Sugar is a carbohydrate made up of two sugar units – fructose and glucose. Sugar provides 4 calories per gram (around 20 calories per teaspoon) but no protein, fat, vitamins or minerals. For this reason sugars are sometimes called ‘empty calories’.
What do we know about sugar and psoriasis?
There are no research studies that have assessed the direct effects of sugar intake in psoriasis, but eating lots of sugar may indirectly aggravate psoriasis in a number of ways.
Diets high in sugar (particularly those from sugary drinks) have been linked with weight gain and higher levels of body fat1,2. Studies show excess body fat increases the risk of psoriasis3, and the severity of the disease 4,5,6,7.
This is because high levels of body fat trigger the release of pro-inflammatory hormones that may aggravate psoriasis and could possibly reduce the effectiveness of treatment 8,9,10.
Aside from body weight, there is evidence that people with psoriasis are more likely to be insulin resistant, a condition where the body does not respond properly to the hormone insulin, which we need to metabolise carbohydrates11,12.
When we eat carbohydrates (including sugars), they are broken down into glucose. Your body must release the hormone insulin to enable the glucose to move into your cells where it can be used for energy. In insulin resistance, the body doesn’t respond to properly to the hormone, so blood glucose remains high, causing more insulin to be released.
Studies show that psoriasis severity is correlated with insulin resistance13, so managing blood sugars by eating fewer sugary foods (which raise blood glucose levels more quickly than wholegrain foods) may be beneficial14.
There are no studies that have looked at this in relation to psoriasis, but as part of an overall change in diet, reducing sugar was shown to be effective in a number of case studies15.
How much sugar is too much?
In 2015 the Scientific Advisory Committee on Nutrition (an independent board of experts who advise the UK government on nutrition), recommended that we consume no more than 5% of our calories from ‘free’ sugars.
‘Free sugars’ are any sugars added to foods by manufacturers or by us – the sugar we add to tea and coffee or found in breakfast cereal for example. It also includes sugars naturally contained in syrup, honey and fruit juice. It doesn’t include the sugars in dairy products (called lactose) or in whole fruits and vegetables (called fructose).
This means if an adult was eating 2000 calories a day, no more than 100 of the calories should come from sugar, which is 24 grams, or 6 teaspoons.
- There are no studies looking at the direct effects of sugar on psoriasis, but diets high in sugar have been linked to weight gain, which may aggravate psoriasis
- People with psoriasis are more likely to be resistant to the hormone insulin, which we need to metabolise sugar and carbohydrates
- As part of an overall strategy, reducing sugar may be helpful in managing psoriasis by reducing body weight, which may help lower inflammation.
You can reduce the amount of sugar you intake by:
- Swapping sugary drinks for water, sparkling water or no added sugar options
- Choosing whole fruit over fruit juice. This is better as the whole fruit contains the fibre, which slows the rate at which the sugars are absorbed by the body.
- Checking food labels – ingredients are listed by weight, so if sugar or syrup is close to the top, it’s one to reduce. If a food has more than 22 grams of sugar per 100 grams and there’s no milk or fruit in the food, it’s high in sugar. If it contains less than 5 grams of sugar per 100 grams it’s low in sugar.
- Swap breakfast cereal for porridge oats, which are a naturally low sugar choice.
- Drewnowski, A. & Bellisle, F. Liquid calories, sugar, and body weight. Am. J. Clin. Nutr. 85, 651–661 (2007).
- Malik, V. S., Schulze, M. B. & Hu, F. B. Intake of sugar-sweetened beverages and weight gain: a systematic review. Am. J. Clin. Nutr. 84, 274–288 (2006).
- Johnston, a. et al. Obesity in psoriasis: Leptin and resistin as mediators of cutaneous inflammation. Br. J. Dermatol. 159, 342–350 (2008).
- Wolkenstein, P. et al. Psoriasis in France and associated risk factors: results of a case-control study based on a large community survey. Dermatology 218, 103–9 (2009).
- Naldi, L., Parazzini, F., Peli, L., Chatenaud, L. & Cainelli, T. Dietary factors and the risk of psoriasis. Results of an Italian case-control study. Br. J. Dermatol. 134, 101–106 (1996).
- Balci, A. et al. Increased amount of visceral fat in patients with psoriasis contributes to metabolic syndrome. Dermatology 220, 32–7 (2010).
- Wolk, K. et al. Excessive body weight and smoking associates with a high risk of onset of plaque psoriasis. Acta Derm. Venereol. 89, 492–497 (2009).
- Fontana, L., Eagon, J. C., Trujillo, M. E., Scherer, P. E. & Klein, S. Visceral Fat Adipokine Secretion Is Associated With Systemic Inflammation in Obese Humans. Diabetes 56, 1010–1013 (2007).
- Hamminga, E. a, van der Lely, a J., Neumann, H. a M. & Thio, H. B. Chronic inflammation in psoriasis and obesity: implications for therapy. Med. Hypotheses 67, 768–73 (2006).
- di Minno, M. N. D. et al. Obesity and the prediction of minimal disease activity: a prospective study in psoriatic arthritis. Arthritis Care Res. (Hoboken). 65, 141–7 (2013).
- Boehncke, S. et al. Psoriasis patients show signs of insulin resistance. Br. J. Dermatol. 157, 1249–1251 (2007).
- Gyldenløve, M. et al. Patients with psoriasis are insulin resistant. J. Am. Acad. Dermatol. 72, 599–605 (2015).
- Fitzgerald, R., Sadlier, M., Connolly, M. & Tobin, A. M. Psoriasis and insulin resistance: a review. J. Diabetes Res. Clin. Metab. 3, 5 (2014).
- Schwingshackl, L. & Hoffmann, G. Long-term effects of low glycemic index/load vs. high glycemic index/load diets on parameters of obesity and obesity-associated risks: A systematic review and meta-analysis. Nutr. Metab. Cardiovasc. Dis. 23, 699–706 (2013).
- Wong, A., Kalinovsky, T., Niedzwiecki, A. & Rath, M. Efficacy of nutritional treatment in patients with psoriasis: A case report. Exp. Ther. Med. 1071–1073 (2015). doi:10.3892/etm.2015.2631