Introduction
When I first decided to write about the humble egg, I thought it would be simple. It turns out there is nothing humble about it. Eggs sit at the centre of debates about nutrition, cholesterol, farming, food labels, public health advice, and online misinformation. There are far too many angles to cover in one article, but I will try to tackle the most common misconceptions. And if you still have questions after reading, please get in touch, I am always happy to dig further into the literature, which is vast!
What pushed me to write this was the confusion I kept seeing online. During my research, I came across two recent videos making almost opposite claims: Eggs Every Day? What Doctors Think from 2025, which was more cautious about egg consumption, and 4 Huge Egg Myths That Refuse to Die from 2023, which took a much more positive view. One framed egg as something to be careful with and the other argued that many fears about eggs are outdated. No wonder people are confused!
So, who is right? As usual in nutrition, the answer is not black and white. To understand where the truth lies, we need to look past the headlines and into the studies behind them.
Egg Anatomy
First things first: what is an egg? Biologically, it begins as the hen’s oocyte, or ovum, the female reproductive cell. In birds, oocytes grow inside the ovary and fill with yolk, a nutrient-rich reserve made from the hen’s diet. Nutrients absorbed from food are processed mainly by the liver, transported through the bloodstream, and deposited into the developing oocyte (Adegbenjo, et al., 2020).
Once mature, the yolk-filled oocyte is released from the ovary into the oviduct, the long tubular structure where the rest of the egg is assembled. In hens, only the left ovary and left oviduct are functional, the right-side regresses early in development. As the oocyte travels down the oviduct, each region adds a different layer, gradually turning it into the egg we recognise (Figure 1. left panel) (Sah and Mishra, 2018; Kaspers, 2016).
The first region is the infundibulum, which catches the ovulated oocyte and is also the site where fertilisation can occur if sperm are present. The egg remains here only briefly, around 15–20 minutes. It then moves into the magnum, where most of the albumen, or egg white, is secreted over the next 2-3 hours. After that, it enters the isthmus (1h), where the inner and outer shell membranes are formed. The egg then spends the longest time in the uterus, also called the shell gland , where the hard calcium carbonate shell is deposited over about 20-21 hours. Shell pigmentation also occurs here, and the outer cuticle, a protective antimicrobial coating, is added near the end of shell formation (Figure 1, right panel) (Wilson, et al., 2017). Finally, the completed egg passes through the vagina which helps turn it so that the blunt end is laid first and push the egg out of the oviduct during oviposition, or egg laying (Sah and Mishra, 2018).
Figure 1: Egg formation in the hen and protective structure of the eggshell.
(Left panel) Hen’s reproductive tract. The developing oocyte is released from the ovary and passes through the oviduct. Each region adds a different part of the egg: the infundibulum captures the ovulated yolk, the magnum secretes most of the albumen, the isthmus forms the shell membranes, and the uterus or shell gland deposits the calcium carbonate shell and pigments before the egg passes through the vagina, cloaca, and vent. (Right panel) Close-up of the eggshell barrier. The shell is porous, allowing gas exchange, but is covered by a thin outer cuticle that helps seal shell pores and reduce bacterial entry, with shell membranes providing an additional internal protective layer (adapted from Adegbenjo et al., 2020).
Nutrients
Eggs are inexpensive, widely available, and nutrient dense. Their exact nutrient composition is not fixed: it can vary with the hen’s breed or strain, age, diet, environment, and even the relative amount of yolk and white in the egg. This is why different food-composition databases and review papers sometimes report slightly different values. As a rough guide, a medium egg weighs about 55 g in total, including the shell, and contains roughly 50 g of edible egg (Figure 2A). This edible portion provides around 65–80 kcal, about 6 g of protein, less than 1 g of carbohydrate, and roughly 4–5 g of fat, including less than 2 g of saturated fat. It also contains about 180–190 mg of cholesterol, almost all of it in the yolk (Kuang et al., 2018; Caffa et al., 2025).
The nutrients are not evenly distributed between the white and the yolk. The egg white is mostly water and protein, with very little fat (Figure 2B). Its main proteins include ovalbumin, ovomucoid, ovotransferrin, lysozyme, and ovomucin, some of which have been studied for antioxidant, antimicrobial, anti-inflammatory, antihypertensive, or immune-related properties (Figure 2C). The yolk is more energy dense. It contains most of the egg’s fat, cholesterol, phospholipids, choline (Box 1), fat-soluble vitamins, carotenoids, and many minerals. Yolk lipids include triglycerides and fatty acids, phospholipids such as phosphatidylcholine, and cholesterol (Figure 2D,E). Eggs also provide several minerals, including calcium, phosphorus, potassium, iron, zinc, selenium, magnesium, copper, and iodine, as well as many vitamins, including B vitamins, vitamin A, vitamin D, and vitamin E. One notable exception is vitamin C, which eggs do not provide in meaningful amounts. (Kuang et al., 2018; Caffa et al., 2025).
Box 1: Choline
Choline is an essential nutrient, officially recognised in 1998, that plays important roles in cell membranes, liver function, nerve signalling, and brain development. Although the body can make small amounts, this is not enough to meet human needs, so choline must also come from the diet. Egg yolks are one of the richest dietary sources, providing about 680 mg of choline per 100 g. Since many people do not reach optimal choline intakes, eggs can be a useful source of this nutrient as part of a balanced diet (Zeisel and da Costa, 2009).
Figure 2. Composition and structure of a hen’s egg.
(A) Basic egg anatomy, showing the shell, albumen or egg white, yolk, and chalazae (yolk anchors), with typical weights for a medium egg: approximately 5 g shell, 35 g white, and 15 g yolk. (B) Macronutrient composition of egg white and yolk, highlighting that egg white is mostly water and protein, while yolk contains more lipids, protein, and nutrient-rich fractions. (C) Major egg-white proteins, including ovalbumin, ovomucoid, ovotransferrin, lysozyme, and ovomucin, alongside the main yolk protein and lipoprotein groups: LDL and HDL lipoproteins, phosvitin, and livetins. (D) Lipid composition of the yolk, dominated by triglycerides and fatty acids, followed by phospholipids and cholesterol. (E) Fatty-acid profile of whole egg lipids, showing the relative proportions of saturated, monounsaturated, and polyunsaturated fatty acids (adapted from Caffa et al., 2025).
The bottom line is that an egg is not just a simple food item. It is the result of an extraordinary reproductive process. The hen’s body gathers, processes, and packages proteins, fats, vitamins, minerals, protective membranes, and a hard shell into one compact structure, essentially providing everything a developing chick would need, straight from her own body.
Is the egg really the ‘’bad egg’’?
For decades, eggs were treated with suspicion in dietary advice because they are naturally rich in cholesterol (186mg/egg). The assumption was simple: if a food contains cholesterol, eating it must raise cholesterol in the blood, and higher the blood cholesterol the higher the chances to develop cardiovascular disease.
But cholesterol itself is not just a harmful substance. It is an essential molecule (Box 2). In other words, cholesterol is not optional; life depends on it. The problem is not cholesterol itself, but cholesterol imbalance and excessive cholesterol can lead to a variety of severe diseases, including atherosclerosis, gallstones, metabolic dysfunction–associated steatotic liver disease (MASLD), cardiovascular disease, type 2 diabetes, cancer, and Alzheimer disease (Zhang et al., 2024).
Box 2: What is Cholesterol?
The word cholesterol comes from the greek chole, meaning bile, and stereos, meaning solid; the compound was named “cholesterine” by Michel Eugène Chevreul in 1815 after being identified in gallstones. The suffix “-ol” was later added because cholesterol is chemically an alcohol (Zhang et al., 2024).
Structurally, cholesterol has both a water-attracting hydroxyl head and a water-repelling sterol body. This unusual structure allows it to sit within cell membranes, where it helps regulate membrane stability and fluidity. Cholesterol is also the starting material for several important molecules, including bile acids, steroid hormones, and vitamin D. It is especially important in the nervous system, where it contributes to myelin formation and synapse function (Zhang et al., 2024).
Figure 3. Cholesterol functions, homeostasis, and the mechanism of statins.
(1) Cholesterol’s essential biological roles. Cholesterol is contributing to cell membrane structure and its use as a precursor for steroid hormones, bile acids, and vitamin D. (2) Cholesterol homeostasis. The body maintains a cholesterol pool by balancing inputs — dietary cholesterol absorbed from food (about 300–500 mg/day) and endogenous or de novo cholesterol synthesis, mainly in the liver (about 600–900 mg/day) — with outputs, including secretion into bile as biliary cholesterol and bile acids and eventual fecal excretion through the intestine (adapted from Zhang et al., 2024). (3) Statins mechanism of action. Statins inhibit HMG-CoA reductase, the rate-limiting enzyme in hepatic cholesterol synthesis, so they reduce cholesterol production in the liver, increase LDL receptor expression on liver cells, enhance removal of LDL particles from the blood, and lower circulating LDL-C.
Between the egg on the plate and cholesterol in the bloodstream sits a major regulatory organ: the liver (Figure 4)!
The liver acts as the central control hub. It can synthesise cholesterol (50% of the endogenous cholesterol biosynthesis takes place in the liver), use cholesterol, store it, convert some into bile acids, release some into bile, or package it into lipoproteins such as VLDL, which can eventually become LDL (Box 3).
Some cholesterol and bile acids return to the intestine through bile; some are reabsorbed, while some leave the body in faeces. This gut–liver recycling system is one reason blood cholesterol does not rise in a simple one-to-one relationship with cholesterol eaten from food.
This is where the egg story becomes more complicated. A medium egg contains around 186 mg of cholesterol, but that does not mean 186 mg of cholesterol simply enters the blood and stays there. When dietary cholesterol intake increases, the body can compensate by absorbing a smaller proportion from the intestine, making less cholesterol internally, or excreting more through bile and faeces. However, this compensation is not perfect and varies between individuals. Some people show little change in blood cholesterol (hypo-responders) after dietary cholesterol, while others show a larger response (hyper-responders) (Herron et. al., 2003). Genetic factors are heavily involved in regulating cholesterol metabolism, explaining the variability of individual responses to dietary cholesterol. For instance, individuals carrying the apoE4 allele are more sensitive to dietary cholesterol, and even a moderate increase in dietary cholesterol resulted in a 10% elevation in serum total cholesterol (Sarkkinen et al., 1998).
Figure 4: Cholesterol transport and the early development of atherosclerosis.
(1) Dietary fat and cholesterol from the gut into the bloodstream. After absorption in the small intestine, cholesterol cannot simply dissolve into blood on its own. First, cholesterol from food mixes with bile acids to form micelles, which help move cholesterol to the surface of intestinal cells. Cholesterol then enters these cells and is packaged into large fat-carrying particles called chylomicrons. These chylomicrons enter the lymphatic system first, then the bloodstream, where they deliver triglycerides to tissues. The remaining cholesterol-rich chylomicron remnants are then taken up by the liver. The liver regulates cholesterol balance by producing VLDL, which can become LDL and deliver cholesterol to tissues, by receiving cholesterol back through HDL, and by converting some cholesterol into bile acids for excretion through the intestine. (2) Beginning of atherosclerosis. Atherosclerosis can begin when excess LDL particles enter the artery wall, become oxidised, and are taken up by macrophages. These macrophages turn into foam cells, forming fatty streaks that can develop into early atherosclerotic plaque.
Box 3: LDL-C vs ApoB — why particle number matters
Cholesterol cannot travel freely in blood, so the body carries it inside particles called lipoproteins. Some of these particles can contribute to atherosclerosis because they are small enough to enter the artery wall and deposit cholesterol. These include VLDL, IDL, LDL, lipoprotein(a), and chylomicron remnants.
ApoB or apolipoprotein B, is a structural protein found on these atherogenic lipoproteins (Figure 5, Left panel). Each particle carries one ApoB molecule, so measuring ApoB gives an estimate of the total number of potentially harmful particles circulating in the blood. HDL particles do not contain ApoB.
In a routine cholesterol blood test, the “LDL” result usually means LDL-C. LDL-C measures the total amount of cholesterol carried inside LDL particles. It is useful, but it does not tell us how many LDL particles are present, and it does not fully capture risk from other atherogenic particles such as VLDL, IDL, lipoprotein(a), or remnants.
This distinction matters because two people can have the same LDL-C but very different ApoB levels. One may have fewer cholesterol-rich particles, while another may have many cholesterol-poor particles. The second person may have higher cardiovascular risk, even if their LDL-C looks normal, because more particles means more opportunities for them to enter the artery wall and contribute to plaque formation (Figure 5, Right panel) (Qiao et al., 2022; De Oliveira-Gomes et al., 2024; Liester and Moore, 2026).
Bottom line: Think of atherosclerosis as a numbers game. It is not only the amount of cholesterol that matters, but the number of ApoB-containing particles repeatedly circulating, colliding with, and entering the artery wall. That is why ApoB can sometimes tell us more about cardiovascular risk than LDL-C alone (Qiao et al., 2022; De Oliveira-Gomes et al., 2024; Liester and Moore, 2026).
Figure 5. ApoB-containing lipoproteins and why ApoB can reveal cardiovascular risk beyond LDL-C.
(Left panel) The structure of an ApoB-containing lipoprotein particle. ApoB-100 wraps around the particle surface, while the outer layer contains phospholipids and free cholesterol, and the core contains triglycerides and cholesteryl esters. (Right panel) Why LDL-C and ApoB can give different information. Two people may have the same LDL-C level, meaning the same total amount of cholesterol carried in LDL particles, but very different ApoB levels. A higher ApoB level reflects a greater number of atherogenic particles, creating more opportunities for particles to enter the artery wall and contribute to plaque formation. Thus, LDL-C reflects cholesterol mass, whereas ApoB better estimates atherogenic particle number.
History of Dietary advice
In 1968, the American Heart Association (AHA) advised people to limit themselves to dietary cholesterol to less than 300 mg/day and restricting egg intake to no more than three egg yolks per week. Later reviews have argued that this recommendation was based on an incomplete understanding of cholesterol metabolism and became much less defensible as better evidence accumulated. The scientific basis for the exact 300 mg/day threshold has never been entirely clear. McNamara notes that the number appears to have been chosen less as a biologically defined safety limit and more as a practical target, it is approximately half of the estimated cholesterol intake of the population at that time (McNamara, 2015).
Later AHA guidelines kept the <300 mg/day cholesterol target but eventually removed the specific egg-yolk restriction. It was recognised that the saturated fat can increase the cholesterol levels more than the dietary cholesterol.
The problematic thing is that most foods that have high cholesterol they also have high saturated fat (e.g. fatty meats, full-fat dairy products, processed meats etc.). The egg yolk and shellfish are important exceptions as they are high in cholesterol and low in saturated fat, so their effects on LDL cholesterol may be smaller than foods high in both (Krauss et al., 2000).
In 2015, Dietary Guidelines Advisory Committee (DGAC) made the most famous change and in its report mentions: ‘’Previously, the Dietary Guidelines for Americans recommended that cholesterol intake be limited to no more than 300 mg/day. The 2015 DGAC will not bring forward this recommendation because available evidence shows no appreciable relationship between consumption of dietary cholesterol and serum cholesterol’’ (US Department of Agriculture, Scientific Report, 2015).
And just like that, a 47-year-old recommendation was finally dropped (valid from 1968). McNamara presents this as the “rehabilitation” of the egg (McNamara, 2015).
Finally, in the updated Scientific Report of the 2020 Dietary Guidelines Advisory Committee mentions that “it seems prudent to recommend lower intake of foods high in dietary cholesterol” (US Department of Agriculture, Scientific Report, 2020).
Bottom line: For decades eggs were once restricted because of their cholesterol content (one yolk could nearly reach the old 300 mg/day cholesterol limit), but later evidence showed that dietary cholesterol is not the only issue, and saturated fat often has a stronger effect on LDL-C. Today, the message is more balanced: eggs can fit into a healthy diet, especially because they are low in saturated fat, but cholesterol-rich foods should still be considered in the context of the whole diet.
What do the large population studies say?
Population studies on eggs and cardiovascular disease have not all reached the same conclusion. Some Western cohorts have found that higher egg or dietary cholesterol intake is associated with higher cardiovascular risk, while several non-Western studies suggest neutral or even lower risk with moderate intake. This is why eggs are difficult to label simply as “good” or “bad”: their effect may depend on the population, the background diet, cooking methods, metabolic health, and what foods eggs are eaten with.
One of the first major long-term population studies was published by Hu et al. in 1999, using data from more than 117,000 men and women. That study found that eating up to one egg per day was not associated with a substantial overall increase in coronary heart disease or stroke among generally healthy men and women, although the findings were less reassuring in people with diabetes. Later epidemiological studies and meta-analyses reported similar neutral findings, helping weaken the old idea that eggs are automatically dangerous for the heart (Hu et al., 1999; McNamara, 2015).
A very different picture came from Qin et al. 2018, using the China Kadoorie Biobank. In more than 460,000 Chinese adults without prior cancer, cardiovascular disease, or diabetes, daily egg consumers — about 0.76 egg per day — had lower risk of cardiovascular disease than people who rarely or never ate eggs. The strongest inverse association was seen for haemorrhagic stroke. However, egg intake was self-reported, cooking methods were not captured, and the findings may not transfer directly to populations with different diets and disease patterns (Qin et al., 2018).
By contrast, Zhong et al pooled data from six US cohorts and found that higher dietary cholesterol and egg intake were associated with higher cardiovascular disease and mortality risk. However, the egg association weakened after adjustment for dietary cholesterol, suggesting that the cholesterol content of eggs may explain much of the association rather than eggs acting independently as a whole food (Zhong et al., 2019). Kalogeropoulos and Papanastasiou praised the study’s design but emphasised that it remained observational, diet was measured only once and dietary patterns are difficult to separate from one food alone (Kalogeropoulos and Papanastasiou, 2019)
Similarly, Zhao et al found that higher egg intake was associated with higher all-cause and cardiovascular mortality in the ATBC cohort of Finnish male smokers. Their updated meta-analysis also found a small positive association between egg intake and cardiovascular disease overall, but the results differed by region: stronger in US cohorts, borderline in Europe, and not significant in Asia (Zhao et al., 2022). Song et al. later argued that these findings should be interpreted cautiously because the ATBC cohort was a very specific population, egg intake was measured only once, cooking methods were not captured, and the dose-response relationship may not be straightforward (Song et al., 2022).
More recent evidence outside Europe and North America also shows why simple answers are difficult. A 2023 Iranian study reported no significant association between egg consumption and overall cardiovascular disease, although some stroke-related outcomes were noted. A 2025 umbrella review of recent meta-analyses concluded that the overall evidence remains inconsistent and too weak to justify broadly discouraging egg consumption, although some analyses still show small increases in LDL cholesterol and total cholesterol (Mohseni et al., 2023; Formisano et al., 2025).
Bottom line: Population studies do not give one simple answer on eggs. Moderate egg intake appears neutral or even favourable in some cohorts, but higher intake has been linked with greater risk in others, especially in Western populations. The safest interpretation is that eggs should not be judged alone: their effect likely depends on the whole diet, metabolic health, cooking method, and what they replace on the plate.
Discussion - where does that leave eggs today?
After reading through decades of research, one thing becomes obvious: eggs are not a simple story. They have been praised, restricted, rehabilitated, and questioned again. Part of the confusion is that nutrition science is not static: new studies keep adding pieces to the puzzle, evidence builds slowly, and recommendations evolve as the bigger picture becomes clearer.
We also need to be honest about bias. Everyone has it, consumers, doctors, scientists and even guideline committees. If someone already believes that eggs are harmful, they can find studies that support that view. If someone believes eggs are a perfect food, they can find studies for that too. That does not mean the science is useless, it means we have to look at the whole body of evidence, not just the papers that confirm what we already think.
This is especially important in nutrition, where studies are rarely perfect. Long-term dietary trials are difficult, expensive, and often unrealistic. Many studies rely on food-frequency questionnaires, which depend on people remembering what they ate. Diet is usually measured only once or a few times, even though people’s habits change over years. Cooking methods are often not captured, and it is hard to separate one food from the wider dietary pattern. Someone eating eggs with vegetables and whole grains is not having the same meal as someone eating eggs with bacon, sausage, butter, and refined bread. Observational studies can show associations, but they cannot fully prove cause and effect.
This helps explain why population studies on eggs and cardiovascular disease have been such a mixed bag. Some Western cohorts have linked higher egg or dietary cholesterol intake with higher cardiovascular risk, while other populations have shown neutral or even favourable associations with moderate egg intake. These differences may reflect background diet, metabolic health, diabetes status, cooking methods, smoking, processed meat intake, and other lifestyle factors. In other words, eggs are difficult to judge in isolation.
The history matters too. Earlier recommendations were shaped by a much simpler view of cholesterol: dietary cholesterol was expected to raise blood cholesterol, and blood cholesterol was expected to raise cardiovascular risk. We now know the biology is more complex. The liver is a major regulator of cholesterol balance, adjusting internal cholesterol production and clearance in response to what comes in from the diet. For many healthy people, this regulation means that moderate egg intake does not dramatically disturb blood cholesterol. But this compensation is not identical in everyone. Some people are more sensitive to dietary cholesterol, and people with diabetes, dyslipidaemia, high LDL-C, or higher cardiovascular risk may need more caution.
That is why the modern message is neither “eggs are dangerous” nor “eat as many as you like.” Current advice has shifted away from treating cholesterol as one number to fear and towards looking at the whole dietary pattern. The AHA describes a heart-healthy diet as one rich in fruits, vegetables, whole grains, nuts, seeds, lean proteins, low-fat or fat-free dairy, and liquid vegetable oils. Within that kind of pattern, one egg per day can be reasonable for healthy adults, and up to two eggs per day may be acceptable for older adults with normal cholesterol. But eggs are not a nutritional loophole. The overall diet still matters, especially saturated fat intake and the foods that come with the eggs (Carson et al., 2020; AHA Here’s the latest on dietary cholesterol and how it fits in with a healthy diet).
So the most balanced conclusion is this: eggs can be part of a healthy diet, but they should not be judged alone. For most healthy people, moderate intake (around one egg per day or less) is unlikely to be a major problem when the rest of the diet is balanced. For people with diabetes, high LDL-C, dyslipidaemia, or high cardiovascular risk, a more cautious and personalised approach makes sense. As usual in nutrition, context is everything. The egg itself is only one part of the plate.
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