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Sugar and Health

Ice Cream Party

As this sweet substance is laced on most of our food products,  it has been made easier for us to overconsume it, making it a huge issue of concern for public health worldwide (2).

People may have been more conscious towards their diets but overall sugar consumption still remains higher than the recommendation.

Statistics have shown that the average American takes in a staggering 83.1 grams of sugar per day (1).

The WHO guideline recommends us to reduce the intake of added sugars to no more than 10% of dietary energy (around 6 to 9 teaspoons). Additionally, the American Heart Association (AHA) recommends no more than 24 grams (6 teaspoons) or 36 grams (9 teaspoons) of added sugar per day for women and men, respectively.

Sugar Conversion

1 gram of sugar = 4 calories

4 grams of sugar = 1 teaspoon of sugar​


Maximum sugar intake/day


2 years

3 years

4 to 6 years

< 13 grams

< 15 grams

< 19 grams

1 to 3

2 to 4

3 to 5

7 to 10 years

11+ years



<24 grams

< 24 grams

< 36 grams

4 to 6



Source: the World Health Organisation (WHO), the UK Scientific Advisory Committee on Nutrition (SACN) and the American Heart Association.


However, even a single can of classic fizzling coke (375 mL or 12oz) alone contains 34.5 grams of sugar which is already over the recommendations for women.

Sources of added sugar in your diet


One study done in 2016 assessed the free sugar content in Canadian prepackaged foods (3).

This chart shows the percentage of free sugar ingredients, sweeteners, a combination of both, or neither contained in prepackaged foods and beverages. As you can see, food sources that contain the most added sugars are often processed.

main sugars

The main sugars

Many sugars are found naturally in plant tissues which are then extracted and processed into various types of sugars. However, the amounts found in nature varies e.g. fructose was rare to be consumed in the past in our ancestors as the sources only contained trace amounts.

Monosaccharides (the Simplest form of sugar)

Glucose (fruits and plants)

Fructose (fruit)

Galactose (milk)


Disaccharides (2 monosaccharides)

Lactose = Glucose + Galactose

Sucrose = Glucose + Fructose

Maltose = Glucose + Glucose

Sugars that should be cut down from your diet (NOTE: NOT AVOID)


Added sugars refer to sugars that do not naturally occur in foods and these consist mainly of sucrose and high fructose corn syrup (HFCS). These appear on the ingredient list on beverages and packaged food products.

Remember to read your labels.

There are 61 names for sugars hidden in the ingredient list!

Some naturally occurring sugars such as agave nectar, honey, coconut sugar though may contain some nutrients, may not appear as healthy as it seems.


Although most of these mentioned sugars have a lower glycaemic index (a number representing the response of blood glucose after the consumption of a particular food), it may not be as simple as that.


These sugars comprise a high percentage of fructose which is metabolised in a different way when compared to glucose (explained later).

Note: The sugar proportions vary depending on the source of the nectar that the manufacturer uses.


While sweeteners such as honey, maple syrup, and coconut sugar may provide traces of micronutrients, it is best to consume them at in moderation as overconsumption will have detrimental effects on health.


Naturally occurring sugars

are sugars found naturally in whole foods

  • whole fruits

  • vegetables

  • dairy

  • some grains


are food additives that are used to provide a sweet taste

  • sugar alcohols (maltitol, xylitol, sorbitol)

  • non-nutritive sweeteners (aspartame, sucralose)

  • cyclamate sweeteners

  • saccharin sweeteners

Added Sugars

are free sugars (no longer occurring in its naturally occurring state) that have been added to foods during preparation

  • any sugar

  • brown sugar

  • syrup, honey

  • fruit juice

  • sweeteners

  • nectars


Sugar & Addiction Debate

It has been argued that back in the old days, we did not have that many options and it was important for us to have a constant energy supply. We hence developed an innate preference for sweetness to increase our chances of survival.


The consumption of sugar activates the reward system by releasing dopamine, a neurotransmitter, in the cerebral cortex of the brain (4). The pleasurable "highs" caused by dopamine makes you want to repeat that behaviour.


Typically, when a normal meal is consumed, dopamine is released but eventually will level out. However, when large amounts of sugar are constantly ingested, the dopamine response does not level out and hence, allows a continuous feeling of “high”,  acting the same as an illicit drug. Overactivation of this reward system eventually kickstarts a series of events: loss of control, craving and increased tolerance to sugar


However,  this paper was widely accused of misinterpreting the evidence. These animals were only allowed to have sugar for 2 hours a day which does not mimic the environment we are living in where sugar is widely available all the time. Without such restriction, addiction-like behaviours are not shown.


What about processed foods?

Most processed foods such as ready meals, snacks, tinned foods, cakes contain high levels of sugar and little nutritional value.


Once high amounts are ingested, complex sugars (disaccharides or polysaccharides) breaks down into simple sugars (monosaccharides such as glucose and fructose) causing insulin and blood glucose levels to hit the roof.

Figure 1. Fructose found in fruits (5).


By looking at the data, we can see that fruits contain a large amount of fructose. So why shouldn’t we swap fruits and indulge in chocolates and cakes instead?


Well, it’s important to focus on the nutritional content of the entire food rather than to target an individual component. Fruits are an excellent source of vitamins and minerals but most importantly, it contains a high amount of soluble fibre. This helps to slow down glucose digestion and absorption and prevents the insulin spike. This slower rate of absorption and high fibre content causes a feeling of satiety.

fruit juice

So what about fruit juice?

Although fruit juice contains vitamins and antioxidants, it contains lacks fibre and is high in sugar.


Just a glass of juice may be equivalent to 10 whole apples which we would not normally eat in one sitting. Thus, there has been more and more evidence that fruit juices are basically made up of fructose and has the same effect on the body as soft drinks.


It is actually advised by the government that one 150ml serving of fruit juice counts towards one of your five-a-day servings and anything above that does not count.


The Action on sugar group is calling for fruit juice to be removed from the recommended five a day list as fruit juices contain a high amount of sugar.

The average amount of fructose in grams found in 100 grams of processed foods.

25-40 grams of fructose per day is safe according to a meta-analysis of clinical trials (6).

Not all sugars have the same effect on your body

effect on body

In a study, it has shown that participants who drank a glucose-sweetened drink felt satiated afterwards while the fructose drinkers felt less satisfied (7).


Glucose is regulated by insulin allowing the ingested glucose to bypass the liver and reach the body’s circulation. This would either be utilised or be stored as glycogen. While glucose is taken up by cells, it's a completely different story with fructose.


Once Fructose is ingested, it is poorly absorbed from the gastrointestinal tract. Most cells cannot metabolise fructose due to the low levels of transporters (GLUT-5).


Unlike glucose, most of the fructose is catalysed by the enzyme called fructokinase which is found in the liver (the small intestinal mucosa and kidney as well) but this is not regulated by the hepatic energy status (8).


It acts as a substrate by providing the backbone for VLDL triacylglycerol (the main predictor of coronary heart disease) and hence, increase fat production.


The increase in fat deposits in the liver will eventually lead to the development of fatty liver disease, an asymptomatic killer which is often associated with insulin resistance (cells become less responsive to insulin). In turn, this exhausts the pancreas resulting in the inability to regulate glucose levels.

Appetite Signalling

A high fructose diet can result in reduced levels of circulating leptin when compared to a high glucose diet as leptin production is regulated by insulin responses to meals (9).


  • Leptin is a hormone involved in the regulation of food intake and energy metabolism through neuropeptides such as neuropeptide-Y and melanocortins.


  • Leptin helps to decrease food intake and induces pathways that activate the periphery involved in promoting energy expenditure and fat oxidation.


In addition, fructose up-regulates the production of ghrelin which could increase appetite possibly contributing to weight gain.

What about weight loss?

Sure, limiting sugar consumption may help you lose weight ONLY if you are mindful of your overall calorie intake. A low- or no-sugar diet will not guarantee weight loss. 

It is important to note that there is always room for some sugar in a healthy diet.

Other Health Concerns?

Needs to be updated**

It has also been suggested that lack of efficiency in the conversion of fructose due to the lack of enzymes will override the other functions of the liver resulting in the production of uric acid -This may increase the risk of type 2 diabetes, kidney stones, gout, and hypertension.

Other than these diseases, many studies have also demonstrated that the consumption of fructose has a led to increased de novo lipogenesis (fat production), dyslipidemia (abnormal levels of lipids in the blood), insulin resistance, metabolic syndrome and even impaired cognitive function (10, 11).

  • References
    Irritable bowel syndrome [Online] Available at: [Accessed: 22 June 2018]. Saha, L. (2014). Irritable bowel syndrome: Pathogenesis, diagnosis, treatment, and evidence-based medicine. World Journal of Gastroenterology, 20(22), p.6759. D. Cashman, M., K. Martin, D., Dhillon, S. and R. Puli, S. (2016). Irritable Bowel Syndrome: A Clinical Review. Current Rheumatology Reviews, 12(1), pp.13-26. Guidelines--Rome III Diagnostic Criteria for Functional Gastrointestinal Disorders. (2006). Journal of Gastrointestinal and Liver Diseases, 15(3), pp.307-12. Drossman, D. (2016). Functional Gastrointestinal Disorders: History, Pathophysiology, Clinical Features, and Rome IV. Gastroenterology, 150(6), pp.1262-1279.e2. Ikechi, R., Fischer, B., DeSipio, J. and Phadtare, S. (2017). Irritable Bowel Syndrome: Clinical Manifestations, Dietary Influences, and Management. Healthcare, 5(2), p.21. Enck, P., Aziz, Q., Barbara, G., Farmer, A., Fukudo, S., Mayer, E., Niesler, B., Quigley, E., Rajilić-Stojanović, M., Schemann, M., Schwille-Kiuntke, J., Simren, M., Zipfel, S. and Spiller, R. (2016). Irritable bowel syndrome. Nature Reviews Disease Primers, 2, p.16014. Chey, W., Kurlander, J. and Eswaran, S. (2015). Irritable Bowel Syndrome. JAMA, 313(9), p.949. Hungin, A., Chang, L., Locke, G., Dennis, E. and Barghout, V. (2005). Irritable bowel syndrome in the United States: prevalence, symptom patterns and impact. Alimentary Pharmacology and Therapeutics, 21(11), pp.1365-1375. Gibson, P., Varney, J., Malakar, S. and Muir, J. (2015). Food Components and Irritable Bowel Syndrome. Gastroenterology, 148(6), pp.1158-1174.e4. Card, T., Canavan, C. and West, J. (2014). The epidemiology of irritable bowel syndrome. Clinical Epidemiology, p.71. Occhipinti, K. and Smith, J. (2012). Irritable Bowel Syndrome: A Review and Update. Clinics in Colon and Rectal Surgery, 25(01), pp.046-052. Chey, W., Kurlander, J. and Eswaran, S. (2015). Irritable Bowel Syndrome. JAMA, 313(9), p.949. Zhou, Q. and Verne, G. (2011). New insights into visceral hypersensitivity—clinical implications in IBS. Nature Reviews Gastroenterology & Hepatology, 8(6), pp.349-355. Ghoshal, U., Kumar, S., Mehrotra, M., Lakshmi, C. and Misra, A. (2010). Frequency of Small Intestinal Bacterial Overgrowth in Patients with Irritable Bowel Syndrome and Chronic Non-Specific Diarrhea. Journal of Neurogastroenterology and Motility, 16(1), pp.40-46. Ghoshal, U., Shukla, R. and Ghoshal, U. (2017). Small Intestinal Bacterial Overgrowth and Irritable Bowel Syndrome: A Bridge between Functional Organic Dichotomy. Gut and Liver, 11(2), pp.196-208. Ghoshal, U. (2014). Irritable bowel syndrome and small intestinal bacterial overgrowth: Meaningful association or unnecessary hype. World Journal of Gastroenterology, 20(10), p.2482. Marshall, J., Thabane, M., Garg, A., Clark, W., Moayyedi, P. and Collins, S. (2010). Eight year prognosis of postinfectious irritable bowel syndrome following waterborne bacterial dysentery. Gut, 59(5), pp.605-611. Marshall, J., Thabane, M., Garg, A., Clark, W., Salvadori, M. and Collins, S. (2006). Incidence and Epidemiology of Irritable Bowel Syndrome After a Large Waterborne Outbreak of Bacterial Dysentery. Gastroenterology, 131(2), pp.445-450. Spiller, R. and Campbell, E. (2006). Post-infectious irritable bowel syndrome. Current Opinion in Gastroenterology, 22(1), pp.13-17. Ericsson, C., Hatz, C. and DuPont, A. (2008). Postinfectious Irritable Bowel Syndrome. Clinical Infectious Diseases, 46(4), pp.594-599. Grenham, S., Clarke, G., Cryan, J. and Dinan, T. (2011). Brain?Gut?Microbe Communication in Health and Disease. Frontiers in Physiology, 2. The Brain-Gut Connection [Online] Available at: [Accessed: 24 June 2018]. Folks, D. (2004). The interface of psychiatry and irritable bowel syndrome. Current Psychiatry Reports, 6(3), pp.210-215. Fichna, J. and Storr, M. (2012). Brain-Gut Interactions in IBS. Frontiers in Pharmacology, 3. El-Salhy, M. and Gundersen, D. (2015). Diet in irritable bowel syndrome. Nutrition Journal, 14(1). Irritable Bowel Syndrome - National Library of Medicine - PubMed Health [Online] Available at: [Accessed: 24 June 2018]. Folks, D. (2004). The interface of psychiatry and irritable bowel syndrome. Current Psychiatry Reports, 6(3), pp.210-215. Ikechi, R., Fischer, B., DeSipio, J. and Phadtare, S. (2017). Irritable Bowel Syndrome: Clinical Manifestations, Dietary Influences, and Management. Healthcare, 5(2), p.21. Rao, S., Yu, S. and Fedewa, A. (2015). Systematic review: dietary fibre and FODMAP-restricted diet in the management of constipation and irritable bowel syndrome. Alimentary Pharmacology & Therapeutics, 41(12), pp.1256-1270. Moayyedi, P., Quigley, E., Lacy, B., Lembo, A., Saito, Y., Schiller, L., Soffer, E., Spiegel, B. and Ford, A. (2014). The Effect of Fiber Supplementation on Irritable Bowel Syndrome: A Systematic Review and Meta-analysis. The American Journal of Gastroenterology, 109(9), pp.1367-1374. FRANCIS, C. (1994). Bran and irritable bowel syndrome: time for reappraisal. The Lancet, 344(8914), pp.39-40. Vazquez–Roque, M., Camilleri, M., Smyrk, T., Murray, J., Marietta, E., O'Neill, J., Carlson, P., Lamsam, J., Janzow, D., Eckert, D., Burton, D. and Zinsmeister, A. (2013). A Controlled Trial of Gluten-Free Diet in Patients With Irritable Bowel Syndrome-Diarrhea: Effects on Bowel Frequency and Intestinal Function. Gastroenterology, 144(5), pp.903-911.e3. Ford, A., Quigley, E., Lacy, B., Lembo, A., Saito, Y., Schiller, L., Soffer, E., Spiegel, B. and Moayyedi, P. (2014). Efficacy of Prebiotics, Probiotics and Synbiotics in Irritable Bowel Syndrome and Chronic Idiopathic Constipation: Systematic Review and Meta-analysis. The American Journal of Gastroenterology, 109(10), pp.1547-1561. Basturk, A., Artan, R. and Yilmaz, A. (2016). Efficacy of synbiotic, probiotic, and prebiotic treatments for irritable bowel syndrome in children: A randomized controlled trial. The Turkish Journal of Gastroenterology, 27(5), pp.439-443. Zhang, Y., Li, L., Guo, C., Mu, D., Feng, B., Zuo, X. and Li, Y. (2016). Effects of probiotic type, dose and treatment duration on irritable bowel syndrome diagnosed by Rome III criteria: a meta-analysis. BMC Gastroenterology, 16(1). Guandalini, S., Magazzù, G., Chiaro, A., La Balestra, V., Di Nardo, G., Gopalan, S., Sibal, A., Romano, C., Canani, R., Lionetti, P. and Setty, M. (2010). VSL#3 Improves Symptoms in Children With Irritable Bowel Syndrome: A Multicenter, Randomized, Placebo-Controlled, Double-Blind, Crossover Study. Journal of Pediatric Gastroenterology and Nutrition, 51(1), pp.24-30. Paineau, D., Payen, F., Panserieu, S., Coulombier, G., Sobaszek, A., Lartigau, I., Brabet, M., Galmiche, J., Tripodi, D., Sacher-Huvelin, S., Chapalain, V., Zourabichvili, O., Respondek, F., Wagner, A. and Bornet, F. (2007). The effects of regular consumption of short-chain fructo-oligosaccharides on digestive comfort of subjects with minor functional bowel disorders. British Journal of Nutrition, 99(02). Khanna, R., MacDonald, J. and Levesque, B. (2013). Peppermint Oil for the Treatment of Irritable Bowel Syndrome. Journal of Clinical Gastroenterology, p.1. Peppermint Oil for IBS: Does it Work? [Online] Available at: [Accessed: 24 June 2018]. Grigoleit, H. and Grigoleit, P. (2005). Peppermint oil in irritable bowel syndrome. Phytomedicine, 12(8), pp.601-606. Khanna, R., MacDonald, J. and Levesque, B. (2013). Peppermint Oil for the Treatment of Irritable Bowel Syndrome. Journal of Clinical Gastroenterology, p.1. IBS Diet: What to Do and What to Avoid [Online] Available at: [Accessed: 24 June 2018]. Johannesson, E., Simrén, M., Strid, H., Bajor, A. and Sadik, R. (2011). Physical Activity Improves Symptoms in Irritable Bowel Syndrome: A Randomized Controlled Trial. The American Journal of Gastroenterology, 106(5), pp.915-922.
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