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Chronic inflammation: The role of sugar

Christine Herbert

Christine Herbert FAMH, DipAET, BA(Hons) qualified as a herbalist in 1997 and has been practising and learning herbal medicine ever since. During the years of her practice, she added many skills, including nutrition, aromatic medicine and flower essence therapy, in order to be best able to help the many people who came to see her. She retired from practice in 2019 so that she could teach and write using all the knowledge she had acquired.

She served on the Association of Master Herbalists council for several years and was awarded an Honorary Fellowship on retirement. Previous to 1997, she worked as a senior biomedical scientist for nineteen years for the NHS. Inflammation, the source of chronic disease: how to treat it with herbs and natural healing was published by Aeon Books.

Listen to Christine Herbert’s Herbcast episode “A herbalist’s approach to treating inflammation“.

As a key driver of chronic inflammation, sugar contributes to metabolic, cardiovascular, immune and mood-related disorders. This article examines mechanisms and health implications.

Inflammation is a key process essential to healthy immune function, as a response to resolve injury and infection. Whilst acute, inflammation is integral to healing, yet sustained inflammation is a cardinal feature of the pathophysiology of  many chronic inflammatory diseases prevalent today. These include: 

Chronic Inflammation The Role Of Sugar
  • Allergies
  • Arthritis
  • Autoimmunity
  • Bladder inflammation
  • Cancer
  • Cardiovascular disease
  • Chronic fatigue
  • Diabetes
  • Fibromyalgia
  • Inflammatory bowl disease
  • Inflammatory lung diseases — e.g., COPD, asthma
  • Inflammatory skin diseases — e.g., eczema, psoriasis, acne
  • Neurodegenerative disease

Inflammation has also been implicated in the neurobiology of mood disorders, such as major depressive disorder.

Chronic inflammatory disease arises from a complex interplay of genetic and environmental factors. Whilst genetics in part determines individual constitutions, strengths and vulnerabilities, epigenetics describes how these genes are expressed according to environmental influences. Environmental factors encompass diet, exercise, climate, toxin or pathogen exposure, gut microbiome composition, digestive function and immune health.

Inflammation is the combination of redness (rubor), heat (calor), swelling (tumor) and often pain (dolor) that occurs after an injury, irritation or infection. Inflammation is a protective, restorative response of the immune system, essential to the healing process of the body. When resolution is reached the body then produces anti-inflammatory chemicals to stop the inflammatory process and restore healthy tissue function. However, if the cause of acute inflammation is sustained — for example, an untreated infection or continued exposure to allergens or toxins — inflammatory activity becomes

Knee Pain Inflammation

an ongoing chronic process that causes tissue damage and dysfunction, and eventually chronic disease. Simply using anti-inflammatory medication to suppress the symptoms will not resolve the problem and will create new issues due to side effects.

A key consideration in managing chronic inflammation is diet (1). A deficiency of foods that reduce inflammation, in particular whole grains, fruit vegetables, nuts and seeds and omega 3 fatty acids can contribute to a rise in inflammation. Another consideration is whether a diet is high in foods  that increase inflammation. 

Pro-inflammatory foods include sugar, ultra-processed foods (UPFs), processed meat products, refined carbohydrates, trans fatty acids, gluten, alcohol, non cold pressed vegetable oils, artificial additives and, for many people, dairy products (2,3). The physiological effects of carbohydrates vary according to their composition and metabolic impact. Glycaemic load (GL) is a measure that reflects both the quality (glycaemic index) and quantity of carbohydrate in a given portion of food, thereby estimating its overall effect on postprandial blood glucose levels. Diets characterised by a lower glycaemic load have been associated with reduced postprandial hyperglycaemia and lower inflammatory markers (4).

Sugar has an especially significant impact on the inflammatory process. Dietary sugars are mainly glucose, fructose, sucrose and high fructose corn syrup (HFCS). Table sugar (sucrose) is composed of equal parts of fructose and glucose. Until the 18th century the human diet contained small amounts of sucrose and fructose, naturally present in fruits, vegetables and honey.

The Romans and Greeks knew of sugar in the first century CE and it very gradually appeared in Europe. Yet, sugar remained rare and expensive until sugar plantations were established in the 18th century on the Caribbean islands, relying on systems of enslavement to sustain production. By the 19th century sugar became a commodity used by all, in Britain, mostly to sweeten tea, but then in confectionery.

The use of sugar beet, starting in Europe in the early 19th century, in sugar production contributed to the reduction in price. In the 1960s, high fructose corn syrup (HFCS) was produced from corn by industrial production, and this became the cheapest form of sugar available, resulting in vastly increased consumption.

HFCS is sweeter and more soluble than sucrose, has a longer shelf life, and does not crystallise as sucrose does. HFCS has become a major component of industrial baked goods (cakes and biscuits) as well as sweetened soft drinks; all of which have become a major component of the modern Western diet (5). 

Sugar Causing Chronic Inflammation

The way fructose is metabolised by the body is important. In nature, sweet foods — such as fruit, vegetables and honey — contain a diverse combination of sugars, with fructose present, but only in small amounts and alongside glucose. This makes all the difference in the effect of fructose on the body, as the metabolism of fructose in the body is very different to that of glucose.

Fructose metabolism for cellular uptake is largely insulin independent and is primarily processed by the liver. The body’s capacity to metabolise  fructose is limited. As such, processing large quantities puts high metabolic demands on the liver, which, if sustained, can increase risk of fatty liver disease or metabolic dysfunction-associated steatotic liver disease (MASLD) (6). MASLD is correlated with metabolic disease and obesity, as well as increased body fat and the amount of secreted pro-inflammatory cytokines and other inflammatory mediators. 

Obesity itself is associated with chronic low-grade inflammation as adipose (fat) tissue functions as an endocrine and immune-modulating organ that secretes a range of inflammatory cytokines and other inflammatory chemicals, such as adipokines, contributing to systemic inflammatory signalling. Central (abdominal) obesity is more strongly associated with inflammation, with increasing visceral adipose tissue mass correlating with increased secretion of pro-inflammatory cytokines (7,8).

Metabolic diseases, including insulin resistance, type II diabetes, cardiovascular diseases and obesity, are all closely associated with chronic inflammation, which both contributes to and is exacerbated by metabolic dysfunction (9). A study of 29 healthy people found that consuming one 375 ml can of a soft drink containing 40 g of sugar per day for three weeks resulted in increased risk factors for cardiovascular disease. These risk factors all involved inflammation with weight gain, increased LDL, inflammatory markers and blood sugar. This is a relatively low intake over a short period of time (10). 

Another study found that people given a single 50 g dose of fructose showed an increase in the inflammatory marker C-reactive protein CRP in just 30 minutes. The CRP level remained high for over two hours (11). Eating high GL foods has a similar result, with a study showing increased inflammatory markers after ingestion of 50 g of refined carbohydrate in the form of white bread (12). Studies have found that this is dose dependent — the greater the quantity of inflammatory foods eaten, the greater the resulting inflammation (13).

Severe inflammatory diseases including rheumatoid arthritis, multiple sclerosis, psoriasis and inflammatory bowel disease have been associated with dietary sugar intake, with higher sugar intake exacerbating symptom severity (14).

Bilberry (Vaccinium myrtillus)
Bilberry (Vaccinium myrtillus)

From the point of view of herbal medicine, an important consideration is the use of sugar in herbal preparations, as syrups. These use sugar in a high concentration (typically 65–70% sucrose) to preserve a herbal extract and also improve its taste, which is especially helpful for children. Historically syrups were often used, especially for cough medicines.

The active compounds are extracted with the water content, not the sugar and the shelf life of syrups is limited. An alternative option for a sweet-tasting herbal medicine is organic vegetable glycerin (glycerol), which both extracts constituents and preserves them, so has a better extraction ability than water, tastes sweet, offers an alcohol-free preparation, is typically stable concentrations greater than 60% (the remainder can be water as infusion or decoction, and/or alcohol), and most importantly in this context, it has much lower glycaemic impact (GI) than sugar (15). 

Owing to the lower GI, glycerine has a lesser effect on blood sugar levels and insulin. So, for palatable, alcohol-free (though technically glycerine is an alcohol) herbal extracts, preparations made with glycerine (glycerites) may be a favoured method.

Evidence associating high sugar intake with metabolic and inflammatory disease informed the UK government’s introduction of the Soft Drinks Industry Levy (SDIL) in 2018, a tiered tax designed to incentivise reduced sugar content of soft drinks (16). However, to satiate consumers’ sugar cravings manufacturers subsequently swapped HFCS and sugar for artificial sweeteners.

Yet, these also cause inflammation, particularly gut inflammation, as well as changes in the gut microbiome. Even stevia, considered to be a healthy non-sugar sweetener, appears to modify the gut microbiome. Saccharin, sucralose and aspartame have all shown deleterious effects on the gut microbiome and the liver, as well as increasing release of lipopolysaccharides (LPS), which contribute tosystemic inflammation (17).

Erythritol has been found to cause endothelial cell inflammation, particularly affecting the microcirculation to the brain, increasing the risk of stroke (18). Despite data that suggests that artificial sweeteners may be helpful for weight reduction, they have contrarily also been found to contribute to weight gain. Disruptions in gut flora can dysregulate glucose metabolism and insulin sensitivity, increasing susceptibility to metabolic syndrome (19,20).  

Changing your diet blood sugar stabilising foods

Advising individuals to remove sugar from their diets, is unlikely to be effective. A substantial body of evidence suggests that high sugar intake promotes addictive-like eating behaviours and is associated with neurobiological alterations in reward and stress pathways.

Diets high in refined sugars have been linked to dysregulation of mood, associated with anxiety, depression, as well as heightened cravings to eat more sweet things (20). Sugar reduction is often more sustainable when implemented gradually and accompanied by clear information about its potential physiological and psychological effects.

In the context of rising rates of inflammatory disease, public health approaches have increasingly focussed on nutritional education and reformulating products with artificial sweeteners. Yet, substituting sugar with non-nutritive sweeteners does not address established preferences for sweet tastes, and may therefore leave underlying patterns of consumption and reward-seeking behaviour largely unchanged.

Evidence implicating chronic inflammation in the pathophysiology of many of the chronic conditions that burden healthcare systems globally today is ever-growing. Similarly, studies are mounting that elucidate the inflammatory pathways and further implications of high dietary sugar intake. These expanding fields of research establish reducing sugar in the diet as a valuable means of supporting chronic inflammatory disease prevention and management.

  1. GBD 2017 Diet Collaborators. Health effects of dietary risks in 195 countries, 1990-2017: a systematic analysis for the Global Burden of Disease Study 2017. Lancet. 2019 May 11;393(10184):1958-1972 Ma X, Nan F, Liang H, et al
  2. Excessive intake of sugar: An accomplice of inflammation. Front Immunol. 2022;13:988481. Published 2022 Aug 31. https://doi.org/10.3389/fimmu.2022.988481 
  3. Tristan Asensi M, Napoletano A, Sofi F, Dinu M. Low-Grade Inflammation and Ultra-Processed Foods Consumption: A Review. Nutrients. 2023;15(6):1546. Published 2023 Mar 22. https://doi.org/10.3390/nu15061546 
  4. Neuhouser ML, Schwarz Y, Wang C, et al. A low-glycemic load diet reduces serum C-reactive protein and modestly increases adiponectin in overweight and obese adults. J Nutr. 2012;142(2):369-374. https://doi.org/10.3945/jn.111.149807 
  5. Agarwal V, Das S, Kapoor N, Prusty B, Das B. Dietary Fructose: A Literature Review of Current Evidence and Implications on Metabolic Health. Cureus. 2024;16(11):e74143. Published 2024 Nov 21. https://doi.org/10.7759/cureus.74143 
  6. Agarwal V, Das S, Kapoor N, Prusty B, Das B. Dietary Fructose: A Literature Review of Current Evidence and Implications on Metabolic Health. Cureus. 2024;16(11):e74143. Published 2024 Nov 21. https://doi.org/10.7759/cureus.74143  
  7. Ferrucci, Luigi, and Elisa Fabbri. “Inflammaging: chronic inflammation in ageing, cardiovascular disease, and frailty.” Nature reviews. Cardiology vol. 15,9 (2018): 505-522. https://doi.org/10.1038/s41569-018-0064-2 
  8. Ellulu, Mohammed S et al. “Obesity and inflammation: the linking mechanism and the complications.” Archives of medical science : AMS vol. 13,4 (2017): 851-863. https://doi.org/10.5114/aoms.2016.58928 
  9. Franceschi, C., Garagnani, P., Parini, P. et al. Inflammaging: a new immune–metabolic viewpoint for age-related diseases. Nat Rev Endocrinol 14, 576–590 (2018). https://doi.org/10.1038/s41574-018-0059-4
  10.  Aeberli I, Gerber PA, Hochuli M, et al. Low to moderate sugar-sweetened beverage consumption impairs glucose and lipid metabolism and promotes inflammation in healthy young men: a randomized controlled trial. Am J Clin Nutr. 2011;94(2):479-485. https://doi.org/10.3945/ajcn.111.013540 
  11. Jameel F, Phang M, Wood LG, Garg ML. Acute effects of feeding fructose, glucose and sucrose on blood lipid levels and systemic inflammation. Lipids Health Dis. 2014;13:195. Published 2014 Dec 16. https://doi.org/10.1186/1476-511x-13-195
  12. Dickinson S, Hancock DP, Petocz P, Ceriello A, Brand-Miller J. High-glycemic index carbohydrate increases nuclear factor-kappaB activation in mononuclear cells of young, lean healthy subjects. Am J Clin Nutr. 2008;87(5):1188-1193. https://doi.org/10.1093/ajcn/87.5.1188 
  13. Buyken AE, Flood V, Empson M, et al. Carbohydrate nutrition and inflammatory disease mortality in older adults. Am J Clin Nutr. 2010;92(3):634-643. https://doi.org/10.3945/ajcn.2010.29390 
  14. Ma X, Nan F, Liang H, et al. Excessive intake of sugar: An accomplice of inflammation. Front Immunol. 2022;13:988481. Published 2022 Aug 31. https://doi.org/10.3389/fimmu.2022.988481 
  15. Personal Communication, Lisa Ganora Herbalist
  16. UK Government. Soft Drinks Industry Levy. GOV.UK. Published April 2018. Available at: https://www.gov.uk/government/publications/soft-drinks-industry-levy/soft-drinks-industry-levy. Accessed February 9, 2026.
  17. Basson AR, Rodriguez-Palacios A, Cominelli F. Artificial Sweeteners: History and New Concepts on Inflammation. Front Nutr. 2021;8:746247. Published 2021 Sep 24. https://doi.org/10.3389/fnut.2021.746247 
  18. Auburn R. Berry, Samuel T. Ruzzene, Emily I. Ostrander, Kendra N. Wegerson, Nathalie C. Orozco-Fersiva, Madeleine F. Stone, Whitney B. Valenti, Joao E. Izaias, Joshua P. Holzer, Jared J. Greiner, Vinicius P. Garcia, and Christopher A. DeSouza The non-nutritive sweetener erythritol adversely affects brain microvascular endothelial cell function Journal of Applied Physiology,2025;138 (6):1571;https://doi.org/10.1152/japplphysiol.00276.2025 
  19. M M, Vellapandian C. Exploring the Long-Term Effect of Artificial Sweeteners on Metabolic Health. Cureus. 2024;16(9):e70043. Published 2024 Sep 23. https://doi.org/10.7759/cureus.70043 
  20. Huimin Xue, Xiping Kang, Kexin Hong, Yunxiao Gao, Yunyu Tang, Yuchen Lin, Xiangjun Liu, Weidong Huang, Jicheng Zhan, Yilin You, Effects of artificial and natural sweeteners on host metabolic health: A double-edged sword, Food Research International, Volume 220, 2025, 117158, ISSN 0963-9969, https://doi.org/10.1016/j.foodres.2025.117158.
  21. Angela Jacques, Nicholas Chaaya, Kate Beecher, Syed Aoun Ali, Arnauld Belmer, Selena Bartlett,The impact of sugar consumption on stress driven, emotional and addictive behaviors,Neuroscience & Biobehavioral Reviews,Volume 103,2019,Pages 178-199,ISSN 0149-7634,https://doi.org/10.1016/j.neubiorev.2019.05.021 

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Christine Herbert
- Herbalist

Christine Herbert FAMH, DipAET, BA(Hons) qualified as a herbalist in 1997 and has been practising and learning herbal medicine ever since.

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