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

Robert H. Lustig is an American 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 4.2 million viewings (as of Jan 27, 2014).[3] In his lecture, Lustig calls fructose a "poison" and equates its metabolic effects with those of ethanol.[3]

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] In 2013, Lustig received a Master of Studies in Law (MSL) degree from 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]

Controversies[edit]

Fructose controversy[edit]

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.[6][7] 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]

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.[10]

Animal research has provided evidence for deleterious effects of excessive fructose consumption,[11] and potential for negative impact on triglycerides, LDL cholesterol and apolipoprotein-B.[12]

One scientific study reports 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] as a particular villain. In fact, small 'catalytic' doses of fructose may improve control of blood glucose.[13] Further, fructose is the normal, natural monosaccharide sugar present in sweet-tasting plant foods.[13][14][15] Lustig argues that the characteristics of processed foods, namely the addition of sugar and the removal of dietary fibre, are two of the main culprits in a global obesity epidemic.[16]

Sugar v. HFCS controversy[edit]

In 2013, Lustig was called upon as an expert witness on behalf of a plaintiff in Buffalo, New York, who claimed her obesity was the result of high-fructose corn syrup in foods. Forbes magazine cited Lustig for his inconsistent statements on sugar and HFCS: "Dr. Lustig’s past writings also inconveniently reflect his scientific opinion that HFCS 'and sucrose are, for all intents and purposes, biochemically and metabolically equivalent.'"[17] The article goes on to vilify the plaintiff's case, but does not seek comment from the plaintiff apart from quotations from Lustig's book. Lustig has made this comparison other times previously. A New York Times Magazine article in 2009 noted Lustig's view that HFCS and sugar "are effectively identical in their biological effects." The author cited a lecture he attended five months earlier, where Lustig stated: "High-fructose corn syrup, sugar — no difference."[18]

Personal[edit]

Prof. Lustig lives in San Francisco. He is married and has two daughters.[19]

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 c 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 Tappy L, Mittendorfer B (2012). "Fructose toxicity: is the science ready for public health actions?". Current Opinion in Clinical Nutrition and Metabolic Care 15 (4): 357–61. doi:10.1097/MCO.0b013e328354727e. PMID 22617566. 
  7. ^ Bremer, A. A., Mietus-Snyder, M., & Lustig, R. H. (2012). "Toward a Unifying Hypothesis of Metabolic Syndrome". Pediatrics 129 (3): 557–70. doi:10.1542/peds.2011-2912. PMID 22351884. 
  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". Annals of Internal Medicine 156 (4): 291–304. doi:10.1059/0003-4819-156-4-201202210-00007. PMID 22351714. 
  10. ^ Johnson RJ, Murray R. "Fructose, exercise, and health". Curr Sports Med Rep 9 (4): 253–8. doi:10.1249/JSR.0b013e3181e7def4. PMID 20622544. 
  11. ^ 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. 
  12. ^ 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. 
  13. ^ a b 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. 
  14. ^ "Is fructose being blamed unfairly for obesity epidemic?". Science Daily. Feb 21, 2012. Retrieved 7 July 2012. 
  15. ^ 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. 
  16. ^ Lustig, Robert H. (2013). Fat Chance: Beating the Odds Against Sugar, Processed Food, Obesity, and Disease (Hardcover ed.). Hudson Street Press. ISBN 978-1594631009. 
  17. ^ "Demonization By Litigation: Food Ingredient Makers Face Frivolous Charges". Forbes. November 14, 2013. Retrieved December 11, 2013. 
  18. ^ "Is Sugar Toxic?". New York Times Magazine. April 13, 2011. Retrieved December 11, 2013. 
  19. ^ http://profiles.ucsf.edu/robert.lustig

External links[edit]