Where did the fat in this blood come from? ~ An Ead-iotic Analysis

NOTE  (8/7/2018):    I've edited this post, originally written/published 5/5/2011, to omit the no longer relevant back story and broken links.  I had referred to a discussion on Jimmy Moore's now-long-defunct LLVLC Discussion Board that made me aware of the Eades' post discussed.

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SUMMARY:  Fat in the blood following a fatty meal is almost entirely due to the fat in the meal.

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Several years ago, Dr. Michael Eades wrote the following post:  ABC’s big meal propaganda.  Sadly, the video is no longer available.  It involved subjects consuming a GIGANTIC meal of 6000 calories, after which blood was drawn two hours later.  This "after" blood was very cloudy, and the technician holds this up and identifies the source of the cloudiness as fat.  The meal was deep fat fried mac&cheese, a bacon cheese burger quesadilla and fries and an ice cream smothered giant cookie.  Yes, high in fat and carbs, but favoring the starches.  While they pointed finger at just the saturated fat -- it was 187g of saturated fat == it's not too much of a stretch to estimate this meal contained around 300-350g total fat or more.

/END EDITS other than formatting

Now, one of the first things Eades does is track down the foods and do his own "gotcha" nutritional analysis.  By his calcs, the calorie count is only ~5700 cals (tsk tsk around 400 some odd cal less than they stated) and the sat fat was 88g vs. 187g bringing total fat in his analysis to 258g.  But something sticks out at me about Eades analysis:

I'm not sure when the last time cheese contained no saturated fat was, and he used livestrong.com data, but something wouldn't have sounded quite right to me.  According to Cheesecake Factory it's even a bit more convoluted because they list around 1500 calories, 63g fat (again no sat fat) but only 77g carb and no protein.  Again, I'm not sure what kind of cheese this is at the CHEESEcake factory ;-)  Seems to me the carbs are rather overstated and the fat slightly understated and the sat fat not properly reported.  Eades also chides the researchers for "stretching the truth" a little on the serving size of the cookie - it's supposed to be shared by 4 people.  Well, I would note that CF lists a 1500 cal portion of the M&C as serving 2-4.   But in the end, folks, this is an example of true picking at fairly irrelevant minutia. 

It was a huge fatty, carby, calorie-laced meal.  Even most VHF low carbers wouldn't come close to 258g fat for a day let alone a meal!!  

But here's the real kicker of the blog post:

It’s pretty impressive when the lab tech holds up the tube of blood taken after the meal and compares it to the one taken before the meal. There is a lot of fat swimming in the serum, that’s for sure. What the producers of this piece (and, sadly, the doctors commenting although they should know better) want you to take away from all this by the way they set it up is that all that saturated fat went directly into the blood. And how can you argue with them? It’s there for all to see.

Problem is, that’s what blood samples look like after almost any meal, especially one that contains carbohydrates. The fat you see isn’t the fat the two reporters ate; it is the fat the liver has made from the carbohydrate. It’s the same picture a tube of blood would show after either of the two doctors had eaten a high-carb, low-fat lunch.

I find this rather startling.  Or maybe doctors don't even have a good idea of what blood samples look like and never have an opportunity to see a variety of such from various sources? I have worked with literally thousands of  blood samples in my former careers and it's really *common knowledge* that cloudy blood results from a fatty meal.   From the fat in that meal.  It's doubtful they could have consumed a low fat high carb lunch approaching 6000 cals, but if they did, no, the blood would not look the same.  I even dug up a citation though for those who might doubt this.

The timeline is not given here, but 170g fat is about 2/3rds of the fat in the ABC test meal.

Doc continues:

The blood samples were taken two hours after the meal. Dietary carbohydrate is absorbed directly into the blood and makes a pass through the liver where it stimulates the production of triglycerides, the fat you see in the blood. Fat, especially long-chain saturated fat digests very slowly, and doesn’t reach the blood until much later than the two hour mark. While carbs go directly into the blood, fats take a different route. The process that breaks down dietary fat into its component fatty acids is a lengthy process as compared to the breakdown of carbs. Once the fat has broken down, it has to combine with bile salts to make it into a form that is water soluble and can be taken up by the intestinal cells. Once taken up, unlike carbs, which are sent directly to the bloodstream, fats go into the lymphatic system, a much smaller and more static transport system than the vasculature. Once in the lymphatics, fats make their way to the thoracic duct, which empties into a large vein in the upper chest. The lymphatics are small vessels and take a long time to move their contents along since there is no heartbeat pushing them as there is with blood. As I say, the fat in the blood you see on the video didn’t come from the saturated fat in the diet, although that was definitely the implication.

And the choir in the echo chamber ate this up for the most part.  The first many many comments are all snarky against ABC and adoring of Dr. Eades for sharing the information and debunking the science.  So in the discussion at LLVLC, I posted that I wonder what Eades would have to say about the following study:

The Elevation of Ingested Lipids within Plasma Chylomicrons Is Prolonged in Men Compared with Women

This is an interesting study on its own, that I may blog on soon.  But what the study did was use radioactive labeled fat, emulsified into a heavy cream "meal"  (likely ~50g fat, it was 0.7g/kg for lean subjects, essentially zero carb), to track it's appearance and clearance from blood.  Below is the timeline for triglycerides and chylomicrons:

In the discussion:

Recovery of the ingested lipid tracer was evident in the CHYLO, VLDL, and fatty acid fractions 2 h after consumption of the meal in both men and women.

Now, the meal consumed in the ABC "study" contained about 5X the fat as this study.  By 2 hrs, as the demonstration showed quite clearly, the blood was swimming with fat.  Fat from the meal.

Far down the comments, "jon" asked Eades the following:

as I understand this meal generates fat into the bloodstream in three ways: first, by de novo lipogenesis as the liver converts CHO into triglycerides. second, fast absorption of medium chain fatty acids into the blood from the small intestine. third, slow release of long chain fatty acids that process through the lymphatic system. I am curious where these three pathways peak and how they overlap in time. so, some general questions on digestion. I understand the answers depend on many things, and will be happy to research it myself if you recommend a good source.

if 700 g of refined sugar is converted to fat, what is the time period for this? if we were to chart rate of lipogenesis over time, would it be sort of a bell curve with a long right tail? is the peak around an hour, 2 hours or what? does consuming fat, fiber, complex carbohydrates together with the refined CHO slow down this process?

how much of this 700g goes to glycogen replenishment and blood sugar, and how much goes to lipogenesis? and then, assuming 700g was all converted to fat, how much fat would it be? is it 700 g or is there some adding or subtracting? are the fatty acids long? medium? saturated?

you write that fats are released slowly into the bloodstream via the lymphatic vessels. is this all fats, or just the LCFAs? if this meal with ~250g of fat from red meat, dairy products and vegetable oil is half LCFA, what is the rate of entry of MCFA into the bloodstream and approximately where does that peak?

other than the amount of time passed since consumption, is there any easy way to tell the source of fat in the blood? I read a study of stable isotope marking which was interesting.

I would imagine this is all basic medical school knowledge, but I am afraid to ask.

Eades' Response:

These questions are far too complex and would require more time than I have available to answer in a comment. Here is a link to a recent study that will get you started on your quest to learn.

Yeah, NOW it's all too complicated, go read a study.  The study is interesting but doesn't answer the question which was, essentially, how fast the liver could feasibly crank out triglycerides derived from de novo lipogenesis.  It should have given anyone pause.  How fast could the liver produce fat to cause that fatty plasma?  That's the first thing that came to my mind after I got past my shock that a doctor would even suggest that the fat in the blood wasn't from the fat in the meal.  But clearly most read what Eades said and presumed he knows what he's talking about.

Now it was 3 months or so after the blog post was made, but Vesna did bring my points to Dr. Eades' attention in the comments, including my references.  One might just presume he didn't read that post, but he did reply to commenter Lucy another 3 months or so later who cited a Dr. Davis post:

Fat absoprtion…in this post you said saturated fat traveled through the lymph system and wouldn’t hit the blood stream until several hours after the 2 hour mark. Yet Dr. Davis, over on the Heart Scan Blog recently posted this statement: “In other words, eat fat, whether it’s saturated, hydrogenated, polyunsaturated, or monounsaturated, and blood levels of triglycerides will go up over the next 6 hours. This remains true if there are carbohydrates in the meal, or if there are NO carbohydrates in the meal. It also remains true if you chronically consume fats.

While fats are the primary determinant of postprandial (after-eating) triglycerides, carbohydrates are the primary determinant of fasting triglycerides.” (and here)

He credits FAT with postprandial triglyceride increases. This seems a pretty fundamental point to be in dispute. What’s your supporting evidence for the lymph path?

Eades response:

My supporting evidence is every medical physiology text in print. Eating fat will increase the triglycerides in the blood after the meal over several hours, but a high intake of carbohydrates keep the fasting triglycerides up. There is nothing I wrote that is in conflict with what Dr. Davis wrote.

Except that he got his timeline wrong.  And he apparently only looked at Davis' first linked post and not the second.   Below is a screenshot of the results of one of Davis' reader's experiments that should have given Eades pause had he seen it.  

He never answered Vesna's inquiry.

Interestingly, Jeff Volek (co-author of the New Atkins) is among many low carb advocates who acknowledges increased circulating triglycerides on a high fat diet:

Repeated ingestion of a VLCD initially increases circulating TAG-rich chylomicrons, which are cleared rapidly by lipoprotein lipase (LPL) bound to the luminal surface of capillary endothelial cells in skeletal muscle and adipose tissue. Although speculative, we suggest that a VLCD increases muscle LPL, enhancing TAG clearance. A VLCD leads to lower glucose and insulin levels, which decrease LPL and increase hormone-sensitive lipase (HSL), promoting TAG hydrolysis and increasing fatty acid (FA) rate of appearance. LPL-mediated lipolysis of chylomicrons results in release of FA that is either taken up by the underlying tissue or escapes into the circulation. Any increase in FA delivery to skeletal muscle is balanced by an increase in fat oxidation as evident from the postabsorptive respiratory exchange ratios near 0.7. Circulating FAs are taken up by the liver and preferentially diverted away from esterification to TAG and toward mitochondrial oxidation to acetyl CoA. Accumulation of acetyl CoA exceeding the capacity for mitochondrial oxidation results in the formation of ketones. Reduced hepatic production of TAG results in less VLDL synthesis and secretion into the circulation.

If memory serves (my Sony ebook reader is not accessing my copy of TNA :( ) in the science section they discuss postprandial vasoconstriction and how it's not an issue with VLC due to more rapid clearance of triglycerides.  {If anyone reading this can provide the citation (or set me straight if I'm remembering wrong) I would appreciate it.}

Eades ends his post with the following:

Anyone with a smattering of knowledge of normal physiology (and apparently an open mind) could predict that the artery in a relaxed arm would narrow after a heavy meal and that that artery would be back to normal six hours later (which it was so reported in this video).

What you’re seeing in this video is normal physiology at work interpreted as being abnormal by a couple of lipophobic doctors who should (and probably do) know better. It makes for dramatic theater, but their interpretation is nothing but prevarication or ignorance or both.

But had they reported the truth, there would have been no story. Kind of sad, isn’t it. 

No.  What was sad about this is that Eades wrote this at all, though he should know the truth to be different.

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