By: Dr. Emeka Enwere Human civilization has been punctuated, every so often, with close, personal, and often deadly interactions with microscopic organisms. These microbes – call them pathogens, or infectious agents, or just germs – are responsible for such moderately-notable events as the Black Death, the 1918 flu, smallpox, and, more recently, the Ebola epidemic. Over the past 150 years, we’ve spent trillions of dollars, and uncountable laboratory research-hours, finding new and better drugs and vaccines with which to control these microbes. It’s safe to say that the idea that “microbes are bad” is universally imprinted upon the human consciousness.
The ability of fructose to raise uric acid levels sheds some light on possible mechanisms in the development of diabetes and metabolic syndrome. This may be a new area where early interventions can be used. In animal and human trials, lowering uric acid improved a number of features of metabolic syndrome, which include renal damage, insulin resistance, high triglycerides and hypertension (Nakagawa et al 2006). It seems that fructose induced damage via uric acid may be a key initiating factor in the cascade of progression in metabolic syndrome since it drives may underlying processes.
The harmful effects of fructose make it clear that reducing intake is a key part of any chronic disease prevention or treatment plan. The most important thing would be to reduce intake from refined foods and drinks such as soft drinks, juices, and candy. Even though fruit contains fructose, ingestion has not been associated with the development of diabetes while fruit juices (added HFCS) have been. Whole fruit contains other nutrients such as fibre and antioxidants that have a protective effect against the damage of fructose (Bazzano et al 2008).
Gout, which is the most well known effect of high levels of uric acid, is a known risk factor for type 2 diabetes (Saggiani et al 1996). Also considering the effect of a diet high in refined sugar and the production of uric acid, measures should be employed to reduce uric acid levels in both gout patients and also diabetics (especially pre-diabetics). This may be a missing link in the progression and initiation of diabetes.
What I find even more interesting is that Mulberry leaf has been herb remedy traditionally used in Chinese medicine to treat diabetes. Research trials have confirmed that mulberry has the ability to reduce insulin resistance (Tanabe et al 2011). Other animal trials have also shown that mulberry leaf has antioxidant, anti-hypertensive, and anti-inflammatory effects. Recent research has also shown that morin, a compound found in mulberry leaf, is a potent xanthine oxidase inhibitor and inhibitor of renal urate reabsorption (Yu Z, et al 2006). The duality in functions peaked my interest as a novel intervention for both diabetes and gout. There is evidence that xanthine oxidase inhibitors can prevent the development of metabolic syndrome induced by fructose (Nakagawa et al 2006). This shows promise for the use of mulberry leaf as an early diabetes and metabolic syndrome intervention.
In addition to reducing your intake of HFCS, sucrose and fructose, someone with metabolic syndrome and a risk for developing type 2 diabetes should reduce their uric acid levels. To reduce the levels, one should also reduce the intake of purine rich foods such as meats and shellfish, which are converted to uric acid. Alcohol, especially beer, can also raise uric acid. Vitamin C has multiple actions to prevent the negative effects of uric acid. It can lower levels by promoting excretion and it can protect against the harmful effects of fructose at the cellular level (Johnson et al, Gao et al, Huang et al. 2008). Through dietary changes, adequate intake of antioxidants and a herbal extract such as mulberry we may be able to effectively tackle the a new underlying process that may be driving diabetes. For more information about the role of fructose, uric acid and diabetes please refer here to the well-written paper by Johnson et al 2009.
Gross LS, Li L, Ford ES, Liu S. Increased consumption of refined carbohydrates and the epidemic of type 2 diabetes in the United States: an ecological assessment. Am J Clin Nutr 2004;79:774–9
Johnson RJ et al. Hypothesis: could excessive fructose intake and uric acid cause type 2 diabetes? Endocr Rev. 2009 Feb;30(1):96-116. Epub 2009 Jan 16.
Bazzano LA, Li TY, Joshipura KJ, Hu FB 2008 Intake of fruit, vegetables, and fruit juices and risk of diabetes in women. Diabetes Care 31:1311–1317
Saggiani F, Pilati S, Targher G, Branzi P, Muggeo M, Bonora E 1996 Serum uric acid and related factors in 500 hospitalized sub- jects. Metabolism 45:1557–1561
Yu Z, et al. The dual actions of morin (3,5,7,2′,4′-pentahydroxyflavone) as a hypouricemic agent: uricosuric effect and xanthine oxidase inhibitory activity. J Pharmacol Exp Ther. 2006 Jan;316(1):169-75
Tanabe K, Nakamura S, Omagari K, Oku T. Repeated ingestion of the leaf extract from Morus alba reduces insulin resistance in KK-Ay mice.
Nutr Res. 2011 Nov;31(11):848-54.
Nakagawa T, Hu H, Zharikov S, Tuttle KR, Short RA, Glushakova
O, Ouyang X, Feig DI, Block ER, Herrera-Acosta J, Patel JM, Johnson RJ 2006 A causal role for uric acid in fructose-induced metabolic syndrome. Am J Physiol 290:F625–F631
Johnson RJ, Gaucher EA, Sautin YY, Henderson GN, Angerhofer AJ, Benner SA 2008 The planetary biology of ascorbate and uric acid and their relationship with the epidemic of obesity and car- diovascular disease. Med Hypotheses 71:22–31
Gao X, Curhan G, Forman JP, Ascherio A, Choi HK 2008 Vitamin C intake and serum uric acid concentration in men. J Rheumatol 35:1853–1858
Huang HY, Appel LJ, Choi MJ, Gelber AC, Charleston J, Norkus EP, Miller 3rd ER 2005 The effects of vitamin C supplementation on serum concentrations of uric acid: results of a randomized controlled trial. Arthritis Rheum 52:1843–1847