Fructose Increases the Rate of Aging
By William Misner, Ph.D.I advise consumers to limit fructose intake to only natural fruits. No research associates whole fruit intake with health issues. There is general agreement that dietary fruit and vegetables are associated with optimal health. However, when live cells are exposed to processed form of fructose, the rate of aging increases dramatically. Skin as the largest organ may profile the state of both external and internal health in man and beast.
Werman & Boaz provide evidence that fructose and its phosphate metabolites can modify DNA faster than glucose and its phosphate metabolites under in vitro conditions. These scientists from the Tehnion-Israeli Institute of Technology report that cell structures of animals fed fructose aged more rapidly and accelerated aging of the collagen content of the skin also occurred. Large quantities of fructose were fed to laboratory rats. The rats subsequently exhibited accelerated cross-linking of the collagen content of their skin and bones. Excessive cross-linking reduces the elasticity of the skin to the extent that wrinkles can result. Their data suggest that long-term fructose consumption induces adverse effects on aging; further studies are required to clarify the precise role of fructose in the aging process (1, 2, 3).
Fructose-drinking rats exhibit higher liver weights compare to the other dietary groups. Control rats excreted significantly less urinary output than all sugar groups, which did not differ from each other. No differences were observed in fasting plasma fructose, glucose, and creatinine levels, or in urinary glucose levels. Fructose consumption resulted in elevated urinary fructose levels, higher creatinine clearance, and marked proteinuria. The tested sugars had influence on the molecular weight distribution of urinary proteins in the ranges of 10 to 16, 25 to 35, and 75 to 85 kd. Histological examination revealed that fructose consumption led to the formation of foci of cortical tubular necrosis with chronic inflammatory infiltrate, accumulation of tubular hyaline casts, thickening of the Bowman's capsule, mesangial thickening due to collagen deposits, and the occurrence of hemosiderin in tubular cells. These data suggest that fructose has a negative impact on kidney function and morphology (4).
HOW MUCH FRUCTOSE?
Rats were fed a commercial diet for 16 months, and had free access either to water (control) or to 250 g/L solutions of fructose, glucose, or sucrose. The typical 250 g rat consumes between 1.5-2.2 fluid ounces per day (45-65 ml). Therefore it requires between 15-22 days to consume a liter solution of 250 grams fructose. Hence, an increased rate of aging occurs with 2-3 teaspoons fructose per day in rats. Data compiled by the U.S. Department of Agriculture show that Americans consume 13 teaspoons (82 g/day) of high-fructose corn syrup daily.
Human intake of naturally occurring fructose from non-processed foods (primarily Fruits and Vegetables) is 15 grams per day. This produces a concentration of Fructose in fasting blood of healthy humans is typically 1 mg/dL or less. More than 66% of these normal, healthy persons may experience fructose intolerance (fructose malabsoprtion) when they consume 50 grams of fructose or more. Every gram of fructose consumed over 50 grams per day may proportionately increase the rate of aging of both within external skin and organ cells.
Processed fructose should be limited by health-conscious persons concerned about either the quality of or length of life.
1) Levi B, Werman MJ. Fructose and related phosphate derivatives impose DNA damage and apoptosis in L5178Y mouse lymphoma cells. J Nutr Biochem. 2003 Jan;14(1):49-60. PMID: 12559477 [PubMed - indexed for MEDLINE]
2) Levi B, Werman MJ. Fructose triggers DNA modification and damage in an Escherichia coli plasmid. J Nutr Biochem. 2001 Apr;12(4):235-241. PMID: 11287219 [PubMed - as supplied by publisher]
3) Levi B, Werman MJ. Long-term fructose consumption accelerates glycation and several age-related variables in male rats. J Nutr. 1998 Sep;128(9):1442-9. PMID: 9732303 [PubMed - indexed for MEDLINE]
4) Kizhner T, Werman MJ. Long-term fructose intake: biochemical consequences and altered renal histology in the male rat. Metabolism. 2002 Dec;51(12):1538-47. PMID: 12489065 [PubMed - indexed for MEDLINE]
Consumption of Fructose May Lead to Elevated Triglyceride and Glucose Concentrations, resulting in metabolic disorders, obesity, diabetes, and cardiovascular disease
In a study involving 7 healthy male subjects, consumption of a high-fructose diet was found to significantly increase fasting plasma concentrations of triglycerides, glucose, lactate and leptin, without appearing to affect insulin sensitivity, intrahepatocellular lipids, intramyocellular lipids, or body weight. For 2 weeks, subjects consumed an isoenergetic diet, containing 55% carbohydrates, 30% fat, and 15% protein, and less than 20 g/day fructose. This was followed by a 4-week period in which subjects were fed a high-fructose diet containing 1.5 g fructose per kg body weight per day. Various lipid and metabolic parameters were measured after 1 and 4 weeks of the high-fructose diet. After 1 week, significant increases were found in fasting plasma concentrations of VLDL-triglycerides (72%), total triglycerides (36%), and leptin (48%).
After 2 weeks, increases in lactate were found (49%) and after 4 weeks, increases in glucose were found (5.5%). No significant changes in fasting insulin, glucagon, cholesterol, or body weight were found. These results differ from results of previous studies in rodents which found a high-sucrose diet to lead to insulin resistance and increased IHCL. The results of this study suggest that high intake of fructose, which is quite prevalent in many countries around the world largely due to consumption of sweetened beverages, may increase the risk of cardiovascular disease by increasing levels of VLDL-triglycerides, total triglycerides, leptin, and glucose.
Le KA, et al, A 4-wk high-fructose diet alters lipid metabolism without affecting insulin sensitivity or ectopic lipids in healthy humans," Am J Clin Nutr, 2006; 84(6): 1374-9.