Sugar can be highly rewarding and palatable in both taste and dietary input. Many times, our excessive sugar consumption triggers neuroadaptations in our reward system. This action decouples our eating behaviour, switching from eating for caloric needs into compulsive eating. This accumulative effect in turn is associated with adverse health conditions, including obesity, inflammatory diseases and metabolic syndrome such as high blood pressure, high fasting blood glucose, high triglycerides and visceral adiposity (1,2) etc that increases the risk of cardiovascular diseases, non-alcoholic fatty liver disease and type 2 diabetes (3).
What is (really) sugar?
Sugar is typically referred to the category of simple carbohydrates. They are differentiated into 2 categories: Monosaccharides (Eg. Glucose and Fructose) and Disaccharides (Eg. Sucrose and Lactose). They each has different effect on our brain and body.
So, what form of sugar should we be most mindful of?
The form of sugar that we would like to highlight today is high fructose corn syrup (HFCS). HFCS is (sadly) predominate in a typical western diet and carries a substantial negative impact on our health compared to others.
HCFS can be easily found in lots of foods that we indulge in during our holiday/festive season. They are:
- Candies
- Packaged sweets
- Sweet drinks
- Sweetened juice
- Ice cream
- Fast foods
- Sauces / Condiments / Salad dressings
- Cereals
- Granola bars
HFCS is a monosaccharide that is made up of 42% or 55% of free fructose and free glucose (4). Monosaccharides are processed by the brain differently and influences brain activity. Most of us might think that fructose is a healthier option as the source itself comes from fruits (5), but this notion is truly misguided. Our body does not break down in the same way fructose found in fruits as compared to added sugar fructose. This article is focusing on the effects of added sugar fructose. When fructose is ingested as an added sugar excessively, it is associated with insulin resistance, hypertension, diabetes, inflammation, metabolic syndrome and associated retinopathy (4,6,7,8,9).
Relatively, fructose naturally obtained from fruit comes with antioxidants, potassium, high in fiber, vitamin C and flavonoids. When eaten moderately, this nutrients available collectively outweighs the negative impact of fructose content (4, 10). Adding on, the quantities of fructose found in fruit compared to a sweetened beverage are drastically different. Eg. The amount of fructose found in a peach is roughly 1% of the weight of the fruit compared to fructose found in HFCS is 50% (7).
How is fructose different from glucose?
The digestion and absorption of sugars takes place in the top half of the digestive tract (11), of which fructose and glucose follows a different metabolic pathway hence causing different health effects.
Glucose - through the act of insulin, passes through the muscle, adipose and other peripheral tissues quickly to be use as energy immediately (11).
Fructose - independent of insulin, is a less direct source of energy. Fructose is converted in glucose, lactate and/or fatty acids by the liver to be oxidase in other tissues for energy (12,13,8).
As compared to glucose, fructose produces a smaller amount of circulating satiety hormones such as insulin and glucagon-like-peptide 1(GLP-1) while at the same time weakens the suppression of ghrelin [an appetite hormone] (14). As such, fructose consumption does not significantly reduce hunger as the body fails to activate the signals to stop eating. Consumption of fructose has also been associated with a higher a fMRI response in the visual cortex to high calorie foods as relative to glucose consumption (12). Thus, this visual response and the sweet taste that fructose delivers without an immediate nutritional input allows overconsumption of calories.
Apart from overconsumption of calories, excess fructose also contributes to inflammation in the body which in turn generates advanced glycation end products (AGE’s), relating to neurodegenerative diseases and chronic inflammatory diseases such as diabetes, asthma and associated cognitive decline (15,9,16,17,18).
With all the adverse health effects, what should we do?
Fret not, because not all forms of sugar reacts the same way in our body (phew!).
Some complex carbohydrates like starches, when broken down into monosaccharides (similar to the ones found in vegetables and fiber-rich whole grains/legumes) follows a different metabolic pathway. Short chain fatty acids (SCFA) found in complex carbohydrates increases the release of peptides and hormones from enteroendocrine cells, leading to increase satiety and thus reducing food seeking behaviour (19). Therefore, the SCFAs produced by the gut microbes during digestion of complex carbohydrates may be a source of protection against the effects of high fructose consumption.
Contrary to fructose, SCFAs brings about more health benefits than adversary. These includes anti-inflammatory effects, decreased body fat and weight, inhibition of fat storage and anti diabetic effects via suppression of insulin signalling. (20,21,11,22). These anti-inflammatory effect also spills over into the brain by regulating the central nervous system via pathways that involves the vagus nerve and immune system (23,22).
In conclusion, added sugar in our dietary inhibits our satiety signals and leads to overconsumption of calories. This accumulative effect can be detrimental to our health by exposing us to a higher risk of inflammation in our bodies and in time, leads to chronic diseases and/or metabolic syndromes. Therefore, it is encouraged to include whole foods into our dietary plans to support satiety, counterbalance the effects of sugar and regulate our immune system.
Importantly, the key is to find the balance between nourishing with what we need, while enjoying with moderation on the foods that we want, especially during this festive season! :)
Merry X'mas and a very very Happy New Year all!!<3
With love,
Ashley
References:
1. Odegaard AO, Choh AC, Czerwinski SA, Towne B, Demerath EW. Sugar-sweetened and diet beverages in relation to visceral adipose tissue. Obesity (Silver Spring) 2012;20(3):689–91.
2. Pollock NK, Bundy V, Kanto W, Davis CL, Bernard PJ, Zhu H, et al. Greater fructose consumption is associated with cardiometabolic risk markers and visceral adiposity in adolescents. J Nutr. 2012;142(2):251–7
3. RH Eckel, SM Grundy, PZ Zimmet: The metabolic syndrome. Lancet 365(9468), 1415-1428 (2005)
4. M Madero, JC Arriaga, D Jalal, C Rivard, K McFann, O Pérez-Méndez, RJ Johnson: The effect of two energy-restricted diets, a low-fructose diet versus a moderate natural fructose diet, on weight loss and metabolic syndrome parameters: a randomized controlled trial. Metabolism 60(11), 1551-1559 (2011)
5. B Sütterlin, M Siegrist: Simply adding the word “fruit” makes sugar healthier: The misleading effect of symbolic information on the perceived healthiness of food. Appetite 95, 252-261 (2015)
6. DI Jalal, G Smits, RJ Johnson, M Chonchol: Increased fructose associates with elevated blood pressure. J Am Soc Neph 21(9), 1543-1549 (2010)
7. JJ DiNicolantonio, JH O’keefe, SC Lucan: Added fructose: a principal driver of type 2 diabetes mellitus and its consequences. Mayo Clin Proc 90(3), 372-381 (2015)
8. VS Malik, FB Hu: Fructose and cardiometabolic health: what the evidence from sugar-sweetened beverages tells us. J Am Coll Cardiol 66(14), 1615-1624 (2015)
9. M Aragno, R Mastrocola: Dietary Sugars and Endogenous Formation of Advanced Glycation Endproducts: Emerging Mechanisms of Disease. Nutrients 9(4), 385 (2017)
10. X Gao, G Curhan, JP Forman, A Ascherio, HK Choi: Vitamin C intake and serum uric acid concentration in men. J Rheumatol 35(9), 1853-1858 (2008)
11. DJA Jenkins, LSA Augustin, A Malick, A Esfahani, CWC Kendall: Glucose: Chemistry and Dietary Sources. Encyc Hum Nutr 2, 390-398 (2013)
12. S Luo, JR Monterosso, K Sarpelleh, KA Page: Differential effects of fructose versus glucose on brain and appetitive responses to food cues and decisions for food rewards. Proc Natl Acad Sci112(20), 6509–6514 (2015)
13. MR Laughlin: Normal roles for dietary fructose in carbohydrate metabolism. Nutrients 6(8), 3117-3129 (2014)
14. KA Page, O Chan, J Arora, R Belfort-Deaguiar, J Dzuira, B Roehmholdt, GW Cline, S Naik, R Sinha, RT Constable, RS Sherwin: Effects of fructose vs glucose on regional cerebral blood flow in brain regions involved with appetite and reward pathways. JAMA 309(1), 63–70 (2013)
15. A Gugliucci: Formation of fructose-mediated advanced glycation end products and their roles in metabolic and inflammatory diseases. Adv Nutr 8(1), 54-62 (2017)
16. R Simó, A Ciudin, O Simó-Servat, C Hernández: Cognitive impairment and dementia: a new emerging complication of type 2 diabetes—The diabetologist’s perspective. Acta diabetologica54(5), 417-424 (2017)
17. Y Bains, A Gugliucci, R Caccavello: Advanced glycation endproducts form during ovalbumin digestion in the presence of fructose: inhibition by chlorogenic acid. Fitoterapia 120, 1-5 (2017)
18. LR DeChristopher: Excess free fructose and childhood asthma. Eur J Clin Nutr 69(12), 1371 (2015)
19. E Sherwin, KV Sandhu, TG Dinan, JF Cryan: May the force be with you: the light and dark sides of the microbiota–gut–brain axis in neuropsychiatry. CNS drugs 30(11), 1019-1041 (2016)
20. V Tremaroli, F Bäckhed: Functional interactions between the gut microbiota and host metabolism. Nature 489(7415), 242-249 (2012)
21. G den Besten, K van Eunen, AK Groen, K Venema, DJ Reijngoud, BM Bakker: The role of short-chain fatty acids in the interplay between diet, gut microbiota, and host energy metabolism. J Lipid Res 54(9), 2325-2340 (2013)
22. MM Kaczmarczyk, MJ Miller, GG Freund: The health benefits of dietary fiber: beyond the usual suspects of type 2 diabetes mellitus, cardiovascular disease and colon cancer. Metabolism 61(8), 1058-1066 (2012)
23. E Sherwin, KV Sandhu, TG Dinan, JF Cryan: May the force be with you: the light and dark sides of the microbiota–gut–brain axis in neuropsychiatry. CNS drugs 30(11), 1019-1041 (2016)