Egg-Yolk and Serum Cholesterol Levels: Importance of Dietary Cholesterol Intake

JAMA ◽  
1963 ◽  
Vol 184 (12) ◽  
pp. 207
Author(s):  
Eridiong O. Onyenweaku ◽  
Henrietta N. Ene-Obong ◽  
Gregory E. Oko ◽  
Ima O. Williams

Aim: Eggs have sometimes been regarded as unhealthy foods due to their relatively high cholesterol content. The aim of this study is to determine contribution of eggs and other    cholesterol containing food to total dietary cholesterol and their influence on serum lipid profile of adults. Study Design: Cross sectional and experimental. Place and Duration of Study: Department of Biochemistry, University of Calabar, Calabar. February to July 2017. Methodology: A cross-sectional survey to determine consumption pattern was carried out on 400 respondents using food frequency questionnaire (FFQ) and 24 hour dietary recall. The respondents were further grouped into four based on their reported weekly egg consumption. A detailed follow-up study was conducted on 50 participants selected from across the 4 groups, using a 3-day repeated 24 hour dietary recall to determine their consumption of egg and other cholesterol-containing foods. Serum blood lipid profile of these 50 participants was also determined using Randox cholesterol test kits. Food composition tables were used to calculate dietary cholesterol intake (DCI). The mean DCI of the 4 groups were cross-tabulated with mean serum cholesterol levels. Percentage contribution of eggs and other frequently consumed cholesterol-containing foods (such as milk and fish) to total DCI was calculated. Statistical significance was accepted at p = .05. Results: For the follow-up participants, it was observed that results of correlations between DCI and the lipid profile parameters showed negative correlation (at p = .01) in both males and females, except slight positive correlations between cholesterol intake and HDL-c (r=0.191) among the males, and cholesterol with TC (r=0.265) among the females. Apart from this, no association was observed between DCI and the lipid profile parameters. Furthermore, the > 5eggs/week group had the lowest TC and LDL-c (4.23±0.19 mmol/L and 2.38±0.10 mmol/L). Based on the respondents’ consumption patterns, eggs (boiled and fried) contributed the highest- 34.8% to total DCI, followed by milk (15.9%); salad cream contributed lowest (0.3%) to total DCI. Conclusion: Increased DCI from cholesterol-containing foods (such as eggs), did not cause an adverse increase in serum cholesterol levels of normocholesterolemic people.


2020 ◽  
Vol 61 (11) ◽  
pp. 1504-1511
Author(s):  
Shaofeng Huo ◽  
Liang Sun ◽  
Geng Zong ◽  
Boyu Song ◽  
He Zheng ◽  
...  

Accompanied with nutrition transition, non-HDL-C levels of individuals in Asian countries has increased rapidly, which has caused the global epicenter of nonoptimal cholesterol to shift from Western countries to Asian countries. Thus, it is critical to underline major genetic and dietary determinants. In the current study of 2,330 Chinese individuals, genetic risk scores (GRSs) were calculated for total cholesterol (TC; GRSTC, 57 SNPs), LDL-C (GRSLDL-C, 45 SNPs), and HDL-C (GRSHDL-C, 65 SNPs) based on SNPs from the Global Lipid Genetics Consortium study. Cholesterol intake was estimated by a 74-item food-frequency questionnaire. Associations of dietary cholesterol intake with plasma TC and LDL-C strengthened across quartiles of the GRSTC (effect sizes: −0.29, 0.34, 2.45, and 6.47; Pinteraction = 0.002) and GRSLDL-C (effect sizes: −1.35, 0.17, 5.45, and 6.07; Pinteraction = 0.001), respectively. Similar interactions with non-HDL-C were observed between dietary cholesterol and GRSTC (Pinteraction = 0.001) and GRSLDL-C (Pinteraction = 0.004). The adverse effects of GRSTC on TC (effect sizes across dietary cholesterol quartiles: 0.51, 0.82, 1.21, and 1.31; Pinteraction = 0.023) and GRSLDL-C on LDL-C (effect sizes across dietary cholesterol quartiles: 0.66, 0.52, 1.12, and 1.56; Pinteraction = 0.020) were more profound in those having higher cholesterol intake compared with those with lower intake. Our findings suggest significant interactions between genetic susceptibility and dietary cholesterol intake on plasma cholesterol profiles in a Chinese population.


2004 ◽  
Vol 286 (2) ◽  
pp. C398-C405 ◽  
Author(s):  
Kerrie A. Buhagiar ◽  
Peter S. Hansen ◽  
Benjamin Y. Kong ◽  
Ronald J. Clarke ◽  
Clyne Fernandes ◽  
...  

A modest diet-induced increase in serum cholesterol in rabbits increases the sensitivity of the sarcolemmal Na+/K+ pump to intracellular Na+, whereas a large increase in cholesterol levels decreases the sensitivity to Na+. To examine the mechanisms, we isolated cardiac myocytes from controls and from rabbits with diet-induced increases in serum cholesterol. The myocytes were voltage clamped with the use of patch pipettes that contained osmotically balanced solutions with Na+ in a concentration of 10 mM and K+ in concentrations ([K+]pip) ranging from 0 to 140 mM. There was no effect of dietary cholesterol on electrogenic Na+/K+ current ( Ip) when pipette solutions were K+ free. A modest increase in serum cholesterol caused a [K+]pip-dependent increase in Ip, whereas a large increase caused a [K+]pip-dependent decrease in Ip. Modeling suggested that pump stimulation with a modest increase in serum cholesterol can be explained by a decrease in the microscopic association constant KK describing the backward reaction E1 + 2K+ → E2(K+)2, whereas pump inhibition with a large increase in serum cholesterol can be explained by an increase in KK. Because hypercholesterolemia upregulates angiotensin II receptors and because angiotensin II regulates the Na+/K+ pump in cardiac myocytes in a [K+]pip-dependent manner, we blocked angiotensin synthesis or angiotensin II receptors in vivo in cholesterol-fed rabbits. This abolished cholesterol-induced pump inhibition. Because the ϵ-isoform of protein kinase C (ϵPKC) mediates effects of angiotensin II on the pump, we included specific ϵPKC-blocking peptide in patch pipette filling solutions. The peptide reversed cholesterol-induced pump inhibition.


1985 ◽  
Vol 63 (5) ◽  
pp. 557-564 ◽  
Author(s):  
Sheila M. Innis

Atherosclerosis is believed to begin early in life and to develop over several decades. Elevated plasma cholesterol is a major contributing factor. Studies in animals have shown that manipulation of cholesterol metabolism during its development in pre-and early post-natal life can permanently alter cholesterol synthesis and catabolism to favour lower plasma cholesterol levels in the adult faced with a high dietary cholesterol intake. Although the mechanisms and pathways involved are likely to be different, "metabolic training" can occur as a result of both the diet fed to the mother during gestation and lactation and from the diet fed to the animal itself in early life. The presence of cholesterol itself in the suckling diet does not appear to confer any lasting improvement to cholesterol handling in either man or animals. Although much research is still required to define the time in development for effective training of specific steps in cholesterol metabolism and the primary site and mechanism of permanently altered metabolism, significant progress has been made. These studies will form the basis of this review.


1980 ◽  
Vol 59 (8) ◽  
pp. 1812-1817 ◽  
Author(s):  
J.S. SIM ◽  
W.D. KITTS ◽  
D.B. BRAGG

2021 ◽  
Vol 8 (4) ◽  
pp. 36
Author(s):  
Piia Simonen ◽  
Elisa Arte ◽  
Helena Gylling

Dietary modifications including plant stanol ester consumption are recommended measures to control serum and low-density lipoprotein (LDL)-cholesterol concentrations, but obesity can affect their responses. We investigated whether body mass index (BMI) affects serum cholesterol levels during plant stanol (mainly sitostanol) ester consumption. This ad hoc analysis was based on earlier results of a cross-over, randomized controlled trial of postmenopausal women consuming rapeseed oil-based margarine without or with plant stanol ester (3 g plant stanols/day) for seven weeks. We classified the subjects as normal-weight (BMI ≤ 25 kg/m2, n = 9, mean 22.6 kg/m2) or overweight/obese (BMI > 25 kg/m2, n = 11, mean 28.4 kg/m2), and recalculated the results, focusing on cholesterol absorption, cholesterol synthesis, and fecal steroid outputs. Serum cholesterol levels were similar in the groups during the control diet. Plant stanol ester reduced serum cholesterol by 0.63 ± 0.19 mmol/L (11%) in normal-weight and by 0.75 ± 0.13 mmol/L (12%) in overweight/obese subjects (p < 0.05 for both), and cholesterol absorption was reduced in both groups. However, relative and dietary cholesterol absorption were more effectively reduced in normal-weight subjects. In conclusion, overweight/obesity did not interfere with the serum cholesterol response to plant stanol ester consumption despite substantial differences in cholesterol metabolism between the groups.


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