Rosell M, Johansson G, Berglund L, Vessby B, de Faire U, Hellénius M-L
Division of Cardiovascular Epidemiology, Institute of Environmental Medicine, Karolinska, Institutet, Stockholm, Sweden.
Int J Obes Relat Metab Disord. 2004 Nov;28(11):1427-34. doi: 10.1038/sj.ijo.0802769.
This study evaluates the association between abdominal obesity and the intake of dairy fat and calcium using information from dietary data and the relative content of the fatty acids 14:0, 15:0, and 17 : 0 in serum phospholipids (PL) and adipose tissue (AT), which are suggested biological markers for dairy fat intake. This study also explores how the associations were affected when under-reporters (URs) were separated from the analyses.
Cross-sectional study.
In all, 301 healthy 63-y-old men with different degrees of fasting-insulin concentrations.
Sagittal abdominal obesity (SAD), dietary intake assessed by a 7-day food registration, and the fatty acid composition in serum PL and AT were measured. URs (n=88) and non-under-reporters (non-URs, n=213) were identified by Goldberg's equation, which compares energy intake with energy expenditure, both expressed as multiples of the basal metabolic rate.
The intake of dairy fat, expressed as g/100 g fat, was inversely correlated with SAD; however, this association was only observed in the URs (r=-0.36, P=0.001) and not in the non-URs (r=-0.04, P=0.59). The intake of calcium was inversely correlated with SAD in both groups, although the association was weaker in the non-URs. The intake of dairy fat was related to the relative content of the fatty acids 14:0, 15:0, and 17 : 0 in serum PL and AT (r ranging between 0.32 and 0.55). When these fatty acids were correlated to SAD, inverse associations were seen except for 14:0 in PL (r ranging between -0.17 and -0.29.
If there is a true inverse association between the intake of dairy fat and SAD, it remains to explain why this association was not seen in the non-URs. The data gave some indications of an inverse association between SAD and the intake of calcium. The diverse findings observed when the URs and non-URs were separated highlight the question of how to use and interpret dietary data in URs when diet-disease relationships are investigated.
本研究利用饮食数据以及血清磷脂(PL)和脂肪组织(AT)中脂肪酸14:0、15:0和17:0的相对含量信息,评估腹部肥胖与乳脂肪及钙摄入量之间的关联,这些脂肪酸被认为是乳脂肪摄入量的生物学标志物。本研究还探讨了在分析中分离出低报者(URs)后,这些关联会受到怎样的影响。
横断面研究。
总共301名63岁的健康男性,其空腹胰岛素浓度各不相同。
测量矢状面腹部肥胖(SAD)、通过7天食物记录评估的饮食摄入量以及血清PL和AT中的脂肪酸组成。通过比较能量摄入量与能量消耗量(均表示为基础代谢率的倍数)的戈德堡方程,识别出低报者(n = 88)和非低报者(非URs,n = 213)。
以每100克脂肪中的克数表示的乳脂肪摄入量与SAD呈负相关;然而,这种关联仅在低报者中观察到(r = -0.36,P = 0.001),在非低报者中未观察到(r = -0.04,P = 0.59)。两组中钙摄入量均与SAD呈负相关,尽管在非低报者中这种关联较弱。乳脂肪摄入量与血清PL和AT中脂肪酸14:0、15:0和17:0的相对含量相关(r在0.32至0.55之间)。当这些脂肪酸与SAD相关时,除了PL中的14:0外,均呈现负相关(r在-0.17至-0.29之间)。
如果乳脂肪摄入量与SAD之间确实存在负相关,仍有待解释为何在非低报者中未观察到这种关联。数据表明SAD与钙摄入量之间存在负相关迹象。当分离低报者和非低报者时观察到的不同结果凸显了在研究饮食与疾病关系时,如何使用和解释低报者的饮食数据这一问题。