Robert Lustig

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Robert H. Lustig, MD
Nationality American
Education MIT, Cornell University Medical College
Medical career
Profession clinical medical practice, teaching and research
Field neuroendocrinology, pediatric endocrinology
Institutions University of California, San Francisco, UCSF Benioff Children's Hospital
Specialism childhood obesity
Research biochemical, neural, hormonal and genetic influences contributing to obesity
This article needs attention from an expert in medicine. Please add a reason or a talk parameter to this template to explain the issue with the article. WikiProject Medicine (or its Portal) may be able to help recruit an expert. (September 2012)

Robert H. Lustig is a pediatric endocrinologist at the University of California, San Francisco (UCSF) where he is a Professor of Clinical Pediatrics.[1] He practices in the field of neuroendocrinology, with an emphasis on the regulation of energy balance by the central nervous system.[2] He also has a special interest in childhood obesity.[2]

Lustig came to public attention through his efforts to establish that fructose can have serious deleterious effects on human (especially children's) health if consumed in too large amounts.[3] On May 26, 2009, he delivered a lecture called "Sugar: The Bitter Truth" which was posted on YouTube the following July and "went viral" with some 3.47 million viewings (as of Apr 28, 2013).[3] In his lecture, Lustig calls fructose a "poison" and equates its metabolic effects with those of ethanol.

Contents

Biography [edit]

Lustig grew up in Brooklyn, New York, and attended Stuyvesant High School in Manhattan.[4] He obtained a bachelors degree from MIT (1976) and an M.D. degree from Cornell University Medical College (1980). He then spent six years as a research associate in neuroendocrinology at Rockefeller University. He completed a pediatric residency at St. Louis Children's Hospital and his clinical fellowship in pediatric endocrinology at UCSF where he joined the teaching staff in 1984.[1][2] Lustig is currently in the Master of Studies in Law program at UC Hastings College of the Law.[5]

Lustig has authored over 85 research articles and 45 book chapters. He is a former chairman of the Obesity Task Force of the Pediatric Endocrine Society, a member of the Obesity Task force of The Endocrine Society, and on the Steering Committee of the International Endocrine Alliance to Combat Obesity.[1]

Controversy over fructose [edit]

Lustig's assertion that the food sugar fructose is a "poison" or "toxin" that augments body fat storage — thus representing a (or the) primary cause of the obesity now prevalent in the Western world — is disputed by some researchers;[6] Tappy and Mittendorfer cite a review by Dolan of the Burdock Group where average-estimated amounts of dietary fructose in a weight-maintaining diet did not appear to harm metabolic health. However, definitive studies are missing, as these trials involved fructose intake approaching 95% of average consumption, while toxicity of dietary fructose is only suspected for above-average consumption that overwhelms metabolic pathways. .[7][6] Some studies have shown that "the long-term consumption of diets high in fat and fructose is likely to lead to increased energy intake, weight gain, and obesity", and "the potential for weight gain from increased fructose consumption may only represent one aspect of its metabolic consequences".[8] Meta-analysis studies have indicated that the clinical trials cited by Lustig, which were aimed at studying carbohydrate consumption, were of only short duration and variable quality, and that study subjects had only modest increases in body weight, thus precluding definitive conclusions.[6][9]

Several studies show that for small doses (less than 10 grams per meal), fructose consumption may actually have a catalytic effect that reduces blood glucose levels with no consequent change in body weight.[10][11]

One controversial issue surrounding fructose consumption is its role in blocking satiety. Lustig's research suggests that fructose consumption reduces satiety leading to over-consumption. Trials that focus on isocaloric diets and on light fructose consumption do not address the issue of satiety and over-consumption.

In athletes requiring sugar to meet their caloric needs, fructose may enhance exercise performance by stimulating nutrient absorption and energy metabolism.[12]

Animal research has provided evidence for deleterious effects of excessive fructose consumption,[13] and potential for negative impact on triglycerides, LDL cholesterol and apolipoprotein-B.[14]

Some scientists report that the combination of medical disorders known as metabolic syndrome (syndrome X) results mainly from excessive caloric intake and that fructose should not be singled out[6][15] as a particular villain. In fact, small 'catalytic' doses of fructose may improve control of blood glucose.[10] Further, fructose is the normal, natural monosaccharide sugar present in sweet-tasting plant foods.[10][15][16]

Publications [edit]

  • Obesity Before Birth: Maternal and Prenatal Influences on the Offspring. Boston: Springer Science, 2010. ISBN 978-1441970336
  • Fat Chance: Beating the Odds against Sugar, Processed Food, Obesity, and Disease. New York: Hudson Street Press, 2013. ISBN 978-1594631009

References [edit]

  1. ^ a b c Robert H. Lustig biography at University of California, San Francisco (UCSF). Accessed April 2011
  2. ^ a b c Robert H. Lustig, M.D. Biography at Benioff Children's Hospital. Accessed April 2011
  3. ^ a b Is Sugar Toxic? Gary Taubes, New York Times, April 13, 2011 . Accessed April 2011
  4. ^ Robert Lustig, MD Professor Pediatric Endocrinology biography at ConnectWell.biz , 2011
  5. ^ Inaugural MSL Class of 2013. Accessed Sept 2012
  6. ^ a b c d Tappy L, Mittendorfer B (2012). "Fructose toxicity: is the science ready for public health actions?". Curr Opin Clin Nutr Metab Care 15 (4): 357–61. doi:10.1097/MCO.0b013e328354727e. PMID 22617566. 
  7. ^ Bremer, A. A., Mietus-Snyder, M., & Lustig, R. H. (2012). [doi:http://www.ncbi.nlm.nih.gov/pubmed/22351884 "Toward a Unifying Hypothesis of Metabolic Syndrome"]. Pediatrics 129 (3): 557–70. 
  8. ^ Elliott SS, Keim NL, Stern JS, Teff K, Havel PJ (2002). "Fructose, weight gain, and the insulin resistance syndrome". Am J Clin Nutr 76 (5): 911–22. PMID 12399260. Retrieved 7 July 2012.  (Quote taken from the conclusion)
  9. ^ Sievenpiper JL, de Souza RJ, Mirrahimi A, Yu ME, Carleton AJ, Beyene J, Chiavaroli L, Di Buono M, Jenkins AL, Leiter LA, Wolever TM, Kendall CW, Jenkins DJ (2012). "Effect of fructose on body weight in controlled feeding trials: a systematic review and meta-analysis". Ann Int Med 156 (4): 291–304. doi:10.1059/0003-4819-156-4-201202210-00007. PMID 22351714. 
  10. ^ a b c Sievenpiper JL, Chiavaroli L, de Souza RJ, Mirrahimi A, Cozma AI, Ha V, Wang DD, Yu ME, Carleton AJ, Beyene J, Di Buono M, Jenkins AL, Leiter LA, Wolever TM, Kendall CW, Jenkins DJ (14 August 2012). "Catalytic doses of fructose may benefit glycaemic control without harming cardiometabolic risk factors: a small meta-analysis of randomised controlled feeding trials". Brit J Nutr 108 (3): 418–23. doi:10.1017/S000711451200013X. PMC 3411192. PMID 22354959. Retrieved 7 July 2012. 
  11. ^ Cozma AI, Sievenpiper JL, de Souza RJ, Chiavaroli L, Ha V, Wang DD, Mirrahimi A, Yu ME, Carleton AJ, Di Buono M, Jenkins AL, Leiter LA, Wolever TM, Beyene J, Kendall CW, Jenkins DJ (2012). "Effect of fructose on glycemic control in diabetes: a systematic review and meta-analysis of controlled feeding trials". Diabetes Care (American Diabetes Association) 35 (7): 1611–20. doi:10.2337/dc12-0073. PMID 22723585. 
  12. ^ Johnson RJ, Murray R. "Fructose, exercise, and health". Curr Sports Med Rep 9 (4): 253–8. doi:10.1249/JSR.0b013e3181e7def4. PMID 20622544. 
  13. ^ Botezelli, José; Cambri, Lucieli; Ghezzi, Ana; Dalia, Rodrigo; Voltarelli, Fabrício; de Mello, Maria Alice (2012). "Fructose-rich diet leads to reduced aerobic capacity and to liver injury in rats". Lipids in Health and Disease 11 (1): 78. doi:10.1186/1476-511X-11-78. ISSN 1476-511X. 
  14. ^ Stanhope, K. L.; Bremer, A. A.; Medici, V.; Nakajima, K.; Ito, Y.; Nakano, T.; Chen, G.; Fong, T. H.; Lee, V.; Menorca, R. I.; Keim, N. L.; Havel, P. J. (2011). "Consumption of Fructose and High Fructose Corn Syrup Increase Postprandial Triglycerides, LDL-Cholesterol, and Apolipoprotein-B in Young Men and Women". Journal of Clinical Endocrinology & Metabolism 96 (10): E1596–E1605. doi:10.1210/jc.2011-1251. ISSN 0021-972X. 
  15. ^ a b "Is fructose being blamed unfairly for obesity epidemic?". Science Daily. Feb 21, 2012. Retrieved 7 July 2012. 
  16. ^ White JS (2008). "Straight talk about high-fructose corn syrup: what it is and what it ain't". Am J Clin Nutr (Am Soc Clin Nutr) 57 (18): 8125–9. doi:10.3945/ajcn.2008.25825B. PMID 19064536. Retrieved 7 July 2012. 

External links [edit]

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