Alan Aragon wrote a pretty damning post on the Lustig lecture on the dangers of fructose and argued that dosage was not considered. From my reading it seems that fructose regarding weight gain probably doesn't happen in a state of caloric deficiency. However I think many of us here are at very little risk of becoming diabetic so it might now apply to us. However what does apply (and is not usually discussed in the blogosphere [except for JLL's blog]) is the concept of glycation. If the study from 1968 is true and fructose glycates at 10x that of glucose then it is still probably more prudent to stay away from fructose.
Biochem Biophys Res Commun. 2010 Jan 7. [Epub ahead of print]
Fructated apolipoprotein A-I showed severe structural modification and loss of beneficial functions in lipid-free and lipid-bound state with acceleration of atherosclerosis and senescence.
Park KH, Jang W, Kim KY, Kim JR, Cho KH.
School of Biotechnology, Aging-associated Vascular Disease Research Center, Yeungnam University, Gyeongsan 712-749, Republic of Korea.
Non-enzymatic glycation of serum apolipoproteins is a main feature of diabetes mellitus under hyperglycemia. Advanced glycation end products are implicated in the development of aging and metabolic syndrome, including premature atherosclerosis in diabetic subjects. ApoA-I is the principal protein constituent of HDL. In this study, glycated human apoA-I (gA-I) by fructation was characterized on functional and structural correlations in lipid-free and lipid-bound states. The gA-I showed more spontaneous multimeric band formation up to pentamer and exhibited slower elution profile with more degraded fragments from fast protein liquid chromatography. The gA-I showed modified secondary structure from fluorescence and circular dichroism analysis. Reconstituted high-density lipoprotein (rHDL) containing the gA-I had less content of phospholipid with a much smaller particle size than those of rHDL-containing nA-I (nA-I-rHDL). The rHDL containing gA-I (gA-I-rHDL) consisted of less molecular number of apoA-I than nA-I-rHDL with decreased alpha-helical content. Treatment of the gA-I-rHDL induced more atherogenic process in macrophage cell and premature senescence in human dermal fibroblast cell. Conclusively, fructose-mediated apoA-I glycation resulted in severe loss of several beneficial functions of apoA-I and HDL regarding anti-senescence and anti-atherosclerosis activities due to a lack of anti-oxidant activity with increased susceptibility of protein degradation and structural modification. Copyright © 2010 Elsevier Inc. All rights reserved.
PMID: 20059975 [PubMed - as supplied by publisher]
I always thought that fructose was always packaged in lipids or converted to something else other than fructose. But that doesn't seem to be the case:
Diabetes Care. 2002 Feb;25(2):353-7.
Increased fructose concentrations in blood and urine in patients with diabetes.
Kawasaki T, Akanuma H, Yamanouchi T.
Department of Internal Medicine, Teikyo University, School of Medicine, 11-1, 2-chome Kaga, Itabashi-ku, Tokyo, Japan 173-0003. t-kawa@med.teikyo-u.ac.jp
OBJECTIVE: To investigate fructose metabolic changes in patients with diabetes. RESEARCH DESIGN AND METHODS: Serum and urinary fructose concentrations were determined in healthy subjects (n = 23) and in nondiabetic (n = 23) and diabetic patients (n = 26). Fructose was measured using our newly developed method, and (13)C(6)-fructose was used as the internal standard. After adding sample to a fixed amount of internal standard, ion-exchange resins and high-performance liquid chromatography pretreatments were performed. Then, the amount of fructose in the sample was measured by gas chromatography-mass spectrometry. RESULTS: Serum fructose concentrations in patients with diabetes (12.0 +/- 3.8 micromol/l) were significantly higher than those in healthy subjects (8.1 +/- 1.0 micromol/l, P < 0.001) and nondiabetic patients (7.7 +/- 1.6 micromol/l, P < 0.001), and daily urinary fructose excretion was significantly greater in patients with diabetes (127.8 +/- 106.7 micromol/day) than in nondiabetic patients (37.7 +/- 23.0 micromol/day, P < 0.001). In patients with diabetes (n = 20), serum fructose concentrations (8.6 +/- 1.8 micromol/l, P < 0.001) and daily urinary fructose excretion (63.4 +/- 63.8 micromol/day, P < 0.01) significantly decreased by week 2 after admission. CONCLUSIONS: The present results differed from those of previous studies in that we found that the serum and urinary fructose concentrations decreased rapidly, concomitant with an improvement in glycemia. Therefore, hyperglycemia was associated with increased serum and urinary fructose concentrations in patients with diabetes.
PMID: 11815509 [PubMed - indexed for MEDLINE]
In the meantime fructose is still something I'll try to limit within reason (such as part of my berry intake).
Edited by Sillewater, 15 February 2010 - 08:10 AM.