Eggs and beyond: is dietary cholesterol no longer important?

Eckel, Robert H.

doi:10.3945/ajcn.115.116905

Cited by 15 publications

(8 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recommendations to reduce the risk of ASCVD in humans include maintaining low cholesterol intake and low plasma cholesterol levels. However, in the last few years, there have been a number of epidemiological studies that do not support a relationship between dietary cholesterol and/or blood cholesterol and ASCVD [Kanter et al, ; Berger et al, ; Eckel, ]. This led to the 2015 USDA guidelines indicating that cholesterol is not a nutrient of concern for overconsumption.…”

Section: Discussionmentioning

confidence: 99%

7‐Dehydrocholesterol (7‐DHC), But Not Cholesterol, Causes Suppression of Canonical TGF‐β Signaling and Is Likely Involved in the Development of Atherosclerotic Cardiovascular Disease (ASCVD)

Huang

Liu

Chen

et al. 2016

J of Cellular Biochemistry

View full text Add to dashboard Cite

For several decades, cholesterol has been thought to cause ASCVD. Limiting dietary cholesterol intake has been recommended to reduce the risk of the disease. However, several recent epidemiological studies do not support a relationship between dietary cholesterol and/or blood cholesterol and ASCVD. Consequently, the role of cholesterol in atherogenesis is now uncertain. Much evidence indicates that TGF-β, an anti-inflammatory cytokine, protects against ASCVD and that suppression of canonical TGF-β signaling (Smad2-dependent) is involved in atherogenesis. We had hypothesized that cholesterol causes ASCVD by suppressing canonical TGF-β signaling in vascular endothelium. To test this hypothesis, we determine the effects of cholesterol, 7-dehydrocholesterol (7-DHC; the biosynthetic precursor of cholesterol), and other sterols on canonical TGF-β signaling. We use Mv1Lu cells (a model cell system for studying TGF-β activity) stably expressing the Smad2-dependent luciferase reporter gene. We demonstrate that 7-DHC (but not cholesterol or other sterols) effectively suppresses the TGF-β-stimulated luciferase activity. We also demonstrate that 7-DHC suppresses TGF-β-stimulated luciferase activity by promoting lipid raft/caveolae formation and subsequently recruiting cell-surface TGF-β receptors from non-lipid raft microdomains to lipid rafts/caveolae where TGF-β receptors become inactive in transducing canonical signaling and undergo rapid degradation upon TGF-β binding. We determine this by cell-surface 125I-TGF-β-cross-linking and sucrose density gradient ultracentrifugation. We further demonstrate that methyl-β-cyclodextrin (MβCD), a sterol-chelating agent, reverses 7-DHC-induced suppression of TGF-β-stimulated luciferase activity by extrusion of 7-DHC from resident lipid rafts/caveolae. These results suggest that 7-DHC, but not cholesterol, promotes lipid raft/caveolae formation, leading to suppression of canonical TGF-β signaling and atherogenesis. J. Cell. Biochem. 118: 1387–1400, 2017. © 2016 Wiley Periodicals, Inc.

show abstract

Section: Discussionmentioning

confidence: 99%

7‐Dehydrocholesterol (7‐DHC), But Not Cholesterol, Causes Suppression of Canonical TGF‐β Signaling and Is Likely Involved in the Development of Atherosclerotic Cardiovascular Disease (ASCVD)

Huang

Liu

Chen

et al. 2016

J of Cellular Biochemistry

View full text Add to dashboard Cite

show abstract

“…On the contrary, there are still examples of advice that contradict this view. One such example, in a recent editorial in the American Journal of Clinical Nutrition , claimed that eggs should be avoided if you have type-2 diabetes, because the absorption of dietary cholesterol in the gut is increased in this condition ( 48 ) . The meta-analysis that was the subject of the editorial that issued this advice concluded that its data were insufficiently robust to absolve eggs from their association with CVD, but it did not study diabetes ( 49 ) .…”

Section: Impact Of Egg Feeding On Serum Ldl-cholesterol In Diabetesmentioning

confidence: 99%

Eggs: good or bad?

Griffin

2016

Proc. Nutr. Soc.

View full text Add to dashboard Cite

Eggs have one of the lowest energy to nutrient density ratios of any food, and contain a quality of protein that is superior to beef steak and similar to dairy. From a nutritional perspective, this must qualify eggs as 'good'. The greater burden of proof has been to establish that eggs are not 'bad', by increasing awareness of the difference between dietary and blood cholesterol, and accumulating sufficient evidence to exonerate eggs from their associations with CVD and diabetes. After 60 years of research, a general consensus has now been reached that dietary cholesterol, chiefly from eggs, exerts a relatively small effect on serum LDL-cholesterol and CVD risk, in comparison with other diet and lifestyle factors. While dietary guidelines have been revised worldwide to reflect this view, associations between egg intake and the incidence of diabetes, and increased CVD risk in diabetes, prevail. These associations may be explained, in part, by residual confounding produced by other dietary components. The strength of evidence that links egg intake to increased CVD risk in diabetes is also complicated by variation in the response of serum LDL-cholesterol to eggs and dietary cholesterol in types 1 and 2 diabetes. On balance, the answer to the question as to whether eggs are 'bad', is probably 'no', but we do need to gain a better understanding of the effects of dietary cholesterol and its association with CVD risk in diabetes. Eggs: Dietary: Cholesterol: CVD: DiabetesAn egg is equipped to support life, with a profile of essential micronutrients that is unparalleled by any other food. Eggs are relatively low in energy (326·35 kJ (78 kcal)/medium egg) and saturated fat (1·7 g/medium egg) in comparison with other animal products, and can boast the highest quality of dietary protein, with certain dairy foods (1) . Eggs also represent the principal source of dietary cholesterol, which has been a major barrier to egg consumption, primarily because of the outdated, but popular misconception that egg cholesterol converts directly into serum cholesterol, and thus increased risk of CVD. While dietary and serum cholesterol are the same chemical entity, the concentration of serum cholesterol (LDL-cholesterol) falls under the physiological control of whole-body cholesterol homeostasis. This process can be influenced by numerous dietary factors, including dietary cholesterol and fatty acids, but depends ultimately on the essential requirement of cells for cholesterol, and reciprocal interplay between the biosynthesis of cholesterol in tissues, and absorption of cholesterol and bile acids in the gut.A growing body of evidence from prospective cohort studies (2)(3)(4) , systematic reviews and meta-analyses (5)(6)(7)(8) have culminated in a consensus that eggs, and dietary cholesterol derived from eggs, exert a relatively small and clinically insignificant effect on serum LDL-cholesterol in comparison with other lifestyle factors. In one study, modifiable lifestyle factors accounted for <40 % of CHD mortality, to which eating one eg...

show abstract

“…In the 1980s, dietary guidelines around the world recommended restricting dietary cholesterol to 300 mg/day because controlled dietary experiments had shown that dietary cholesterol increased LDL cholesterol 3. In a meta-analysis of four small prospective cohort studies dietary cholesterol was positively associated with Netherlands and the US indicated that the average cholesterol intake was about 200 mg/day, considerably less than the recommended maximum of 300 mg/day.…”

mentioning

confidence: 99%