To understand fructose well, let’s start from first principles: how is it metabolised, how does its metabolism differ from glucose, and what are the implications?
Fructose Metabolic Pathway = damaging positive feedback loop, energy depletion and cellular stress
FRUCTOSE METABOLISM & ITS CONSEQUENCES
- Fructose is metabolised by the small intestine, kidneys, skeletal muscle and adipose tissue, although the majority of excess fructose is metabolised by the liver, with a similar pathway to alcohol (ethanol), i.e. as a toxin. Research indicates that amounts >30g fructose for an adult weighing 60kg leads to rapid pressure upon the liver to deal with the fructose, wherein it goes through the pathway described below that has many negative consequences, not only upon liver function: inducing non-alcoholic fatty liver disease over time (i).
- As shown above, fructose enters the cell (via GLUT2) and is metabolised by fructokinase into Fructose-1-P. This first step in fructose metabolism reduces ATP (the main energy carrier in the body) and creates uric acid (UA) (ii). Increasing UA in the body has harmful effects, including increasing blood pressure, disrupting the immune system and increasing cardiovascular disease risks (iii).
- Fructose’s metabolic pathway leads directly towards the creation of FAT: triglycerides (fatty acids), mainly packaged in very low-density lipoproteins (vLDL).
- Unlike with glucose metabolism (right side), when there is an influx of fructose, there is no automatic negative feedback loop to regulate what is happening. Thus, with a large intake, fructose metabolism can proceed unabated, generating uric acid and triglycerides, while depleting ATP.
- Some of the consequences of fructose metabolism:
- Increased UA: this triggers endothelial (blood vessel wall) dysfunction, increases blood pressure and impairs UA excretion, further increasing UA. UA turns on fat creation and fat storage.
- Increased Triglycerides: increased fats travelling in the blood and increased visceral fat creation (fat in and around vital organs such as the liver and the pancreas).
- Depletion of ATP outstripping ATP generation: energy is depleted, rather than net increased, by eating fructose. This in itself creates significant intracellular stress.
- Increased oxidative stress: ageing of tissues and tissue dysfunction.
- Direct and epigenetic impacts that promote insulin resistance and thus disturbed blood sugar balance (i.e. the beginnings of Type II Diabetes), leptin (fullness hormone) resistance (i.e. one doesn’t feel full as normal) and fat storage.
i) Jang, C. et al. (2018) ‘The Small Intestine Converts Dietary Fructose into Glucose and Organic Acids’, Cell Metabolism, 27(2), pp. 351-361
ii) Mayes, P. (1993), ‘Intermediary Metabolism of Fructose’, The American Journal of Clinical Nutrition, 58, pp. 754-765
iii) Ali, N. et al. (2018) ‘Prevalence of hyperuricemia and the relationship between serum uric acid and obesity: A study on Bangladeshi adults’, PLoS ONE, 13(11)
Fructose and Harmful Fat Creation
- The fructose metabolic pathway leads to de novo lipogenesis: fat generation (i).
- Fructose metabolism also has epigenetic effects that switch on fat storage and suppress fat burning (ii, iii).
- Fructose leads to increased visceral fat accumulating between / around organs, especially around the waist. This type of fat tissue is harmful and disrupts the functioning of those organs (particularly the pancreas and the liver) (iv, v, vi, vii).
- Fat tissue is biologically active and secretes inflammatory cytokines. Visceral fat in particular secretes interleukin-6 (il-6), which induces inflammation and plasminogen activator inhibitor 1 (PAI-1), high levels of which can contribute to atherosclerosis / thrombosis, in fact a key link between abdominal fat and heart disease (viii). Visceral fat secretes tumour necrosis factor-alpha (TNF-α) and fructose itself elevates this inflammatory marker (ix, x).
- TNF-α stimulates insulin resistance and is strongly implicated in the pathology of diabetes, obesity, metabolic syndrome (xi, xii).
- This fat tissue also secretes resistin, which further impairs insulin’s efficacy by impairing insulin signalling and promoting hepatic gluconeogenesis: generation of glucose by the liver, i.e. higher blood sugar (xiii).
- Fructose metabolism increases uric acid, which itself is a key predictor and mediator of weight gain and obesity (xiv).
(i) Tappy, L. and Le, K-A. (2010) ‘Metabolic Effects of Fructose and the Worldwide Increase in Obesity’, Physiology Review, 90, pp. 23-46
(ii) Foufelle, F. and Ferre, P. (2002) ‘New perspectives in the regulation of hepatic glycolytic and lipogenic genes by insulin and glucose : a role for the transcription factor sterol regulatory element binding protein-1c’, Biochem. J, 366, pp. 377-391
(iii) Koo, H. Y. et al. (2009) ‘Replacing dietary glucose with fructose increases ChREBP activity and SREBP-1 protein in rat liver nucleus’, Biochemical and Biophysical Research Communications, 390(2), pp. 285–289
(iv) Stanhope K. et al. (2009) ‘Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans’, Journal of Clinical Investigations, 119 (5), pp. 1322-1334
(v) DiNicolantonio, J. J. et al. (2018) ‘Fructose-induced inflammation and increased cortisol: A new mechanism for how sugar induces visceral adiposity’, Progress in Cardiovascular Diseases. W.B. Saunders, pp. 3–9
(vi) Baena, M. et al. (2016) ‘Fructose, but not glucose, impairs insulin signaling in the three major insulinsensitive tissues’, Scientific Reports, 6.
(vii) Sousa, G. J. et al. (2017) ‘Fructose intake exacerbates the contractile response elicited by norepinephrine in mesenteric vascular bed of rats via increased endothelial prostanoids’, Journal of Nutritional Biochemistry, 48, pp. 21–28
(viii) Barnard S. et al. (2016) The contribution of different adipose tissue depots to plasma plasminogen activator inhibitor-1 (PAI-1) levels,
Blood Reviews, 30:6, 421-429
(ix) Nier, A. et al. (2018) ‘Non-Alcoholic Fatty Liver Disease in Overweight Children: Role of Fructose Intake and Dietary Pattern’, Nutrients, 10, p. 1329.
(x) Saygin, M. et al. (2016) ‘The impact of high fructose on cardiovascular system: Role of α-lipoic acid’, Human and Experimental Toxicology, 35(2), pp. 194–204
(xi) Walsh, J. et al. (2013) ‘The association between TNF-α and insulin resistance in euglycemic women’, Cytokine, 64:1, 208-212.
(xii) Dragut R. et al, (2014) ‘Relationship between TNF alpha, IL-6 and cardiovascular risk in patients with type 2 diabetes and metabolic syndrome’, 235:2, 239
(xiii) Hashimoto, H. et al. (2020) ‘Expression of MCP-1 in white adipose tissues induce the resistin-hypersecretion in type 2 diabetes’, Obesity Medicine, 20; 100286
Turns on Fat Creating
Turns on Fat Creating (Lipogenic) and Turns off Fat Burning (FA-Oxidation) Genes and Proteins
Makes us hungry
WE EAT MORE
FRUCTOSE CONSUMPTION: INCREASES GHRELIN: the HUNGER hormone, this causes LEPTIN resistance and the FULLNESS hormone STOPS WORKING.
- Fructose consumption activates the endocannabinoid system: makes us crave more dopamine-releasing, highly energy-dense foods (more sugary foods).
- Fructose is the only food that bypasses our fullness (satiety)-signalling system. We can eat large (calorific) amounts of it, without feeling full – we often feel hungrier! This is because it increases ghrelin (hunger hormone) levels and creates leptin (fullness hormone) resistance (i, ii).
- Research also indicates that fructose influences the types of foods we choose to eat: by influencing the endocannabinoid system, we crave more ‘rewarding’ (more energy-dense carbohydrate) foods (iii). Thus, we inevitably tend to eat more and gain body-fat when our diet is high in fructose, since we feel hungrier.
- Meanwhile, the high-fructose foods we tend to eat are nutrient-poor, so not only do we ingest excess calories, but we do not get the nutrients we need. We are left overfed, yet hungry, and undernourished.
- Calories: unlike some inaccurate messaging of the past, calories are not made equal at all. Calories are only equal when they are literally put into a fire and burnt in a lab to count them. 100kcal from broccoli and 100kcal from date syrup will behave completely differently inside the human body. The composition of the food will send different signals to the body, switching on/off certain genes’ expression, be used as components to build structures, be used for energy, stored as glycogen or fat, etc.
- That fructose bypasses our satiety is super important when discussing the ‘calories-in, calories-out’ thermodynamic equation that is spoken of as the answer to weight-control. Over time, one cannot override the deepest human instinct – hunger – that is controlled by our hunger and satiety hormones. This is why for example a low calorie, low fat (thus higher carbohydrate) diet is notoriously difficult/impossible to maintain.
- Bottom-line: a high-fructose diet makes us hungrier (and crave more dopamine-releasing sugar), so we almost inevitably overeat. If we do not over-consume much fructose, our hunger-fullness hormonal regulatory system keeps the equation in balance naturally. There should be no need to count calories – on a healthy diet without sugar’s impacts, our biology easily takes care of this balance for us naturally, and it is easy.
(i) LIndqvist, A. et al, (2008), ‘Effects of sucrose, glucose and fructose on peripheral and central appetite signals’, Regulatory Peptides, 150(1–3), pp. 26–32
(ii) Ibarro-Reynoso, L. et al. (2017), ‘Effect of Restriction of Foods with High Fructose Corn Syrup Content on Metabolic Indices and Fatty Liver in Obese Children’, Obesity Facts, 10(4), pp. 332-340
(iii) Page, K. A. et al. (2013) ‘Effects of fructose vs glucose on regional cerebral blood flow in brain regions involved with appetite and reward pathways’, JAMA, 309(1), pp. 63–70
Fructose, Sucrose and Gut health
Fructose alters the composition and metabolism of gut microbiota and is causally associated with colitis (chronic inflammation of the colonic internal lining) and inflammatory bowel disease (i).
Fructose induces epithelial barrier (intestinal lining) dysfunction (ii). The intestinal lining is one of the most critical interfaces in our bodies, responsible for absorbing nutrients and keeping toxins and pathogens out of the body. Its health and optimal functioning is thus critical to our digestion, energy generation and immune system function (a large percentage of our immune cells surround the gut). When there is any abnormal functioning and/or intestinal permeability, these essential functions are likely to become disrupted, resulting in inflammatory, autoimmune, allergic and/or malabsorption problems and disease.
Fructose combined with glucose (e.g. in sucrose, found in varying combinations in honey, maple syrup, agave syrup, coconut sugar etc.) fuels intestinal (colon) cancer growth (iii) and increases metastasis (spreading to other tissue) of liver cancer (iv).
(i) Montrose, D. et al, (2020), ‘Dietary Fructose Alters the Composition, Localization, and Metabolism of Gut Microbiota in Association With Worsening Colitis’, Cellular and Molecular Gastroenterology and Hepatology, 2020, ISSN 2352-345X
(ii) Kawabata, K. et al, (2019), ‘A high fructose diet induces epithelial barrier dysfunction and exacerbates the severity of dextran sulfate sodium induced colitis’, Int J Mol Med, 43 (2019), pp. 1487-1496
(iii) Goncalves, M. et al, (2019), ‘High-fructose corn syrup enhances intestinal tumor growth in mice’, Science, 363, pp. 1345–1349
(iv) Bu, P. et al, (2019), ‘Aldolase B-Mediated Fructose Metabolism Drives Metabolic Reprogramming of Colon Cancer Liver Metastasis’, Cell Metabolism, 27(6)
Fructose, Sucrose & Immune Dysfunction
Dietary sugars, especially fructose, negatively impact the innate immune system, in multiple ways, including by significantly inhibiting the binding of pattern recognition molecules, a critical step that initiates immune signaling cascades. This reduces the immune system’s defense against both viral and bacterial pathogens. Research demonstrates that this is the case in a dose-dependent manner (i.e. the more fructose ingested, the worse the effect) (i).
Sucrose increases the risk of allergic inflammation in the lungs, and higher sugar intake is associated with asthma. (ii, iii)
Sucrose and fructose have negative impacts on the gut microbiome, including increasing the relative abundance of Proteobacteria, and reducing the abundance of Bacteroidetes, thus reducing the latter’s positive influence on maintaining the gut barrier. Thus, both the integrity of the epithelium and mucosal immunity may decrease with sugar intake, increasing systemic inflammation and metabolic endotoxemia. (iv) The gut microbiome plays an integral role in immune system function, and it is evident that the amounts of sugar we are consuming is not what we are evolved for, with evident detrimental impacts on our microbiome.
Sucrose causes micronutrient deficiencies in Calcium, Magnesium, Vitamin C, Vitamin D and Chromium.
(i) Takahashi K. et al, (2011) ‘Dietary sugars inhibit biologic functions of the pattern recognition molecule, mannose-binding lectin’, Open Journal of Immunology, 01(02)
(ii) Kierstein, S. et al (2008) ‘Sugar Consumption Increases Susceptibility to AllergicAirway Inflammation and Activates the Innate ImmuneSystem in the Lung’, J Allergy Clin Immunol, S196(754)
(iii) Park, S. et al (2016) ‘Association of Sugar-Sweetened Beverage Intake Frequency and Asthma Among US Adults’, Journal of Nutrition Education and Behaviour, 48(7)
(iv) Satokari, R., (2020) ‘High Intake of Sugar and the Balance between Pro- and Anti-Inflammatory Gut Bacteria’, Nutrients, 12(5), pp. 1348
Fructose and skin
Sugar (fructose and sucrose) consumption leads to increased production of advanced glycation end products (AGEs) in the body, including in the skin. These cross-linked sugar-proteins reduced the ability of the skin to heal and regenerate, thus accelerating the formation of wrinkles and general skin ageing (i, ii, iii, iv, v, vi).
Fructose leads to a reduction in the anti-inflammatory hormone adiponectin, and lower levels of adiponectin in subcutaneous adipose tissue (fat tissue beneath the skin) is associated with cellulite in those areas. Cellulite is also linked to glycation, another risk factor for cellulite (vii, viii).
Sugar consumption and high blood glucose are associated with acne development and exacerbation (ix, x), and populations that follow a very low sugar diet appear to have no cases of acne whatsoever (xi). Low adiponectin (which fructose decreases) appears to play a role in acne pathophysiology.
(i) Rodrigo, S. et al. (2019) ‘Effects of maternal fructose intake on perinatal ER-stress: A defective XBP1s nuclear translocation affects the ER-stress resolution’, Nutrients, 11(8)
(ii) Sotokawauchi, A. et al. (2019) ‘Fructose causes endothelial cell damage via activation of advanced glycation end products–receptor system’, Diabetes and Vascular Disease Research, 16(6), pp. 556–561
(iii) Levi, B. and Werman, M. J. (1998) Biochemical and Molecular Roles of Nutrients Long-Term Fructose Consumption Accelerates Glycation and Several Age-Related Variables in Male Rats, J. Nutr, 128, pp. 1442-1449
(iv) Sakai, M. et al. (2002) ‘Experimental Studies on the Role of Fructose in the Development of Diabetic Complications’, Kobe Journal of Medical. Sciences, 48(5), pp. 125-136
(v) Takeuchi, M. et al. (2010) ‘Immunological detection of fructose-derived advanced glycation endproducts’, Laboratory Investigation, 90(7), pp. 1117–1127.
(vi) Danby, F. W. (2010),‘Nutrition and ageing skin: sugar and glycation’, Clinics in Dermatology, 28(4), pp. 409-411
(vii) Emmanuele, E. et al. (2011) ‘Adiponectin expression in subcutaneous adipose tissue is reduced in women with cellulite’, International Journal of Dermatology, 50(4)
(viii) Marek, G. et al. (2015) ‘Adiponectin Resistance and Proinflammatory Changes in the Visceral Adipose Tissue Induced by Fructose Consumption via Ketohexokinase-Dependent Pathway’, Diabetes, 64(2)
(ix) Cerman, A, et al. (2016) ‘Dietary glycemic factors, insulin resistance, and adiponectin levels in acne vulgaris’, Journal of the American Academy of Dermatology, 75(1), pp. 155-62
(x) Mahmood S.N. et al. (2014) ‘Diet and Acne Update: Carbohydrates Emerge as the Main Culprit’, 13(4), pp. 428-435
(xi) Cordain, L. et al. (2002), ‘Acne Vulgaris: a disease of Western civilisation’, Archives of Dermatology, 138(12), pp. 1584-90
Fructose and Mental Health
Sugar (sucrose and fructose) impacts the brain negatively. Via various mechanisms, it may increase the risk of depression (i) and have other detrimental brain health consequences, including increasing the risk of and accelerating the pathophysiology of neurodegenerative disorders such as Alzheimer’s disease (ii, iii).
A high sugar diet has been linked to cognitive impairment, including hippocampal dysfunction and negative neuroplasticity (iv, v, vi).
Fructose reduces blood flow to numerous important brain regions (vii) and interferes with the function of dopamine, a key hormone in regulating motivation and mood (viii).
Sugar sweetened beverages consumption increases stress levels (ix) and sucrose consumption from infancy creates abnormalities in the adrenal glands (x).
Sugar consumption has been linked to depression and suicidal tendencies in multiple studies (xi, xii, xiii) and its addictiveness in combination with its mechanistic associations with stress driven and emotional behaviours continues to be researched (xiv).
(i) Reis, D. et al. (2020) ‘The depressogenic potential of added dietary sugars’, Medical Hypotheses, 134: 109421
(ii) Dineley, K. et al. (2014) ‘Insulin Resistance in Alzheimer’s Disease’, Neurobiology of Disease, 72, pp. 92-103
(iii) Stephan, B.C.M. et al. (2010) ‘Increased Fructose Intake as a Risk Factor For Dementia’, J Gerontol A Biol Sci Med Sci.;65(8), pp. 809–814
(iv) Noble, E. E. et al. (2017) ‘Early-life sugar consumption has long-term negative effects on memory function in male rats’, Nutr. Neurosci., pp. 1-11
(v) Kanoski, S. E. et al. (2011) ‘Western diet consumption and cognitive impairment: links to hippocampal dysfunction and obesity, Physiol. Behav., 103, pp. 59-68
(vi) Peet, M. (2004) ‘International variations in the outcome of schizophrenia and the prevalence of depression in relation to national dietary practices: an ecological analysis’, Br. J. Psychiatry, 184, pp. 404-408
(vii) Page, K.A. et al (2013), ‘Effects of fructose vs glucose on regional cerebral blood flow in brain regions involved with appetite and reward pathways’, 309, pp. 63-70
(viii) Naneix, F. et al. (2018), ‘Protracted motivational dopamine-related deficits following adolescence sugar overconsumption’, Neuropharmacology, 129, pp. 16-25
(ix) Shearrer, G. et al. (2016) ‘Associations among sugar sweetened beverage intake, visceral fat, and cortisol awakening response in minority youth’, Physiol. Behav., 167, pp. 188-193
(x) Díaz-Aguila, Y. et al. (2016) ‘Consumption of sucrose from infancy increases the visceral fat accumulation, concentration of triglycerides, insulin and leptin, and generates abnormalities in the adrenal gland’, Anat. Sci. Int., 91, pp. 151-162
(xi) Pan, X. et al. (2011) ‘Soft drink and sweet food consumption and suicidal behaviours among Chinese adolescents’, Acta Paediatr., 100, pp. e215-e222
(xii) Lien, L. et al. (2006) ‘Consumption of soft drinks and hyperactivity, mental distress, and conduct problems among adolescents in Oslo, Norway’, Am. J. Public Health, 96, pp. 1815-1820
(xiii) Gueye, A.B. et al. (2018) ‘Unlimited sucrose consumption during adolescence generates a depressive-like phenotype in adulthood’, Neuropsychopharmacology, Am. J. Public Health, 96, pp. 1815-1820
(xiv) Jacques, A. et al. (2019) ‘The impact of sugar consumption on stress driven, emotional and addictivebehaviors’, Neuroscience and Behavioural Reviews, 103, pp. 178-199
Fructose and Chronic Diseases
High fructose consumption has adverse impacts on various tissue structures and organ functions, and indirectly and directly plays a role in the pathophysiology of various chronic diseases.
High sugar and fructose intake directly contribute to the development of Type 2 diabetes, obesity and hypertension.
Fructose has been demonstrated to be a causal factor in tumour growth in colorectal cancer, particularly when fructose is ingested in liquid form (i).
Fructose plays a role in pancreatic cancer growth, as the pancreatic cancer cells specifically utilise fructose metabolism to fuel the creation of nucleic acids, the building units of RNA and DNA, to enable the cancer to grow (ii).
Non-alcoholic fatty liver disease (NAFLD) is becoming more widespread, including in younger populations, where fatty liver disease used to be absent. NAFLD impairs the function of this critical fat-regulating and detoxification organ. Increased sugar intake appears to be a leading factor, with fructose being directly implicated, particularly in how it initiates fat generation and storage in the liver. Fructose intake has been associated with liver cancer, and NAFLD can be an initiating pathophysiology leading to liver cancer (iii, iv).
Sugar (sucrose and fructose) impacts the brain negatively. Via various mechanisms, it may increase the risk of depression (v) and have other detrimental brain health consequences, including increasing the risk of and accelerating the pathophysiology of neurodegenerative disorders such as Alzheimer’s disease (vi, vii).
Dietary sugar and fructose in particular, appears to play a causal role in increasing the risk of and accelerating cardiovascular disease (CVD), directly by increasing atherogenic particles (viii, ix) in the blood, creating liver and kidney dysfunction (a symptom of which is higher blood pressure) (x, xi, xii), and indirectly by increasing the risk of obesity, type II diabetes and metabolic syndrome (xiii, xiv). CVD is still the leading cause of death globally, accounting for 1/3rd of deaths, more than any other disease by far (xv).
(i) Goncalves M. et al, (2019) ‘High-fructose corn syrup enhances intestinal tumor growth in mice’, Science. 2019 March 22; 363(6433), pp. 1345–1349
(ii) Liu H. et al, (2010) ‘Fructose Induces Transketolase Flux to Promote Pancreatic Cancer Growth’, Cancer Research, 70, pp. 6368-6376
(iii) Jensen T. et al, (2018) ‘Fructose and Sugar: A Major Mediator of Nonalcoholic Fatty Liver Disease’, J Hepatol. 2018 May ; 68(5), pp. 1063–1075
(iv) Basaranoglu M. et al, (2013) ‘Fructose as a key player in the development of fatty liver disease’, World J Gastroenterol, 19(8), pp. 1166-1172
(v) Reis D. et al, (2020) ‘The depressogenic potential of added dietary sugars’, Medical Hypotheses, 134: 109421
(vi) Dineley K. et al, (2014) ‘Insulin Resistance in Alzheimer’s Disease’, Neurobiology of Disease, 72, pp. 92-103
(vii) Stephan B.C.M. et al (2010) ‘Increased Fructose Intake as a Risk Factor For Dementia’, J Gerontol A Biol Sci Med Sci.;65(8), pp. 809–814
(viii) Koo, H. Y. et al. (2009) ‘Replacing dietary glucose with fructose increases ChREBP activity and SREBP-1 protein in rat liver nucleus’, Biochemical and Biophysical Research Communications, 390(2), pp. 285–289
(ix) Karasawa, T. et al. (2011) ‘Sterol regulatory element-binding protein-1 determines plasma remnant lipoproteins and accelerates atherosclerosis in low-density lipoprotein receptor-deficient mice’, Arteriosclerosis, Thrombosis, and Vascular Biology, 31(8), pp. 1788–1795
(x) Johnson, R. J., Sanchez-Lozada, L. G. and Nakagawa, T. (2010) ‘The effect of fructose on renal biology and disease’, Journal of the American Society of Nephrology, 21(12), pp. 2036–2039
(xi) Johnson, R. J. et al. (2003) ‘Is there a pathogenetic role for uric acid in hypertension and cardiovascular and renal disease?’, Hypertension, pp. 1183–1190
(xii) Jiang, Z. G., Robson, S. C. and Yao, Z. (2013) ‘Lipoprotein metabolism in nonalcoholic fatty liver disease’, Journal of Biomedical Research, 27(1), pp. 1–13
(xiii) Perez-Pozo, S. E. et al. (2010) ‘Excessive fructose intake induces the features of metabolic syndrome in healthy adult men: Role of uric acid in the hypertensive response’, International Journal of Obesity, 34(3), pp. 454–461
(xiv) Johnson, R. J. et al. (2015) ‘Causal or noncausal relationship of uric acid with diabetes’, Diabetes, pp. 2720–2722.
(xv) WHO Institute of Health Metrics and Evaluation (IHME) (2017). The Global Burden of Disease 2017
What amount is ok? How can I see?
What amounts of fructose are problematic, and how can I check nutrition labels to avoid overconsuming it?
Exactly how much fructose, over what durations, and in what forms (liquid forms are very problematic) are pathological? Recent research demonstrates that even levels of c. 0.25g/kg body weight per day (e.g. 15g of fructose per day for a 60kg person) can be harmful (i). This is equivalent to a small glass (150ml) of apple juice. A typical ‘date ball’ snack on the market has >15g of sugar (50% of which is fructose), so two of these will put you over this level. True, date balls have some fibre, typically c. 3g per ball, but on balance, the fibre content therein is unlikely to offset fructose’s negative health consequences.
Advice on Checking Labels: On the nutrition table on packaged foods, check ‘Sugars’, per 100g. If the ‘Sugars’ content is 40g/100g, you know that essentially the product you are holding is 40% sugar by weight (10 cubes of sugar per 100g)! You would be surprised how many products are this high in sugar, including sauces and products you wouldn’t expect to contain sugar. As a rule of thumb, try to avoid products that are >5g/100g sugars. If it is a drink, avoid any drink with >5g/100g sugars – ideally, avoid all sugar-containing and artificially-sweetened drinks.
Trust your tastebuds! Fructose is sweet. Cauliflower and grapes are both carbohydrates. Which one is sweet? Cauliflower contains mainly glucose as its carbohydrate, while grapes contain mainly fructose. You can guess the level of fructose by how sweet a food is, unless it is artificially sweetened or naturally sweetened by a healthy sweetening, non-sugar ingredient. The metabolic consequences of eating different carbohydrates are different. There is some confusion generated by labels, primarily with dairy products. Milk – which is not sweet – contains lactose (glucose + galactose), and no fructose. Yet, you may find a milk-product that has to be labelled c. 5g/100g sugars, despite having none of the health consequences of fructose-containing drinks.
Ask: Do I know how much sugar I’m consuming? Is there a healthier way to enjoy sweetness?
(i) Jang, C. et al. (2018) ‘The Small Intestine Converts Dietary Fructose into Glucose and Organic Acids’, Cell Metabolism, 27(2), pp. 351-361.