Heterogeneity of cholesterol homeostasis in man. Response to changes in dietary fat quality and cholesterol quantity.

McNamara, Donald J.; Kolb, R; Parker, Thomas S.; Batwin, H; Samuel, Paul; Brown, Clinton D.; Ahrens, E. H.

doi:10.1172/jci113013

Cited by 281 publications

(99 citation statements)

References 77 publications

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“…Other studies in free-living subjects, including our previous study, 13 ' 24 -28 failed to demonstrate significant rises in plasma cholesterol with supplements of 250 to 750 mg of cholesterol, although between 21% to 40% of subjects experienced at least a 5% rise. In the present study, half of all subjects experienced a rise of 5% or more in plasma cholesterol with dietary cholesterol.…”

Section: Discussionmentioning

confidence: 58%

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Relationship between sensitivity to dietary fat and dietary cholesterol.

et al. 1990

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A group of 56 hypercholesterolemic and normocholesterolemic men and women were given approximately 700 mg a day of egg yolk cholesterol In a double-blind, crossover study while they were on a background diet containing approximately 30% of energy as fat. Overall there was a 0.23 mmol/l rise In plasma cholesterol (3.7%, p<0.001) after 4 weeks, a 0.19 mmol/l rise in low density lipoprotein (LDL) cholesterol (4.9%, p=0.002), and a 0.07 mmol/l rise In high density lipoprotein (HDL) cholesterol (5.4%, p<0.001). Plasma trlglycerides fell by 0.07 mmol/l (5.1%). Normocholesterolemic Individuals (plasma cholesterol <5.2 mmol/l) experienced small, nonsignificant rises of 0.06, 0.02, and 0.05 mmol/l In total, LDL, and HDL cholesterol, respectively. Hypercholesterolemic sub|ects were classified on the basis of their response to a low fat diet. Diet-sensitive sub|ects were defined by a > 10% fall In plasma cholesterol on a 25% fat, low cholesterol (<200 mg/day) diet These individuals were found to be more responsive to the effect of dietary cholesterol than were dlet-insensltlve subjects; the respective changes In the two groups were rises of 0. A n increase in dietary cholesterol produces a small, but significant, increase in plasma cholesterol in most large experimental groups, but there is great individual variability.1 -8 The response to a change in saturated fat intake tends to be much larger than the response to dietary cholesterol, and although individual variability occurs, few people are truly unresponsive. 9 -13 McNamara et al. 13 in an extensive trial of free-living subjects, found that 70% of people could effectively compensate for an increase in dietary cholesterol by down-regulating cholesterol synthesis. A similar proportion of metabolic "compensators" had earlier been reported by Nestel and Poyser.14 In the former study, only 10% of the individuals had a significant (10%) increase in plasma cholesterol, and these individuals failed to downregulate cholesterol synthesis and tended to have high cholesterol absorption rates. A possible genetic basis has been suggested by Kesaniemi et al. 16 who demonstrated that subjects with the E4 allele for apolipoprotein (apo) E had a higher fractional cholesterol absorption From the CSIRO Division of Human Nutrition, Adelaide, South Australia.This work was partly supported by the National Heart Foundation of Australia and the Egg Industry Research Council of Australia.Address for reprints: Dr. P.J. Nestel, CSIRO Division of Human Nutrition, Kintore Avenue, Adelaide SA 5000, Australia.Received August 3, 1989; revision accepted December 11, 1989. than did subjects with the E2 allele. Individuals carrying an apo E4 allele had a much higher low density lipoprotein (LDL) cholesterol concentration than did those with the E2 allele. 16 Katan et al. 17 have recently shown that there may be a correlation between sensitivity to changes in dietary saturated fat intake and sensitivity to dietary cholesterol in normocholesterolemic individuals. However, hypercholesterolemic ind...

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Section: Discussionmentioning

confidence: 58%

“…9 -13 McNamara et al 13 in an extensive trial of free-living subjects, found that 70% of people could effectively compensate for an increase in dietary cholesterol by down-regulating cholesterol synthesis. A similar proportion of metabolic "compensators" had earlier been reported by Nestel and Poyser.…”

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confidence: 99%

Relationship between sensitivity to dietary fat and dietary cholesterol.

et al. 1990

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“…The concept of respondersanonresponders to hypercholesterolemic diets is not new (Ginsberg et al, 1981;McNamara et al, 1987;Glatz et al, 1993). According to Glatz et al (1993) variations in response may be partly random in nature and partly due to metabolic differences among subjects.…”

Section: Effects On Serum Lipoprotein Concentrationsmentioning

confidence: 99%

Effect of synthetic triglycerides of myristic, palmitic, and stearic acid on serum lipoprotein metabolism

et al. 1999

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Objectives: To determine relative effects of diets high in synthetic sources of myristic (14:0), palmitic (16:0) or stearic (18:0) acid on concentrations and metabolism of serum lipoproteins. Design: Eighteen healthy women participated in a three-way cross-over study for ®ve week periods separated by seven week washout periods, diets were assigned in random order. Subjects: Premenopausal women, not on medication, were from three races (Caucasian, African-American, Asian) and four apolipoprotein E phenotype groups (3a3, 3a2, 4a3, and 4a2). Intervention: During the ®rst week the subjects consumed a baseline diet providing 11 energy (en)% saturated fat, 10 en% polyunsaturated fat and 14 en% monounsaturated fat. Followed by test diets with 19 en% saturated fat (including 14 en% test saturated fatty acid), 3 en% polyunsaturated fat, and 14 en% monounsaturated fat for four weeks. Synthetic fats (trimyristin, tripalmitin, and tristearin) were used in blends with natural fats and oils. Results: Mean concentrations of serum total, esteri®ed and LDL cholesterol were signi®cantly lower after 18:0 than after 16:0 (n 16 ± 18, P`0.01 for treatment effect). Myristic acid (14:0) had an intermediate effect.Receptor-mediated degradation of 125 I-LDL in mononuclear cells obtained from the subjects was lower after 16:0 than after 14:0 and 18:0 (n 16 ± 18, P 0.05 for treatment effect). Differences in the digestibilities of the fats were not a major factor in the results. Strong cholesterolemic responses to the 16:0 diet were partly explained by apoE phenotype. Conclusions: As noted previously, stearic acid was neutral compared to 14:0 and 16:0. In contrast to studies involving natural fats, 14:0, fed as a synthetic triglyceride, was less cholesterolemic than 16:0 in a majority of subjects. ApoE phenotype in¯uenced the cholesterolemic response particularly when diets high in 16:0 were eaten.

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“…However, a consistent finding from study after study was the high degree of variability in plasma cholesterol responses to dietary cholesterol challenges between patients (24) . In order to explain this variability, and its significance in the dietary cholesterol -heart disease question, it is necessary to consider the inter-individual differences in cholesterol metabolism.…”

Section: Clinical Interventionsmentioning

confidence: 70%

Dietary cholesterol, heart disease risk and cognitive dissonance

McNamara¹

2014

Proc. Nutr. Soc.

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In the 1960s, the thesis that dietary cholesterol contributes to blood cholesterol and heart disease risk was a rational conclusion based on the available science at that time. Fifty years later the research evidence no longer supports this hypothesis yet changing the dietary recommendation to limit dietary cholesterol has been a slow and at times contentious process. The preponderance of the clinical and epidemiological data accumulated since the original dietary cholesterol restrictions were formulated indicate that: (1) dietary cholesterol has a small effect on the plasma cholesterol levels with an increase in the cholesterol content of the LDL particle and an increase in HDL cholesterol, with little effect on the LDL: HDL ratio, a significant indicator of heart disease risk, and (2) the lack of a significant relationship between cholesterol intake and heart disease incidence reported from numerous epidemiological surveys. Over the last decade, many countries and health promotion groups have modified their dietary recommendations to reflect the current evidence and to address a now recognised negative consequence of ineffective dietary cholesterol restrictions (such as inadequate choline intake). In contrast, health promotion groups in some countries appear to suffer from cognitive dissonance and continue to promote an outdated and potentially hazardous dietary recommendation based on an invalidated hypothesis. This review evaluates the evidence for and against dietary cholesterol restrictions and the potential consequences of such restrictions.

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Heterogeneity of cholesterol homeostasis in man. Response to changes in dietary fat quality and cholesterol quantity.

Cited by 281 publications

References 77 publications

Relationship between sensitivity to dietary fat and dietary cholesterol.

Relationship between sensitivity to dietary fat and dietary cholesterol.

Effect of synthetic triglycerides of myristic, palmitic, and stearic acid on serum lipoprotein metabolism

Dietary cholesterol, heart disease risk and cognitive dissonance

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