Antonino De Lorenzo

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Antonino De Lorenzo (born 3 September 1954) is a Specialist in Gastroenterology and Digestive Endoscopy, a Full Professor of Human Nutrition and Director of the School of Specialization in Food Science at the University of Rome "Tor Vergata", where he is also Director of the PhD Research in "Physiology of Districts Corporeal" and director of the Unit "Service of Clinical Nutrition, and Parenteral Therapy Anorexia Nervosa". During his long research and studies on body composition, he discovered the "Normal Weight Obese Syndrome". He holds positions of scientific responsibility for national and international research projects and is a member of several scientific societies including: Member of the Executive Committee and Head of Research of the Italian Society of Human Nutrition, member of the American College of Nutrition (European Chapter). He is the author of over 250 articles in international journals with "peer revision" in PubMed, 54 chapters of national and international treaties and 150 articles in journals and conference proceedings in Italy and abroad. President of the National Institute for the Mediterranean diet and the Nutrigenomics (INDi.M).

Mediterranean diet[edit | hide all | hide | edit source]

The Mediterranean diet is a modern nutritional recommendation originally inspired by the dietary patterns of Greece, Southern Italy, and Spain in the 1940s and 1950s.[1] The principal aspects of this diet include proportionally high consumption of olive oil, legumes, unrefined cereals, fruits, and vegetables, moderate to high consumption of fish, moderate consumption of dairy products (mostly as cheese and yogurt), moderate wine consumption, and low consumption of non-fish meat products.[2]

De Lorenzo Syndrome[edit | hide | edit source]

In 2006, De Lorenzo A. et al.[3] have identified the Normal Weight Obese (NWO)syndrome, characterized by normal body weight and BMI, but high TBFat accumulation.[4] The frequency of NWO syndrome is typically found in females. A study was conducted at the University of Rome Tor Vergata, Human Nutrition Unit, on a sample of Caucasian women from Centre-South of Italy. In the study was included a complete and clear medical history of women. The subjects were also categorized into BMI subgroups according to World Health Organization (WHO) criteria, other study parameters were: gender, age, anthropometric measurements, Dual-energy X-ray absorptiometry (DXA), statistical analysis. The following predictive equation of PBF was derived:

PBF= 0.920 x weight (Kg) – 0.004 x (weight (Kg))2 - 0.326 x height (cm)+ 0.263 x hip (cm) + 147.110 x log (waist (cm)) – 32.309 x sqrt (waist (cm)) - 332.116

This equation allows the prediction of individual PBF on the base of easily available measures: height, weight, hip and waist circumference.[5] Based on BMI levels and predicted values of PBF women were classified into underweight, normal, pre-obese and obese. All the 10 obese women incorrectly classified by predicted values of PBF were considered pre-obese. Among the 62 obese women incorrectly classified by BMI, 29 were identified as pre-obese but 33 were regarded as normal. The majority of women misclassified as normal by BMI were found to be pre-obese or obese by PBF. Moreover, it is important to recognize that some subjects, while having a BMI of up to 26 kg/m2, actually had a PBF of <30%, probably due to a greater percentage of muscular mass seen in athletic individuals. In post-menopausal women was reported that both BMI and WC (waist circumference, it reflects abdominal fat levels ) were associated with mortality. In the Nurses’ Health Study, waist circumference were also strongly associated with increased risk of coronary heart disease among women with a BMI of <25 kg/m2.[6] Waist and hip measurements are useful to know different physical and metabolic characteristics of these two regions and therefore the diverse clinical outcomes in subjects with a gynoid or android body conformation. Early inflammation and genetic predisposition characterizes the syndrome.[7] A cross-sectional study carried out to assess the prevalence of NWO in Switzerland. The classical perception of adipose tissue and skeletal muscle as an energy storage has been replaced by the notion that these tissues have a role in lipid and glucose metabolism by producing a large number of adipokines (that have a great role in the pathogenesis of obesity, insulin resistance, hypercholesterolaemia, hypertriglyceridaemia, low levels of HDL cholesterol, hypertension, glucose intolerance and CVD) and myokines.[8][9][10]

References[edit | hide | edit source]

  1. Alberto Capatti et al., Italian Cuisine: A Cultural History, p. 106.; Silvano Serventi and Francoise Sabban, Pasta, p. 162.
  2. ^
  3. Prof. A. De Lorenzo Division of Human Nutrition, Department of Biomedicine and Prevention, University of Tor Vergata, Italy
  4. De Lorenzo A, Martinoli R, Vaia F, Di Renzo L. "Normal Weight Obese (NWO) Women: an evaluation of candidate new syndrome. Nutrition Metabolism and Cardiovascular Diseases 2006; 16, 8: 513-23.
  5. De Lorenzo, A; Del Gobbo, V; Premrov, MG; Bigioni, M; Galvano, F; Di Renzo, L (2007). "Normal-weight obese syndrome: early inflammation?". Am. J. Clin. Nutr. 85: 40–5. PMID 17209175.
  6. Rexrode, KM; Carey, VJ; Hennekens, CH; et al. (1998). "Abdominal adiposity and coronary heart disease in women". JAMA. 280: 1843–1848. doi:10.1001/jama.280.21.1843.
  7. "Normal weight obese (NWO) women: an evaluation of a candidate new syndrome". Nutr Metab Cardiovasc Dis. 16: 513–23. Dec 2006. doi:10.1016/j.numecd.2005.10.010. PMID 17126766.
  8. Hajer, GR; van Haeften, TW; Visseren, FL (2008). "Adipose tissue dysfunction in obesity, diabetes, and vascular diseases". Eur Heart J. 29 (24): 2959–71. doi:10.1093/eurheartj/ehn387.
  9. Romero-Corral, A; Lopez-Jimenez, F; Sierra-Johnson, J; Somers, VK (2008). "Differentiating between body fat and lean mass-how should we measure obesity?". Nature Clinical Practice Endocrinology & Metabolism. 4: 322–323.
  10. Shah, A; Mehta, N; Reilly, MP (2008). "Adipose inflammation, insulin resistance, and cardiovascular disease". JPEN J Parenter Enteral Nutr. 32 (6): 638–44.