{'fraction_non_alphanumeric': 0.05483625285605483, 'fraction_numerical': 0.051028179741051026, 'mean_word_length': 4.639484978540772, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Familial aggregation of LDL oxidation.

The "oxidation hypothesis" states that oxidative modification of low-density lipoprotein (LDL) is important in the pathogenesis of the atherosclerotic lesion. We studied 15 families (fathers, mothers and male twins of 16 to 18 years of age) to investigate the familial aggregation of LDL oxidation. As an indicator of LDL oxidation products we measured baseline levels of conjugated dienes extracted from LDL (LDL-BDC). For this analysis LDL was first isolated by rapid precipitation with buffered heparin. LDL-BDC was highest in fathers (mean 673 delta Abs per mg LDL cholesterol, 95% confidence interval (CI) 547-800) followed by mothers (500, 95% CI 408-592) and twins (383, 95% CI 337-430). There was a high correlation in the LDL-BDC between the identical twins (r = 0.81, 95% CI 0.44-0.95), but no correlation between the parents (r = -0.36). The LDL-BDC of boys correlated positively with that of fathers (r = 0.49, 95% CI 0.16-0.72), but not with that of mothers (r = 0.00). Highly significant positive correlations were observed between LDL-BDC and serum lipid risk factors among parents, but among twins the correlations were usually weaker. Our study suggests that inherited factors contribute to interindividual variability in the oxidative modification of LDL.