The internet has no shortage of information about eggs. Unfortunately, there exists a paucity of sources that have looked in detail at the actual scientific research as a whole. While I went through it myself, it became clear that this information should be condensed into a post in hopes that eggs, and their most feared constituent, cholesterol, are better understood. As stated by Dr. Elizabeth Applegate (19): “…the evidence that eating eggs is unrelated to heart disease risk needs to be widely disseminated to health professionals and the public so that everyone can benefit from including eggs in the diet.” Indeed, many other authors are speaking up for eggs, but they aren’t being heard by the masses.
Earlier this month marked Easter for some theists. As part of a long tradition, many people consume eggs which apparently represent the resurrection of Jesus. As a food that is deeply integrated into various diets through historical and cultural influences, it is important to garner a general understanding of food habits when considering the big picture, in combination with the scientific evidence. Eggs have been consumed for millennia, back to at least the Neolithic period. As a part of (some) diets for that long, it bodes more confidence in their role in a healthy diet; it has been demonstrated that genetic adaptations to foods can occur within this timespan, though our understanding is still limited and may not be directly applicable to eggs. Bolstering this, overwhelming research is clear that eggs are indeed good to eat.
Chicken or Egg?
Chicken eggs have somewhat of an unhealthy stigma attached to them, but this wasn’t always so. It stems from food scares in the 1960’s; in this case, the eggs/cholesterol/heart disease hypothesis. Prominent organizations like the American Heart Association can be credited partly for solidifying cholesterol fears into Americans, but scientists, the media, and industry itself all contributed. Though eggs were far from the first food scare victim, this one perpetuated through the years because of misinterpretations of the limited scientific data available. Fortunately, from the 1980’s until today, trends from written material suggest that the fear of eggs is much reduced from earlier decades, but the the American Heart Association (AHA) and American Dietetic Association (ADA) still recommend lowering the consumption of cholesterol containing foods like eggs without much further direction in how to do this or offering evidence-based substantiation. The Mayo Clinic also demonizes the cholesterol content. Eggs have been on a consumption roller coaster, declining in the 1950’s but now rising in the last couple of decades, which may be explained by perception changes in the healthiness of eggs (15). Yet as of 2000, they only contribute approximately 1.3% of total calories in the American diet (19). In fact, from 1970 to 1995, per capita consumption decreased 24%, from 310 eggs to 235 per year (20). Public policy worked, but it was wrong.
Out of the Shell
Eggs are a rich source of many nutrients. Two eggs are a good source (as defined by 10-19% of Daily Value) of B12, D, A, Folate, and Phosphorous, and an excellent source (20+% of DV) of Riboflavin, Protein, K, and Selenium. They can technically be defined as a “functional food,” under one of the ADA’s definitions of an “unmodified whole food with physiologically active components.” (19) Though I dislike nutritionism and celebritizing specific foods, many of these nutrients are consumed in low amounts by most Americans, who are increasingly choosing taste and convenience over nutrition (19). Eggs are inexpensive, and already widely available in stores. Based on these data as well as other research outlined in this article, I believe they should be promoted, yolk and all.
Dietary Guidelines for the U.S. recommend consuming less than 300 mg of dietary cholesterol per day. As eggs contain over 200 mg per (50 g) egg, this only allows for several eggs per week, since many other foods contain cholesterol as well (8). As noted previously, the AHA and ADA also both suggest limiting cholesterol, even from eggs. Recent publications have been questioning these recommendations (e.g. refs 18-20), and nutrition professionals should be aware of the large body of evidence that suggests that they may be doing more harm than good.
Though I will focus on the egg-specific research, cholesterol alone has been studied intensely for decades. Dr. Donald McNamara has done a superb job at summarizing cholesterol studies (20). I summarize some of his conclusions below.
Epidemiological studies are complicated by confounding nutrients that may not be relevant to eggs, which unlike other sources of cholesterol, have a very different macronutrient composition. Even then, analysis of surveys and prospective studies overwhelmingly suggest that cholesterol is not related to coronary heart disease (CHD).
As of 2000, 167 cross-over cholesterol feeding studies in which cholesterol was the only variable were analyzed by McNamara. Varying designs and doses were used, in context of varying diet pattterns. Together, the data do show that plasma cholesterol level does increased with increasing dietary cholesterol (but not linearly). His results corroborated other meta-analyses and predictive equations developed back to 1965. The equation suggests that for every 100mg/day change of dietary cholesterol, the plasma cholesterol will change approximately 2.2 mg/dL. This is a small change, and is highly individual. Total body cholesterol is about 150 grams, with absorption from the diet ranging widely from 20%-80%, which regulates endogenous synthesis that ranges from about 11-13 mg/kg/day. Feedback mechanisms are in strict control of the whole process, so inconsistent intakes don’t dramatically alter cholesterol homeostasis.
So the assumption used to be that changes in plasma cholesterol may reflect risks in CHD. Now we know it is much more complex. For instance, cholesterol is contained in lipoprotein fractions, HDL & LDL. Though one egg as predicted by an equation can increase total cholesterol on average by 5 mg/dL, cholesterol in LDL would be predicted to increase by 4.1 mg/dL and in HDL by .9 mg/dL, which doesn’t change the ratio of LDL:HDL by much. Indeed, the ratio is better correlated in studies to relate to CHD (18). As I detail later, several studies show that eggs do not alter this ratio. In addition, there are different subfractions of LDL and HDL, which are examined later.
Note: Gary Taubes has described the cholesterol research with a historical context in his recent book (I do not necessarily agree with the book in its entirety, but the cholesterol part is to my knowledge a fair representation).
There have been many observational studies specifically looking at egg consumption and CVD risk. They paint a still complicated picture.
In the large Nurses’ Health Study, the consumption of 1 egg per day does not increase relative risk for CHD, except in diabetics. Another study (controlled) found that 2 eggs per day found that lipoprotein fractions may differ somewhat in hyperlipidemic subjects, suggesting that in certain disease contexts, egg or cholesterol reduction may be warranted. In the Physicians’ Health Study, CVD risk was not affected, but was linked to all-cause mortality, and most strongly in diabetics. However, as pointed out by Robert Eckel in an editorial, the consumption patterns are patterns are much different for these physicians compared to “average” people: only 8% consumed more than 1 egg per day, compared to other studies that have found this number to be in the 30’s. Many unknowns remain unanswered. Another study adds concern to diabetic consumption, but not healthy people.
Many other large studies, however, report no risk for CHD or mortality: Framingham, NIPPON DATA80, Japan Public Health Center-based prospective study.
Several other studies exist; a good review by Kritchevsky is recommended to better understand the difficulties in making solid conclusions. The majority suggest that eggs are not related to cardiovascular disease or mortality.
Observational studies can be difficult to interpret with many possible confounders, and should not be a basis for policy. But they are good starting points to get a sense of what should be studied in a controlled fashion. If enough data point in one direction, they may give a sense of risk. For a clearer picture, we look to the controlled studies.
Recent studies by Maria Luz Fernandez, Jeff Volek, and others have given us important insights into dietary context. Because we have an incomplete understanding of interactions at the molecular level, many misinterpretations have arisen that demonize certain foods when they haven’t been studied appropriately as a whole food item (in this case, eggs represented as cholesterol), or in context with various dietary patterns (macronutrient variations). These studies use similar designs and show consistent results in each.
Non-Low Carbohydrate/Non-Calorie Restricted Studies
Herron et al. (1) gave 91 subjects (between 20-50 years old) either 3 whole (liquid) eggs (~ 640 mg additional cholesterol) or a placebo (cholesterol & fat-free egg substitute) every day for 30 days in a crossover trial and examined a number of biomarkers of CVD risk. Subjects were classified as hyperresponders if their total serum cholesterol increased more than 15 mg/dL, and hyporesponders if they experienced an increase of less than that or no increase. This was determined based on an equation developed from other studies which have found large individual variations in serum cholesterol changes. 28 hyperresponders and 26 hyporesponders were analyzed for LDL particle size. Plasma insulin concentrations were apparently not significantly different between groups. Of these subjects, 29 were classified as pattern B (LDL-3+) and 25 pattern A (LDL-1,2). Pattern B correlates more strongly to an increased risk for atherosclerosis. Following egg consumption, hyperresponders had greater increases in total LDL-C & LDL-C1 than hyporesponders. Because LDL-C itself doesn’t have a strong prognostic value for cardiovascular disease (CVD), as discussed previously, the increase in LDL-C1 in the hyperresponders suggests actually a decreased risk for CVD. Thus, this study may suggest that an increase in fat and cholesterol (and possibly other constituents) from the consumption of 3 eggs daily may reduce CVD risk. It should be noted that total fat and saturated fat intake was slightly higher in the egg group (31.4% +/- 5.5%, 10.9% +/-2.5%) versus the placebo (26.6% +/- 7.1%, 9.4% +/-2.6%). However, these amounts approximated a typical “western” diet. Plasma triglycerides did not change significantly between groups.
A similar group (2) tested the same protocol in an older group of 42 subjects (men were above 60 years old, women menopausal for at least 1 year). This population also contained hyper and hyporesponders, but in general, total cholesterol, LDL-C, and HDL-C increased in the group consuming the eggs. The LDL:HDL ratio and plasma triglycerides did not differ between the 2 groups (eggs vs. placebo). As with the first experiment, the LDL particle size increased with egg consumption, suggesting a reduced risk for CVD. As before, total fat, saturated fat, cholesterol, and also monounsaturated fat increased in the egg group, but the authors speculate that the effect on lipids was mostly from the dietary cholesterol itself.
A separate group examined (16) a different lipoprotein: chylomicrons. Chylomicrons carry fats and cholesterol absorbed in the intestine into circulation. After lipolysis of the triglycerides contained in chylomicrons at the tissues, particles called chylomicron remnants remain in circulation and are eventually taken up in the liver. This is all done quickly; chylomicrons have a half-life of about 15 to 20 minutes. As noted by the authors, evidence suggests that delayed chylomicron catabolism is related to an acceleration of atherosclerosis. They studied 25 males who consumed approximately 2 types of meals, each with about 60% carbohydrate, 15% protein, and 25% fat (7% saturated and 18% mono/polyunsaturated) for 15 days. 1 of the meals was low in cholesterol plus 3 egg whites, and the other was high in cholesterol with 3 whole eggs per day. All meals were provided, however in the high cholesterol group, according to table 1, the average energy intake per day was slightly over 400 kcal greater. Total cholesterol in the high cholesterol group was over 800 mg/day, versus over 170 mg/day in the low cholesterol group. The authors state no difference in baseline measures, however for serum triglycerides, there was approximately a 30 mg/dL difference. After the treatment period, the high cholesterol diet increased serum cholesterol, LDL-C, and HDL-C compared to the low cholesterol diet. Triglycerides and Lp(a) did not differ, but Apo B was greater in the high cholesterol group. Cholesterol ester removal from plasma was decreased, and triglyceride removal was not. VLDL shares a common metabolic pathway, thus if they are also altered (reduced clearance), it could explain the increase in LDL-C with higher cholesterol intake, because it is the precursor to LDL. This is supported by the increase in ApoB, which is the primary apolipoprotein of LDL. One earlier study by Ginsberg et al. on 0,1,2, or 4 eggs per day for 8 weeks in 20 subjects found that the number of eggs did not alter chylomicron metabolism, so I have to wonder if the energy intake difference in this study influenced this, though the authors suggest that it may be because of a superior measurement approach. This issue needs to be further examined.
Some studies have suggested that carotenoids such as lutein and zeaxanthin can protect against age-related macular degeneration. Clark et al. (3), using 3 eggs (~640 mg cholesterol + ~600 µg lutein + zeaxanthin) or placebo (~ 568 µg ß-carotene) per day, and (4) using the same except without ß-carotene elucidated relationships between cholesterol and carotenoids. Interestingly, subjects classified as hyperresponders to dietary cholesterol had higher plasma baseline concentrations of several carotenoids and greater increases in plasma lutein (but not necessarily ß-carotene) after consumption of eggs. In hyporesponders, however, a consistent pattern was evident after egg consumption: ß-carotene nor lutein increased as significantly as in hyperresponders. The authors speculate this is because carotenoids and cholesterol share several steps during absorption and transport. Another (4) found similar relationships in older subjects, as well as an association between BMI and baseline lutein, and that the size of LDL and HDL affects plasma lutein, rather than the number. It is unknown if these findings are clinically relevant yet, but it is plausible that because different carotenoids are concentrated differently in the various lipoprotein subclasses, it suggests that dietary patterns that shift these classes could influence how carotenoids are distributed.
Low-Carbohydrate/Calorie Restricted Egg Studies
Mutungi et al. (5) studied subjects for 12 weeks who consumed again 3 additional eggs per day or a placebo, but who limited carbohydrate consumption to a target of 10-15%, while protein was kept at 30-35%, and 55-60% fat. Total cholesterol in plasma was not affected significantly by the diets. In these subjects, LDL-C was not increased from baseline or between the egg and placebo groups. However, HDL-C was increased only in the group that consumed the eggs. The investigators also examined the expressions of 2 genes’ mRNA that are involved in cholesterol homeostasis; HMG-CoA reductase and LDL-r were downregulated in the group consuming the eggs, and upregulated in the placebo group. These suggest that the additional cholesterol downregulated genes involved in the synthesis and uptake of cholesterol because of an increased intracellular content. The lack of an increase in LDL-C, unlike studies discussed previously, may be because of a reduction in weight in the subjects.
In a similar study (6), 31 men between the age of 40 and 70 with BMIs of 26-37 kg/m^2 were studied. These subjects were also subjected a low carbohydrate diet, at the same target ratios used in (5). Body weights, BMI, and waist circumferences were all reduced after 12 weeks because of a reduction in total caloric intake by an average of 22% (it seems difficult for subjects to adapt quickly to new foods), and systolic and diastolic blood pressure decreased. Total plasma cholesterol and LDL-C, as well as LDL:HDL did not change, as expected (weight loss). The carbohydrate restriction lowered triglyceride concentration in both groups (by about ~45%). In 13/15 subjects consuming eggs, HDL-C increased, while only 3/13 in the placebo group increased in HDL. Fasting glucose concentrations did not change in the groups. Importantly, there was a dramatic reduction in subjects classified with metabolic syndrome following the diet, 100% of which was ameliorated in the low carbohydrate group + egg consumption. A separate report from the study (7) explored the same subjects in more detail. LCAT activity increased in the egg group only (suggesting greater HDL concentrations and size). Both groups experienced similar changes in apolipoproteins. The group consuming eggs had a more consistent plasma lutein and zeaxanthin increase, suggesting that the food matrix, possibly from the lipids in the yolk, may increase their absorption. VLDL was reduced similarly in both groups.
These studies tell us is that subjects who (unintentionally) restrict calories because of a low carbohydrate diet do not experience lipoprotein differences that are evident in studies showing hyper and hyporesponders to dietary cholesterol. They are important to consider for dieters, however, and apparently especially for people with metabolic problems, as eggs may help ameliorate characteristics of metabolic syndrome. For other reasons as discussed below, eggs can be very helpful for dieters.
Curious Case of the Egg Man
To demonstrate one extreme of responsiveness to dietary cholesterol, there is a case study of an 88 year old “egg man” who compulsively consumed 20 to 30 eggs for at least 15 years, yet had normal lipid values. It was found that he absorbed a substantially reduced amount of the cholesterol, an increased conversion of cholesterol to bile acids, a reduced cholesterol synthesis, and a possible increase in biliary cholesterol secretion compared to subjects in a trial at the time. But this does not mean everyone could handle this amount, and consuming the majority of calories from a single food source is risky.
Eggs for Breakfast & Weight Control?
Various studies suggest that eggs with breakfast are superior for weight control over some other foods.
The first (9) studied 28 overweight or obese women who consumed a breakfast of either: 1) 2 scrambled eggs, 2 slices of toast, and 1 Tbsp of reduced calorie fruit spread, or 2) a 3.5 inch diameter bagel, 2 Tbsp cream cheese, and 3 oz. non-fat yogurt. Both the weight and energy content of each of the meals was similar. 3.5 hours after each breakfast, the subjects consumed similar lunches, ad libitum. The energy intake for the rest of the day following the egg breakfast was on average ~264 kcal lower than the bagel breakfast, and ~420 kcal lower until noon of the next day. Subjective measures of satiety suggest that the egg breakfast is more satiating compared to the bagel breakfast, which corroborates earlier research, which established a satiety index of various foods. The specific macronutrient or other component responsible for these effects were not established.
The results of a longer trial were published in 2008 (10). 152 overweight or obese subjects completed the study (131 women, 21 men). Subjects were randomly divided into 4 groups: a bagel, bagel diet, egg, or egg diet. Breakfasts were consumed on weekdays. In the bagel and egg groups, subjects continued normal eating and activity patterns except for the breakfasts, and in the bagel diet and egg diet groups, subjects were suggested (and not strictly monitored) to lower energy intake by 1000 kcal per day based on (initial) BMI. The nutritional compositions of each diet are available here. Over 8 weeks, the weight loss, waist circumference, BMI, and body fat % didn’t differ significantly between the groups that weren’t recommended to restrict calories. In the groups that did restrict calories, weight and BMI were decreased more in the egg diet group compared to the bagel group, with a trend toward a decreased waist circumference. Although, the weight difference was only ~1kg (the egg diet group lost about 2.5kg on average). Chart available here. Considering energy intakes were not strictly controlled, this may follow the predictions of the short term study. But for obese people who have 10s or more pounds to lose, this may not be clinically significant in the long run, as long term dieters often plateau after months in clinical studies, and it is unknown if the weight loss advantage with eggs would be sustained. Plasma LDL, HDL, total cholesterol, and triglycerides did not differ significantly between the groups. Subjective analyses for a number of quality of life factors suggested that egg breakfast improved energy, decreased fatigue, and improved pain compared to the other breakfast.
The most recent, published this year (11) aimed to further understand the mechanism for why eggs are more satiating. Ghrelin, insulin, leptin, glucagons-like peptide 1 (GLP-1) and peptide YY (PYY) were examined, all which have been found to influence appetite. The authors studied 21 men in a crossover fashion consuming each breakfast, which consisted of: ~396 kcal, the egg breakfast with 3 scrambled eggs and 1.5 pieces of white toast (macronutrient %’s: ~22 CHO/23 PRO/55 FAT), and a bagel breakfast with 1 white bagel, 1/2 Tbsp. low-fat cream cheese, and 6 oz of low-fat yogurt (~72 CHO/16 PRO/12 FAT). 3 hours after the breakfast, an ad libitum buffet lunch was served, and food records were taken for the next 24 hours. Subjects consuming the egg breakfast consumed a little over 100 kcal less than when they consumed the bagel breakfast, and about 400 kcal less over the next 24 hours. This is consistent with the a previously discussed study (9) which reported ~420 kcal less the next day using similar breakfast meals. The egg breakfast had a lower AUC for glucose, insulin, and ghrelin compared to the bagel breakfast. Importantly, glucose was back to baseline in the egg breakfast group and insulin elevated, while glucose was still below baseline for the bagel group and insulin lower, suggesting that the elevated insulin perhaps reduced subsequent energy intake. There were no significant differences between plasma leptin, GLP-1, or PYY between time points or breakfasts. Hunger was measured with a VAS (visual analog scales), which found a reduced AUC for hunger and an increased AUC for satisfaction with the egg breakfast, and less hunger and more satisfaction after 3 hours compared to the bagel breakfast. Subjective measures and blood markers are difficult to interpret at this stage, as these results seem to conflict even with a recent study that I reported on, regarding eating speed and appetite. As protein and fat seem to impact ghrelin, but not glucose or insulin, the higher intake of these in the egg breakfast may be responsible for the reduction in energy intake, along with a potential independent effect from elevated insulin. These will need further study to be sure.
These are promising findings and may be relevant for nutrition professionals to include in dietary recommendations for weight control.
Raw Egg: A Rocky Idea
Downing raw eggs was made famous perhaps largely in part to the Rocky series, but may go back even to the late 1800′s. A hardcore boxer with an inspirational dedication to his training and nutrition is no doubt to be emulated by aspiring athletes. But Rocky didn’t know what we know today, and it certainly isn’t ideal.
Many people may have the perception that raw foods are healthier and better digested than cooked. But in many cases, including eggs, this just isn’t true. Evenepoel et al. (12) tested the assimilation of egg protein in 5 ileostomy patients using a novel (and more accurate than previous) method of nitrogen and carbon labeling. They found that for a 25 gram load of egg protein, ileal digestibility was approximately 91% for microwave cooked egg, and only 51% for raw egg. This is about half of the protein going to waste compared to over 90% being utilized after heat treatment. Not only that, but malabsorbed proteins in the colon are theorized to influence the development of certain diseases such as colon cancer or ulcerative colitis.
The phenomenon of “egg white injury”, characterized by certain symptoms and metabolic derangements when animal or human subjects are fed unheated egg protein was explained 70 years ago (and documented well before that); a glyco-protein called avidin (and likely others) irreversibly binds biotin, creating a deficiency. Cooking denatures the avidin. So not only do raw eggs lack the biotin that cooked eggs do, the avidin can bind biotin in the GI tract as well (it is produced by bacteria in the intestine, providing a significant source, or from food), inducing a deficiency at a high enough intake. I won’t detail the potential consequences of biotin deficiency, which have been thoroughly studied, but even if symptoms are not obvious, a subclinical deficiency may still exist and result in problems later in life. Though human studies are difficult to interpret at this point with different designs and such, raw egg white consumption clearly can cause biotin deficiency with as little as 2 eggs per day for an extended period of time. See Table 3 in this paper (also recent case study).
Salmonella enteritidis can cause intestinal illness and is present in some eggs. Very detailed reports have been produced on this, but the contamination may be as low as 1 in every 30,000 eggs. You can risk by following CDC guidelines as listed here. Cooking the egg will reduce the risk of infection even more. Given the protein and biotin issues, it doesn’t make sense to not cook them.
It seems a waste to throw out egg shells if you know how nutrient rich they are. Indeed, our stone-age ancestors may have consumed the shells as a source of calcium, though this may seem carnal in modern times.
Interestingly, there are studies on egg shells for osteoporotic subjects; I won’t go into detail at this point as I don’t think people without clinical supervision should try this yet, so experiment at your own risk.
Because they are rich in calcium, and contain minerals and potential bioactive substances that are involved in bone metabolism, they may be superior to other preparations. For a review of in vitro, animal, and clinical experiments, see (17).
If nothing else, it is a decent and inexpensive antacid if you have nothing else on hand.
Eggs are one of the best sources of dietary choline (13) at approximately 251 mg/100 g. Choline is needed for phospholipid synthesis, methyl donation, cholinergic neurotransmission, as a precursor to betaine, and more. Interventional studies in animals and humans have showed that a deficiency results in poor development in various tissues, and damage (especially the liver). The AI for choline is 550 mg/day for men, and 425 mg/day, though based on still limited data, seems to be around the average intakes (14). Though a deficiency of choline is certainly harmful, more research is needed to elucidate an optimal intake. Chronic subclinical deficiency is likely a contributer to disease pathologies, given the importance of membrane phospholipid metabolism in many functions, and will likely be officially classified as an essential nutrient eventually; the consumption of whole foods, including eggs, may contribute to an more ideal intake than most Americans consume, but more research is necessary before we can make appropriate evidence-based conclusions.
Athletes require a greater intake of protein than non-athletes, and eggs are a decent source of it. Eggs also a high content of branched chain amino acids (BCAA), and specifically 1 of those, leucine, is important for protein synthesis. Egg protein is sometimes used in studies post workout, and is a popular choice in the bodybuilding culture.
All of these studies achieved dietary intakes of cholesterol averaging above 800 mg per day. This is substantially higher than than recommendations to limit intake below 300 mg. Although this recommendation may curb the intake of other less healthy choices, it also does this for eggs, for which the evidence suggests is not necessary.
Considering that multiple lines of evidence, from a rich cultural history to long term observational studies to short term interventional studies on cardiovascular biomarkers suggest that eggs are healthy. Based on all of the data, I have no problem suggesting that up to 3 or 4 eggs per day is perfectly fine, and perhaps in many people even more. Though some short term research suggests that eggs may be beneficial in people with metabolic problems, observational data suggest that diabetics may benefit from a lower cholesterol intake, as they have an altered cholesterol metabolism. Thus, this is the only caveat I see at the moment.
Short term controlled studies have found that indeed consuming cholesterol increases serum cholesterol, but it is highly individual on to what extent, if any. And this itself should not be a reason to avoid eggs. When other markers of cardiovascular health are examined, they suggest that eggs may are either benign or beneficial. Triglycerides do not change, and LDL:HDL ratio does not change significantly, as both increase. Examining subfractions of these finds that eggs actually promote a less atherogenic LDL profile.
The research on satiation and subsequent calorie intake is extremely fascinating. There are not many interventions as simple as replacing dull, high carbohydrate foods with eggs for breakfast that may make significant long term differences in weight.
One last thing to emphasize is that the yolk must also be consumed for benefits, as the majority of the nutrients are contained there.
1. Herron KL, Lofgren IE, Sharman M, Volek JS, & Fernandez ML (2004). High intake of cholesterol results in less atherogenic low-density lipoprotein particles in men and women independent of response classification. Metabolism: clinical and experimental, 53 (6), 823-30 PMID: 15164336
2. Greene CM, Zern TL, Wood RJ, Shrestha S, Aggarwal D, Sharman MJ, Volek JS, & Fernandez ML (2005). Maintenance of the LDL cholesterol:HDL cholesterol ratio in an elderly population given a dietary cholesterol challenge. The Journal of nutrition, 135 (12), 2793-8 PMID: 16317122
3. Clark RM, Herron KL, Waters D, & Fernandez ML (2006). Hypo- and hyperresponse to egg cholesterol predicts plasma lutein and beta-carotene concentrations in men and women. The Journal of nutrition, 136 (3), 601-7 PMID: 16484531
4. Waters D, Clark RM, Greene CM, Contois JH, & Fernandez ML (2007). Change in plasma lutein after egg consumption is positively associated with plasma cholesterol and lipoprotein size but negatively correlated with body size in postmenopausal women. The Journal of nutrition, 137 (4), 959-63 PMID: 17374661
5. Mutungi G, Torres-Gonzalez M, McGrane MM, Volek JS, & Fernandez ML (2007). Carbohydrate restriction and dietary cholesterol modulate the expression of HMG-CoA reductase and the LDL receptor in mononuclear cells from adult men. Lipids in health and disease, 6 PMID: 18045475
6. Mutungi G, Ratliff J, Puglisi M, Torres-Gonzalez M, Vaishnav U, Leite JO, Quann E, Volek JS, & Fernandez ML (2008). Dietary cholesterol from eggs increases plasma HDL cholesterol in overweight men consuming a carbohydrate-restricted diet. The Journal of nutrition, 138 (2), 272-6 PMID: 18203890
7. Mutungi G, Waters D, Ratliff J, Puglisi M, Clark RM, Volek JS, & Fernandez ML (2010). Eggs distinctly modulate plasma carotenoid and lipoprotein subclasses in adult men following a carbohydrate-restricted diet. The Journal of nutritional biochemistry, 21 (4), 261-7 PMID: 19369056
8. Vorster HH, Beynen AC, Berger GM, & Venter CS (1995). Dietary cholesterol–the role of eggs in the prudent diet. South African medical journal = Suid-Afrikaanse tydskrif vir geneeskunde, 85 (4), 253-6 PMID: 7777999
9. Vander Wal JS, Marth JM, Khosla P, Jen KL, & Dhurandhar NV (2005). Short-term effect of eggs on satiety in overweight and obese subjects. Journal of the American College of Nutrition, 24 (6), 510-5 PMID: 16373948
10. Vander Wal JS, Gupta A, Khosla P, & Dhurandhar NV (2008). Egg breakfast enhances weight loss. International journal of obesity (2005), 32 (10), 1545-51 PMID: 18679412
11. Ratliff J, Leite JO, de Ogburn R, Puglisi MJ, VanHeest J, & Fernandez ML (2010). Consuming eggs for breakfast influences plasma glucose and ghrelin, while reducing energy intake during the next 24 hours in adult men. Nutrition research (New York, N.Y.), 30 (2), 96-103 PMID: 20226994
12. Evenepoel P, Geypens B, Luypaerts A, Hiele M, Ghoos Y, & Rutgeerts P (1998). Digestibility of cooked and raw egg protein in humans as assessed by stable isotope techniques. The Journal of nutrition, 128 (10), 1716-22 PMID: 9772141
13. Zeisel SH, Mar MH, Howe JC, & Holden JM (2003). Concentrations of choline-containing compounds and betaine in common foods. The Journal of nutrition, 133 (5), 1302-7 PMID: 12730414
14. Fischer LM, Scearce JA, Mar MH, Patel JR, Blanchard RT, Macintosh BA, Busby MG, & Zeisel SH (2005). Ad libitum choline intake in healthy individuals meets or exceeds the proposed adequate intake level. The Journal of nutrition, 135 (4), 826-9 PMID: 15795442
15. McIntosh WA (2000). The symbolization of eggs in American culture: a sociologic analysis. Journal of the American College of Nutrition, 19 (5 Suppl) PMID: 11023004
16. César TB, Oliveira MR, Mesquita CH, & Maranhão RC (2006). High cholesterol intake modifies chylomicron metabolism in normolipidemic young men. The Journal of nutrition, 136 (4), 971-6 PMID: 16549459
17. Rovenský J, Stancíková M, Masaryk P, Svík K, & Istok R (2003). Eggshell calcium in the prevention and treatment of osteoporosis. International journal of clinical pharmacology research, 23 (2-3), 83-92 PMID: 15018022
18. Herron KL, & Fernandez ML (2004). Are the current dietary guidelines regarding egg consumption appropriate? The Journal of nutrition, 134 (1), 187-90 PMID: 14704316
19. Applegate E (2000). Introduction: nutritional and functional roles of eggs in the diet. Journal of the American College of Nutrition, 19 (5 Suppl) PMID: 11022998
20. McNamara DJ (2000). The impact of egg limitations on coronary heart disease risk: do the numbers add up? Journal of the American College of Nutrition, 19 (5 Suppl) PMID: 11023005