IF YOU SEEK THRIVING HEALTH, HAVE YOU CONSIDERED YOUR SUGAR EXPOSURE?

WHAT IS SUGAR?

Sugar (sucrose) is a disaccharide made of the monosaccharide glucose and the monosaccharide fructose, bound together. GLUCOSE + FRUCTOSE = SUCROSE.

FRUCTOSE is a monosaccharide that tastes sweet. Examples of carbohydrates made mostly of fructose are apple juice, honey, and agave syrup. Fructose does not immediately spike blood sugar or insulin, BUT excess fructose generates uric acid, triglycerides (fat), visceral fat, and leads to insulin resistance over time, along with other harmful effects.

GLUCOSE = NOT so sweet. Examples of carbohydrates made mostly of glucose are rice and potatoes. Glucose raises blood sugar and insulin in the short-term, but can be attenuated by eating fiber and having a healthy metabolism. Glucose is found in varying quantities in most plant foods. Excess glucose in the form of low fiber carbohydrates is unhelpful partly because that excess glucose generates fructose.

WHAT IS BLOOD SUGAR? Continuous Glucose Monitor

Blood Sugar is Blood GLUCOSE - the amount of glucose circulating in the blood. Glucose is used by many of the body’s cells for energy, and the body has an intricate system of regulating how glucose from the food we eat gets into the cells to be used as energy. The system keeps blood glucose levels in a tight range, and it depends partly on the effective functioning of hormones such as insulin, and glucose transporters on cell membranes.

When a food causes a high spike in blood glucose, it has a high ‘glycemic load’ (GL). Higher blood glucose over time is harmful. What makes it high?

Fructose does NOT cause an immediate spike (i.e. it would count as ‘low GL’, which is why GL is not enough to consider), yet over time, chronic high-fructose consumption causes constantly higher blood glucose. High fructose diets promote insulin resistance. This leads to elevated blood glucose and insulin, driving metabolic dysfunction, and ultimately Type 2 diabetes. Type 2 diabetes is when specific cells in the body stop responding appropriately to insulin signaling. The result? Chronically elevated blood glucose and insulin, triggering many harmful effects and increasing the risk of the major chronic diseases.

DO YOU KNOW THE COMMON SOURCES OF SUGAR?

These added sugars are biochemically almost identical. They all contain high amounts of fructose. We do NOT need them to survive, and it is best for our health to minimize or avoid them.

Tappy L. and Le, K-A (2010) “Metabolic Effects of Fructose and the Worldwide Increase in Obesity” Physiology Review 90 pp. 23-46

METABOLIC PATHWAY: WHAT HAPPENS WHEN YOU EAT SUGAR?

The sugar (sucrose) cleaved into fructose and glucose. Fructose enters its metabolic pathway and glucose will enter its metabolic pathway.

Fructose is metabolized by the small intestine, kidneys, skeletal muscle, adipose tissue, and liver, wherein it has a similar pathway to ethanol. Research indicates that amounts of >30g fructose for an adult weighing 60kg leads to rapid pressure on the liver to deal with the fructose, wherein it goes through the following pathway, triggering multiple negative consequences, including on liver function in which it can induce liver disease (MASLD) over time (i).

As shown in the diagram, fructose enters the cell via GLUT2 and is metabolized by fructokinase into Fructose-1-P. This first step in fructose metabolism lowers ATP (the main energy carrier in the body) and creates uric acid (UA) (ii). Higher UA 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 glucose metabolism (right side of diagram), when there is an influx of fructose, there is no automatic feedback loop to regulate what is happening. Thus, with a large intake, fructose metabolism can proceed unabated, depleting ATP and generating uric acid and triglycerides.

Some of fructose metabolism’s consequences:

a. Increased UA: triggers endothelial (blood vessel wall) dysfunction, raises blood pressure, and impairs UA excretion, further increasing UA. UA turns on fat creation and fat storage.

b. Increased Triglycerides: increased fats travelling in the blood and visceral fat generation (fat in and around vital organs such as the liver and the pancreas).

c. Depletion of ATP outstripping ATP generation: intracellular energy is depleted acutely, rather than increased, creating intracellular stress.

d. Increased oxidative stress: tissue ageing and dysfunction.

e. Direct and epigenetic impacts that promote insulin resistance and thus disturbed blood sugar balance (i.e. the start 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)
(iv) Tappy L. and Le, K-A. (2010) ‘Metabolic Effects of Fructose and the Worldwide Increase in Obesity’, Physiology Review, 90, pp. 23-46.

SUGAR CREATES FAT

The fructose metabolic pathway leads to de novo lipogenesis: fat generation (i).

Fructose metabolism has epigenetic effects: switching on fat storage and suppressing fat burning (ii, iii).

Fructose leads to increased visceral fat accumulating between and around organs, especially central adiposity. Visceral fat disrupts the functioning of key organs (such as the pancreas and liver) (iv, v, vi, vii).

Fat tissue is biologically active and secretes inflammatory cytokines. Visceral fat secretes interleukin-6 (il-6), which induces inflammation and plasminogen activator inhibitor 1 (PAI-1), high levels of which contribute to atherosclerosis and thrombosis. This is a key link between abdominal fat and heart disease (viii). Visceral fat secretes tumor necrosis factor-alpha (TNF-α) and fructose itself elevates this inflammatory biomarker (ix, x).

TNF-α encourages insulin resistance and is strongly implicated in the pathology of diabetes, obesity, and metabolic syndrome (xi, xii).

The 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).

Fructose: Turns on Fat Creating (Lipogenic) and Turns off Fat Burning (FA-Oxidation) Genes and Proteins

Fructose-supplementation increases liver weight and triglycerides. Fructose-supplementation upregulates lipogenic genes and proteins while downregulating fatty acid oxidation genes and proteins.

(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 insulin-sensitive 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
(xiv) Rebollo, A. et al. (2014) ‘Liquid fructose downregulates Sirt1 expression and activity and impairs the oxidation of fatty acids in rat and human liver cells’, Biochimica et Biophysica Acta - Molecular and Cell Biology of Lipids, 1841(4), pp. 514–524

SUGAR KEEPS US HUNGRY → WE EAT MORE

Fructose bypasses our fullness (satiety) signalling system. We can consume many calories of fructose, without feeling full. This is because it fails to suppress ghrelin, the hunger hormone, and creates leptin (fullness hormone) resistance (i, ii, iii, iv, v). You can easily drink >2 cups of apple juice, but not >2 cups of milk, which contains satiating protein and fat.

Research also indicates that fructose influences the types of foods we choose: by influencing the endocannabinoid system, we crave more 'rewarding' (more energy-dense) foods (vi). Thus, we 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 fiber and micronutrient-poor, so not only do we ingest excess calories, but we do not get the fiber and nutrients we need. We are left overfed, hungry, and undernourished.

A vicious cycle: research in humans indicates that the impact of fructose not suppressing hunger gets worse in the obese state (vii). Despite excess body weight, one feels hungry for longer after eating fructose.

Calories: calories are not made equal. Calories are only equal when they are literally put into a fire and burnt in a lab to count them. Eating 100kcal of broccoli vs. 100kcal of date syrup is a completely different experience. The composition of the food will make you feel satiated or not, send different signals, switch on/off certain genes’ expression, be used as components to build structures, be used for energy, stored as glycogen, and/or generate visceral fat.

That fructose bypasses 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 one of the deepest human instincts - hunger. This is why a low calorie diet with a high % of sugar is notoriously hard to maintain.

A high-fructose diet leaves us hungrier (and crave more dopamine-releasing sugar), so we almost inevitably overeat. If we do not over-consume sugar, our hunger-fullness hormonal regulatory system keeps the equation in balance naturally. On a healthy, satiating diet with functioning metabolism, without excess sugar, our biology easily takes care of this balance for us naturally – no need for calorie counting.

(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) Shapiro, A. et al (2008), ‘Fructose-induced leptin resistance exacerbates weight gain in response to subsequent high-fat feeding,’ Am J Physiol Regul Integr Comp Physiol 295: R1370–R1375
(iii) Äijälä, M. et al, (2013), ‘Long-term fructose feeding changes the expression of leptin receptors and autophagy genes in the adipose tissue and liver of male rats: a possible link to elevated triglycerides’, Genes Nutr (2013) 8:623–635
(iv) Teff, K.L. et al, (2004), ‘Dietary Fructose Reduces Circulating Insulin and Leptin, Attenuates Postprandial Suppression of Ghrelin, and Increases Triglycerides in Women’, The Journal of Clinical Endocrinology & Metabolism, Volume 89, Issue 6, 1 June 2004, Pages 2963–2972
(v) 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
(vi) 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
(vii) Van Name, M. (2015), ‘Blunted Suppression of Acyl-Ghrelin in Response to Fructose Ingestion in Obese Adolescents: the Role of Insulin Resistance’, Obesity (Silver Spring). 2015 Mar;23(3):653-61

SUGAR HARMS THE GUT

Excess fructose alters the composition and metabolism of gut microbiota to states associated with chronic diseases 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 body, responsible for absorbing nutrients and keeping toxins and pathogens out. Its health and optimal functioning are critical to our digestion, energy generation, and immune system function (a large percentage of our immune cells surround the gut). When there is intestinal permeability, these essential functions become disrupted, resulting in inflammatory, autoimmune, allergic, and/or malabsorption problems and disease.

Sugar 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)

SUGAR DISRUPTS THE IMMUNE SYSTEM

Sugar negatively impacts the innate immune system, in multiple ways, incl. 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 works 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, reducing the latter’s positive influence on maintaining the gut barrier. 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 function, and it is evident that the amounts of sugar we are exposed to are not what we 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 Allergic Airway Inflammation and Activates the Innate Immune System 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

SUGAR AGES AND DISRUPTS 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 reduce the ability of the skin to heal and regenerate, 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) are associated with cellulite in those areas. Cellulite is also linked to glycation (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 drives) appears to play a role in acne pathophysiology.

Even the best topical skincare regime will not be effective if you have a high sugar diet.

(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

SUGAR vs. YOUR BRAIN AND MOOD

Sugar (sucrose and fructose) impacts the brain negatively. Via various mechanisms, it may increase the risk of depression (i) and have other detrimental 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 behaviors 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’, JAMA, 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
(xiv) Jacques, A. et al. (2019) ‘The impact of sugar consumption on stress driven, emotional and addictive behaviors’, Neuroscience and Behavioural Reviews, 103, pp. 178-199

SUGAR DEPLETES ESSENTIAL MICRONUTRIENTS: VITAMINS, MINERALS

Vitamin C: the uncharged form of Vitamin C enters cells via glucose transporters. Higher blood glucose thus outcompetes vitamin C, robbing your cells from this vital anti-oxidant (i).

Magnesium: the kidneys excrete more Magnesium in states of hyperglycemia. Low Magnesium appears to further exacerbate insulin resistance and hyperglycemia (ii, iii, iv, v).

Vitamin D3 and Calcium: high fructose diets drive down Vitamin D3 levels, resulting in less Calcium absorption and damage to bone health (vi, vii, viii).

Increased Reactive Oxidation Species and Advanced Glycation End Products (AGEs) → Increased Inflammation → Antioxidant Depletion (ix).

(i) Chen L, et al (2005) ‘Hyperglycemia inhibits the uptake of dehydroascorbate in tubular epithelial cell’, Am J Nephrol. 2005 Sep-Oct;25(5):459-65.
(ii) Djurhuus, M.S. et al. (2000) ‘Hyperglycaemia enhances renal magnesium excretion in type 1 diabetic patients’, Scand J Clin Lab Invest. 2000 Aug;60(5):403-9.
(iii) Xu, Eric J. et al. (2025) ‘Hypomagnesemia With Metformin Use in Diabetes Mellitus: A Case and Narrative Review’, Kidney Medicine, Volume 7, Issue 7, 101030
(iv) Ebrahimi Mousavi, S. et al. (2021) ‘Association between magnesium concentrations and prediabetes: a systematic review and meta-analysis’, Sci Rep 11, 24388.
(v) Giuseppe P, et al. (1997) ‘Hypertension, Diabetes Mellitus, and Insulin Resistance: The Role of Intracellular Magnesium’, American Journal of Hypertension, Volume 10, Issue 3, March 1997, Pages 346–355
(vi) Douard V, et al. (2014) ‘Chronic high fructose intake reduces serum 1,25 (OH)2D3 levels in calcium-sufficient rodents.’ PLoS One. 2014 Apr 9;9(4):e93611.
(vii) Douard V, et al. (2013) ‘Excessive fructose intake causes 1, 25-(OH) 2D 3-dependent inhibition of intestinal and renal calcium transport in growing rats’, American Journal of Physiology-Endocrinology and Metabolism. 2013 Jun 15;304(12):E1303–13.
(viii) Tjäderhane L. (1996) ‘The effect of high sucrose diet on dentin minerals measured by electron probe microanalyzer (EPMA) in growing rat molars’. In: Shimono S, Maeda T, Suda H, Takahashi K, editors. Dentin/Pulp Complex. Quintessence Publishing; Tokyo, Japan: 1996. pp. 293–296.
(ix) Prasad, K. (2014) ‘Oxidative stress as a mechanism of added sugar-induced cardiovascular disease’, Int J Angiol. 2014 Dec;23(4):217-26.

SUGAR DRIVES AND ACCELERATES AGEING AND THE MAJOR CHRONIC DISEASES

Hypertension

Insulin Resistance, Type 2 Diabetes

Obesity

Dementia and Alzheimer’s Disease

Cardiovascular Disease

Acne, Cellulite, Ageing Skin, Wrinkles

Colon Cancer

Pancreatic Cancer

Hypertriglyceridemia

Metabolic Dysfunction Associated Liver Disease (MASLD)

Liver Cancer

Depression

Osteoporosis

Tooth Decay

Hair Loss

Candida

Polycystic Ovarian Syndrome

Inflammatory Bowel Disease

High fructose consumption has adverse impacts on various tissue structures and organ functions, and directly plays a role in the pathophysiology of various chronic diseases.

High sugar intake directly contributes to the development of Type 2 diabetes, obesity, and hypertension.

Fructose has been demonstrated to be a causal factor in tumor growth in colorectal cancer, especially when ingested in liquid form (i).

Fructose plays a role in pancreatic cancer growth, as the pancreatic cancer cells specifically utilize fructose metabolism to fuel the creation of nucleic acids, the building units of RNA and DNA, to enable the cancer to grow (ii).

Metabolic Dysfunction-Associated Liver Disease (MASLD) is becoming more widespread, including in younger populations, where this disease used to be absent. MASLD impairs the function of this critical fat-regulating and detoxification organ – the liver. 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 is associated with liver cancer, and MASLD 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 neurodegeneration such as Alzheimer’s disease (vi, vii).

Excess sugar 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).

Osteoporosis: in addition to depleting Vitamin D3 and calcium, excess sugar exacerbates bone loss by allowing cholesterol build up in bones (xvi, xvii, xviii).

(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.
(xvi) DiNicolantonio, J. J. et al (2018) ‘Not Salt But Sugar As Aetiological In Osteoporosis: A Review’, Mo Med. 2018 May-Jun;115(3):247-252.
(xvii) Chen, J. et al (2025) ‘A high-fructose diet leads to osteoporosis by suppressing the expression of Thrb and facilitating the accumulation of cholesterol’, Cell Death Discov. 11, 159 (2025).
(xviii) Ahn, H. (2021) ‘Sugar-sweetened beverage consumption and bone health: a systematic review and meta-analysis’, Nutr J 20, 41 (2021).

HOW MUCH IS PROBLEMATIC?

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 sweetened bar has >15g of sugar (50% of which is fructose), so two of these will put you over this level. True, a date bar has some fiber, typically c. 3g per serving, but on balance, the fiber content therein is unlikely to offset the negative health consequences of the sugar.

WHAT CAN YOU DO?

AVOID LIQUID SUGAR: sugar-sweetened drinks (e.g. sodas, 'energy' drinks, sweet cocktails, fruit-juices, fruit-containing smoothies).

AVOID ADDED SUGARS:. such as agave syrup, maple syrup, date syrup, corn syrup, honey, coconut sugar, cane sugar, fruit concentrate.

CHECK THE LABEL: do not buy if >5g/100g sugar, unless it is an exception that is delicious!

LIMIT TOTAL SUGAR to <5%/daily-kcal = <c. 25g/day for an average adult. (e.g. 1 cup of strawberries).

CROWD CARBS OUT (CCO): Start your meal with fiber and protein. These are satiating. Leave white carbs or dessert for last, if you still want them.

AVOID DRIED FRUIT: Eat 1 portion of fruit per day (no need to have fruit daily). Eat plenty of VEGETABLES for micronutrients and fiber. Eat berries rather than grapes. You can tell how much fructose is in the fruit by its sweetness.

DETECT THE SUGAR. TREAT AS A TREAT: Sugar tastes sweet because of the FRUCTOSE. Unless sweetened with artificial sweeteners or natural healthy sweeteners (stevia, erythritol, xylitol, allulose, monk fruit extract, katemfe extract (thaumatin) and others), if something you are eating tastes sweet, it contains fructose. Usually, the sweeter it tastes, the more fructose it contains. For example, a ripe brown banana has formed more fructose than a green one. Fresh grapes contain c. 8% fructose, but after drying to become raisins, the fructose quadruples to c. 32% fructose, and the total sugars (fructose, glucose, sucrose, maltose (two glucoses bonded together)) make up 67-80% of the raisins (ii).

CHOOSE HEALTHY SWEET INGREDIENTS from nature’s healthy sweetness pantry: organic stevia, organic erythritol, organic monk fruit extract, katemfe fruit extract, and/or allulose. Make sure the sweetening product you buy is not mixed with artificial sweeteners (often happens) and go for certified organic versions of all if possible.

ADDITIONAL LABEL READING TIPS

Net Carbs: if considering carbohydrates, look out for Net Carbs which subtracts fiber and other non-caloric, no glycemic load carbohydrates.
Dairy: dairy has no fructose. The carbohydrates in milk are lactose: glucose and galactose. Unless you are lactose intolerant, these do not need to be counted towards your daily sucrose (sugar) intake.

ASK: ‘What is the cost-benefit of the amount of sugar I choose to eat, now and long term? Is there a way to enjoy healthy sweetness that tastes equally good?’

(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) Alnuwaiser M.A., (2017), Content of Sugars in Fresh Grapes and Raisins, and Fresh and Dried Apricot: A Comparative Study. Int. j. res. granthaalayah. 5, pp. 1770186

EVOLUTION AND THE FAT SWITCH

Human beings have not evolved to adapt to the high-sugar environment we live in. Fruits were not cross-bred to increase their sweetness (sugar-content) as they are now, and we ate what we could find, allowing us to store fat, useful ahead of a cold, food-scarce winter. Our Paleolithic ancestors are unlikely to have had regular access to honey, dates, or maple syrup.

One mechanism by which fructose increases fat generation and storage, and reduces fat-burning, is via its generation of uric acid. While many mammals have an enzyme (uricase) that helps them to break down uric acid, humans do not. Genetic research reveals that our ancestors lost the uricase enzyme during the early Miocene period, when progressive climate-cooling challenged early hominids’ diets. Losing uricase – elevating uric acid levels – likely provided a substantial survival advantage by increasing fructose’s fat-storage effects in the then-frugivorous species (i, ii).

In human history, the time during which sugar consumption began to increase until now is less than c. 0.1% of our existence as a species: the biology of human beings has not had time to evolve to deal with the large quantities of sugar we currently consume. In fact, our biology is still geared towards reacting to fructose by storing body fat, a great survival mechanism in the food-scarce past, a harmful one in the sugar-filled present.

(i) Kratzer, J. et al (2014), ‘Evolutionary history and metabolic insights of ancient mammalian uricases’, Proc. Natl. Acad. Sci. U.S.A. 111 (10) 3763-3768.

(ii) Johnson, RJ. et al (2023), ‘The fructose survival hypothesis for obesity’, Philos Trans R Soc Lond B Biol Sci. 2023 Sep 11;378(1885):20220230

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