scholarly journals Risk of metabolic syndrome in adults exposed to the great Chinese famine during the fetal life and early childhood

2011 ◽  
Vol 66 (2) ◽  
pp. 231-236 ◽  
Author(s):  
X Zheng ◽  
Y Wang ◽  
W Ren ◽  
R Luo ◽  
S Zhang ◽  
...  
2020 ◽  
Vol 76 (2) ◽  
pp. 140-146 ◽  
Author(s):  
Yue Peng ◽  
Miaomiao Hai ◽  
Pengcheng Li ◽  
Yongjie Chen

Objective: To explore the association of famine exposure in early life with the risk of metabolic syndrome (MS) in the ­Chinese adults. Methods: Data were obtained from the wave 2009 of the China Health and Nutrition Survey. MS was identified when 3 or more of the following components happened: (1) waist circumference >90 cm in males or >85 cm in females; (2) fasting glucose ≥6.1 mmol/L; (3) systolic blood pressure ≥130 mm Hg/diabolic blood pressure ≥85 mm Hg; (4) fasting triglyceride ≥1.70 mmol/L; and (5) high-density lipids cholesterol <1.04 mmol/L. All participants were divided into 5 groups: no exposure, born after 1961; fetal life exposure, between 1959 and 1961; early childhood exposure, between 1956 and 1958; mid-childhood exposure, between 1953 and 1955; and late childhood exposure, between 1949 and 1952. A total of 2,080 subjects were included in this study. Results: In rural, famine exposure in fetal life and early childhood was associated with the lower risk of MS (p = 0.0491 and 0.0245; OR 0.583 and 0.703; and OR, 95% CI 0.341–0.998 and 0.517–0.956, respectively). But famine exposure in late childhood was associated with the higher risk of MS (p = 0.0140; OR 3.096; and OR, 95% CI 1.257–7.625). Famine exposure in early childhood was associated with the lower risk of MS (p = 0.0120; OR 0.633; and OR, 95% CI 0.443–0.904) in males. Conclusions: Famine exposure in mid- and late-childhood was associated with the higher risk of MS, especially in rural, males, and severe famine areas.


2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Noelle Ma ◽  
Daniel B. Hardy

Epidemiological studies have suggested that metabolic programming begins during fetal life and adverse eventsin uteroare a critical factor in the etiology of chronic diseases and overall health. While the underlying molecular mechanisms linking impaired fetal development to these adult diseases are being elucidated, little is known about how we can intervene early in life to diminish the incidence and severity of these long-term diseases. This paper highlights the latest clinical and pharmaceutical studies addressing how dietary intervention in fetal and neonatal life may be able to prevent aspects of the metabolic syndrome associated with IUGR pregnancies.


PEDIATRICS ◽  
2016 ◽  
Vol 137 (6) ◽  
pp. e20154661-e20154661 ◽  
Author(s):  
R. D. Goldstein ◽  
H. C. Kinney ◽  
M. Willinger

2014 ◽  
Vol 81 (1) ◽  
pp. 43-49 ◽  
Author(s):  
Miranda de Jong ◽  
Harrie N. Lafeber ◽  
Anneke Cranendonk ◽  
Mirjam M. van Weissenbruch

2012 ◽  
Vol 90 (9) ◽  
pp. 1171-1183 ◽  
Author(s):  
Ram B. Singh ◽  
Siddharth Gupta ◽  
Parinita Dherange ◽  
Fabien De Meester ◽  
Agnieszka Wilczynska ◽  
...  

Recent research indicates an association between brain dysfunction and the pathogenesis of metabolic syndrome. To investigate this, we created a Medline search (up to December 2011) of articles in PubMed. The results indicated that refined carbohydrates, saturated and total fat, high levels of ω-6 fatty acids, and low levels of ω-3 fatty acids and other long chain polyunsaturated fatty acids (PUFA), all in conjunction with sedentary behaviour and mental stress can predispose to inflammation. Increased sympathetic activity, with increased secretion of catecholamine, cortisol, and serotonin can cause oxidative stress, which may damage the arcuate nucleus as well as the hypothalamus and macrophages, and the liver may release pro-inflammatory cytokines. These, in conjunction with an underlying deficiency in long chain PUFA, may damage the arcuate nucleus as well as neuropeptide-Y and pro-opiomelanocortin neurons and insulin receptors in the brain, especially during fetal life, infancy, and childhood, resulting in their dysfunction. Of the fatty acids in the brain, 30%–50% are long chain PUFA, which are incorporated in the cell membrane phospholipids. Hence, ω-3 fatty acids, which are also known to enhance parasympathetic activity and increase the secretion of anti-inflammatory cytokines interleukin (IL)-4 and IL-10 as well as acetylcholine in the hippocampus, may be protective. Therefore, treatment with ω-3 fatty acids may be applied for the prevention of metabolic syndrome.


Nutrition ◽  
2016 ◽  
Vol 32 (6) ◽  
pp. 620-627 ◽  
Author(s):  
Daria A. Kashtanova ◽  
Anna S. Popenko ◽  
Olga N. Tkacheva ◽  
Alexander B. Tyakht ◽  
Dimitry G. Alexeev ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document