Egg Fanatic

2 Whole eggs have 422 mg Cholesterol. My goals says you should only have 300 mg in a whole day.
That's why I switched to whites. It's not just about calories.

Unless you have a cholesterol problem. Whole eggs are actually shown to lower bad cholesterol and raise good cholesterol. Again I eat 6 whole a day. And my blood work is perfect!

Do you have cholesterol checked regularly.

2 Whole eggs have 422 mg Cholesterol. My goals says you should only have 300 mg in a whole day.
That's why I switched to whites. It's not just about calories.

my concern, too. the fat and calories don't bother me..the cholesterol does.

No offense Joe, you and I think alike on a lot of things but this (Clinical Chemistry) is an area of expertise for me.

The above ahajournails study proves nothing. People ate a diet before the first cholesterol, then ate about the same diet and surprisingly had no significant change in cholesterol levels. What else did they expect.

There are people who can eat anything they want and they will have a normal cholesterol and there will be others who will have a high cholesterol no matter what they eat or what medications they are on. Because of this variation in lipid metabolism, it is imparative to have compared differing diet's affects on cholesterol levels on an individaul basis.

Fernandez ML. Dietary cholesterol provided by eggs and plasma lipoproteins in healthy populations. Curr Opin Clin Nutr Metab Care. 2006 Jan;9(1):8-12.

PURPOSE OF REVIEW: Extensive research has not clearly established a link between egg consumption and risk for coronary heart disease. The effects of egg intake on plasma lipids and low-density lipoprotein (LDL) atherogenicity in healthy populations need to be addressed. RECENT FINDINGS: The lack of connection between heart disease and egg intake could partially be explained by the fact that dietary cholesterol increases the concentrations of both circulating LDL and high-density lipoprotein (HDL) cholesterol in those individuals who experience an increase in plasma cholesterol following egg consumption (hyperresponders). It is also important to note that 70% of the population experiences a mild increase or no alterations in plasma cholesterol concentrations when challenged with high amounts of dietary cholesterol (hyporesponders). Egg intake has been shown to promote the formation of large LDL, in addition to shifting individuals from the LDL pattern B to pattern A, which is less atherogenic. Eggs are also good sources of antioxidants known to protect the eye; therefore, increased plasma concentrations of lutein and zeaxanthin in individuals consuming eggs are also of interest, especially in those populations susceptible to developing macular degeneration and eye cataracts. SUMMARY: For these reasons, dietary recommendations aimed at restricting egg consumption should not be generalized to include all individuals. We need to acknowledge that diverse healthy populations experience no risk in developing coronary heart disease by increasing their intake of cholesterol but, in contrast, they may have multiple beneficial effects by the inclusion of eggs in their regular diet.

Kritchevsky SB. A review of scientific research and recommendations regarding eggs. J Am Coll Nutr. 2004 Dec;23(6 Suppl):596S-600S.

For much of the past 40 years, the public has been warned away from eggs because of a concern over coronary heart disease risk. This concern is based on three observations: 1. eggs are a rich source of dietary cholesterol; 2. when fed experimentally, dietary cholesterol increases serum cholesterol and; 3. high serum cholesterol predicts the onset of coronary heart disease. However, data from free-living populations show that egg consumption is not associated with higher cholesterol levels. Furthermore, as a whole, the epidemiologic literature does not support the idea that egg consumption is a risk factor for coronary disease. Within the nutritional community there is a growing appreciation that health derives from an overall pattern of diet rather than from the avoidance of particular foods, and there has been a shift in the tone in recent dietary recommendations away from "avoidance" messages to ones that promote healthy eating patterns. The most recent American Heart Association guidelines no longer include a recommendation to limit egg consumption, but recommend the adoption of eating practices associated with good health. Based on the epidemiologic evidence, there is no reason to think that such a healthy eating pattern could not include eggs.

Herron KL, Lofgren IE, Sharman M, Volek JS, Fernandez ML. Metabolism. 2004 Jun;53(6):823-30. High intake of cholesterol results in less atherogenic low-density lipoprotein particles in men and women independent of response classification.

The influence of a high-cholesterol diet on the atherogenicity of the low-density lipoprotein (LDL) particle was examined by measuring LDL peak diameter and composition, LDL susceptibility to oxidation, and the distribution of cholesterol between LDL subclasses. The crossover intervention randomly assigned 27 premenopausal women and 25 men (18 to 50 years) to an egg (640 mg/d additional dietary cholesterol) or placebo (0 mg/d additional dietary cholesterol) diet for 30 days, followed by a 3-week washout period. Subjects were classified as either hyperresponders (>2.5 mg/dL increase in plasma cholesterol for each 100 mg additional dietary cholesterol consumed) or hyporesponders to dietary cholesterol. Sex was found to have a significant effect on 3 of the parameters examined. LDL peak diameter was significantly larger (P <.005) in females (26.78 +/- 0.59 nm, n = 27) as compared with males (26.52 +/- 0.49 nm, n = 25), regardless of response to dietary cholesterol. The LDL particles of the male participants also had a higher number of triglyceride (TG) and cholesteryl ester (CE) molecules (P <.01); however, cholesterol ester transfer protein (CETP) activity was higher in females (P <.05). Response classification also revealed significant differences in the determination of LDL subclasses. Independent of sex, the LDL-1 particle (P <.05), which is considered to be less atherogenic, was predominant in hyperresponders and this finding was associated with increased cholesterol intake (interactive effect, P <.001). In addition, CETP and lecithin: cholesterol acyltransferase (LCAT) activities were higher in hyperresponders during the egg period (interactive effect, P <.05). Sex, response to cholesterol intake, and diet were not found to affect the susceptibility of LDL to oxidation (P > 0.5). Because LDL peak diameter was not decreased and the larger LDL-1 subclass was greater in hyperresponders following egg intake, these data indicate that the consumption of a high-cholesterol diet does not negatively influence the atherogenicity of the LDL particle.

Herron KL, Vega-Lopez S, Conde K, Ramjiganesh T, Shachter NS, Fernandez ML. Men classified as hypo- or hyperresponders to dietary cholesterol feeding exhibit differences in lipoprotein metabolism. J Nutr. 2003 Apr;133(4):1036-42.

The purpose of this study was to evaluate the differences that occur within the plasma compartment of normolipidemic men, classified on the basis of their response to prolonged consumption of additional dietary cholesterol. Using a crossover design, 40 men aged 18-57 y were randomly allocated to an egg (640 mg/d additional dietary cholesterol) or placebo group (0 mg/d additional dietary cholesterol), for two 30-d periods, which were separated by a 3-wk washout period. Subjects were classified as hypo- [increase in plasma total cholesterol (TC) of <0.05 mmol/L for each additional 100 mg of dietary cholesterol consumed] or hyperresponders (increase in TC of > or =0.06 mmol/L for each additional 100 mg of dietary cholesterol consumed) on the basis of their plasma reaction to the additional dietary cholesterol provided. Male hyporesponders did not experience an increase in LDL cholesterol (LDL-C) or HDL cholesterol (HDL-C) during the egg period, whereas both lipoproteins were significantly (P < 0.0001 and P < 0.05, respectively) elevated in hyperresponders. Although the LDL/HDL ratio was increased in male hyperresponders after the high cholesterol period, the mean increase experienced by this population was still within National Cholesterol Education Program guidelines. Furthermore, male hyperresponders had higher lecithin cholesterol acyltransferase (P < 0.05) and cholesteryl ester transfer protein (P < 0.05) activities during the egg period, which suggests an increase in reverse cholesterol transport. These data suggest that additional dietary cholesterol does not increase the risk of developing an atherogenic lipoprotein profile in healthy men, regardless of their response classification.

Not to beat the dead horse, but these were quotes that Alan Aragon used himself.

Fernandez ML. Dietary cholesterol provided by eggs and plasma lipoproteins in healthy populations. Curr Opin Clin Nutr Metab Care. 2006 Jan;9(1):8-12.

PURPOSE OF REVIEW: Extensive research has not clearly established a link between egg consumption and risk for coronary heart disease. The effects of egg intake on plasma lipids and low-density lipoprotein (LDL) atherogenicity in healthy populations need to be addressed. RECENT FINDINGS: The lack of connection between heart disease and egg intake could partially be explained by the fact that dietary cholesterol increases the concentrations of both circulating LDL and high-density lipoprotein (HDL) cholesterol in those individuals who experience an increase in plasma cholesterol following egg consumption (hyperresponders). It is also important to note that 70% of the population experiences a mild increase or no alterations in plasma cholesterol concentrations when challenged with high amounts of dietary cholesterol (hyporesponders). Egg intake has been shown to promote the formation of large LDL, in addition to shifting individuals from the LDL pattern B to pattern A, which is less atherogenic. Eggs are also good sources of antioxidants known to protect the eye; therefore, increased plasma concentrations of lutein and zeaxanthin in individuals consuming eggs are also of interest, especially in those populations susceptible to developing macular degeneration and eye cataracts. SUMMARY: For these reasons, dietary recommendations aimed at restricting egg consumption should not be generalized to include all individuals. We need to acknowledge that diverse healthy populations experience no risk in developing coronary heart disease by increasing their intake of cholesterol but, in contrast, they may have multiple beneficial effects by the inclusion of eggs in their regular diet.

Kritchevsky SB. A review of scientific research and recommendations regarding eggs. J Am Coll Nutr. 2004 Dec;23(6 Suppl):596S-600S.

For much of the past 40 years, the public has been warned away from eggs because of a concern over coronary heart disease risk. This concern is based on three observations: 1. eggs are a rich source of dietary cholesterol; 2. when fed experimentally, dietary cholesterol increases serum cholesterol and; 3. high serum cholesterol predicts the onset of coronary heart disease. However, data from free-living populations show that egg consumption is not associated with higher cholesterol levels. Furthermore, as a whole, the epidemiologic literature does not support the idea that egg consumption is a risk factor for coronary disease. Within the nutritional community there is a growing appreciation that health derives from an overall pattern of diet rather than from the avoidance of particular foods, and there has been a shift in the tone in recent dietary recommendations away from "avoidance" messages to ones that promote healthy eating patterns. The most recent American Heart Association guidelines no longer include a recommendation to limit egg consumption, but recommend the adoption of eating practices associated with good health. Based on the epidemiologic evidence, there is no reason to think that such a healthy eating pattern could not include eggs.

Herron KL, Lofgren IE, Sharman M, Volek JS, Fernandez ML. Metabolism. 2004 Jun;53(6):823-30. High intake of cholesterol results in less atherogenic low-density lipoprotein particles in men and women independent of response classification.

The influence of a high-cholesterol diet on the atherogenicity of the low-density lipoprotein (LDL) particle was examined by measuring LDL peak diameter and composition, LDL susceptibility to oxidation, and the distribution of cholesterol between LDL subclasses. The crossover intervention randomly assigned 27 premenopausal women and 25 men (18 to 50 years) to an egg (640 mg/d additional dietary cholesterol) or placebo (0 mg/d additional dietary cholesterol) diet for 30 days, followed by a 3-week washout period. Subjects were classified as either hyperresponders (>2.5 mg/dL increase in plasma cholesterol for each 100 mg additional dietary cholesterol consumed) or hyporesponders to dietary cholesterol. Sex was found to have a significant effect on 3 of the parameters examined. LDL peak diameter was significantly larger (P <.005) in females (26.78 +/- 0.59 nm, n = 27) as compared with males (26.52 +/- 0.49 nm, n = 25), regardless of response to dietary cholesterol. The LDL particles of the male participants also had a higher number of triglyceride (TG) and cholesteryl ester (CE) molecules (P <.01); however, cholesterol ester transfer protein (CETP) activity was higher in females (P <.05). Response classification also revealed significant differences in the determination of LDL subclasses. Independent of sex, the LDL-1 particle (P <.05), which is considered to be less atherogenic, was predominant in hyperresponders and this finding was associated with increased cholesterol intake (interactive effect, P <.001). In addition, CETP and lecithin: cholesterol acyltransferase (LCAT) activities were higher in hyperresponders during the egg period (interactive effect, P <.05). Sex, response to cholesterol intake, and diet were not found to affect the susceptibility of LDL to oxidation (P > 0.5). Because LDL peak diameter was not decreased and the larger LDL-1 subclass was greater in hyperresponders following egg intake, these data indicate that the consumption of a high-cholesterol diet does not negatively influence the atherogenicity of the LDL particle.

Herron KL, Vega-Lopez S, Conde K, Ramjiganesh T, Shachter NS, Fernandez ML. Men classified as hypo- or hyperresponders to dietary cholesterol feeding exhibit differences in lipoprotein metabolism. J Nutr. 2003 Apr;133(4):1036-42.

The purpose of this study was to evaluate the differences that occur within the plasma compartment of normolipidemic men, classified on the basis of their response to prolonged consumption of additional dietary cholesterol. Using a crossover design, 40 men aged 18-57 y were randomly allocated to an egg (640 mg/d additional dietary cholesterol) or placebo group (0 mg/d additional dietary cholesterol), for two 30-d periods, which were separated by a 3-wk washout period. Subjects were classified as hypo- [increase in plasma total cholesterol (TC) of <0.05 mmol/L for each additional 100 mg of dietary cholesterol consumed] or hyperresponders (increase in TC of > or =0.06 mmol/L for each additional 100 mg of dietary cholesterol consumed) on the basis of their plasma reaction to the additional dietary cholesterol provided. Male hyporesponders did not experience an increase in LDL cholesterol (LDL-C) or HDL cholesterol (HDL-C) during the egg period, whereas both lipoproteins were significantly (P < 0.0001 and P < 0.05, respectively) elevated in hyperresponders. Although the LDL/HDL ratio was increased in male hyperresponders after the high cholesterol period, the mean increase experienced by this population was still within National Cholesterol Education Program guidelines. Furthermore, male hyperresponders had higher lecithin cholesterol acyltransferase (P < 0.05) and cholesteryl ester transfer protein (P < 0.05) activities during the egg period, which suggests an increase in reverse cholesterol transport. These data suggest that additional dietary cholesterol does not increase the risk of developing an atherogenic lipoprotein profile in healthy men, regardless of their response classification.