain cholinergic receptors and Na+,K+-ATPase in rats Pharmacol Biochem Behav. May;78(1):121-127.

[vii] Chattopadhyay S, Raychaudhuri U, Chakraborty R. (2014). Artificial sweeteners-a review. J Food Sci Technol. Apr;51(4):611-621.

[viii] Qurrat-ul-Ain, Khan SA. (2015). Artificial sweeteners: safe or unsafe? J Pak Med Assoc. Feb;65(2):225-227.

[ix] Fernstrom JD. (2015). Non-nutritive sweeteners and obesity. Annu Rev Food Sci Technol. 2015;6:119-136.

[x] Roberts JR. (2015). The paradox of artificial sweeteners in managing obesity. Curr Gastroenterol Rep. Jan;17(1):423.

[xi] Schiffman SS, Rother KI. (2013). Sucralose, a synthetic organochlorine sweetener: overview of biological issues J Toxicol Environ Health B Crit Rev. 2013;16(7):399-451  


[i] Howarth C, Gleeson P, Attwell D. (2013). Updated energy budgets for neural computation in the neocortex and cerebellum. J Cereb Blood Flow Metab. Jul; 32(7):1222-32.

[ii] Dienel GA. (2012). Fueling and imaging brain activation. ASN Neuro.  Jul 20; 4(5):e00093.

[iii] Ishibashi K, Sakurai K, Shimoji K, Takumaru AM, Ishii K. (2018). Altered functional connectivity of the default mode network by glucose loading in young, healthy participants.

[iv] Walsh EI, Shaw M, Sachdev P, Anstey KJ, Cherbuin N. (2018). Brain atrophy in aging: Estimating effects of blood glucose levels vs. other type 2 diabetes effects. Diabetes Metab. Feb;44(1):80-83.

[v] Croteau E, Castellano CA, Fortier M, Bocti C, Fulop T, et al. (2018). A cross-sectional comparison of brain glucose and ketone metabolism in cognitively healthy older adults, mild cognitive impairment and early Alzheimer’s disease. Exp Gerontol. Jul 1;107:18-26.

[vi] Edwards S. (2019). Sugar and the Brain. Retrieved Jun 18 2019 from https://neuro.hms.harvard.edu/harvard-mahoney-neuroscience-institute/brain-newsletter/and-brain-series/sugar-and-brain.

[vii] Crane PK, Walker R, Hubbard RA, Li G, Nathan DM, et al. (2013). Glucose levels and risk of dementia. N Engl J Med. Aug 8;369(6):540-548.

[viii] An Y, Varma VR, Varma S, Casanova R, Dammer E, et al. (2018). Evidence for brain glucose dysregulation in Alzheimer’s disease. Mar;14(3):318-329.

[ix] An Y, Varma VR, Varma S, Casanova R, Dammer E, et al. (2018). Evidence for brain glucose dysregulation in Alzheimer’s disease. Alzheimers Dement. Mar;14(3):318-329.

[x] Doheny K. (2012). Americans Sweet on Sugar: Time to Regulate? WebMD. Retrieved from https://www.webmd.com/diet/news/20120201/americans-sweet-on-sugar-time-to-regulate#1

[xi] Leung CW, Laraia BA, Needham BL, Rehkopf DH, Adler NE, et al. (2014). Soda and cell aging: associations between sugar-sweetened beverage consumption an leukocyte telomere length in healthy adults from the National Health and Nutrition Examination Surveys. Am J Public Health. Dec;104(12):2425-31.