Sugar and Arthrosis: Could What We Eat Be Changing Our Joints?

Written by N. Streawbridge| 29 April 2026

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Fructose, uric acid, liver fat and cartilage ageing — the surprising connections between sugar consumption and osteoarthritis.



Research in Focus | Joint Health Series

When we think about arthrosis, or osteoarthritis, we usually imagine years of wear and tear. Perhaps our knees have carried us through decades of walking, our hands have worked hard, or our hips have gradually become stiffer with age.


But what if the health of our joints is influenced by more than how much we use them?

What if some of the changes taking place in cartilage are also connected to what we eat — particularly the sugars hidden in everyday foods?


Research into osteoarthritis is increasingly revealing the importance of metabolism, inflammation and cellular function. The relationship between sugar and joint health is particularly interesting because several processes may be involved simultaneously: the way fructose is metabolised, the production of uric acid, the accumulation of fat in the liver, and the gradual alteration of cartilage proteins through glycation. Understanding these connections gives us another perspective on protecting our joints as we age.


Arthrosis is more than worn-out cartilage


Cartilage is not simply a protective covering over the ends of our bones. It is a highly organised living tissue designed to distribute pressure, absorb mechanical forces and enable smooth movement.


Its remarkable properties come from a matrix of collagen fibres, proteoglycans and water. Within this structure live specialised cells called chondrocytes, responsible for maintaining the surrounding tissue.


Unlike many other tissues, cartilage has a limited capacity for repair. Its collagen network turns over extremely slowly, making it particularly vulnerable to changes that accumulate over many years.


In osteoarthritis, the balance between tissue maintenance and deterioration becomes disrupted. Changes occur not only in cartilage but also in the synovial lining, underlying bone and surrounding muscles.


Mechanical stress is important, but it is not the only influence. Researchers are increasingly examining the role of metabolic dysfunction, inflammatory signalling, oxidative stress and changes in cellular energy regulation. This is where sugar enters the picture.


Glucose and fructose: two sugars, different metabolic pathways


Ordinary table sugar, or sucrose, consists of approximately equal parts glucose and fructose. Although both supply energy, they are metabolised differently.


Glucose can be taken up and used as an energy source by many cells throughout the body. Its metabolism is regulated through several interconnected pathways that help balance energy production, storage and blood glucose concentrations.


Fructose, on the other hand, undergoes substantial initial processing in the small intestine and liver. When fructose enters these cells, an enzyme called fructokinase converts it rapidly into fructose-1-phosphate. This reaction consumes ATP, the molecule used by cells to store and transfer energy.


Unlike an important regulatory step in glucose metabolism, this initial fructose reaction is not controlled by phosphofructokinase-1. At sufficiently high fructose exposure, rapid phosphorylation can temporarily reduce intracellular ATP and phosphate. This can accelerate the breakdown of purine nucleotides and increase the production of uric acid.


This is an important distinction: uric acid does not come only from purine-rich foods such as meat and offal. Our own metabolism can increase its production in response to fructose.


Fructose, uric acid and inflammation in the joints


Most people associate elevated uric acid with gout, a condition in which monosodium urate crystals can accumulate in joints and provoke intense inflammatory attacks.

However, the biological activity of uric acid extends beyond gout. Urate participates in antioxidant defence in extracellular fluids. Yet intracellular urate and associated metabolic pathways have also been investigated for their potential influence on oxidative stress, mitochondrial function and inflammatory signalling.


Of particular interest is the relationship between urate and the NLRP3 inflammasome, a protein complex involved in activating inflammatory responses, especially in response to urate crystals.


Researchers have also investigated associations between uric acid concentrations in synovial fluid, inflammatory mediators such as interleukin-1β and interleukin-18, and the severity of osteoarthritis.


The precise contribution of uric acid to osteoarthritis remains unresolved. Unlike gout, osteoarthritis is not defined by urate crystal deposition, and higher uric acid does not necessarily cause cartilage deterioration. Nevertheless, the findings raise an interesting possibility: disturbances in urate metabolism may influence the inflammatory environment in which joint tissues function.


From sweet foods to liver fat: another important pathway


One of the most significant consequences of excessive fructose consumption concerns what happens in the liver. Fructose is widely present in confectionery, biscuits, cakes, sweetened breakfast cereals, soft drinks, syrups and many other manufactured foods.

Not all of it becomes fat. A substantial proportion is converted into glucose, lactate or glycogen, which can contribute to energy metabolism.


However, high fructose intake can also stimulate the liver to manufacture new fatty acids through a process called de novo lipogenesis. These fatty acids can be assembled into triglycerides, released into the bloodstream or stored within liver cells.


When this process contributes to the accumulation of liver fat, particularly alongside excess calorie intake and other metabolic disturbances, it may become part of the development of metabolic dysfunction-associated steatotic liver disease, often known as fatty liver disease.


Fructose is especially interesting because its metabolism is linked to both increased uric acid generation and pathways that promote fat synthesis.Experimental research suggests that uric acid-related oxidative signalling may also interfere with aspects of mitochondrial metabolism and fat oxidation, potentially reinforcing metabolic disturbances.


The liver is therefore not simply a passive processing station for dietary sugar. It is an important metabolic organ whose responses may influence the rest of the body.


Why does liver fat matter for arthrosis?


The connection is partly systemic. Fatty liver disease, insulin resistance and excess abdominal adiposity frequently coexist with low-grade inflammation and altered metabolic signalling.


These changes can influence tissues throughout the body, including blood vessels, adipose tissue and potentially the structures within joints. The synovial membrane, chondrocytes and underlying bone all respond to their metabolic environment.

Researchers are therefore investigating whether the disturbances associated with metabolic disease may contribute to a particular pattern of osteoarthritis sometimes described as metabolic osteoarthritis.


This is one reason the relationship between sugar and joint health cannot be explained solely by body weight.


Sugar can also change the physical properties of cartilage


There is another fascinating connection between sugar and arthrosis: glycation.

Glycation is a chemical process in which sugars or reactive sugar-derived compounds interact with proteins without the involvement of enzymes. Over time, these reactions can produce advanced glycation end-products, commonly called AGEs.


AGEs are especially relevant to tissues containing long-lived proteins. Cartilage collagen is one such example. The collagen network that provides cartilage with tensile strength and structural organisation is renewed very slowly. Over many years, AGE-related cross-links can accumulate within this matrix. These cross-links may increase stiffness and reduce the ability of cartilage to deform and recover under repeated mechanical loading.


In addition to modifying the cartilage matrix, certain AGEs can interact with cellular receptors, including RAGE, activating pathways associated with inflammatory signalling and oxidative stress.


Chondrocytes may consequently find themselves maintaining a matrix whose mechanical properties and biochemical environment have changed.


Ageing itself contributes to AGE accumulation, and diabetes or persistent hyperglycaemia may accelerate aspects of the process.


The intriguing possibility is that metabolic conditions can influence not only how joint cells behave, but also the physical characteristics of the tissue they maintain.


This does not mean that eating a sweet dessert immediately damages cartilage. Glycation is a complex, cumulative process influenced by many factors, including ageing and long-term glucose regulation. It does, however, provide another reason to consider metabolic health when thinking about joint ageing.


Where is fructose hiding in our everyday diet?


Fructose is not confined to fruit. It is present in table sugar, honey, agave syrup, glucose-fructose syrups, invert sugar and various fruit juice concentrates used in manufactured foods.


In confectionery and processed products, sugars are added not only for sweetness but also for texture, moisture retention, browning and shelf-life characteristics.

Some products may contain several different sugar ingredients, making their total contribution less obvious at first glance.


Foods to pay particular attention to


Sweetened beverages. Fizzy drinks, energy drinks, sweetened iced teas and fruit drinks can deliver substantial amounts of sugar rapidly, often without producing the same feeling of fullness as solid food.


Confectionery. Sweets, gummies, chocolate fillings, chewy candies and other products may contain sucrose, glucose-fructose syrup or invert sugar. Their exact fructose content depends on the recipe.


Cakes, pastries and biscuits. These often combine added sugar with refined flour and substantial amounts of fat, making them energy-dense foods.


Breakfast cereals and snack bars. Even products marketed as wholesome may contain sugar, honey, syrups or concentrated fruit juice.


Sweetened yoghurts and dairy desserts. Some contain considerable amounts of added sugar despite being presented as healthy snacks.


Fruit juices and smoothies. Even without added sugar, these may contain substantial free sugars in a form that is easy to consume quickly.


Sauces and dressings. Ketchup, barbecue sauce, sweet chilli sauce and some ready-made salad dressings can contain added sugars.


Natural sweeteners. Honey, agave syrup and fruit concentrates are still sources of free sugars, even when they are marketed as alternatives to refined sugar.


Understanding food labels


The ingredients list may identify fructose-containing ingredients under several names:


  • Fructose
  • Glucose-fructose syrup or fructose-glucose syrup
  • High-fructose corn syrup
  • Invert sugar syrup
  • Sucrose or ordinary sugar
  • Honey and agave syrup
  • Fruit juice concentrates


These ingredients do not all contain the same proportion of fructose. For example, ordinary table sugar is approximately half fructose, whereas the composition of commercial syrups varies.


Also look at the nutrition declaration for total sugars per 100 g or 100 mL. This figure does not distinguish naturally occurring from added sugars, which is why reading the ingredient list alongside it is useful.


Whole fruit is not the same as a sweetened drink


An important distinction must be made between fructose consumed in whole fruit and fructose supplied by concentrated sweeteners.


Whole fruit contains water, fibre, vitamins, minerals and numerous plant compounds.

The cellular structure and fibre content of fruit influence how sugars are released and absorbed. Whole fruit is also generally more filling than juice.


Berries, citrus fruits, apples, plums and other fruits contribute polyphenols and other nutrients that form part of a varied, health-supportive diet. It would therefore be misguided to advise people to avoid whole fruit simply because it contains fructose.


The more useful target is the frequent consumption of concentrated free sugars, particularly in sweetened beverages. Fruit juices deserve moderation. Although they may provide some vitamins and plant compounds, a large glass can contain the sugars from several pieces of fruit without the equivalent fibre or satiety.


Better Alternatives for Everyday Eating


Reducing added sugar need not mean giving up sweetness or pleasure in food. A few thoughtful changes can reduce our intake of concentrated sugars while improving overall nutritional quality.


1. Sweetened fizzy drinks

Better alternative: Sparkling water with lemon, fresh mint or berries.


2. Sweetened iced tea

Better alternative: Chilled hibiscus, rosehip, mint or lemon balm infusion without added sugar.


3. Sugary breakfast cereals

Better alternative: Porridge with nuts, cinnamon, seeds and fresh berries.


4. Sweetened fruit yoghurts

Better alternative: Plain natural or Greek yoghurt with fresh fruit.


5. Sweets, gummies and confectionery

Better alternative: Fresh fruit with a handful of nuts or seeds.


6. Cakes, pastries and biscuits

Better alternative: Smaller portions or homemade versions with less sugar, oats, nuts and warming spices.


7. Fruit juices and sweetened smoothies

Better alternative: Whole fruit accompanied by water or an unsweetened herbal infusion.


8. Sweetened granola and cereal bars

Better alternative: Homemade oat, nut and seed bars with minimal added sweeteners.


9. Jams and sweet spreads

Better alternative: Fresh berries, crushed fruit or unsweetened fruit compote.


10. Sweetened sauces and dressings

Better alternative: Extra virgin olive oil, lemon juice, herbs and homemade tomato sauces without added sugar.


11. Flavoured milk drinks

Better alternative: Plain milk or unsweetened plant-based drinks with cinnamon or vanilla.


12. Large quantities of honey, agave or syrups

Better alternative: Smaller amounts of sweetener, complemented by cinnamon, cardamom, vanilla or citrus zest.


A useful tip


Aromatic ingredients such as cinnamon, cardamom, vanilla, orange zest and fresh herbs can enhance the perception of sweetness, helping us enjoy foods and drinks with less added sugar.


The aim is not to eliminate sweetness, but to reduce habitual exposure to concentrated free sugars, particularly those found in sweetened beverages and heavily processed foods.


How much sugar is too much?


The World Health Organization recommends keeping free sugars below 10% of total daily energy intake, with additional health benefits associated with reducing intake below 5%.


For an adult consuming approximately 2,000 calories daily, 5% represents about 25 g of free sugars.


In the United Kingdom, the NHS recommends that adults consume no more than 30 g of free sugars daily.


Free sugars include those added to foods and drinks, as well as sugars naturally present in honey, syrups and fruit juices. They do not include the sugars contained within intact whole fruit or plain milk.


These recommendations concern overall health, not a specifically established threshold for preventing osteoarthritis. Nevertheless, they provide a useful practical guide.


Can reducing sugar improve arthrosis?


There are several reasons why reducing excessive added-sugar consumption may be beneficial.

  • It can help limit unnecessary energy intake and support a healthier body weight, reducing mechanical stress on weight-bearing joints.
  • It may improve aspects of metabolic health, particularly when sugary drinks and highly processed foods are replaced with more nutritious alternatives.
  • Reducing high fructose intake may also help limit excessive uric acid production in susceptible individuals.
  • Better long-term glucose regulation may be relevant to processes such as protein glycation, although reducing dietary sugar has not been proven to reverse established AGE cross-links in cartilage.


What remains to be established is how strongly these individual mechanisms influence the progression of osteoarthritis in people, and whether dietary sugar reduction can directly slow structural joint deterioration.


Diet is one part of joint care. Appropriate physical activity, muscle strengthening, management of relevant medical conditions and individualised clinical treatment remain important.


Looking after our joints from within


The most interesting lesson from this developing field of research is that arthrosis cannot be understood purely as a consequence of mechanical wear. Our joints are living structures whose health depends upon the interaction between cellular energy, inflammatory regulation, structural proteins and the mechanical forces of everyday life.


Excessive sugar consumption, particularly through concentrated fructose-containing foods and drinks, can influence several of these processes. It can alter liver fat production, increase uric acid generation, affect metabolic regulation and contribute to conditions associated with long-term tissue glycation.


These are not identical processes, nor do they prove that sugar is the sole cause of osteoarthritis. But together they illustrate how closely nutrition and tissue health may be connected.


Perhaps the most useful message is also the simplest: we do not need to eliminate every sweet food, but we should be more aware of the sugars we consume habitually, particularly those hidden in processed foods and drinks.


Looking after our joints means more than reducing wear and tear. It also means nourishing the living tissues that allow us to keep moving.



References


1. Johnson, R. J., et al. (2013). Sugar, uric acid, and the etiology of diabetes and obesity. Diabetes, 62(10), 3307–3315. https://doi.org/10.2337/db12-1814

2. Jang, C., et al. (2018). The small intestine converts dietary fructose into glucose and organic acids. Cell Metabolism, 27(2), 351–361.e3. https://doi.org/10.1016/j.cmet.2017.12.016

3. Geidl-Flueck, B., et al. (2021). Fructose- and sucrose- but not glucose-sweetened beverages promote hepatic de novo lipogenesis: A randomized controlled trial. Journal of Hepatology, 75(1), 46–54. https://doi.org/10.1016/j.jhep.2021.02.027

4. Choi, H. K., & Curhan, G. (2008). Soft drinks, fructose consumption, and the risk of gout in men: Prospective cohort study. BMJ, 336, 309–312. https://doi.org/10.1136/bmj.39449.819271.BE

5. Choi, H. K., Willett, W., & Curhan, G. (2010). Fructose-rich beverages and risk of gout in women. JAMA, 304(20), 2270–2278. https://doi.org/10.1001/jama.2010.1638

6. Denoble, A. E., et al. (2011). Uric acid is a danger signal of increasing risk for osteoarthritis through inflammasome activation. Proceedings of the National Academy of Sciences, 108(5), 2088–2093. https://doi.org/10.1073/pnas.1012743108

7. Verzijl, N., et al. (2002). Crosslinking by advanced glycation end products increases the stiffness of the collagen network in human articular cartilage: A possible mechanism through which age is a risk factor for osteoarthritis. Arthritis & Rheumatism, 46(1), 114–123. https://doi.org/10.1002/1529-0131(200201)46:1%3C114::AID-ART10025%3E3.0.CO;2-P

8. DeGroot, J., et al. (2003). Advanced glycation endproducts and osteoarthritis. Current Opinion in Rheumatology, 15(5), 545–551.

9. Loeser, R. F., Goldring, S. R., Scanzello, C. R., & Goldring, M. B. (2012). Osteoarthritis: A disease of the joint as an organ. Arthritis & Rheumatism, 64(6), 1697–1707. https://doi.org/10.1002/art.34453

10. Scanzello, C. R., & Goldring, S. R. (2012). The role of synovitis in osteoarthritis pathogenesis. Bone, 51(2), 249–257. https://doi.org/10.1016/j.bone.2012.02.012

11. Binvignat, M., et al. (2024). The role of obesity and adipose tissue dysfunction in osteoarthritis pain. Nature Reviews Rheumatology, 20, 565–584. https://doi.org/10.1038/s41584-024-01143-3

12. Chiu, S., et al. (2014). Effect of fructose on markers of non-alcoholic fatty liver disease (NAFLD): A systematic review and meta-analysis of controlled feeding trials. European Journal of Clinical Nutrition, 68, 416–423. https://doi.org/10.1038/ejcn.2014.8

13. Asadi, S., et al. (2025). The effectiveness of dietary intervention in osteoarthritis management: A systematic review and meta-analysis of randomized clinical trials. European Journal of Clinical Nutrition, 79, 959–971. https://doi.org/10.1038/s41430-025-01622-0

14. World Health Organization. (2015). Guideline: Sugars intake for adults and children. Geneva: World Health Organization. https://www.who.int/publications/i/item/9789241549028

15. National Health Service (NHS). How to cut down on sugar in your diet. https://www.nhs.uk/live-well/eat-well/how-to-eat-a-balanced-diet/how-to-cut-down-on-sugar-in-your-diet/

16. National Institute for Health and Care Excellence (NICE). (2022). Osteoarthritis in over 16s: Diagnosis and management. NICE Guideline NG226. https://www.nice.org.uk/guidance/ng226


Disclaimer


This article is intended for educational and informational purposes only and does not replace individual medical advice, diagnosis or treatment. The research discussed includes established findings as well as emerging scientific evidence, and the mechanisms described may not have been conclusively demonstrated to affect osteoarthritis progression in humans.


Dietary changes, herbal medicines and supplements should be considered in the context of individual health needs, existing medical conditions and prescribed medications. Do not discontinue or alter prescribed treatment without consulting your healthcare professional.



At Wildberry Clinic, we provide personalised clinical herbal medicine, nutritional and lifestyle guidance, working alongside your GP or specialist consultants where appropriate.


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