Wednesday, May 29, 2013

"Eggs" - 4-Letter Food Improves Both Cholesterol Particle & Phospholipid Profile + HDL-Driven Lipid Reverse-Transport

In addition to the previously reported improvements in cholesterol particle profile, the regular consumption of whole eggs increases HDL's ability to carry lipids out of the macrophages. If these accumulate, they will turn the macrophage into pro-atherogenic foam cells (cf. Eckardstein. 2001).
You will probably remember the long-boycotted(*) 2012 study by Blesso et al. which showed quite conclusively that daily whole egg consumption has a  beneficial impact on the HDL-C levels and the particle size profile of overweight and obese patients following a diet with a moderate amount of carbohydrates (read all about the study in the SuppVersity article from October 2012)

(*) I obviously have no evidence that the publication of the Blesso study was mischievously delayed, but it is unquestionably conspicuous that a paper with 100% convincing data that the witch hunt on eggs of the medical establishment is totally unwarranted was postponed from September 2012 (date of the online publication) to March 2013, isn't it?

Be that as it may, let's now after devoting our precious time to the always popular conspiracy theories, take a look at the actual news - news, which come right from the labs of the same laboratory, but this time with a slight twist:
"We recently demonstrated that daily whole egg consumption during moderate carbohydrate restriction leads to greater increases in plasma HDL-cholesterol (HDL-C) and improvements in HDL profiles in metabolic syndrome (MetS) when compared to intake of a yolk-free egg substitute. We further investigated the effects of this intervention on HDL composition and function, hypothesizing that the phospholipid species present in egg yolk modulate HDL lipid composition to increase the cholesterol-accepting capacity of subject serum." (Anderson. 2013)
As you gather from the above citation the dataset, or I should say the blood samples the scientists from the University of Connecticut analyzed to gather their data, were the same as in the previous study accordingly, there is little I could tell you about the 37 subjects (25 women; 12 men) classified with MetS who were recruited to participate in the previously described 12-week parallel, randomized, single-blind diet intervention.
Figure 1: Phospholipid composition of whole egg and egg substitute products; data displayed in mg/serving x 10,  y-axis logarithmically scaled (Anderson. 2013)
"During the 12-week study, subjects were instructed to follow an ad libitum moderate carbohydrate-restricted diet (25–30%) of energy from carbohydrates) in addition to consuming either three whole eggs (EGG group) or the equivalent amount of egg yolk-free egg substitute (SUB group) each day. The egg substitute product consisted of egg whites (99 %), 1 % xanthan and guar gums, beta-carotene for color, and provided 0 mg of cholesterol, whereas the daily serving of whole egg contained 534 mg of cholesterol." (Andersen. 2013)
In the course of the intervention the HDL-cholesteryl ester content in the blood of all subjects increased (relative to other forms of HDL). This increase was, as the data in figure 2 goes to show you, more pronounced in the SUB [=no egg yolks] group. The HDL triacylglycerol content, on the other hand, was reduced in the subjects receiving the whole eggs, only (EGG group). Consequently, the egg intervention resulted in an increases in HDL-CE/TAG ratios in both groups. More importantly, though, ...
Figure 2: Effects of egg feeding on HDL-phospholipid class distribution during moderate carbohydrate restriction  (Andersen. 2013)
"[...p]hospholipid analysis [ (PtdCho phosphatidyl-choline, PtdEtn phosphatidyl-ethanolamine, CerPCho sphingomyelin, LysoPtdCho lysophosphatidyl-choline, PtdIns phosphatidyl-inositol; cf. figure 2] by mass spectrometry revealed that HDL became enriched in phosphatidylethanolamine in the EGG group, and that EGG group HDL better reflected sphingomyelin species present in the whole egg product at week 12 compared to baseline." (Andersen. 2013)
In addition, and in line with previous results suggesting that greater enrichment of HDL in phospholipids—such as PtdCho and CerPCho—are associated with a greater lipid-accepting capacity
of HDL and/or human serum (Fournier. 1996 & 1997), the macrophage cholesterol efflux of the subject in the EGG group increased from baseline to week 12 (+2.4% from baseline). This physiologically highly relevant effect which correspond to the previously reported improvements in HDL particle profiles (see post from October, 2012) is the actual news this re-analysis of the blood samples has to offer, as it goes to show us that the beneficial effects of daily consumption of the "4-letter" food "eggs" does not only promotes favorable shifts in the particle size distribution of the lipoproteins in a patient group with a high baseline risk for cardiovascular diseases. No, the "bad" eggs also improve the HDL lipid composition (lowering the triglyceride content) and the function of the HDL molecules.

Bottom line: If you have been following the SuppVersity Facebook News over the past couple of weeks, you will now probably be thinking: "Wait a minute.. wasn't there..."? And yes, there was. Scientists from the IMIM-Research Institut Hospital del Mar in Barcelona, Spain (Farràs. 2013), have observed very similar effect in a rodent study in response to the consumption of the phenols from a highly praised "8-letter food": Olive Oil!
  "If we have not somehow pimped it, it can never be good enough!" appears to be one of the credos with which mankind approaches almost every natural health-remedy. In the past this approach was not particularly healthy, though... is phenol-enriched olive oil going to be the exception to the rule? (learn more)
I know that parts of the medical establishment are not going to like it, but a  short and concise bottom line of the study at hand could thus well be:  

Eggs and olive oil belong to the same category of health foods whose beneficial effects on lipid metabolism go well beyond promoting a more favorable lipoprotein profile. They will also boost the ability of the "good" cholesterol to do it's job and clear the otherwise plaque forming cholesterol from the cells... 

whether this message will ever make it into the headlines of the "science" colums of mainstream media is unfortunately highly questionable.

  • Andersen CJ, Blesso CN, Lee J, Barona J, Shah D, Thomas MJ, Fernandez ML. Egg Consumption Modulates HDL Lipid Composition and Increases the Cholesterol-Accepting Capacity of Serum in Metabolic Syndrome. Lipids. 2013 Jun;48(6):557-67.
  • Blesso CN, Andersen CJ, Barona J, Volek JS, Fernandez ML. Whole egg consumption improves lipoprotein profiles and insulin sensitivity to a greater extent than yolk-free egg substitute in individuals with metabolic syndrome. Metabolism. 2012 Sep 26.
  • von Eckardstein A, Nofer JR, Assmann G. High density lipoproteins and arteriosclerosis. Role of cholesterol efflux and reverse cholesterol transport. Arterioscler Thromb Vasc Biol. 2001 Jan;21(1):13-27. 
  • Farràs M, Valls RM, Fernández-Castillejo S, Giralt M, Solà R, Subirana I, Motilva MJ, Konstantinidou V, Covas MI, Fitó M. Olive oil polyphenols enhance the expression of cholesterol efflux related genes in vivo in humans. A randomized controlled trial. J Nutr Biochem. 2013 Jan 17.
  • Fournier N, de la Llera Moya M, Burkey BF, Swaney JB, Paterniti J Jr, Moatti N, Atger V, Rothblat GH. Role of HDL phospholipid in efflux of cell cholesterol to whole serum: studies with human apoA-I transgenic rats. J Lipid Res. 1996 Aug;37(8):1704-11. 
  • Fournier N, Paul JL, Atger V, Cogny A, Soni T, de la Llera-Moya M, Rothblat G, Moatti N. HDL phospholipid content and composition as a major factor determining cholesterol efflux capacity from Fu5AH cells to human serum. Arterioscler Thromb Vasc Biol. 1997 Nov;17(11):2685-91.


  1. What would be very interesting is to know whether conclusions would be different for APOE 4/4 carriers...

    1. interesting question. If I had to bet, I'd say yes: In APO-E4 carriers everything appears to be reversed (e.g. fish oil wreaking havoc on the lipoprotein profile) and fat in general is pretty much a no-go

    2. How do you know if you're an APO-E4 carrier?

  2. Many foods which had been deemed "bad" for the last decades are slowly gaining scientific evidence for their role in human nutrition: do you think saturated fats from other animal products (e.g. meat, whole milk and dairy) will follow the same line?

    Thank you for everything you do for us :)

    1. I would not say that the beneficial effects of eggs are a result of their saturated fat content (at least not exclusively) and a major problem I see here is that many "high SFA foods" are actually / have actually become high N-6 foods. Take lard as an example...

      on the other hand the general condemnation of saturated fats is bullocks; so is the condemnation of omega-6s you need SOME - the problem is that we have turned the ratios around

    2. To expand on this, while condemnation of saturated fats is complete bullsh*t, there is rationale to keep the intake to a minimum if you are very lean and looking to gain weight ==>

      Basically, if you are gaining weight, you are eating in a surplus. The fat you eat will become stored, and saturated fats are the hardest for you body to mobilize when you decide to diet again. So while mostly theoretical (and probably insignificant for most people), bulking with mainly monounsaturated fats and fish oils are your best bet.

      Similarly with the high N-6, while we do need some, they are so widespread in the typical diet that most people get more than enough. Even fatty salmon and grass-fed beef has them.

      Just some random thoughts I had while reading this...

    3. Primalkid,

      How would MCT's/Coconut oil change what you have mentioned? I know that they are not stored as efficiently as other fats and I am wondering about the liberation of these in a calorie deficit?

    4. MCTs are preferentially dealt with by the liver in a manner similar to carbohydrates simply because they are small enough to be absorbed directly into the bloodstream. If you overeat MCTs, then not only will you have massive diarrhea but I would bet that your body would find some way of storing them in fat tissue as well. MCTs are the exception, not the rule and most of this is irrelevant because nobody could consume significant amounts of MCTs.

      With regard to coconut oil, I make the discrepancy because people commonly assume it is on par with MCTs. This is not the case as only 2/3 of coconut oil is MCTs and the remainder is Myristic and Palmitic acid, both of which are readily stored in adipose tissue.

    5. on a side note:MCTs may not be stored as fat, but if they are used the rest of what you eat will be stored - makes no sense (if you asked me) to waste your money on them (you can't live of MCTs only)

    6. Completely understood. I was just trying to wrap my head around the process. I definitely don't rely on one source of fat for all of my intake. I try and vary it through several sources (GF beef, fish, avocados, coconut, etc...)

      If I read you correctly comparing 2 eucaloric diets with one having a greater percentage of MCT's, would it not theoretically decrease calorie intake over the other diet including more of a different fat?

    7. No, a eucaloric diet provides exactly the number of calories your body needs. Because MCTs only provide about 8.5 kcal/g, you would actually have more fat in the diet containing MCTs compared to the other.

    8. good point, Alex (Primalkid). Also, I wrote about the fallacy of MCTs (their touted benefits disappear over time) before =>

  3. Adel, I am a little confused with the HDL composition.

    "No, the "bad" eggs also improve the HDL lipid composition (lowering the triglyceride content) and the function of the HDL molecules."

    So HDL with higher protein, lower triglyceride composition is a good thing?

    From what I understand the "density" is the ratio of protein to triglyceride. So HDL is by definition of a higher density than other lipoproteins, but ideally we want its density even higher?

    But is not the improved function the lipid accepting, and thus the density is reduced the more it carries?

    1. hold on HDL with protein content? HDL with phospholipids vs. trigs is what the scientists are looking at here. And density increases the more it carries not reduced (that's by the way simple physics not even biology ;-)

    2. Sorry not understanding to well.

      The density of what increases? The amount of triglyceride the HDL carries? Is this a good thing or bad thing?

      "The density of lipoproteins increases in proportion to their ratio of proteins to lipids."

    3. Toma,

      I don't know how to answer the specificity of your question, but all you need to keep in mind is that you want a ratio with higher HDL than LDL, because you are then getting rid of more cholesterol than you take in...correct me if I'm wrong guys?

    4. Nick you are right, but scientists are finally realizing what they knew all along: HDL is a carrier - so the health effects will depend not just on its presence, but also on what it carries and @Toma, I did answer your question in the article

      "In addition, and in line with previous results suggesting that greater enrichment of HDL in phospholipids—such as PtdCho and CerPCho—are associated with a greater lipid-accepting capacity of HDL and/or human serum (Fournier. 1996 & 1997),"

      so if you are not guilty of headline only "reading", you must have overread it ;-)

    5. To be honest I am not entirely sure what I am asking!

      OK but this "getting rid of more cholesterol than you take in" is not really correct since we eat around 300 - 500 mg, but our body produces 800 - 1200 mg. From what I understand the more HDL you have the better your reverse cholesterol transport is: "a multi-step process resulting in the net movement of cholesterol from peripheral tissues back to the liver via the plasma", so I suppose you are wanting greater cholesterol carrying capacity of HDL but apparently even drugs that increase HDL cholesterol density do nothing if LDL numbers are low.

    6. right, if you don't have HDL improving it''s efficacy is worthless. Ah,... but is there a question involved?

  4. Olive oil is the richest dietary source of squalene, squalene is a cholesterol precursor... is olive oil the vegetarian's egg?

    1. Hardly, olive oil doesn't contain the choline, vitamin A, the B's, K2 and great quality protein that eggs do.
      Not that olive oil is a bad source of fats and vitamin E, it is just that eggs are a nutritional powerhouse.

    2. witchcraft! "vegetarian eggs" ;-)

    3. Screw olive oil, go with avocados ;)